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Biological insights from 108 schizophrenia-associated genetic loci

     * Schizophrenia Working Group of the Psychiatric Genomics Consortium

     * Affiliations
     * Contributions
     * Corresponding author

   Journal name:
          Nature

   Volume:
          511,

   Pages:
          421–427

   Date published:
          (24 July 2014)

   DOI:
          doi:10.1038/nature13595

   Received
          06 March 2014

   Accepted
          18 June 2014

   Published online
          22 July 2014

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Abstract

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Schizophrenia is a highly heritable disorder. Genetic risk is conferred
   by a large number of alleles, including common alleles of small effect
   that might be detected by genome-wide association studies. Here we
   report a multi-stage schizophrenia genome-wide association study of up
   to 36,989 cases and 113,075 controls. We identify 128 independent
   associations spanning 108 conservatively defined loci that meet
   genome-wide significance, 83 of which have not been previously
   reported. Associations were enriched among genes expressed in brain,
   providing biological plausibility for the findings. Many findings have
   the potential to provide entirely new insights into aetiology, but
   associations at DRD2 and several genes involved in glutamatergic
   neurotransmission highlight molecules of known and potential
   therapeutic relevance to schizophrenia, and are consistent with leading
   pathophysiological hypotheses. Independent of genes expressed in brain,
   associations were enriched among genes expressed in tissues that have
   important roles in immunity, providing support for the speculated link
   between the immune system and schizophrenia.

Subject terms:

     * Genome-wide association studies

At a glance

Figures

   View all figures
    1. Manhattan plot showing schizophrenia associations. Figure 1:
       Manhattan plot showing schizophrenia associations.
       Manhattan plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). The x axis is chromosomal position and
       the y axis is the significance (–log[10] P; 2-tailed) of
       association derived by logistic regression. The red line shows the
       genome-wide significance level (5 × 10^−8). SNPs in green are in
       linkage disequilibrium with the index SNPs (diamonds) which
       represent independent genome-wide significant associations.
       Full size image
       View in article
    2. Enrichment in enhancers of credible SNPs. Figure 2: Enrichment in
       enhancers of credible SNPs.
       Cell and tissue type specific enhancers were identified using
       ChIP-seq data sets (H3K27ac signal) from 56 cell line and tissue
       samples (y axis). We defined cell and tissue type enhancers as the
       top 10% of enhancers with the highest ratio of reads in that cell
       or tissue type divided by the total number of reads. Enrichment of
       credible causal associated SNPs from the schizophrenia GWAS was
       compared with frequency matched sets of 1000 Genomes SNPs
       (Supplementary Methods). The x axis is the –log[10] P for
       enrichment. P values are uncorrected for the number of tissues or
       cells tested. A –log[10] P of roughly 3 can be considered
       significant after Bonferroni correction. Descriptions of cell and
       tissue types at the Roadmap Epigenome website
       (http://www.roadmapepigenomics.org).
       Full size image
       View in article
    3. Odds ratio by risk score profile. Figure 3: Odds ratio by risk
       score profile.
       Odds ratio for schizophrenia by risk score profile (RPS) decile in
       the Sweden (Sw1-6), Denmark (Aarhus), and Molecular Genetics of
       Schizophrenia studies (Supplementary Methods). Risk alleles and
       weights were derived from ‘leave one out’ analyses in which those
       samples were excluded from the GWAS meta-analysis (Supplementary
       Methods). The threshold for selecting risk alleles was P[T] < 0.05.
       The RPS were converted to deciles (1 = lowest, 10 = highest RPS),
       and nine dummy variables created to contrast deciles 2-10 to decile
       1 as the reference. Odds ratios and 95% confidence intervals (bars)
       were estimated using logistic regression with PCs to control for
       population stratification.
       Full size image
       View in article
    4. Homogeneity of effects across studies. Extended Data Fig. 1:
       Homogeneity of effects across studies.
       Plot of the first two principal components (PCs) from principal
       components analysis (PCA) of the logistic regression β coefficients
       for autosomal genome-wide significant associations. The input data
       were the β coefficients from 52 samples for 112 independent SNP
       associations (excluding 3 chrX SNPs and 13 SNPs with missing values
       in Asian samples). PCAs were weighted by the number of cases. Each
       circle shows the location of a study on PC1 and PC2. Circle size
       and colour are proportional to the number of cases in each sample
       (larger and darker red circles correspond to more cases). Most
       samples cluster. Outliers had either small numbers of cases
       (‘small’) or were genotyped on older arrays. Abbreviations: a500
       (Affymetrix 500K); a5 (Affymetrix 5.0). Studies that did not use
       conventional research interviews are in the central cluster
       (CLOZUK, Sweden, and Denmark-Aarhus studies, see Supplementary
       Methods for sample descriptions).
       Full size image
       View in article
    5. Quantile-quantile plot. Extended Data Fig. 2: Quantile-quantile
       plot.
       Quantile-quantile plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). Expected –log[10] P values are those
       expected under the null hypothesis. Observed are the GWAS
       association results derived by logistic regression (2-tailed) as in
       Fig. 1. For clarity, we avoided expansion of the y axis by setting
       the smallest association P values to 10^−12. The shaded area
       surrounded by a red line indicates the 95% confidence interval
       under the null. λ[GC] is the observed median χ^2 test statistic
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       View in article
    6. Linkage disequilibrium score regression consistent with polygenic
       inheritance. Extended Data Fig. 3: Linkage disequilibrium score
       regression consistent with polygenic inheritance.
       The relationship between marker χ^2 association statistics and
       linkage disequilibrium (LD) as measured by the linkage
       disequilibrium score. Linkage disequilibrium score is the sum of
       the r^2 values between a variant and all other known variants
       within a 1 cM window, and quantifies the amount of genetic
       variation tagged by that variant. Variants were grouped into 50
       equal-sized bins based on linkage disequilibrium score rank.
       Linkage disequilibrium score bin and mean χ^2 denotes mean linkage
       disequilibrium score and test statistic for markers each bin. a, b,
       We simulated (Supplementary Methods) test statistics under two
       scenarios: a, no true association, inflation due to population
       stratification; and b, polygenic inheritance (λ = 1.32), in which
       we assigned independent and identically distributed
       per-normalized-genotype effects to a randomly selected subset of
       variants. c, Results from the PGC schizophrenia GWAS (λ = 1.48).
       The real data are strikingly similar to the simulated data
       summarized in b but not a. The intercept estimates the inflation in
       the mean χ^2 that results from confounding biases, such as cryptic
       relatedness or population stratification. Thus, the intercept of
       1.066 for the schizophrenia GWAS suggests that ~90% of the
       inflation in the mean χ^2 results from polygenic signal. The
       results of the simulations are also consistent with theoretical
       expectation (see Supplementary Methods). λ is the median χ^2 test
       statistic from the simulations (a, b) or the observed data (c)
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       View in article
    7. Enrichment of associations in tissues and cells. Extended Data Fig.
       4: Enrichment of associations in tissues and cells.
       Genes whose transcriptional start is nearest to the most associated
       SNP at each schizophrenia-associated locus were tested for enriched
       expression in purified brain cell subsets obtained from mouse
       ribotagged lines^41 using enrichment analysis described in the
       Supplementary Methods. The red dotted line indicates P = 0.05.
       Full size image
       View in article
    8. MGS risk profile score analysis. Extended Data Fig. 5: MGS risk
       profile score analysis.
       Polygenic risk profile score (RPS) analyses using the MGS^18 sample
       as target, and deriving risk alleles from three published
       schizophrenia data sets (x axis): ISC (2,615 cases and 3,338
       controls)^10, PGC1 (excluding MGS, 9,320 cases and 10,228
       controls)^16, and the current meta-analysis (excluding MGS) with
       32,838 cases and 44,357 controls. Samples sizes differ slightly
       from the original publications due to different analytical
       procedures. This shows the increasing RPS prediction with
       increasing training data set size reflecting improved precision of
       estimates of the SNP effect sizes. The proportion of variance
       explained (y axis; Nagelkerke’s R^2) was computed by comparison of
       a full model (covariates + RPS) score to a reduced model
       (covariates only). Ten different P value thresholds (P[T]) for
       selecting risk alleles are denoted by the colour of each bar
       (legend above plot). For significance testing, see the bottom
       legend which denotes the P value for the test that R^2 is different
       from zero. All numerical data and methods used to generate these
       plots are available in Supplementary Table 6 and Supplementary
       Methods.
       Full size image
       View in article
    9. Risk profile score analysis. Extended Data Fig. 6: Risk profile
       score analysis.
       We defined 40 target subgroups of the primary GWAS data set and
       performed 40 leave-one-out GWAS analyses (see Supplementary Methods
       and Supplementary Table 7) from which we derived risk alleles for
       RPS analysis (x axis) for each target subgroup. a, The proportion
       of variance explained (y axis; Nagelkerke’s R^2) was computed for
       each target by comparison of a full model (covariates + RPS) score
       to a reduced model (covariates only). For clarity, 3 different P
       value thresholds (P[T]) are presented denoted by the colour of each
       bar (legend above plot) as for Extended Data Fig. 5, but for
       clarity we restrict to fewer P value thresholds (P[T] of 5 × 10^−8,
       1 × 10^−4 and 0.05) and removed the significance values. b, The
       proportion of variance on the liability scale from risk scores
       calculated at the P[T] 0.05 with 95% CI bar assuming baseline
       population disease risk of 1%. c, Area under the receiver operating
       curve (AUC). All numerical data and methods used to generate these
       plots are available in Supplementary Table 7 and Supplementary
       Methods.
       Full size image
       View in article
   10. Pairwise epistasis analysis of significant SNPs. Extended Data Fig.
       7: Pairwise epistasis analysis of significant SNPs.
       Quantile-quantile plot for all pair-wise (n = 7,750) combinations
       of the 125 independent autosomal genome-wide significant SNPs
       tested for non-additive effects on risk using case-control data
       sets of European ancestry (32,405 cases and 42,221 controls). We
       included as covariates the principal components from the main
       analysis as well as a study indicator. The interaction model is
       described by:
       and are genotypes at the two loci, is the interaction between the
       two genotypes modelled in a multiplicative fashion, is the vector
       of principal components, is the vector of study indicator
       variables. Each is the regression coefficient in the generalized
       linear model using logistic regression. The overall distribution of
       P values did not deviate from the null and the smallest P value
       (4.28 × 10^−4) did not surpass the Bonferroni correction threshold
       (P = 0.05/7750 = 6.45 × 10^−6). The line x = y indicates the
       expected null distribution with the grey area bounded by red lines
       indicating the expected 95% confidence interval for the null.
       Full size image
       View in article

Tables

   View all tables
    1. ALIGATOR and INRICH Extended Data Table 1: ALIGATOR and INRICH
       Full size image
       View in article
    2. de novo overlap Extended Data Table 2: de novo overlap
       Full size image
       View in article

Introduction

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Schizophrenia has a lifetime risk of around 1%, and is associated with
   substantial morbidity and mortality as well as personal and societal
   costs^1, 2, 3. Although pharmacological treatments are available for
   schizophrenia, their efficacy is poor for many patients^4. All
   available antipsychotic drugs are thought to exert their main
   therapeutic effects through blockade of the type 2 dopaminergic
   receptor^5, 6 but, since the discovery of this mechanism over 60 years
   ago, no new antipsychotic drug of proven efficacy has been developed
   based on other target molecules. Therapeutic stasis is in large part a
   consequence of the fact that the pathophysiology of schizophrenia is
   unknown. Identifying the causes of schizophrenia is therefore a
   critical step towards improving treatments and outcomes for those with
   the disorder.

   High heritability points to a major role for inherited genetic variants
   in the aetiology of schizophrenia^7, 8. Although risk variants range in
   frequency from common to extremely rare^9, estimates^10, 11 suggest
   half to a third of the genetic risk of schizophrenia is indexed by
   common alleles genotyped by current genome-wide association study
   (GWAS) arrays. Thus, GWAS is potentially an important tool for
   understanding the biological underpinnings of schizophrenia.

   To date, around 30 schizophrenia-associated loci^10, 11, 12, 13, 14,
   15, 16, 17, 18, 19, 20, 21, 22, 23 have been identified through GWAS.
   Postulating that sample size is one of the most important limiting
   factors in applying GWAS to schizophrenia, we created the Schizophrenia
   Working Group of the Psychiatric Genomics Consortium (PGC). Our primary
   aim was to combine all available schizophrenia samples with published
   or unpublished GWAS genotypes into a single, systematic analysis^24.
   Here we report the results of that analysis, including at least 108
   independent genomic loci that exceed genome-wide significance. Some of
   the findings support leading pathophysiological hypotheses of
   schizophrenia or targets of therapeutic relevance, but most of the
   findings provide new insights.

108 independent associated loci

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   We obtained genome-wide genotype data from which we constructed 49
   ancestry matched, non-overlapping case-control samples (46 of European
   and three of east Asian ancestry, 34,241 cases and 45,604 controls) and
   3 family-based samples of European ancestry (1,235 parent
   affected-offspring trios) (Supplementary Table 1 and Supplementary
   Methods). These comprise the primary PGC GWAS data set. We processed
   the genotypes from all studies using unified quality control procedures
   followed by imputation of SNPs and insertion-deletions using the 1000
   Genomes Project reference panel^25. In each sample, association testing
   was conducted using imputed marker dosages and principal components
   (PCs) to control for population stratification. The results were
   combined using an inverse-variance weighted fixed effects model^26.
   After quality control (imputation INFO score ≥ 0.6, MAF ≥ 0.01, and
   successfully imputed in ≥ 20 samples), we considered around 9.5 million
   variants. The results are summarized in Fig. 1. To enable acquisition
   of large samples, some groups ascertained cases via clinician diagnosis
   rather than a research-based assessment and provided evidence of the
   validity of this approach (Supplementary Information)^11, 13. Post hoc
   analyses revealed the pattern of effect sizes for associated loci was
   similar across different assessment methods and modes of ascertainment
   (Extended Data Fig. 1), supporting our a priori decision to include
   samples of this nature.
   Figure 1: Manhattan plot showing schizophrenia associations.
   Manhattan plot showing schizophrenia associations.

   Manhattan plot of the discovery genome-wide association meta-analysis
   of 49 case control samples (34,241 cases and 45,604 controls) and 3
   family based association studies (1,235 parent affected-offspring
   trios). The x axis is chromosomal position and the y axis is the
   significance (–log[10] P; 2-tailed) of association derived by logistic
   regression. The red line shows the genome-wide significance level (5 ×
   10^−8). SNPs in green are in linkage disequilibrium with the index SNPs
   (diamonds) which represent independent genome-wide significant
   associations.
     * Full size image (230 KB)
     * Download PowerPoint slide (376 KB)

     * Figures/tables index
     * Next

   For the subset of linkage-disequilibrium-independent single nucleotide
   polymorphisms (SNPs) with P < 1 × 10^−6 in the meta-analysis, we next
   obtained results from deCODE genetics (1,513 cases and 66,236 controls
   of European ancestry). We define linkage-disequilibrium-independent
   SNPs as those with low linkage disequilibrium (r^2 < 0.1) to a more
   significantly associated SNP within a 500-kb window. Given high linkage
   disequilibrium in the extended major histocompatibility complex (MHC)
   region spans ~8 Mb, we conservatively include only a single MHC SNP to
   represent this locus. The deCODE data were then combined with those
   from the primary GWAS to give a data set of 36,989 cases and 113,075
   controls. In this final analysis, 128
   linkage-disequilibrium-independent SNPs exceeded genome-wide
   significance (P ≤ 5 × 10^−8) (Supplementary Table 2).

   As in meta-analyses of other complex traits which identified large
   numbers of common risk variants^27, 28, the test statistic distribution
   from our GWAS deviates from the null (Extended Data Fig. 2). This is
   consistent with the previously documented polygenic contribution to
   schizophrenia^10, 11. The deviation in the test statistics from the
   null (λ[GC] = 1.47, λ[1000] = 1.01) is only slightly less than expected
   (λ[GC] = 1.56) under a polygenic model given fully informative
   genotypes, the current sample size, and the lifetime risk and
   heritability of schizophrenia^29.

   Additional lines of evidence allow us to conclude the deviation between
   the observed and null distributions in our primary GWAS indicates a
   true polygenic contribution to schizophrenia. First, applying a novel
   method^30 that uses linkage disequilibrium information to distinguish
   between the major potential sources of test statistic inflation, we
   found our results are consistent with polygenic architecture but not
   population stratification (Extended Data Fig. 3). Second, the
   schizophrenia-associated alleles at 78% of 234
   linkage-disequilibrium-independent SNPs exceeding P < 1 × 10^−6 in the
   case-control GWAS were again overrepresented in cases in the
   independent samples from deCODE. This degree of consistency between the
   case-control GWAS and the replication data is highly unlikely to occur
   by chance (P = 6 × 10^−19). The tested alleles surpassed the P < 10^−6
   threshold in our GWAS before we added either the trios or deCODE data
   to the meta-analysis. This trend test is therefore independent of the
   primary case-control GWAS. Third, analysing the 1,235 parent-proband
   trios, we again found excess transmission of the
   schizophrenia-associated allele at 69% of the 263
   linkage-disequilibrium-independent SNPs with P < 1 × 10^−6 in the
   case-control GWAS. This is again unlikely to occur by chance (P = 1 ×
   10^−9) and additionally excludes population stratification as fully
   explaining the associations reaching our threshold for seeking
   replication. Fourth, we used the trios trend data to estimate the
   expected proportion of true associations at P < 1 × 10^−6 in the
   discovery GWAS, allowing for the fact that half of the index SNPs are
   expected to show the same allelic trend in the trios by chance, and
   that some true associations will show opposite trends given the limited
   number of trio samples (Supplementary Methods). Given the observed
   trend test results, around 67% (95% confidence interval: 64–73%) or n =
   176 of the associations in the scan at P < 1 × 10^−6 are expected to be
   true, and therefore the number of associations that will ultimately be
   validated from this set of SNPs will be considerably more than those
   that now meet genome-wide significance. Taken together, these analyses
   indicate that the observed deviation of test statistics from the null
   primarily represents polygenic association signal and the considerable
   excess of associations at the tail of extreme significance largely
   correspond to true associations.

   Independently associated SNPs do not translate to well-bounded
   chromosomal regions. Nevertheless, it is useful to define physical
   boundaries for the SNP associations to identify candidate risk genes.
   We defined an associated locus as the physical region containing all
   SNPs correlated at r^2 > 0.6 with each of the 128 index SNPs.
   Associated loci within 250 kb of each other were merged. This resulted
   in 108 physically distinct associated loci, 83 of which have not been
   previously implicated in schizophrenia and therefore harbour potential
   new biological insights into disease aetiology (Supplementary Table 3;
   regional plots in Supplementary Fig. 1). The significant regions
   include all but 5 loci previously reported to be genome-wide
   significant in large samples (Supplementary Table 3).

Characterization of associated loci

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Of the 108 loci, 75% include protein-coding genes (40%, a single gene)
   and a further 8% are within 20 kb of a gene (Supplementary Table 3).
   Notable associations relevant to major hypotheses of the aetiology and
   treatment of schizophrenia include DRD2 (the target of all effective
   antipsychotic drugs) and many genes (for example, GRM3, GRIN2A, SRR,
   GRIA1) involved in glutamatergic neurotransmission and synaptic
   plasticity. In addition, associations at CACNA1C, CACNB2 and CACNA1I,
   which encode voltage-gated calcium channel subunits, extend previous
   findings implicating members of this family of proteins in
   schizophrenia and other psychiatric disorders^11, 13, 31, 32. Genes
   encoding calcium channels, and proteins involved in glutamatergic
   neurotransmission and synaptic plasticity have been independently
   implicated in schizophrenia by studies of rare genetic variation^33,
   34, 35, suggesting convergence at a broad functional level between
   studies of common and rare genetic variation. We highlight in the
   Supplementary Discussion genes of particular interest within associated
   loci with respect to current hypotheses of schizophrenia aetiology or
   treatment (although we do not imply that these genes are necessarily
   the causal elements).

   For each of the schizophrenia-associated loci, we identified a credible
   causal set of SNPs (for definition, see Supplementary Methods)^36. In
   only 10 instances (Supplementary Table 4) was the association signal
   credibly attributable to a known non-synonymous exonic polymorphism.
   The apparently limited role of protein-coding variants is consistent
   both with exome sequencing findings^33 and with the hypothesis that
   most associated variants detected by GWAS exert their effects through
   altering gene expression rather than protein structure^37, 38 and with
   the observation that schizophrenia risk loci are enriched for
   expression quantitative trait loci (eQTL)^39.

   To try to identify eQTLs that could explain associations with
   schizophrenia, we merged the credible causal set of SNPs defined above
   with eQTLs from a meta-analysis of human brain cortex eQTL studies (n =
   550) and an eQTL study of peripheral venous blood (n = 3,754)^40
   (Supplementary Methods). Multiple schizophrenia loci contained at least
   one eQTL for a gene within 1 Mb of the locus (Supplementary Table 4).
   However, in only 12 instances was the eQTL plausibly causal (two in
   brain, and nine in peripheral blood, one in both). This low proportion
   suggests that if most risk variants are regulatory, available eQTL
   catalogues do not yet provide power, cellular specificity, or
   developmental diversity to provide clear mechanistic hypotheses for
   follow-up experiments.

The brain and immunity

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   To further explore the regulatory nature of the schizophrenia
   associations, we mapped the credible sets (n = 108) of causal variants
   onto sequences with epigenetic markers characteristic of active
   enhancers in 56 different tissues and cell lines (Supplementary
   Methods). Schizophrenia associations were significantly enriched at
   enhancers active in brain (Fig. 2) but not in tissues unlikely to be
   relevant to schizophrenia (for example, bone, cartilage, kidney and
   fibroblasts). Brain tissues used to define enhancers consist of
   heterogeneous populations of cells. Seeking greater specificity, we
   contrasted genes enriched for expression in neurons and glia using
   mouse ribotagged lines^41. Genes with strong expression in multiple
   cortical and striatal neuronal lineages were enriched for associations,
   providing support for an important neuronal pathology in schizophrenia
   (Extended Data Fig. 4) but this is not statistically more significant
   than, or exclusionary of, contributions from other lineages^42.
   Figure 2: Enrichment in enhancers of credible SNPs.
   Enrichment in enhancers of credible SNPs.

   Cell and tissue type specific enhancers were identified using ChIP-seq
   data sets (H3K27ac signal) from 56 cell line and tissue samples (y
   axis). We defined cell and tissue type enhancers as the top 10% of
   enhancers with the highest ratio of reads in that cell or tissue type
   divided by the total number of reads. Enrichment of credible causal
   associated SNPs from the schizophrenia GWAS was compared with frequency
   matched sets of 1000 Genomes SNPs (Supplementary Methods). The x axis
   is the –log[10] P for enrichment. P values are uncorrected for the
   number of tissues or cells tested. A –log[10] P of roughly 3 can be
   considered significant after Bonferroni correction. Descriptions of
   cell and tissue types at the Roadmap Epigenome website
   (http://www.roadmapepigenomics.org).
     * Full size image (266 KB)
     * Download PowerPoint slide (504 KB)

     * Previous
     * Figures/tables index
     * Next

   Schizophrenia associations were also strongly enriched at enhancers
   that are active in tissues with important immune functions,
   particularly B-lymphocyte lineages involved in acquired immunity (CD19
   and CD20 lines, Fig. 2). These enrichments remain significant even
   after excluding the extended MHC region and regions containing brain
   enhancers (enrichment P for CD20 < 10^−6), demonstrating that this
   finding is not an artefact of correlation between enhancer elements in
   different tissues and not driven by the strong and diffuse association
   at the extended MHC. Epidemiological studies have long hinted at a role
   for immune dysregulation in schizophrenia, the present findings provide
   genetic support for this hypothesis^43.

   To develop additional biological hypotheses beyond those that emerge
   from inspection of the individual loci, we further undertook a limited
   mining of the data through gene-set analysis. However, as there is no
   consensus methodology by which such analyses should be conducted, nor
   an established optimal significance threshold for including loci, we
   sought to be conservative, using only two of the many available
   approaches^44, 45 and restricting analyses to genes within genome-wide
   significant loci. Neither approach identified gene-sets that were
   significantly enriched for associations after correction for the number
   of pathways tested (Supplementary Table 5) although nominally
   significantly enrichments were observed among several predefined
   candidate pathways (Extended Data Table 1). A fuller exploratory
   analysis of the data will be presented elsewhere.

Overlap with rare mutations

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   CNVs associated with schizophrenia overlap with those associated with
   autism spectrum disorder (ASD) and intellectual disability^9, as do
   genes with deleterious de novo mutations^34. Here we find significant
   overlap between genes in the schizophrenia GWAS associated intervals
   and those with de novo non-synonymous mutations in schizophrenia (P =
   0.0061) (Extended Data Table 2), suggesting that mechanistic studies of
   rare genetic variation in schizophrenia will be informative for
   schizophrenia more widely. We also find evidence for overlap between
   genes in schizophrenia GWAS regions and those with de novo
   non-synonymous mutations in intellectual disability (P = 0.00024) and
   ASD (P = 0.035), providing further support for the hypothesis that
   these disorders have partly overlapping pathophysiologies^9, 34.

Polygenic risk score profiling

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Previous studies have shown that risk profile scores (RPS) constructed
   from alleles showing modest association with schizophrenia in a
   discovery GWAS can predict case-control status in independent samples,
   albeit with low sensitivity and specificity^10, 11, 16. This finding
   was robustly confirmed in the present study. The estimate of Nagelkerke
   R^2 (a measure of variance in case-control status explained) depends on
   the specific target data set and threshold (P[T]) for selecting risk
   alleles for RPS analysis (Extended Data Fig. 5 and 6a). However, using
   the same target sample as earlier studies and P[T] = 0.05, R^2 is now
   increased from 0.03 (ref. 10) to 0.184 (Extended Data Fig. 5). Assuming
   a liability-threshold model, a lifetime risk of 1%, independent SNP
   effects, and adjusting for case-control ascertainment, RPS now explains
   about 7% of variation on the liability scale^46 to schizophrenia across
   the samples (Extended Data Fig. 6b), about half of which (3.4%) is
   explained by genome-wide significant loci.

   We also evaluated the capacity of RPS to predict case-control status
   using a standard epidemiological approach to a continuous risk factor.
   We illustrate this in three samples, each with different ascertainment
   schemes (Fig. 3). The Danish sample is population-based (that is,
   inpatient and outpatient facilities), the Swedish sample is based on
   all cases hospitalized for schizophrenia in Sweden, and the Molecular
   Genetics of Schizophrenia (MGS) sample was ascertained specially for
   genetic studies from clinical sources in the US and Australia. We
   grouped individuals into RPS deciles and estimated the odds ratios for
   affected status for each decile with reference to the lowest risk
   decile. The odds ratios increased with greater number of schizophrenia
   risk alleles in each sample, maximizing for the tenth decile in all
   samples: Denmark 7.8 (95% confidence interval (CI): 4.4–13.9), Sweden
   15.0 (95% CI: 12.1–18.7) and MGS 20.3 (95% CI: 14.7–28.2). Given the
   need for measures that index liability to schizophrenia^47, 48, the
   ability to stratify individuals by RPS offers new opportunities for
   clinical and epidemiological research. Nevertheless, we stress that the
   sensitivity and specificity of RPS do not support its use as a
   predictive test. For example, in the Danish epidemiological sample, the
   area under the receiver operating curve is only 0.62 (Extended Data
   Fig. 6c, Supplementary Table 6).
   Figure 3: Odds ratio by risk score profile.
   Odds ratio by risk score profile.

   Odds ratio for schizophrenia by risk score profile (RPS) decile in the
   Sweden (Sw1-6), Denmark (Aarhus), and Molecular Genetics of
   Schizophrenia studies (Supplementary Methods). Risk alleles and weights
   were derived from ‘leave one out’ analyses in which those samples were
   excluded from the GWAS meta-analysis (Supplementary Methods). The
   threshold for selecting risk alleles was P[T] < 0.05. The RPS were
   converted to deciles (1 = lowest, 10 = highest RPS), and nine dummy
   variables created to contrast deciles 2-10 to decile 1 as the
   reference. Odds ratios and 95% confidence intervals (bars) were
   estimated using logistic regression with PCs to control for population
   stratification.
     * Full size image (100 KB)
     * Download PowerPoint slide (298 KB)

     * Previous
     * Figures/tables index

   Finally, seeking evidence for non-additive effects on risk, we tested
   for statistical interaction between all pairs of 125 autosomal SNPs
   that reached genome-wide significance. P values for the interaction
   terms were distributed according to the null, and no interaction was
   significant after correction for multiple comparisons. Thus, we find no
   evidence for epistatic or non-additive effects between the significant
   loci (Extended Data Fig. 7). It is possible that such effects could be
   present between other loci, or occur in the form of higher-order
   interactions.

Discussion

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   In the largest (to our knowledge) molecular genetic study of
   schizophrenia, or indeed of any neuropsychiatric disorder, ever
   conducted, we demonstrate the power of GWAS to identify large numbers
   of risk loci. We show that the use of alternative ascertainment and
   diagnostic schemes designed to rapidly increase sample size does not
   inevitably introduce a crippling degree of heterogeneity. That this is
   true for a phenotype like schizophrenia, in which there are no
   biomarkers or supportive diagnostic tests, provides grounds to be
   optimistic that this approach can be successfully applied to GWAS of
   other clinically defined disorders.

   We further show that the associations are not randomly distributed
   across genes of all classes and function; rather they converge upon
   genes that are expressed in certain tissues and cellular types. The
   findings include molecules that are the current, or the most promising,
   targets for therapeutics, and point to systems that align with the
   predominant aetiological hypotheses of the disorder. This suggests that
   the many novel findings we report also provide an aetiologically
   relevant foundation for mechanistic and treatment development studies.
   We also find overlap between genes affected by rare variants in
   schizophrenia and those within GWAS loci, and broad convergence in the
   functions of some of the clusters of genes implicated by both sets of
   genetic variants, particularly genes related to abnormal glutamatergic
   synaptic and calcium channel function. How variation in these genes
   impact function to increase risk for schizophrenia cannot be answered
   by genetics, but the overlap strongly suggests that common and rare
   variant studies are complementary rather than antagonistic, and that
   mechanistic studies driven by rare genetic variation will be
   informative for schizophrenia.

References

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

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Acknowledgements

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Core funding for the Psychiatric Genomics Consortium is from the US
   National Institute of Mental Health (U01 MH094421). We thank T. Lehner
   (NIMH). The work of the contributing groups was supported by numerous
   grants from governmental and charitable bodies as well as philanthropic
   donation. Details are provided in the Supplementary Notes. Membership
   of the Wellcome Trust Case Control Consortium and of the Psychosis
   Endophenotype International Consortium are provided in the
   Supplementary Notes.

Author information

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

Affiliations

    1. Analytic and Translational Genetics Unit, Massachusetts General
       Hospital, Boston, Massachusetts 02114, USA.
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Kai-How Farh,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + Hailiang Huang,
          + Menachem Fromer,
          + Jacqueline I. Goldstein &
          + Mark J. Daly
    2. Stanley Center for Psychiatric Research, Broad Institute of MIT and
       Harvard, Cambridge, Massachusetts 02142, USA.
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + Richard A. Belliveau Jr,
          + Sarah E. Bergen,
          + Elizabeth Bevilacqua,
          + Kimberly D. Chambert,
          + Menachem Fromer,
          + Giulio Genovese,
          + Colm O’Dushlaine,
          + Edward M. Scolnick,
          + Jordan W. Smoller,
          + Steven A. McCarroll,
          + Jennifer L. Moran,
          + Aarno Palotie,
          + Tracey L. Petryshen &
          + Mark J. Daly
    3. Medical and Population Genetics Program, Broad Institute of MIT and
       Harvard, Cambridge, Massachusetts 02142, USA.
          + Benjamin M. Neale,
          + Hailiang Huang,
          + Tune H. Pers,
          + Jacqueline I. Goldstein,
          + Joel N. Hirschhorn,
          + Alkes Price,
          + Eli A. Stahl,
          + Tõnu Esko &
          + Mark J. Daly
    4. Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts
       General Hospital, Boston, Massachusetts 02114, USA.
          + Benjamin M. Neale,
          + Phil Lee,
          + Menachem Fromer,
          + Jordan W. Smoller &
          + Aarno Palotie
    5. Neuropsychiatric Genetics Research Group, Department of Psychiatry,
       Trinity College Dublin, Dublin 8, Ireland.
          + Aiden Corvin,
          + Paul Cormican,
          + Gary Donohoe,
          + Derek W. Morris &
          + Michael Gill
    6. MRC Centre for Neuropsychiatric Genetics and Genomics, Institute of
       Psychological Medicine and Clinical Neurosciences, School of
       Medicine, Cardiff University, Cardiff CF24 4HQ, UK.
          + James T. R. Walters,
          + Peter A. Holmans,
          + Noa Carrera,
          + Nick Craddock,
          + Valentina Escott-Price,
          + Lyudmila Georgieva,
          + Marian L. Hamshere,
          + David Kavanagh,
          + Sophie E. Legge,
          + Andrew J. Pocklington,
          + Alexander L. Richards,
          + Douglas M. Ruderfer,
          + Nigel M. Williams,
          + George Kirov,
          + Michael J. Owen &
          + Michael C. O’Donovan
    7. National Centre for Mental Health, Cardiff University, Cardiff CF24
       4HQ, UK.
          + Peter A. Holmans,
          + Nick Craddock,
          + Michael J. Owen &
          + Michael C. O’Donovan
    8. Eli Lilly and Company Limited, Erl Wood Manor, Sunninghill Road,
       Windlesham, Surrey GU20 6PH, UK.
          + David A. Collier &
          + Younes Mokrab
    9. Social, Genetic and Developmental Psychiatry Centre, Institute of
       Psychiatry, King’s College London, London SE5 8AF, UK.
          + David A. Collier
   10. Center for Biological Sequence Analysis, Department of Systems
       Biology, Technical University of Denmark, DK-2800, Denmark.
          + Tune H. Pers
   11. Division of Endocrinology and Center for Basic and Translational
       Obesity Research, Boston Children’s Hospital, Boston, Massachusetts
       02115, USA.
          + Tune H. Pers,
          + Joel N. Hirschhorn &
          + Tõnu Esko
   12. Department of Clinical Neuroscience, Psychiatry Section, Karolinska
       Institutet, SE-17176 Stockholm, Sweden.
          + Ingrid Agartz,
          + Erik Söderman &
          + Erik G. Jönsson
   13. Department of Psychiatry, Diakonhjemmet Hospital, 0319 Oslo,
       Norway.
          + Ingrid Agartz
   14. NORMENT, KG Jebsen Centre for Psychosis Research, Institute of
       Clinical Medicine, University of Oslo, 0424 Oslo, Norway.
          + Ingrid Agartz,
          + Srdjan Djurovic,
          + Morten Mattingsdal,
          + Ingrid Melle,
          + Ole A. Andreassen &
          + Erik G. Jönsson
   15. Centre for Integrative Register-based Research, CIRRAU, Aarhus
       University, DK-8210 Aarhus, Denmark.
          + Esben Agerbo &
          + Preben B. Mortensen
   16. National Centre for Register-based Research, Aarhus University,
       DK-8210 Aarhus, Denmark.
          + Esben Agerbo &
          + Preben B. Mortensen
   17. The Lundbeck Foundation Initiative for Integrative Psychiatric
       Research, iPSYCH, Denmark.
          + Esben Agerbo,
          + Ditte Demontis,
          + Thomas Hansen,
          + Manuel Mattheisen,
          + Ole Mors,
          + Line Olsen,
          + Henrik B. Rasmussen,
          + Anders D. Børglum,
          + Preben B. Mortensen &
          + Thomas Werge
   18. State Mental Hospital, 85540 Haar, Germany.
          + Margot Albus
   19. Department of Psychiatry and Behavioral Sciences, Stanford
       University, Stanford, California 94305, USA.
          + Madeline Alexander,
          + Claudine Laurent &
          + Douglas F. Levinson
   20. Department of Psychiatry and Behavioral Sciences, Atlanta Veterans
       Affairs Medical Center, Atlanta, Georgia 30033, USA.
          + Farooq Amin
   21. Department of Psychiatry and Behavioral Sciences, Emory University,
       Atlanta, Georgia 30322, USA.
          + Farooq Amin
   22. Virginia Institute for Psychiatric and Behavioral Genetics,
       Department of Psychiatry, Virginia Commonwealth University,
       Richmond, Virginia 23298, USA.
          + Silviu A. Bacanu,
          + Tim B. Bigdeli,
          + Bradley T. Webb &
          + Brandon K. Wormley
   23. Clinical Neuroscience, Max Planck Institute of Experimental
       Medicine, Göttingen 37075, Germany.
          + Martin Begemann,
          + Christian Hammer,
          + Sergi Papiol &
          + Hannelore Ehrenreich
   24. Department of Medical Genetics, University of Pécs, Pécs H-7624,
       Hungary.
          + Judit Bene &
          + Bela Melegh
   25. Szentagothai Research Center, University of Pécs, Pécs H-7624,
       Hungary.
          + Judit Bene &
          + Bela Melegh
   26. Department of Medical Epidemiology and Biostatistics, Karolinska
       Institutet, Stockholm SE-17177, Sweden.
          + Sarah E. Bergen,
          + Anna K. Kähler,
          + Patrik K. E. Magnusson,
          + Christina M. Hultman &
          + Patrick F. Sullivan
   27. Department of Psychiatry, University of Iowa Carver College of
       Medicine, Iowa City, Iowa 52242, USA.
          + Donald W. Black
   28. University Medical Center Groningen, Department of Psychiatry,
       University of Groningen NL-9700 RB, The Netherlands.
          + Richard Bruggeman
   29. School of Nursing, Louisiana State University Health Sciences
       Center, New Orleans, Louisiana 70112, USA.
          + Nancy G. Buccola
   30. Athinoula A. Martinos Center, Massachusetts General Hospital,
       Boston, Massachusetts 02129, USA.
          + Randy L. Buckner &
          + Joshua L. Roffman
   31. Center for Brain Science, Harvard University, Cambridge,
       Massachusetts 02138, USA.
          + Randy L. Buckner
   32. Department of Psychiatry, Massachusetts General Hospital, Boston,
       Massachusetts 02114, USA.
          + Randy L. Buckner &
          + Joshua L. Roffman
   33. Department of Psychiatry, University of California at San
       Francisco, San Francisco, California 94143, USA.
          + William Byerley
   34. University Medical Center Utrecht, Department of Psychiatry, Rudolf
       Magnus Institute of Neuroscience, 3584 Utrecht, The Netherlands.
          + Wiepke Cahn,
          + René S. Kahn,
          + Eric Strengman &
          + Roel A. Ophoff
   35. Department of Human Genetics, Icahn School of Medicine at Mount
       Sinai, New York, New York 10029, USA.
          + Guiqing Cai &
          + Joseph D. Buxbaum
   36. Department of Psychiatry, Icahn School of Medicine at Mount Sinai,
       New York, New York 10029, USA.
          + Guiqing Cai,
          + Kenneth L. Davis,
          + Elodie Drapeau,
          + Joseph I. Friedman,
          + Vahram Haroutunian,
          + Elena Parkhomenko,
          + Abraham Reichenberg,
          + Jeremy M. Silverman &
          + Joseph D. Buxbaum
   37. Centre Hospitalier du Rouvray and INSERM U1079 Faculty of Medicine,
       76301 Rouen, France.
          + Dominique Campion
   38. Department of Human Genetics, David Geffen School of Medicine,
       University of California, Los Angeles, California 90095, USA.
          + Rita M. Cantor &
          + Roel A. Ophoff
   39. Schizophrenia Research Institute, Sydney NSW 2010, Australia.
          + Vaughan J. Carr,
          + Stanley V. Catts,
          + Frans A. Henskens,
          + Carmel M. Loughland,
          + Patricia T. Michie,
          + Christos Pantelis,
          + Ulrich Schall,
          + Rodney J. Scott &
          + Assen V. Jablensky
   40. School of Psychiatry, University of New South Wales, Sydney NSW
       2031, Australia.
          + Vaughan J. Carr
   41. Royal Brisbane and Women’s Hospital, University of Queensland,
       Brisbane, St Lucia QLD 4072, Australia.
          + Stanley V. Catts
   42. Institute of Psychology, Chinese Academy of Science, Beijing
       100101, China.
          + Raymond C. K. Chan
   43. Department of Psychiatry, Li Ka Shing Faculty of Medicine, The
       University of Hong Kong, Hong Kong, China.
          + Ronald Y. L. Chen,
          + Eric Y. H. Chen,
          + Miaoxin Li,
          + Hon-Cheong So,
          + Emily H. M. Wong &
          + Pak C. Sham
   44. State Key Laboratory for Brain and Cognitive Sciences, Li Ka Shing
       Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
          + Eric Y. H. Chen,
          + Miaoxin Li &
          + Pak C. Sham
   45. Department of Computer Science, University of North Carolina,
       Chapel Hill, North Carolina 27514, USA.
          + Wei Cheng
   46. Castle Peak Hospital, Hong Kong, China.
          + Eric F. C. Cheung
   47. Institute of Mental Health, Singapore 539747, Singapore.
          + Siow Ann Chong,
          + Jimmy Lee Chee Keong,
          + Kang Sim &
          + Mythily Subramaniam
   48. Department of Psychiatry, Washington University, St. Louis,
       Missouri 63110, USA.
          + C. Robert Cloninger &
          + Dragan M. Svrakic
   49. Department of Child and Adolescent Psychiatry, Assistance Publique
       Hopitaux de Paris, Pierre and Marie Curie Faculty of Medicine and
       Institute for Intelligent Systems and Robotics, Paris 75013,
       France.
          + David Cohen
   50. Blue Note Biosciences, Princeton, New Jersey 08540, USA
          + Nadine Cohen
   51. Department of Genetics, University of North Carolina, Chapel Hill,
       North Carolina 27599-7264, USA.
          + James J. Crowley,
          + Martilias S. Farrell,
          + Paola Giusti-Rodríguez,
          + Yunjung Kim,
          + Jin P. Szatkiewicz,
          + Stephanie Williams &
          + Patrick F. Sullivan
   52. Department of Psychological Medicine, Queen Mary University of
       London, London E1 1BB, UK.
          + David Curtis
   53. Molecular Psychiatry Laboratory, Division of Psychiatry, University
       College London, London WC1E 6JJ, UK.
          + David Curtis,
          + Jonathan Pimm,
          + Hugh Gurling &
          + Andrew McQuillin
   54. Sheba Medical Center, Tel Hashomer 52621, Israel.
          + Michael Davidson &
          + Mark Weiser
   55. Department of Genomics, Life and Brain Center, D-53127 Bonn,
       Germany.
          + Franziska Degenhardt,
          + Stefan Herms,
          + Per Hoffmann,
          + Andrea Hofman,
          + Sven Cichon &
          + Markus M. Nöthen
   56. Institute of Human Genetics, University of Bonn, D-53127 Bonn,
       Germany.
          + Franziska Degenhardt,
          + Stefan Herms,
          + Per Hoffmann,
          + Andrea Hofman,
          + Sven Cichon &
          + Markus M. Nöthen
   57. Applied Molecular Genomics Unit, VIB Department of Molecular
       Genetics, University of Antwerp, B-2610 Antwerp, Belgium.
          + Jurgen Del Favero
   58. Centre for Integrative Sequencing, iSEQ, Aarhus University, DK-8000
       Aarhus C, Denmark.
          + Ditte Demontis,
          + Manuel Mattheisen,
          + Ole Mors &
          + Anders D. Børglum
   59. Department of Biomedicine, Aarhus University, DK-8000 Aarhus C,
       Denmark.
          + Ditte Demontis,
          + Manuel Mattheisen &
          + Anders D. Børglum
   60. First Department of Psychiatry, University of Athens Medical
       School, Athens 11528, Greece.
          + Dimitris Dikeos &
          + George N. Papadimitriou
   61. Department of Psychiatry, University College Cork, Co. Cork,
       Ireland.
          + Timothy Dinan
   62. Department of Medical Genetics, Oslo University Hospital, 0424
       Oslo, Norway.
          + Srdjan Djurovic
   63. Cognitive Genetics and Therapy Group, School of Psychology and
       Discipline of Biochemistry, National University of Ireland Galway,
       Co. Galway, Ireland.
          + Gary Donohoe &
          + Derek W. Morris
   64. Department of Psychiatry and Behavioral Neuroscience, University of
       Chicago, Chicago, Illinois 60637, USA.
          + Jubao Duan,
          + Alan R. Sanders &
          + Pablo V. Gejman
   65. Department of Psychiatry and Behavioral Sciences, NorthShore
       University HealthSystem, Evanston, Illinois 60201, USA.
          + Jubao Duan,
          + Alan R. Sanders &
          + Pablo V. Gejman
   66. Department of Non-Communicable Disease Epidemiology, London School
       of Hygiene and Tropical Medicine, London WC1E 7HT, UK.
          + Frank Dudbridge
   67. Department of Child and Adolescent Psychiatry, University Clinic of
       Psychiatry, Skopje 1000, Republic of Macedonia.
          + Naser Durmishi
   68. Department of Psychiatry, University of Regensburg, 93053
       Regensburg, Germany.
          + Peter Eichhammer
   69. Department of General Practice, Helsinki University Central
       Hospital, University of Helsinki P.O. Box 20, Tukholmankatu 8 B,
       FI-00014, Helsinki, Finland
          + Johan Eriksson
   70. Folkhälsan Research Center, Helsinki, Finland, Biomedicum Helsinki
       1, Haartmaninkatu 8, FI-00290, Helsinki, Finland.
          + Johan Eriksson
   71. National Institute for Health and Welfare, P.O. Box 30, FI-00271
       Helsinki, Finland.
          + Johan Eriksson &
          + Veikko Salomaa
   72. Translational Technologies and Bioinformatics, Pharma Research and
       Early Development, F. Hoffman-La Roche, CH-4070 Basel, Switzerland.
          + Laurent Essioux
   73. Department of Psychiatry, Georgetown University School of Medicine,
       Washington DC 20057, USA.
          + Ayman H. Fanous
   74. Department of Psychiatry, Keck School of Medicine of the University
       of Southern California, Los Angeles, California 90033, USA.
          + Ayman H. Fanous
   75. Departmentof Psychiatry, Virginia Commonwealth University School of
       Medicine, Richmond, Virginia 23298, USA.
          + Ayman H. Fanous
   76. Mental Health Service Line, Washington VA Medical Center,
       Washington DC 20422, USA.
          + Ayman H. Fanous
   77. Department of Genetic Epidemiology in Psychiatry, Central Institute
       of Mental Health, Medical Faculty Mannheim, University of
       Heidelberg, Heidelberg , D-68159 Mannheim, Germany.
          + Josef Frank,
          + Sandra Meier,
          + Thomas G. Schulze,
          + Jana Strohmaier,
          + Stephanie H. Witt &
          + Marcella Rietschel
   78. Department of Genetics, University of Groningen, University Medical
       Centre Groningen, 9700 RB Groningen, The Netherlands.
          + Lude Franke &
          + Juha Karjalainen
   79. Department of Psychiatry, University of Colorado Denver, Aurora,
       Colorado 80045, USA.
          + Robert Freedman &
          + Ann Olincy
   80. Center for Neurobehavioral Genetics, Semel Institute for
       Neuroscience and Human Behavior, University of California, Los
       Angeles, California 90095, USA.
          + Nelson B. Freimer &
          + Roel A. Ophoff
   81. Department of Psychiatry, University of Halle, 06112 Halle,
       Germany.
          + Marion Friedl,
          + Ina Giegling,
          + Annette M. Hartmann,
          + Bettina Konte &
          + Dan Rujescu
   82. Division of Psychiatric Genomics, Department of Psychiatry, Icahn
       School of Medicine at Mount Sinai, New York, New York, New York
       10029, USA.
          + Menachem Fromer,
          + Shaun M. Purcell,
          + Panos Roussos,
          + Douglas M. Ruderfer,
          + Eli A. Stahl &
          + Pamela Sklar
   83. Department of Psychiatry, University of Munich, 80336, Munich,
       Germany.
          + Ina Giegling &
          + Dan Rujescu
   84. Departments of Psychiatry and Human and Molecular Genetics, INSERM,
       Institut de Myologie, Hôpital de la Pitiè-Salpêtrière, Paris 75013,
       France.
          + Stephanie Godard
   85. Mental Health Research Centre, Russian Academy of Medical Sciences,
       115522 Moscow, Russia.
          + Vera Golimbet
   86. Neuroscience Therapeutic Area, Janssen Research and Development,
       Raritan, New Jersey 08869, USA.
          + Srihari Gopal,
          + Dai Wang &
          + Qingqin S. Li
   87. Queensland Brain Institute, The University of Queensland, Brisbane,
       Queensland, QLD 4072, Australia.
          + Jacob Gratten,
          + S. Hong Lee,
          + Naomi R. Wray,
          + Peter M. Visscher &
          + Bryan J. Mowry
   88. Academic Medical Centre University of Amsterdam, Department of
       Psychiatry, 1105 AZ Amsterdam, The Netherlands.
          + Lieuwe de Haan &
          + Carin J. Meijer
   89. Illumina, La Jolla, California, California 92122, USA.
          + Mark Hansen
   90. Institute of Biological Psychiatry, Mental Health Centre Sct. Hans,
       Mental Health Services Copenhagen, DK-4000, Denmark.
          + Thomas Hansen,
          + Line Olsen,
          + Henrik B. Rasmussen &
          + Thomas Werge
   91. Friedman Brain Institute, Icahn School ofMedicine at Mount Sinai,
       New York, New York 10029, USA.
          + Vahram Haroutunian,
          + Joseph D. Buxbaum &
          + Pamela Sklar
   92. J. J. Peters VA Medical Center, Bronx, New York, New York 10468,
       USA.
          + Vahram Haroutunian
   93. Priority Research Centre for Health Behaviour, University of
       Newcastle, Newcastle NSW 2308, Australia.
          + Frans A. Henskens
   94. School of Electrical Engineering and Computer Science, University
       of Newcastle, Newcastle NSW 2308, Australia.
          + Frans A. Henskens
   95. Division of Medical Genetics, Department of Biomedicine, University
       of Basel, Basel CH-4058, Switzerland.
          + Stefan Herms,
          + Per Hoffmann &
          + Sven Cichon
   96. Department of Genetics, Harvard Medical School, Boston,
       Massachusetts, Massachusetts 02115, USA.
          + Joel N. Hirschhorn,
          + Tõnu Esko &
          + Steven A. McCarroll
   97. Section of Neonatal Screening and Hormones, Department of Clinical
       Biochemistry, Immunology and Genetics, Statens Serum Institut,
       Copenhagen DK-2300, Denmark.
          + Mads V. Hollegaard &
          + David M. Hougaard
   98. Department of Psychiatry, Fujita Health University School of
       Medicine, Toyoake, Aichi,470-1192, Japan.
          + Masashi Ikeda &
          + Nakao Iwata
   99. Regional Centre for Clinical Research in Psychosis, Department of
       Psychiatry, Stavanger University Hospital, 4011 Stavanger, Norway.
          + Inge Joa
   100. Rheumatology Research Group, Vall d'Hebron Research Institute,
       Barcelona 08035, Spain.
          + Antonio Julià &
          + Sara Marsal
   101. Centre for Medical Research, The University of Western Australia,
       Perth WA6009, Australia.
          + Luba Kalaydjieva
   102. The Perkins Institute for Medical Research, The University of
       Western Australia, Perth WA6009, Australia.
          + Luba Kalaydjieva &
          + Assen V. Jablensky
   103. Department of Medical Genetics, Medical University, Sofia 1431,
       Bulgaria.
          + Sena Karachanak-Yankova &
          + Draga Toncheva
   104. Department of Psychology, University of Colorado Boulder, Boulder,
       Colorado 80309, USA.
          + Matthew C. Keller
   105. Campbell Family Mental Health Research Institute, Centre for
       Addiction and Mental Health, Toronto, Ontario M5T 1R8, Canada.
          + James L. Kennedy,
          + Clement C. Zai &
          + Jo Knight
   106. Department of Psychiatry, University of Toronto, Toronto, Ontario
       M5T 1R8, Canada.
          + James L. Kennedy,
          + Clement C. Zai &
          + Jo Knight
   107. Institute of Medical Science, University of Toronto, Toronto,
       Ontario M5S 1A8, Canada.
          + James L. Kennedy &
          + Jo Knight
   108. Institute of Molecular Genetics, Russian Academy of Sciences,
       Moscow 123182, Russia.
          + Andrey Khrunin,
          + Svetlana Limborska &
          + Petr Slominsky
   109. Latvian Biomedical Research and Study Centre, Riga, LV-1067,
       Latvia.
          + Janis Klovins &
          + Liene Nikitina-Zake
   110. Department of Psychiatry and Zilkha Neurogenetics Institute, Keck
       School of Medicine at University of Southern California, Los
       Angeles, California 90089, USA.
          + James A. Knowles,
          + Michele T. Pato &
          + Carlos N. Pato
   111. Faculty of Medicine, Vilnius University, LT-01513 Vilnius,
       Lithuania.
          + Vaidutis Kucinskas &
          + Zita Ausrele Kucinskiene
   112. Department of Biology and Medical Genetics, 2nd Faculty of
       Medicine and University Hospital Motol, 150 06 Prague, Czech
       Republic.
          + Hana Kuzelova-Ptackova &
          + Milan Macek Jr
   113. Department of Child and Adolescent Psychiatry, Pierre and Marie
       Curie Faculty of Medicine, Paris 75013, France.
          + Claudine Laurent
   114. Duke-NUS Graduate Medical School, Singapore 169857.
          + Jimmy Lee Chee Keong
   115. Department of Psychiatry, Hadassah-Hebrew University Medical
       Center, Jerusalem 91120, Israel.
          + Bernard Lerer
   116. Centre for Genomic Sciences, The University of Hong Kong, Hong
       Kong, China.
          + Miaoxin Li &
          + Pak C. Sham
   117. Mental Health Centre and Psychiatric Laboratory, West China
       Hospital, Sichuan University, Chengdu, 610041 Sichuan, China.
          + Tao Li &
          + Qiang Wang
   118. Department of Biostatistics, Johns Hopkins University Bloomberg
       School of Public Health, Baltimore, Maryland 21205, USA.
          + Kung-Yee Liang
   119. Department of Psychiatry, Columbia University, New York, New York
       10032, USA.
          + Jeffrey Lieberman &
          + T. Scott Stroup
   120. Priority Centre for Translational Neuroscience and Mental Health,
       University of Newcastle, Newcastle NSW 2300, Australia.
          + Carmel M. Loughland &
          + Ulrich Schall
   121. Department of Genetics and Pathology, International Hereditary
       Cancer Center, Pomeranian Medical University in Szczecin, 70-453
       Szczecin, Poland.
          + Jan Lubinski
   122. Department of Mental Health and Substance Abuse Services; National
       Institute for Health and Welfare, P.O. BOX 30, FI-00271 Helsinki,
       Finland.
          + Jouko Lönnqvist &
          + Jaana Suvisaari
   123. Department of Mental Health, Bloomberg School of Public Health,
       Johns Hopkins University, Baltimore, Maryland 21205, USA.
          + Brion S. Maher
   124. Department of Psychiatry, University of Bonn, D-53127 Bonn,
       Germany.
          + Wolfgang Maier
   125. Centre National de la Recherche Scientifique, Laboratoire de
       Génétique Moléculaire de la Neurotransmission et des Processus
       Neurodégénératifs, Hôpital de la Pitié Salpêtrière, 75013 Paris,
       France.
          + Jacques Mallet
   126. Department of Genomics Mathematics, University of Bonn, D-53127
       Bonn, Germany.
          + Manuel Mattheisen
   127. Research Unit, Sørlandet Hospital, 4604 Kristiansand, Norway.
          + Morten Mattingsdal
   128. Department of Psychiatry, Harvard Medical School, Boston,
       Massachusetts 02115, USA.
          + Robert W. McCarley,
          + Raquelle I. Mesholam-Gately,
          + Larry J. Seidman &
          + Tracey L. Petryshen
   129. VA Boston Health Care System, Brockton, Massachusetts 02301, USA.
          + Robert W. McCarley
   130. Department of Psychiatry, National University of Ireland Galway,
       Co. Galway, Ireland.
          + Colm McDonald
   131. Centre for Cognitive Ageing and Cognitive Epidemiology, University
       of Edinburgh, Edinburgh EH16 4SB, UK.
          + Andrew M. McIntosh
   132. Division of Psychiatry, University of Edinburgh, Edinburgh EH16
       4SB, UK.
          + Andrew M. McIntosh &
          + Douglas H. R. Blackwood
   133. Division of Mental Health and Addiction, Oslo University Hospital,
       0424 Oslo, Norway.
          + Ingrid Melle &
          + Ole A. Andreassen
   134. Massachusetts Mental Health Center Public Psychiatry Division of
       the Beth Israel Deaconess Medical Center, Boston, Massachusetts
       02114, USA.
          + Raquelle I. Mesholam-Gately &
          + Larry J. Seidman
   135. Estonian Genome Center, University of Tartu, Tartu 50090, Estonia.
          + Andres Metspalu,
          + Lili Milani,
          + Mari Nelis &
          + Tõnu Esko
   136. School of Psychology, University of Newcastle, Newcastle NSW 2308,
       Australia.
          + Patricia T. Michie
   137. First Psychiatric Clinic, Medical University, Sofia 1431,
       Bulgaria.
          + Vihra Milanova
   138. Department P, Aarhus University Hospital, DK-8240 Risskov,
       Denmark.
          + Ole Mors &
          + Anders D. Børglum
   139. Department of Psychiatry, Royal College of Surgeons in Ireland,
       Dublin 2, Ireland.
          + Kieran C. Murphy
   140. King’s College London, London SE5 8AF, UK.
          + Robin M. Murray &
          + John Powell
   141. Maastricht University Medical Centre, South Limburg Mental Health
       Research and Teaching Network, EURON, 6229 HX Maastricht, The
       Netherlands.
          + Inez Myin-Germeys &
          + Jim Van Os
   142. Institute of Translational Medicine, University of Liverpool,
       Liverpool L69 3BX, UK.
          + Bertram Müller-Myhsok
   143. Max Planck Institute of Psychiatry, 80336 Munich, Germany.
          + Bertram Müller-Myhsok
   144. Munich Cluster for Systems Neurology (SyNergy), 80336 Munich,
       Germany.
          + Bertram Müller-Myhsok
   145. Department of Psychiatry and Psychotherapy, Jena University
       Hospital, 07743 Jena, Germany.
          + Igor Nenadic
   146. Department of Psychiatry, Queensland Brain Institute and
       Queensland Centre for Mental Health Research, University of
       Queensland, Brisbane, Queensland, St Lucia QLD 4072, Australia.
          + Deborah A. Nertney
   147. Department of Psychiatry and Behavioral Sciences, Johns Hopkins
       University School of Medicine, Baltimore, Maryland 21205, USA.
          + Gerald Nestadt &
          + Ann E. Pulver
   148. Department of Psychiatry, Trinity College Dublin, Dublin 2,
       Ireland.
          + Kristin K. Nicodemus
   149. Eli Lilly and Company,Lilly Corporate Center, Indianapolis, 46285
       Indiana, USA.
          + Laura Nisenbaum
   150. Department of Clinical Sciences, Psychiatry, Umeå University,
       SE-901 87 Umeå, Sweden.
          + Annelie Nordin &
          + Rolf Adolfsson
   151. DETECT Early Intervention Service for Psychosis, Blackrock, Co.
       Dublin, Ireland.
          + Eadbhard O’Callaghan
   152. Centre for Public Health, Institute of Clinical Sciences, Queen’s
       University Belfast, Belfast BT12 6AB, UK.
          + F. Anthony O’Neill
   153. Lawrence Berkeley National Laboratory, University of California at
       Berkeley, Berkeley, California 94720, USA.
          + Sang-Yun Oh
   154. Institute of Psychiatry, King’s College London, London SE5 8AF,
       UK.
          + Jim Van Os
   155. A list of authors and affiliations appear in the Supplementary
       Information.
          + Psychosis Endophenotypes International Consortium
   156. Melbourne Neuropsychiatry Centre, University of Melbourne &
       Melbourne Health, Melbourne, Vic 3053, Australia.
          + Christos Pantelis
   157. Department of Psychiatry, University of Helsinki, P.O. Box 590,
       FI-00029 HUS, Helsinki, Finland.
          + Tiina Paunio
   158. Public Health Genomics Unit, National Institute for Health and
       Welfare, P.O. BOX 30, FI-00271 Helsinki, Finland
          + Tiina Paunio &
          + Olli Pietiläinen
   159. Medical Faculty, University of Belgrade, 11000 Belgrade, Serbia.
          + Milica Pejovic-Milovancevic
   160. Department of Psychiatry, University of North Carolina, Chapel
       Hill, North Carolina 27599-7160, USA.
          + Diana O. Perkins &
          + Patrick F. Sullivan
   161. Institute for Molecular Medicine Finland, FIMM, University of
       Helsinki, P.O. Box 20FI-00014, Helsinki, Finland
          + Olli Pietiläinen &
          + Aarno Palotie
   162. Department of Epidemiology, Harvard School of Public Health,
       Boston, Massachusetts 02115, USA.
          + Alkes Price
   163. Department of Psychiatry, University of Oxford, Oxford, OX3 7JX,
       UK.
          + Digby Quested
   164. Virginia Institute for Psychiatric and Behavioral Genetics,
       Virginia Commonwealth University, Richmond, Virginia 23298, USA.
          + Mark A. Reimers &
          + Aaron R. Wolen
   165. Institute for Multiscale Biology, Icahn School of Medicine at
       Mount Sinai, New York, New York 10029, USA.
          + Panos Roussos &
          + Pamela Sklar
   166. PharmaTherapeutics Clinical Research, Pfizer Worldwide Research
       and Development, Cambridge, Massachusetts 02139, USA.
          + Christian R. Schubert &
          + Jens R. Wendland
   167. Department of Psychiatry and Psychotherapy, University of
       Gottingen, 37073 Göttingen, Germany.
          + Thomas G. Schulze
   168. Psychiatry and Psychotherapy Clinic, University of Erlangen, 91054
       Erlangen, Germany.
          + Sibylle G. Schwab
   169. Hunter New England Health Service, Newcastle NSW 2308, Australia.
          + Rodney J. Scott
   170. School of Biomedical Sciences, University of Newcastle, Newcastle
       NSW 2308, Australia.
          + Rodney J. Scott
   171. Division of Cancer Epidemiology and Genetics, National Cancer
       Institute, Bethesda, Maryland 20892, USA.
          + Jianxin Shi
   172. University of Iceland, Landspitali, National University Hospital,
       101 Reykjavik, Iceland.
          + Engilbert Sigurdsson
   173. Department of Psychiatry and Drug Addiction, Tbilisi State Medical
       University (TSMU), N33, 0177 Tbilisi, Georgia.
          + Teimuraz Silagadze
   174. Research and Development, Bronx Veterans Affairs Medical Center,
       New York, New York 10468, USA.
          + Jeremy M. Silverman
   175. Wellcome Trust Centre for Human Genetics, Oxford OX3 7BN, UK.
          + ChrisC. A. Spencer
   176. deCODE Genetics, 101 Reykjavik, Iceland.
          + Hreinn Stefansson,
          + Stacy Steinberg &
          + Kari Stefansson
   177. Department of Clinical Neurology, Medical University of Vienna,
       1090 Wien, Austria.
          + Elisabeth Stogmann &
          + Fritz Zimprich
   178. Lieber Institute for Brain Development, Baltimore, Maryland 21205,
       USA.
          + Richard E. Straub &
          + Daniel R. Weinberger
   179. Department of Medical Genetics, University Medical Centre Utrecht,
       Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands.
          + Eric Strengman
   180. Berkshire Healthcare NHS Foundation Trust, Bracknell RG12 1BQ, UK.
          + Srinivas Thirumalai
   181. Section of Psychiatry, University of Verona, 37134 Verona, Italy.
          + Sarah Tosato
   182. Department of Psychiatry, University of Oulu, P.O. Box 5000,
       90014, Finland.
          + Juha Veijola
   183. University Hospital of Oulu, P.O. Box 20, 90029 OYS, Finland.
          + Juha Veijola
   184. Molecular and Cellular Therapeutics, Royal College of Surgeons in
       Ireland, Dublin 2, Ireland.
   185. Health Research Board, Dublin 2, Ireland.
          + Dermot Walsh
   186. School of Psychiatry and Clinical Neurosciences, The University of
       Western Australia, Perth WA6009, Australia.
          + Dieter B. Wildenauer &
          + Assen V. Jablensky
   187. Computational Sciences CoE, Pfizer Worldwide Research and
       Development, Cambridge, Massachusetts 02139, USA.
          + Hualin Simon Xi
   188. Human Genetics, Genome Institute of Singapore, A*STAR, Singapore
       138672.
          + Jianjun Liu
   189. A list of authors and affiliations appear in the Supplementary
       Information.
          + Wellcome Trust Case-Control Consortium
   190. University College London, London WC1E 6BT, UK.
   191. Department of Neuroscience, Icahn School of Medicine at Mount
       Sinai, New York, New York 10029, USA.
          + Joseph D. Buxbaum
   192. Institute of Neuroscience and Medicine (INM-1), Research Center
       Juelich, 52428 Juelich, Germany.
          + Sven Cichon
   193. Department of Genetics, The Hebrew University of Jerusalem, 91905
       Jerusalem, Israel.
          + Ariel Darvasi
   194. Neuroscience Discovery and Translational Area, Pharma Research and
       Early Development, F. Hoffman-La Roche, CH-4070 Basel, Switzerland.
          + Enrico Domenici
   195. Centre for Clinical Research in Neuropsychiatry, School of
       Psychiatry and Clinical Neurosciences, The University of Western
       Australia, Medical Research Foundation Building, Perth WA6000,
       Australia.
          + Assen V. Jablensky
   196. Virginia Institute for Psychiatric and Behavioral Genetics,
       Departments of Psychiatry and Human and Molecular Genetics,
       Virginia Commonwealth University, Richmond, Virginia 23298, USA.
          + Kenneth S. Kendler &
          + Brien P. Riley
   197. The Feinstein Institute for Medical Research, Manhasset, New York
       11030, USA.
          + Todd Lencz &
          + Anil K. Malhotra
   198. The Hofstra NS-LIJ School of Medicine, Hempstead, New York 11549,
       USA.
          + Todd Lencz &
          + Anil K. Malhotra
   199. The Zucker Hillside Hospital, Glen Oaks, New York 11004, USA.
          + Todd Lencz &
          + Anil K. Malhotra
   200. Saw Swee Hock School of Public Health, National University of
       Singapore, Singapore 117597, Singapore.
          + Jianjun Liu
   201. Queensland Centre for Mental Health Research, University of
       Queensland, Brisbane 4076, Queensland, Australia.
          + Bryan J. Mowry
   202. Center for Human Genetic Research and Department of Psychiatry,
       Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
          + Tracey L. Petryshen
   203. Department of Child and Adolescent Psychiatry, Erasmus University
       Medical Centre, Rotterdam 3000, The Netherlands.
          + Danielle Posthuma
   204. Department of Complex Trait Genetics, Neuroscience Campus
       Amsterdam, VU University Medical Center Amsterdam, Amsterdam 1081,
       The Netherlands.
          + Danielle Posthuma
   205. Department of Functional Genomics, Center for Neurogenomics and
       Cognitive Research, Neuroscience Campus Amsterdam, VU University,
       Amsterdam 1081, The Netherlands.
          + Danielle Posthuma
   206. University of Aberdeen, Institute of Medical Sciences, Aberdeen
       AB25 2ZD, UK.
          + David St Clair
   207. Departments of Psychiatry, Neurology, Neuroscience and Institute
       of Genetic Medicine, Johns Hopkins School of Medicine, Baltimore,
       Maryland 21205, USA.
          + Daniel R. Weinberger
   208. Department of Clinical Medicine, University of Copenhagen,
       Copenhagen 2200, Denmark.
          + Thomas Werge

Consortia

    1. Schizophrenia Working Group of the Psychiatric Genomics Consortium
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Aiden Corvin,
          + James T. R. Walters,
          + Kai-How Farh,
          + Peter A. Holmans,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + David A. Collier,
          + Hailiang Huang,
          + Tune H. Pers,
          + Ingrid Agartz,
          + Esben Agerbo,
          + Margot Albus,
          + Madeline Alexander,
          + Farooq Amin,
          + Silviu A. Bacanu,
          + Martin Begemann,
          + Richard A. Belliveau Jr,
          + Judit Bene,
          + Sarah E. Bergen,
          + Elizabeth Bevilacqua,
          + Tim B. Bigdeli,
          + Donald W. Black,
          + Richard Bruggeman,
          + Nancy G. Buccola,
          + Randy L. Buckner,
          + William Byerley,
          + Wiepke Cahn,
          + Guiqing Cai,
          + Dominique Campion,
          + Rita M. Cantor,
          + Vaughan J. Carr,
          + Noa Carrera,
          + Stanley V. Catts,
          + Kimberly D. Chambert,
          + Raymond C. K. Chan,
          + Ronald Y. L. Chen,
          + Eric Y. H. Chen,
          + Wei Cheng,
          + Eric F. C. Cheung,
          + Siow Ann Chong,
          + C. Robert Cloninger,
          + David Cohen,
          + Nadine Cohen,
          + Paul Cormican,
          + Nick Craddock,
          + James J. Crowley,
          + David Curtis,
          + Michael Davidson,
          + Kenneth L. Davis,
          + Franziska Degenhardt,
          + Jurgen Del Favero,
          + Ditte Demontis,
          + Dimitris Dikeos,
          + Timothy Dinan,
          + Srdjan Djurovic,
          + Gary Donohoe,
          + Elodie Drapeau,
          + Jubao Duan,
          + Frank Dudbridge,
          + Naser Durmishi,
          + Peter Eichhammer,
          + Johan Eriksson,
          + Valentina Escott-Price,
          + Laurent Essioux,
          + Ayman H. Fanous,
          + Martilias S. Farrell,
          + Josef Frank,
          + Lude Franke,
          + Robert Freedman,
          + Nelson B. Freimer,
          + Marion Friedl,
          + Joseph I. Friedman,
          + Menachem Fromer,
          + Giulio Genovese,
          + Lyudmila Georgieva,
          + Ina Giegling,
          + Paola Giusti-Rodríguez,
          + Stephanie Godard,
          + Jacqueline I. Goldstein,
          + Vera Golimbet,
          + Srihari Gopal,
          + Jacob Gratten,
          + Lieuwe de Haan,
          + Christian Hammer,
          + Marian L. Hamshere,
          + Mark Hansen,
          + Thomas Hansen,
          + Vahram Haroutunian,
          + Annette M. Hartmann,
          + Frans A. Henskens,
          + Stefan Herms,
          + Joel N. Hirschhorn,
          + Per Hoffmann,
          + Andrea Hofman,
          + Mads V. Hollegaard,
          + David M. Hougaard,
          + Masashi Ikeda,
          + Inge Joa,
          + Antonio Julià,
          + René S. Kahn,
          + Luba Kalaydjieva,
          + Sena Karachanak-Yankova,
          + Juha Karjalainen,
          + David Kavanagh,
          + Matthew C. Keller,
          + James L. Kennedy,
          + Andrey Khrunin,
          + Yunjung Kim,
          + Janis Klovins,
          + James A. Knowles,
          + Bettina Konte,
          + Vaidutis Kucinskas,
          + Zita Ausrele Kucinskiene,
          + Hana Kuzelova-Ptackova,
          + Anna K. Kähler,
          + Claudine Laurent,
          + Jimmy Lee Chee Keong,
          + S. Hong Lee,
          + Sophie E. Legge,
          + Bernard Lerer,
          + Miaoxin Li,
          + Tao Li,
          + Kung-Yee Liang,
          + Jeffrey Lieberman,
          + Svetlana Limborska,
          + Carmel M. Loughland,
          + Jan Lubinski,
          + Jouko Lönnqvist,
          + Milan Macek Jr,
          + Patrik K. E. Magnusson,
          + Brion S. Maher,
          + Wolfgang Maier,
          + Jacques Mallet,
          + Sara Marsal,
          + Manuel Mattheisen,
          + Morten Mattingsdal,
          + Robert W. McCarley,
          + Colm McDonald,
          + Andrew M. McIntosh,
          + Sandra Meier,
          + Carin J. Meijer,
          + Bela Melegh,
          + Ingrid Melle,
          + Raquelle I. Mesholam-Gately,
          + Andres Metspalu,
          + Patricia T. Michie,
          + Lili Milani,
          + Vihra Milanova,
          + Younes Mokrab,
          + Derek W. Morris,
          + Ole Mors,
          + Kieran C. Murphy,
          + Robin M. Murray,
          + Inez Myin-Germeys,
          + Bertram Müller-Myhsok,
          + Mari Nelis,
          + Igor Nenadic,
          + Deborah A. Nertney,
          + Gerald Nestadt,
          + Kristin K. Nicodemus,
          + Liene Nikitina-Zake,
          + Laura Nisenbaum,
          + Annelie Nordin,
          + Eadbhard O’Callaghan,
          + Colm O’Dushlaine,
          + F. Anthony O’Neill,
          + Sang-Yun Oh,
          + Ann Olincy,
          + Line Olsen,
          + Jim Van Os,
          + Psychosis Endophenotypes International Consortium,
          + Christos Pantelis,
          + George N. Papadimitriou,
          + Sergi Papiol,
          + Elena Parkhomenko,
          + Michele T. Pato,
          + Tiina Paunio,
          + Milica Pejovic-Milovancevic,
          + Diana O. Perkins,
          + Olli Pietiläinen,
          + Jonathan Pimm,
          + Andrew J. Pocklington,
          + John Powell,
          + Alkes Price,
          + Ann E. Pulver,
          + Shaun M. Purcell,
          + Digby Quested,
          + Henrik B. Rasmussen,
          + Abraham Reichenberg,
          + Mark A. Reimers,
          + Alexander L. Richards,
          + Joshua L. Roffman,
          + Panos Roussos,
          + Douglas M. Ruderfer,
          + Veikko Salomaa,
          + Alan R. Sanders,
          + Ulrich Schall,
          + Christian R. Schubert,
          + Thomas G. Schulze,
          + Sibylle G. Schwab,
          + Edward M. Scolnick,
          + Rodney J. Scott,
          + Larry J. Seidman,
          + Jianxin Shi,
          + Engilbert Sigurdsson,
          + Teimuraz Silagadze,
          + Jeremy M. Silverman,
          + Kang Sim,
          + Petr Slominsky,
          + Jordan W. Smoller,
          + Hon-Cheong So,
          + ChrisC. A. Spencer,
          + Eli A. Stahl,
          + Hreinn Stefansson,
          + Stacy Steinberg,
          + Elisabeth Stogmann,
          + Richard E. Straub,
          + Eric Strengman,
          + Jana Strohmaier,
          + T. Scott Stroup,
          + Mythily Subramaniam,
          + Jaana Suvisaari,
          + Dragan M. Svrakic,
          + Jin P. Szatkiewicz,
          + Erik Söderman,
          + Srinivas Thirumalai,
          + Draga Toncheva,
          + Sarah Tosato,
          + Juha Veijola,
          + John Waddington,
          + Dermot Walsh,
          + Dai Wang,
          + Qiang Wang,
          + Bradley T. Webb,
          + Mark Weiser,
          + Dieter B. Wildenauer,
          + Nigel M. Williams,
          + Stephanie Williams,
          + Stephanie H. Witt,
          + Aaron R. Wolen,
          + Emily H. M. Wong,
          + Brandon K. Wormley,
          + Hualin Simon Xi,
          + Clement C. Zai,
          + Xuebin Zheng,
          + Fritz Zimprich,
          + Naomi R. Wray,
          + Kari Stefansson,
          + Peter M. Visscher,
          + Wellcome Trust Case-Control Consortium,
          + Rolf Adolfsson,
          + Ole A. Andreassen,
          + Douglas H. R. Blackwood,
          + Elvira Bramon,
          + Joseph D. Buxbaum,
          + Anders D. Børglum,
          + Sven Cichon,
          + Ariel Darvasi,
          + Enrico Domenici,
          + Hannelore Ehrenreich,
          + Tõnu Esko,
          + Pablo V. Gejman,
          + Michael Gill,
          + Hugh Gurling,
          + Christina M. Hultman,
          + Nakao Iwata,
          + Assen V. Jablensky,
          + Erik G. Jönsson,
          + Kenneth S. Kendler,
          + George Kirov,
          + Jo Knight,
          + Todd Lencz,
          + Douglas F. Levinson,
          + Qingqin S. Li,
          + Jianjun Liu,
          + Anil K. Malhotra,
          + Steven A. McCarroll,
          + Andrew McQuillin,
          + Jennifer L. Moran,
          + Preben B. Mortensen,
          + Bryan J. Mowry,
          + Markus M. Nöthen,
          + Roel A. Ophoff,
          + Michael J. Owen,
          + Aarno Palotie,
          + Carlos N. Pato,
          + Tracey L. Petryshen,
          + Danielle Posthuma,
          + Marcella Rietschel,
          + Brien P. Riley,
          + Dan Rujescu,
          + Pak C. Sham,
          + Pamela Sklar,
          + David St Clair,
          + Daniel R. Weinberger,
          + Jens R. Wendland,
          + Thomas Werge,
          + Mark J. Daly,
          + Patrick F. Sullivan &
          + Michael C. O’Donovan
    2.

Contributions

   The individual studies or consortia contributing to the GWAS
   meta-analysis were led by R.A., O.A.A., D.H.R.B., A.D.B., E. Bramon,
   J.D.B., A.C., D.A.C., S.C., A.D., E. Domenici, H.E., T.E., P.V.G.,
   M.G., H.G., C.M.H., N.I., A.V.J., E.G.J., K.S.K., G.K., J. Knight, T.
   Lencz, D.F.L., Q.S.L., J. Liu, A.K.M., S.A.M., A. McQuillin, J.L.M.,
   P.B.M., B.J.M., M.M.N., M.C.O’D., R.A.O., M.J.O., A. Palotie, C.N.P.,
   T.L.P., M.R., B.P.R., D.R., P.C.S, P. Sklar. D.St.C., P.F.S., D.R.W.,
   J.R.W., J.T.R.W. and T.W. Together with the core statistical analysis
   group led by M.J.D. comprising S.R., B.M.N. and P.A.H., this group
   comprised the management group led by M.C.O’D. who were responsible for
   the management of the study and the overall content of the manuscript.
   Additional analyses and interpretations were contributed by E.A.,
   B.B.-S., D.K., K.-H.F., M. Fromer, H.H., P.L., P.B.M., S.M.P., T.H.P.,
   N.R.W. and P.M.V. The phenotype supervisory group comprised A.C.,
   A.H.F., P.V.G., K.K.K. and B.J.M. D.A.C. led the candidate selected
   genes subgroup comprised of M.J.D., E. Dominici, J.A.K., A.M.H.,
   M.C.O’D, B.P.R., D.R., E.M.S. and P. Sklar. Replication results were
   provided by S.S., H.S. and K.S. The remaining authors contributed to
   the recruitment, genotyping, or data processing for the contributing
   components of the meta-analysis. A.C., M.J.D., B.M.N., S.R., P.F.S. and
   M.C.O’D. took responsibility for the primary drafting of the manuscript
   which was shaped by the management group. All other authors saw, had
   the opportunity to comment on, and approved the final draft.

Competing financial interests

   CFI statement–Several of the authors are employees of the following
   pharmaceutical companies; Pfizer (C.R.S., J.R.W., H.S.X.), F.Hoffman-La
   Roche (E.D., L.E.), Eli Lilly (D.A.C., Y.M., L.N.) and Janssen (S.G.,
   D.W., Q.S.L.; also N.C. an ex-employee). Others are employees of deCODE
   genetics (S.S, H.S., K.S.). None of these companies influenced the
   design of the study, the interpretation of the data, or the amount of
   data reported, or financially profit by publication of the results
   which are pre-competitive. The other authors declare no competing
   interests.

Corresponding author

   Correspondence to:
     * Michael C. O’Donovan

   Results can be downloaded from the Psychiatric Genomics Consortium
   website (http://pgc.unc.edu) and visualized using Ricopili
   (http://www.broadinstitute.org/mpg/ricopili). Genotype data for the
   samples where the ethics permit deposition are available upon
   application from the NIMH Genetics Repository
   (https://www.nimhgenetics.org).

Author details

Extended data figures and tables

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

Extended Data Figures

    1.

        Extended Data Figure 1: Homogeneity of effects across studies. (87
                KB)
                Plot of the first two principal components (PCs) from
                principal components analysis (PCA) of the logistic
                regression β coefficients for autosomal genome-wide
                significant associations. The input data were the β
                coefficients from 52 samples for 112 independent SNP
                associations (excluding 3 chrX SNPs and 13 SNPs with
                missing values in Asian samples). PCAs were weighted by
                the number of cases. Each circle shows the location of a
                study on PC1 and PC2. Circle size and colour are
                proportional to the number of cases in each sample (larger
                and darker red circles correspond to more cases). Most
                samples cluster. Outliers had either small numbers of
                cases (‘small’) or were genotyped on older arrays.
                Abbreviations: a500 (Affymetrix 500K); a5 (Affymetrix
                5.0). Studies that did not use conventional research
                interviews are in the central cluster (CLOZUK, Sweden, and
                Denmark-Aarhus studies, see Supplementary Methods for
                sample descriptions).

    2.

        Extended Data Figure 2: Quantile-quantile plot. (111 KB)
                Quantile-quantile plot of the discovery genome-wide
                association meta-analysis of 49 case control samples
                (34,241 cases and 45,604 controls) and 3 family based
                association studies (1,235 parent affected-offspring
                trios). Expected –log[10] P values are those expected
                under the null hypothesis. Observed are the GWAS
                association results derived by logistic regression
                (2-tailed) as in Fig. 1. For clarity, we avoided expansion
                of the y axis by setting the smallest association P values
                to 10^−12. The shaded area surrounded by a red line
                indicates the 95% confidence interval under the null.
                λ[GC]is the observed median χ^2 test statistic divided by
                the median expected χ^2 test statistic under the null
                hypothesis.

    3.

        Extended Data Figure 3: Linkage disequilibrium score regression
                consistent with polygenic inheritance. (273 KB)
                The relationship between marker χ^2 association statistics
                and linkage disequilibrium (LD) as measured by the linkage
                disequilibrium score. Linkage disequilibrium score is the
                sum of the r^2 values between a variant and all other
                known variants within a 1 cM window, and quantifies the
                amount of genetic variation tagged by that variant.
                Variants were grouped into 50 equal-sized bins based on
                linkage disequilibrium score rank. Linkage disequilibrium
                score bin and mean χ^2 denotes mean linkage disequilibrium
                score and test statistic for markers each bin. a, b, We
                simulated (Supplementary Methods) test statistics under
                two scenarios: a, no true association, inflation due to
                population stratification; and b, polygenic inheritance (λ
                = 1.32), in which we assigned independent and identically
                distributed per-normalized-genotype effects to a randomly
                selected subset of variants. c, Results from the PGC
                schizophrenia GWAS (λ = 1.48). The real data are
                strikingly similar to the simulated data summarized in b
                but not a. The intercept estimates the inflation in the
                mean χ^2 that results from confounding biases, such as
                cryptic relatedness or population stratification. Thus,
                the intercept of 1.066 for the schizophrenia GWAS suggests
                that ~90% of the inflation in the mean χ^2 results from
                polygenic signal. The results of the simulations are also
                consistent with theoretical expectation (see Supplementary
                Methods). λ is the median χ^2 test statistic from the
                simulations (a, b) or the observed data (c) divided by the
                median expected χ^2 test statistic under the null
                hypothesis.

    4.

        Extended Data Figure 4: Enrichment of associations in tissues and
                cells. (259 KB)
                Genes whose transcriptional start is nearest to the most
                associated SNP at each schizophrenia-associated locus were
                tested for enriched expression in purified brain cell
                subsets obtained from mouse ribotagged lines^41 using
                enrichment analysis described in the Supplementary
                Methods. The red dotted line indicates P = 0.05.

    5.

        Extended Data Figure 5: MGS risk profile score analysis. (110 KB)
                Polygenic risk profile score (RPS) analyses using the
                MGS^18 sample as target, and deriving risk alleles from
                three published schizophrenia data sets (x axis): ISC
                (2,615 cases and 3,338 controls)^10, PGC1 (excluding MGS,
                9,320 cases and 10,228 controls)^16, and the current
                meta-analysis (excluding MGS) with 32,838 cases and 44,357
                controls. Samples sizes differ slightly from the original
                publications due to different analytical procedures. This
                shows the increasing RPS prediction with increasing
                training data set size reflecting improved precision of
                estimates of the SNP effect sizes. The proportion of
                variance explained (y axis; Nagelkerke’s R^2) was computed
                by comparison of a full model (covariates + RPS) score to
                a reduced model (covariates only). Ten different P value
                thresholds (P[T]) for selecting risk alleles are denoted
                by the colour of each bar (legend above plot). For
                significance testing, see the bottom legend which denotes
                the P value for the test that R^2 is different from zero.
                All numerical data and methods used to generate these
                plots are available in Supplementary Table 6 and
                Supplementary Methods.

    6.

        Extended Data Figure 6: Risk profile score analysis. (448 KB)
                We defined 40 target subgroups of the primary GWAS data
                set and performed 40 leave-one-out GWAS analyses (see
                Supplementary Methods and Supplementary Table 7) from
                which we derived risk alleles for RPS analysis (x axis)
                for each target subgroup. a, The proportion of variance
                explained (y axis; Nagelkerke’s R^2) was computed for each
                target by comparison of a full model (covariates + RPS)
                score to a reduced model (covariates only). For clarity, 3
                different P value thresholds (P[T]) are presented denoted
                by the colour of each bar (legend above plot) as for
                Extended Data Fig. 5, but for clarity we restrict to fewer
                P value thresholds (P[T] of 5 × 10^−8, 1 × 10^−4 and 0.05)
                and removed the significance values. b, The proportion of
                variance on the liability scale from risk scores
                calculated at the P[T] 0.05 with 95% CI bar assuming
                baseline population disease risk of 1%. c, Area under the
                receiver operating curve (AUC). All numerical data and
                methods used to generate these plots are available in
                Supplementary Table 7 and Supplementary Methods.

    7.

        Extended Data Figure 7: Pairwise epistasis analysis of significant
                SNPs. (106 KB)
                Quantile-quantile plot for all pair-wise (n = 7,750)
                combinations of the 125 independent autosomal genome-wide
                significant SNPs tested for non-additive effects on risk
                using case-control data sets of European ancestry (32,405
                cases and 42,221 controls). We included as covariates the
                principal components from the main analysis as well as a
                study indicator. The interaction model is described by:

                and are genotypes at the two loci, is the interaction
                between the two genotypes modelled in a multiplicative
                fashion, is the vector of principal components, is the
                vector of study indicator variables. Each is the
                regression coefficient in the generalized linear model
                using logistic regression. The overall distribution of P
                values did not deviate from the null and the smallest P
                value (4.28 × 10^−4) did not surpass the Bonferroni
                correction threshold (P = 0.05/7750 = 6.45 × 10^−6). The
                line x = y indicates the expected null distribution with
                the grey area bounded by red lines indicating the expected
                95% confidence interval for the null.

Extended Data Tables

    1.

        Extended Data Table 1: ALIGATOR and INRICH (182 KB)

    2.

        Extended Data Table 2: de novo overlap (213 KB)

Supplementary information

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

PDF files

    1.

        Supplementary Information (1.7 MB)
                This file contains Supplementary Text, Supplementary
                Tables 1-3, Supplementary References and Supplementary
                Notes (including a list of consortium members and
                acknowledgements) – see contents page for details.

    2.

        Supplementary Figure (2.1 MB)
                This file contains Supplementary Figure 1.

Excel files

    1.

        Supplementary Table 4 (106 KB)
                Credible causal schizophrenia SNPs, coding variants, and
                eQTLs. Worksheet 1: Coding variants: Index SNP is the
                schizophrenia associated SNP defining the schizophrenia
                associated region. Coding variant, R2, and gene denotes a
                coding credible SNP and the R2 with the index SNP, and the
                gene containing the coding variant. CHR (chromosome), BP
                (base position), A1A2 (alleles 1 and 2), frequencies of
                allele 1 (FRQ_A1), INFO (imputation quality) and P
                (P-value) refer to the index SNP in the discovery GWAS. P
                (incl rep) refers to replication P value for index SNP.
                Worksheets 2 and 3: Brain and blood eQTL: Credible SNP
                denotes a SNP within the schizophrenia credible set
                (defined in supplementary material) that is also a cis
                eQTL (transcript within 1Mb, PeQTL<1x10-4). P(cSCZ) is the
                schizophrenia (discovery) GWAS association P-value for the
                credible SNP. The Prob(cSCZ) is the normalized probability
                of the credible variant being causal for schizophrenia.
                N(cSCZ) is the number of variants in the credible set of
                schizophrenia variants within a region spanned by eQTLs at
                P<10-4. eQTL SNP is the most significant expression
                associated SNP in the region for the gene in next column
                (N.B., many regions have an eQTL for more than 1 gene).
                eQTLgene is the gene that is linked to the eQTL SNP.
                P(eQTL) is the association P-value between the eQTL SNP
                and the eQTLgene in the previous two columns. Prob(eQTL)
                is the normalized probability that the eQTL SNP is also
                the causal SNP for schizophrenia (high values mean higher
                probability of being causal). eQTLcumsum is the cumulative
                sum of the probability of all SNPs into the region, up to
                the inclusion of the max eQTL in locus ordered by
                probability of being the functional SNP. PeQTL(SCZ) is the
                schizophrenia association P-value for the eQTL SNP. R2
                (cSCZ/ eQTL) is the R2 between the credibleSNP and eQTL
                SNP. Associations to schizophrenia that are plausibly
                explained by an eQTL are in bold. Separate worksheets
                provide information on brain and blood eQTL analyses.
                Distinct loci are alternately shaded/unshaded.

    2.

        Supplementary Table 5 (173 KB)
                Pathway analyses by ALIGATOR and INRICH. Enrichment
                analyses using ALIGATOR and INRICH were performed as
                described in Supplementary Text. Pathway ID denotes the
                pathway source: GO (Gene ontology;
                http://www.geneontology.org), KEGG (Kyoto Encyclopaedia of
                Genes and Genomes; http://www.genome.jp/kegg), PAN-PW
                (PANTHER; http://www.pantherdb.org/pathway), Reactome
                (http://www.reactome.org/download), BioCarta (downloaded
                from the Molecular Signatures Database v4.0
                http://www.broadinstitute.org/gsea/msigdb/index.jsp), MGI
                (Mouse Genome Informatics;
                http://www.informatics.jax.org), and NCI pathways (NCI:
                http://pid.nci.nih.gov).

    3.

        Supplementary Table 7 (96 KB)
                Risk Profile Score Analyses. Risk Profile Score (RPS)
                analysis was performed as described in supplementary text.
                RPS datasets tab provides the name given for sample in
                which RPS was performed (target label) and the datasets
                included (defined in Supplementary Table 1). The GWAS data
                used to define the risk alleles for RPS analysis
                represents the remaining GWAS samples. For various GWAS
                P-value thresholds (denoted PT), we calculated: 1) the
                significance of the case-control score difference was
                analyzed (P tab), 2) the proportion of variance explained
                (Nagelkerke’s R2, R2 tab), 3) the proportion of variance
                on the liability scale explained by RPS (h2I tab) with
                standard error in brackets, 4) area under the receiver
                operator characteristic curve (AUC tab), and 5) odds ratio
                for the 10th RPS decile group compared with lowest decile
                with confidence interval in brackets. Ncases tab denotes
                number of cases in each target set.

    4.

        Supplementary Table 6 (32 KB)
                RPS analysis of MGS sample. Risk Profile Score (RPS)
                analyses was performed using the MGS dataset as target,
                using three distinct published results for SCZ GWAS, from
                the (1) ISC (2009) study of 2615 cases and 3338 controls11
                (denoted ISC columns) (2) PGC1 (excluding MGS, denoted
                PGC1 columns) with 9320 cases and 10228 controls22, (3)
                current meta analysis (excluding MGS, denoted Current
                columns) with 32838 cases and 44357 controls. For various
                GWAS P value thresholds (denoted PT), we calculated 1) the
                significance of the case-control score difference was
                analyzed (P tab) 2) The proportion of variance explained
                (Nagelkerke’s R2, R2 tab) 3) The proportion of variance on
                the liability scale explained by RPS (h2I tab) with
                standard error in brackets 4) Area under the receiver
                operator characteristic curve (AUC tab) and 5) Odds ratio
                for 10th RPS decile group compared with lowest decile with
                confidence interval in brackets. Ncases tab denotes number
                of cases in each target set.

Comments

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

    1. 2014-08-09 06:42 AM
       Report this comment #63705

        Hugh Fletcher said:
                This suggests two things: 1/ That studies of
                neurotransmission are easier than studies of the immune
                system, and the known involvement of the immune system in
                autism, OCD and schizophrenia has been largely ignored,
                just as APOE was neglected for amyloid precursor in
                studies of Alzheimer's. Stoner shows evidence of focal
                damage to layers of the cortex of brains of children with
                autism (N Engl J Med 2014; 370:1209-1219 March 27, 2014).
                These look similar to viral plaques and could easily
                involve the immune system, either failing to prevent
                infection or locally causing autoimune damage to specific
                cell types. Overgrowth could be a response to specific
                deficiencies. 2/ That mental health is subject to chaos
                theory. None of these alleles are necessary or sufficient.
                Particular combinations of tiny factors, many
                unpredictable, produce deviations from the norm. When
                these exceed a threshold they can be described as illness.
                If you think of human brains distributed as a pile of
                sand, most are in the central heap and are in the normal
                range. Near the edge is a line around which the difference
                from normal becomes noticable and diagnosis of a disorder
                becomes more likely. The line is nearer the centre in
                countries with a well developed health system and poor
                support for individuals. The designation of the disorder
                depends on where on the rim of the mound it falls; the
                exact location and severity of the lesions. This huge
                collection of data may be distracting. In type II
                diabetes, any loci affecting the immune system, insulin
                production or response, or glucose metabolism are risk
                factors. When a system approaches a state of failure any
                little thing that agrevates the situation may appear as a
                cause of collapse. Hopefully a unified picture of the
                primary system failure will emerge. It may be cell loss,
                rather than synaptic problems.

    2. 2014-08-20 08:23 AM
       Report this comment #63843

        Michael Lerman said:
                The CALL/CHL1 gene on 3p26 (first gene on 3p discovered by
                MH Wei and myself) was found strongly associated with
                schizophrenia in Japanese (Sakurai et al Mol Psychiatry,
                7,412, 2002) and Chinese populations (Chen QY et al,
                Schizophrenia Research, 73, 269, 2005). However a brief
                survey of Table 3 of the Supplementary Information did not
                show the CALL/CHL1 gene. Does this mean this gene is
                specific for the Chinese and Japanese populations? Michael
                Lerman, Ph.D., M.D.

   Subscribe to comments

Additional data

     * Extended Data Figure 1: Homogeneity of effects across studies.
       Hover over figure to zoom
       Plot of the first two principal components (PCs) from principal
       components analysis (PCA) of the logistic regression β coefficients
       for autosomal genome-wide significant associations. The input data
       were the β coefficients from 52 samples for 112 independent SNP
       associations (excluding 3 chrX SNPs and 13 SNPs with missing values
       in Asian samples). PCAs were weighted by the number of cases. Each
       circle shows the location of a study on PC1 and PC2. Circle size
       and colour are proportional to the number of cases in each sample
       (larger and darker red circles correspond to more cases). Most
       samples cluster. Outliers had either small numbers of cases
       (‘small’) or were genotyped on older arrays. Abbreviations: a500
       (Affymetrix 500K); a5 (Affymetrix 5.0). Studies that did not use
       conventional research interviews are in the central cluster
       (CLOZUK, Sweden, and Denmark-Aarhus studies, see Supplementary
       Methods for sample descriptions).
       Full size image
       Enable zoom
     * Extended Data Figure 2: Quantile-quantile plot.
       Hover over figure to zoom
       Quantile-quantile plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). Expected –log[10] P values are those
       expected under the null hypothesis. Observed are the GWAS
       association results derived by logistic regression (2-tailed) as in
       Fig. 1. For clarity, we avoided expansion of the y axis by setting
       the smallest association P values to 10^−12. The shaded area
       surrounded by a red line indicates the 95% confidence interval
       under the null. λ[GC] is the observed median χ^2 test statistic
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       Enable zoom
     * Extended Data Figure 3: Linkage disequilibrium score regression
       consistent with polygenic inheritance.
       Hover over figure to zoom
       The relationship between marker χ^2 association statistics and
       linkage disequilibrium (LD) as measured by the linkage
       disequilibrium score. Linkage disequilibrium score is the sum of
       the r^2 values between a variant and all other known variants
       within a 1 cM window, and quantifies the amount of genetic
       variation tagged by that variant. Variants were grouped into 50
       equal-sized bins based on linkage disequilibrium score rank.
       Linkage disequilibrium score bin and mean χ^2 denotes mean linkage
       disequilibrium score and test statistic for markers each bin. a, b,
       We simulated (Supplementary Methods) test statistics under two
       scenarios: a, no true association, inflation due to population
       stratification; and b, polygenic inheritance (λ = 1.32), in which
       we assigned independent and identically distributed
       per-normalized-genotype effects to a randomly selected subset of
       variants. c, Results from the PGC schizophrenia GWAS (λ = 1.48).
       The real data are strikingly similar to the simulated data
       summarized in b but not a. The intercept estimates the inflation in
       the mean χ^2 that results from confounding biases, such as cryptic
       relatedness or population stratification. Thus, the intercept of
       1.066 for the schizophrenia GWAS suggests that ~90% of the
       inflation in the mean χ^2 results from polygenic signal. The
       results of the simulations are also consistent with theoretical
       expectation (see Supplementary Methods). λ is the median χ^2 test
       statistic from the simulations (a, b) or the observed data (c)
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       Enable zoom
     * Extended Data Figure 4: Enrichment of associations in tissues and
       cells.
       Hover over figure to zoom
       Genes whose transcriptional start is nearest to the most associated
       SNP at each schizophrenia-associated locus were tested for enriched
       expression in purified brain cell subsets obtained from mouse
       ribotagged lines^41 using enrichment analysis described in the
       Supplementary Methods. The red dotted line indicates P = 0.05.
       Full size image
       Enable zoom
     * Extended Data Figure 5: MGS risk profile score analysis.
       Hover over figure to zoom
       Polygenic risk profile score (RPS) analyses using the MGS^18 sample
       as target, and deriving risk alleles from three published
       schizophrenia data sets (x axis): ISC (2,615 cases and 3,338
       controls)^10, PGC1 (excluding MGS, 9,320 cases and 10,228
       controls)^16, and the current meta-analysis (excluding MGS) with
       32,838 cases and 44,357 controls. Samples sizes differ slightly
       from the original publications due to different analytical
       procedures. This shows the increasing RPS prediction with
       increasing training data set size reflecting improved precision of
       estimates of the SNP effect sizes. The proportion of variance
       explained (y axis; Nagelkerke’s R^2) was computed by comparison of
       a full model (covariates + RPS) score to a reduced model
       (covariates only). Ten different P value thresholds (P[T]) for
       selecting risk alleles are denoted by the colour of each bar
       (legend above plot). For significance testing, see the bottom
       legend which denotes the P value for the test that R^2 is different
       from zero. All numerical data and methods used to generate these
       plots are available in Supplementary Table 6 and Supplementary
       Methods.
       Full size image
       Enable zoom
     * Extended Data Figure 6: Risk profile score analysis.
       Hover over figure to zoom
       We defined 40 target subgroups of the primary GWAS data set and
       performed 40 leave-one-out GWAS analyses (see Supplementary Methods
       and Supplementary Table 7) from which we derived risk alleles for
       RPS analysis (x axis) for each target subgroup. a, The proportion
       of variance explained (y axis; Nagelkerke’s R^2) was computed for
       each target by comparison of a full model (covariates + RPS) score
       to a reduced model (covariates only). For clarity, 3 different P
       value thresholds (P[T]) are presented denoted by the colour of each
       bar (legend above plot) as for Extended Data Fig. 5, but for
       clarity we restrict to fewer P value thresholds (P[T] of 5 × 10^−8,
       1 × 10^−4 and 0.05) and removed the significance values. b, The
       proportion of variance on the liability scale from risk scores
       calculated at the P[T] 0.05 with 95% CI bar assuming baseline
       population disease risk of 1%. c, Area under the receiver operating
       curve (AUC). All numerical data and methods used to generate these
       plots are available in Supplementary Table 7 and Supplementary
       Methods.
       Full size image
       Enable zoom
     * Extended Data Figure 7: Pairwise epistasis analysis of significant
       SNPs.
       Hover over figure to zoom
       Quantile-quantile plot for all pair-wise (n = 7,750) combinations
       of the 125 independent autosomal genome-wide significant SNPs
       tested for non-additive effects on risk using case-control data
       sets of European ancestry (32,405 cases and 42,221 controls). We
       included as covariates the principal components from the main
       analysis as well as a study indicator. The interaction model is
       described by:
       and are genotypes at the two loci, is the interaction between the
       two genotypes modelled in a multiplicative fashion, is the vector
       of principal components, is the vector of study indicator
       variables. Each is the regression coefficient in the generalized
       linear model using logistic regression. The overall distribution of
       P values did not deviate from the null and the smallest P value
       (4.28 × 10^−4) did not surpass the Bonferroni correction threshold
       (P = 0.05/7750 = 6.45 × 10^−6). The line x = y indicates the
       expected null distribution with the grey area bounded by red lines
       indicating the expected 95% confidence interval for the null.
       Full size image
       Enable zoom

     * Extended Data Table 1: ALIGATOR and INRICH
       Hover over figure to zoom
       Gene sets that have been reported to be enriched for schizophrenia
       associations and or rare mutations were tested for enrichment for
       genome-wide significant associations using ALIGATOR^44 and
       INRICH^45. Specifically, we tested the glutamatergic postsynaptic
       proteins comprising activity-regulated cytoskeleton-associated
       protein (ARC) and N-methyl-d-aspartate receptor (NMDAR)
       complexes^33, 34, 35, other curated synaptic gene-sets^14, 49,
       targets of fragile X mental retardation protein (FMRP)^33, 34, 35,
       calcium channels^11, 33, and TargetScan predicted MIR137 sets^11,
       16. The MIR137 TargetScan sets contain computationally predicted
       conserved miRNA target sites in 3′ UTRs of human genes^50. The
       current version is v6, but the version used in the prior PGC SCZ
       report^16 was based on v5 (filtered for a probability of conserved
       targeting > 0.9). We report the results of both analyses for
       consistency with previous work. The association at the extended MHC
       complex was not included given the extensive linkage disequilibrium
       at this region spans large numbers of genes. NA means that the
       pathway in question contained fewer than 2 significant genes (for
       ALIGATOR) or regions (INRICH).
       Full size table
       Enable zoom
     * Extended Data Table 2: de novo overlap
       Hover over figure to zoom
       Test of overlap between genes mapping to schizophrenia-associated
       loci in the present study and genes affected by non-synonymous (NS)
       de novo mutations. Enrichment was calculated using the dnenrich
       permutation framework as described^34. Genes within the GWS loci
       (Supplementary Table 3) were weighted by 1/N, where N is the number
       of coding genes within each associated locus. The observed test
       statistic (stat) is the sum of weights of genes impacted by de novo
       mutations. The expected test statistics are calculated by averaging
       over 50,000 permuted de novo mutation sets. Genes within
       schizophrenia-associated loci affected by de novo mutations are
       listed (multiple hits listed in parentheses). Cohorts: SCZ,
       schizophrenia; ID, intellectual disability; ASD, autism spectrum
       disorder. All mutations analysed annotated according to a unified
       system (see Supplementary Tables 1 and 2 of ref. 34). Genes with
       loss-of-function de novo mutations are underlined and in italics.
       Full size table
       Enable zoom

Editor's summary in العربية

   Although schizophrenia is a highly heritable disorder, its complex
   polygenic nature has impeded attempts to establish its genetic basis.
   This paper reports a genome-wide association study of more than 36,000
   schizophrenia patients and 100,000 controls. The study identifies 128
   independent associations in 108 loci, 83 of them new. Among them are
   many genes involved in glutamatergic neurotransmission, highlighting a
   potential therapeutic avenue. In addition, the results provide support
   for the hypothesized link between the immune system and schizophrenia.

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   Home > Health & Education > Mental Health Information

Schizophrenia

     * What Is Schizophrenia?
     * Causes
     * Who Is At Risk?
     * Signs & Symptoms
     * Treatments
     * Living With
     * Clinical Trials

   More
     * What Is Schizophrenia?
     * Causes
     * Who Is At Risk?
     * Signs & Symptoms
     * Treatments
     * Living With
     * Clinical Trials

What Is Schizophrenia?

   Schizophrenia is a chronic, severe, and disabling brain disorder that
   has affected people throughout history.

   People with the disorder may hear voices other people don't hear. They
   may believe other people are reading their minds, controlling their
   thoughts, or plotting to harm them. This can terrify people with the
   illness and make them withdrawn or extremely agitated.

   People with schizophrenia may not make sense when they talk. They may
   sit for hours without moving or talking. Sometimes people with
   schizophrenia seem perfectly fine until they talk about what they are
   really thinking.

   Families and society are affected by schizophrenia too. Many people
   with schizophrenia have difficulty holding a job or caring for
   themselves, so they rely on others for help.

   Treatment helps relieve many symptoms of schizophrenia, but most people
   who have the disorder cope with symptoms throughout their lives.
   However, many people with schizophrenia can lead rewarding and
   meaningful lives in their communities. Researchers are developing more
   effective medications and using new research tools to understand the
   causes of schizophrenia. In the years to come, this work may help
   prevent and better treat the illness.

Causes

   Experts think schizophrenia is caused by several factors.

   Genes and environment. Scientists have long known that schizophrenia
   runs in families. The illness occurs in 1 percent of the general
   population, but it occurs in 10 percent of people who have a
   first-degree relative with the disorder, such as a parent, brother, or
   sister. People who have second-degree relatives (aunts, uncles,
   grandparents, or cousins) with the disease also develop schizophrenia
   more often than the general population. The risk is highest for an
   identical twin of a person with schizophrenia. He or she has a 40 to 65
   percent chance of developing the disorder.

   We inherit our genes from both parents. Scientists believe several
   genes are associated with an increased risk of schizophrenia, but that
   no gene causes the disease by itself. In fact, recent research has
   found that people with schizophrenia tend to have higher rates of rare
   genetic mutations. These genetic differences involve hundreds of
   different genes and probably disrupt brain development.

   Other recent studies suggest that schizophrenia may result in part when
   a certain gene that is key to making important brain chemicals
   malfunctions. This problem may affect the part of the brain involved in
   developing higher functioning skills. Research into this gene is
   ongoing, so it is not yet possible to use the genetic information to
   predict who will develop the disease.

   Despite this, tests that scan a person's genes can be bought without a
   prescription or a health professional's advice. Ads for the tests
   suggest that with a saliva sample, a company can determine if a client
   is at risk for developing specific diseases, including schizophrenia.
   However, scientists don't yet know all of the gene variations that
   contribute to schizophrenia. Those that are known raise the risk only
   by very small amounts. Therefore, these "genome scans" are unlikely to
   provide a complete picture of a person's risk for developing a mental
   disorder like schizophrenia.

   In addition, it probably takes more than genes to cause the disorder.
   Scientists think interactions between genes and the environment are
   necessary for schizophrenia to develop. Many environmental factors may
   be involved, such as exposure to viruses or malnutrition before birth,
   problems during birth, and other not yet known psychosocial factors.

   Different brain chemistry and structure. Scientists think that an
   imbalance in the complex, interrelated chemical reactions of the brain
   involving the neurotransmitters dopamine and glutamate, and possibly
   others, plays a role in schizophrenia. Neurotransmitters are substances
   that allow brain cells to communicate with each other. Scientists are
   learning more about brain chemistry and its link to schizophrenia.

   Also, in small ways the brains of people with schizophrenia look
   different than those of healthy people. For example, fluid-filled
   cavities at the center of the brain, called ventricles, are larger in
   some people with schizophrenia. The brains of people with the illness
   also tend to have less gray matter, and some areas of the brain may
   have less or more activity.

   Studies of brain tissue after death also have revealed differences in
   the brains of people with schizophrenia. Scientists found small changes
   in the distribution or characteristics of brain cells that likely
   occurred before birth. Some experts think problems during brain
   development before birth may lead to faulty connections. The problem
   may not show up in a person until puberty. The brain undergoes major
   changes during puberty, and these changes could trigger psychotic
   symptoms. Scientists have learned a lot about schizophrenia, but more
   research is needed to help explain how it develops.

Who Is At Risk?

   About 1% of Americans have this illness.

   Schizophrenia affects men and women equally. It occurs at similar rates
   in all ethnic groups around the world. Symptoms such as hallucinations
   and delusions usually start between ages 16 and 30. Men tend to
   experience symptoms a little earlier than women. Most of the time,
   people do not get schizophrenia after age 45. Schizophrenia rarely
   occurs in children, but awareness of childhood-onset schizophrenia is
   increasing.

   It can be difficult to diagnose schizophrenia in teens. This is because
   the first signs can include a change of friends, a drop in grades,
   sleep problems, and irritability—behaviors that are common among teens.
   A combination of factors can predict schizophrenia in up to 80% of
   youth who are at high risk of developing the illness. These factors
   include isolating oneself and withdrawing from others, an increase in
   unusual thoughts and suspicions, and a family history of psychosis. In
   young people who develop the disease, this stage of the disorder is
   called the "prodromal" period.

Signs & Symptoms

   The symptoms of schizophrenia fall into three broad categories:
   positive symptoms, negative symptoms, and cognitive symptoms.

   Positive symptoms

   Positive symptoms are psychotic behaviors not seen in healthy people.
   People with positive symptoms often "lose touch" with reality. These
   symptoms can come and go. Sometimes they are severe and at other times
   hardly noticeable, depending on whether the individual is receiving
   treatment. They include the following:

   Hallucinations are things a person sees, hears, smells, or feels that
   no one else can see, hear, smell, or feel. "Voices" are the most common
   type of hallucination in schizophrenia. Many people with the disorder
   hear voices. The voices may talk to the person about his or her
   behavior, order the person to do things, or warn the person of danger.
   Sometimes the voices talk to each other. People with schizophrenia may
   hear voices for a long time before family and friends notice the
   problem.

   Other types of hallucinations include seeing people or objects that are
   not there, smelling odors that no one else detects, and feeling things
   like invisible fingers touching their bodies when no one is near.

   Delusions are false beliefs that are not part of the person's culture
   and do not change. The person believes delusions even after other
   people prove that the beliefs are not true or logical. People with
   schizophrenia can have delusions that seem bizarre, such as believing
   that neighbors can control their behavior with magnetic waves. They may
   also believe that people on television are directing special messages
   to them, or that radio stations are broadcasting their thoughts aloud
   to others. Sometimes they believe they are someone else, such as a
   famous historical figure. They may have paranoid delusions and believe
   that others are trying to harm them, such as by cheating, harassing,
   poisoning, spying on, or plotting against them or the people they care
   about. These beliefs are called "delusions of persecution."

   Thought disorders are unusual or dysfunctional ways of thinking. One
   form of thought disorder is called "disorganized thinking." This is
   when a person has trouble organizing his or her thoughts or connecting
   them logically. They may talk in a garbled way that is hard to
   understand. Another form is called "thought blocking." This is when a
   person stops speaking abruptly in the middle of a thought. When asked
   why he or she stopped talking, the person may say that it felt as if
   the thought had been taken out of his or her head. Finally, a person
   with a thought disorder might make up meaningless words, or
   "neologisms."

   Movement disorders may appear as agitated body movements. A person with
   a movement disorder may repeat certain motions over and over. In the
   other extreme, a person may become catatonic. Catatonia is a state in
   which a person does not move and does not respond to others. Catatonia
   is rare today, but it was more common when treatment for schizophrenia
   was not available.

   Negative symptoms

   Negative symptoms are associated with disruptions to normal emotions
   and behaviors. These symptoms are harder to recognize as part of the
   disorder and can be mistaken for depression or other conditions. These
   symptoms include the following:
     * "Flat affect" (a person's face does not move or he or she talks in
       a dull or monotonous voice)
     * Lack of pleasure in everyday life
     * Lack of ability to begin and sustain planned activities
     * Speaking little, even when forced to interact.

   People with negative symptoms need help with everyday tasks. They often
   neglect basic personal hygiene. This may make them seem lazy or
   unwilling to help themselves, but the problems are symptoms caused by
   the schizophrenia.

   Cognitive symptoms

   Cognitive symptoms are subtle. Like negative symptoms, cognitive
   symptoms may be difficult to recognize as part of the disorder. Often,
   they are detected only when other tests are performed. Cognitive
   symptoms include the following:
     * Poor "executive functioning" (the ability to understand information
       and use it to make decisions)
     * Trouble focusing or paying attention
     * Problems with "working memory" (the ability to use information
       immediately after learning it).

   Cognitive symptoms often make it hard to lead a normal life and earn a
   living. They can cause great emotional distress.

Treatments

   Because the causes of schizophrenia are still unknown, treatments focus
   on eliminating the symptoms of the disease. Treatments include
   antipsychotic medications and various psychosocial treatments.

   Antipsychotic medications

   Antipsychotic medications have been available since the mid-1950's. The
   older types are called conventional or "typical" antipsychotics. Some
   of the more commonly used typical medications include:
     * Chlorpromazine (Thorazine)
     * Haloperidol (Haldol)
     * Perphenazine (Etrafon, Trilafon)
     * Fluphenazine (Prolixin).

   In the 1990's, new antipsychotic medications were developed. These new
   medications are called second generation, or "atypical" antipsychotics.

   One of these medications, clozapine (Clozaril) is an effective
   medication that treats psychotic symptoms, hallucinations, and breaks
   with reality. But clozapine can sometimes cause a serious problem
   called agranulocytosis, which is a loss of the white blood cells that
   help a person fight infection. People who take clozapine must get their
   white blood cell counts checked every week or two. This problem and the
   cost of blood tests make treatment with clozapine difficult for many
   people. But clozapine is potentially helpful for people who do not
   respond to other antipsychotic medications.

   Other atypical antipsychotics were also developed. None cause
   agranulocytosis. Examples include:
     * Risperidone (Risperdal)
     * Olanzapine (Zyprexa)
     * Quetiapine (Seroquel)
     * Ziprasidone (Geodon)
     * Aripiprazole (Abilify)
     * Paliperidone (Invega).

   What are the side effects?

   Some people have side effects when they start taking these medications.
   Most side effects go away after a few days and often can be managed
   successfully. People who are taking antipsychotics should not drive
   until they adjust to their new medication. Side effects of many
   antipsychotics include:
     * Drowsiness
     * Dizziness when changing positions
     * Blurred vision
     * Rapid heartbeat
     * Sensitivity to the sun
     * Skin rashes
     * Menstrual problems for women.

   Atypical antipsychotic medications can cause major weight gain and
   changes in a person's metabolism. This may increase a person's risk of
   getting diabetes and high cholesterol. A person's weight, glucose
   levels, and lipid levels should be monitored regularly by a doctor
   while taking an atypical antipsychotic medication.

   Typical antipsychotic medications can cause side effects related to
   physical movement, such as:
     * Rigidity
     * Persistent muscle spasms
     * Tremors
     * Restlessness.

   Long-term use of typical antipsychotic medications may lead to a
   condition called tardive dyskinesia (TD). TD causes muscle movements a
   person can't control. The movements commonly happen around the mouth.
   TD can range from mild to severe, and in some people the problem cannot
   be cured. Sometimes people with TD recover partially or fully after
   they stop taking the medication.

   TD happens to fewer people who take the atypical antipsychotics, but
   some people may still get TD. People who think that they might have TD
   should check with their doctor before stopping their medication.

   How are antipsychotics taken and how do people respond to them?

   Antipsychotics are usually in pill or liquid form. Some anti-psychotics
   are shots that are given once or twice a month.

   Symptoms of schizophrenia, such as feeling agitated and having
   hallucinations, usually go away within days. Symptoms like delusions
   usually go away within a few weeks. After about six weeks, many people
   will see a lot of improvement.

   However, people respond in different ways to antipsychotic medications,
   and no one can tell beforehand how a person will respond. Sometimes a
   person needs to try several medications before finding the right one.
   Doctors and patients can work together to find the best medication or
   medication combination, as well as the right dose.

   Some people may have a relapse-their symptoms come back or get worse.
   Usually, relapses happen when people stop taking their medication, or
   when they only take it sometimes. Some people stop taking the
   medication because they feel better or they may feel they don't need it
   anymore. But no one should stop taking an antipsychotic medication
   without talking to his or her doctor. When a doctor says it is okay to
   stop taking a medication, it should be gradually tapered off, never
   stopped suddenly.

   How do antipsychotics interact with other medications?

   Antipsychotics can produce unpleasant or dangerous side effects when
   taken with certain medications. For this reason, all doctors treating a
   patient need to be aware of all the medications that person is taking.
   Doctors need to know about prescription and over-the-counter medicine,
   vitamins, minerals, and herbal supplements. People also need to discuss
   any alcohol or other drug use with their doctor.

   To find out more about how antipsychotics work, the National Institute
   of Mental Health (NIMH) funded a study called CATIE (Clinical
   Antipsychotic Trials of Intervention Effectiveness). This study
   compared the effectiveness and side effects of five antipsychotics used
   to treat people with schizophrenia. In general, the study found that
   the older typical antipsychotic perphenazine (Trilafon) worked as well
   as the newer, atypical medications. But because people respond
   differently to different medications, it is important that treatments
   be designed carefully for each person. More information about CATIE is
   on the NIMH website.

   Psychosocial treatments

   Psychosocial treatments can help people with schizophrenia who are
   already stabilized on antipsychotic medication. Psychosocial treatments
   help these patients deal with the everyday challenges of the illness,
   such as difficulty with communication, self-care, work, and forming and
   keeping relationships. Learning and using coping mechanisms to address
   these problems allow people with schizophrenia to socialize and attend
   school and work.

   Patients who receive regular psychosocial treatment also are more
   likely to keep taking their medication, and they are less likely to
   have relapses or be hospitalized. A therapist can help patients better
   understand and adjust to living with schizophrenia. The therapist can
   provide education about the disorder, common symptoms or problems
   patients may experience, and the importance of staying on medications.
   For more information on psychosocial treatments, see the
   psychotherapies section on the NIMH website.

   Illness management skills. People with schizophrenia can take an active
   role in managing their own illness. Once patients learn basic facts
   about schizophrenia and its treatment, they can make informed decisions
   about their care. If they know how to watch for the early warning signs
   of relapse and make a plan to respond, patients can learn to prevent
   relapses. Patients can also use coping skills to deal with persistent
   symptoms.

   Integrated treatment for co-occurring substance abuse. Substance abuse
   is the most common co-occurring disorder in people with schizophrenia.
   But ordinary substance abuse treatment programs usually do not address
   this population's special needs. When schizophrenia treatment programs
   and drug treatment programs are used together, patients get better
   results.

   Rehabilitation. Rehabilitation emphasizes social and vocational
   training to help people with schizophrenia function better in their
   communities. Because schizophrenia usually develops in people during
   the critical career-forming years of life (ages 18 to 35), and because
   the disease makes normal thinking and functioning difficult, most
   patients do not receive training in the skills needed for a job.

   Rehabilitation programs can include job counseling and training, money
   management counseling, help in learning to use public transportation,
   and opportunities to practice communication skills. Rehabilitation
   programs work well when they include both job training and specific
   therapy designed to improve cognitive or thinking skills. Programs like
   this help patients hold jobs, remember important details, and improve
   their functioning.

   Family education. People with schizophrenia are often discharged from
   the hospital into the care of their families. So it is important that
   family members know as much as possible about the disease. With the
   help of a therapist, family members can learn coping strategies and
   problem-solving skills. In this way the family can help make sure their
   loved one sticks with treatment and stays on his or her medication.
   Families should learn where to find outpatient and family services.

   Cognitive behavioral therapy. Cognitive behavioral therapy (CBT) is a
   type of psychotherapy that focuses on thinking and behavior. CBT helps
   patients with symptoms that do not go away even when they take
   medication. The therapist teaches people with schizophrenia how to test
   the reality of their thoughts and perceptions, how to "not listen" to
   their voices, and how to manage their symptoms overall. CBT can help
   reduce the severity of symptoms and reduce the risk of relapse.

   Self-help groups. Self-help groups for people with schizophrenia and
   their families are becoming more common. Professional therapists
   usually are not involved, but group members support and comfort each
   other. People in self-help groups know that others are facing the same
   problems, which can help everyone feel less isolated. The networking
   that takes place in self-help groups can also prompt families to work
   together to advocate for research and more hospital and community
   treatment programs. Also, groups may be able to draw public attention
   to the discrimination many people with mental illnesses face.

Living With

   How can you help a person with schizophrenia?

   People with schizophrenia can get help from professional case managers
   and caregivers at residential or day programs. However, family members
   usually are a patient's primary caregivers.

   People with schizophrenia often resist treatment. They may not think
   they need help because they believe their delusions or hallucinations
   are real. In these cases, family and friends may need to take action to
   keep their loved one safe. Laws vary from state to state, and it can be
   difficult to force a person with a mental disorder into treatment or
   hospitalization. But when a person becomes dangerous to himself or
   herself, or to others, family members or friends may have to call the
   police to take their loved one to the hospital.

   Treatment at the hospital. In the emergency room, a mental health
   professional will assess the patient and determine whether a voluntary
   or involuntary admission is needed. For a person to be admitted
   involuntarily, the law states that the professional must witness
   psychotic behavior and hear the person voice delusional thoughts.
   Family and friends can provide needed information to help a mental
   health professional make a decision.

   After a loved one leaves the hospital. Family and friends can help
   their loved ones get treatment and take their medication once they go
   home. If patients stop taking their medication or stop going to
   follow-up appointments, their symptoms likely will return. Sometimes
   symptoms become severe for people who stop their medication and
   treatment. This is dangerous, since they may become unable to care for
   themselves. Some people end up on the street or in jail, where they
   rarely receive the kind of help they need.

   Family and friends can also help patients set realistic goals and learn
   to function in the world. Each step toward these goals should be small
   and taken one at a time. The patient will need support during this
   time. When people with a mental illness are pressured and criticized,
   they usually do not get well. Often, their symptoms may get worse.
   Telling them when they are doing something right is the best way to
   help them move forward.

   It can be difficult to know how to respond to someone with
   schizophrenia who makes strange or clearly false statements. Remember
   that these beliefs or hallucinations seem very real to the person. It
   is not helpful to say they are wrong or imaginary. But going along with
   the delusions is not helpful, either. Instead, calmly say that you see
   things differently. Tell them that you acknowledge that everyone has
   the right to see things his or her own way. In addition, it is
   important to understand that schizophrenia is a biological illness.
   Being respectful, supportive, and kind without tolerating dangerous or
   inappropriate behavior is the best way to approach people with this
   disorder.

   Are people with schizophrenia violent?

   People with schizophrenia are not usually violent. In fact, most
   violent crimes are not committed by people with schizophrenia. However,
   some symptoms are associated with violence, such as delusions of
   persecution. Substance abuse may also increase the chance a person will
   become violent. If a person with schizophrenia becomes violent, the
   violence is usually directed at family members and tends to take place
   at home.

   The risk of violence among people with schizophrenia is small. But
   people with the illness attempt suicide much more often than others.
   About 10 percent (especially young adult males) die by suicide. It is
   hard to predict which people with schizophrenia are prone to suicide.
   If you know someone who talks about or attempts suicide, help him or
   her find professional help right away.

   What about substance abuse?

   Some people who abuse drugs show symptoms similar to those of
   schizophrenia. Therefore, people with schizophrenia may be mistaken for
   people who are affected by drugs. Most researchers do not believe that
   substance abuse causes schizophrenia. However, people who have
   schizophrenia are much more likely to have a substance or alcohol abuse
   problem than the general population.

   Substance abuse can make treatment for schizophrenia less effective.
   Some drugs, like marijuana and stimulants such as amphetamines or
   cocaine, may make symptoms worse. In fact, research has found
   increasing evidence of a link between marijuana and schizophrenia
   symptoms. In addition, people who abuse drugs are less likely to follow
   their treatment plan.

   Schizophrenia and smoking

   Addiction to nicotine is the most common form of substance abuse in
   people with schizophrenia. They are addicted to nicotine at three times
   the rate of the general population (75 to 90 percent vs. 25 to 30
   percent).

   The relationship between smoking and schizophrenia is complex. People
   with schizophrenia seem to be driven to smoke, and researchers are
   exploring whether there is a biological basis for this need. In
   addition to its known health hazards, several studies have found that
   smoking may make antipsychotic drugs less effective.

   Quitting smoking may be very difficult for people with schizophrenia
   because nicotine withdrawal may cause their psychotic symptoms to get
   worse for a while. Quitting strategies that include nicotine
   replacement methods may be easier for patients to handle. Doctors who
   treat people with schizophrenia should watch their patients' response
   to antipsychotic medication carefully if the patient decides to start
   or stop smoking.

Clinical Trials

   NIMH supports research studies on mental health and disorders. See
   also: A Participant's Guide to Mental Health Clinical Research.

   Participate, refer a patient or learn about results of studies in
   ClinicalTrials.gov , the NIH/National Library of Medicine's registry of
   federally and privately funded clinical trials for all disease.

   Find NIH-funded studies currently recruiting participants with
   schizophrenia.

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                           Types of Schizophrenia

                          By Michael Bengston, M.D.
                                ~ 5 min read

   Pages: 1 2All

   The kinds of symptoms that are utilized to make a diagnosis of
   schizophrenia differ between affected people and may change from one
   year to the next within the same person as the disease progresses.
   Different subtypes of schizophrenia are defined according to the most
   significant and predominant characteristics present in each person at
   each point in time. The result is that one person may be diagnosed with
   different subtypes over the course of his illness.

Schizophrenia: Paranoid Subtype

   The defining feature of the paranoid subtype (also known as paranoid
   schizophrenia) is the presence of auditory hallucinations or prominent
   delusional thoughts about persecution or conspiracy. However, people
   with this subtype may be more functional in their ability to work and
   engage in relationships than people with other subtypes of
   schizophrenia. The reasons are not entirely clear, but may partly
   reflect that people suffering from this subtype often do not exhibit
   symptoms until later in life and have achieved a higher level of
   functioning before the onset of their illness. People with the paranoid
   subtype may appear to lead fairly normal lives by successful management
   of their disorder.

   Paranoid schizophrenia is the most common subtype.

   People diagnosed with the paranoid subtype may not appear odd or
   unusual and may not readily discuss the symptoms of their illness.
   Typically, the hallucinations and delusions revolve around some
   characteristic theme, and this theme often remains fairly consistent
   over time. A person’s temperaments and general behaviors often are
   related to the content of the disturbance of thought. For example,
   people who believe that they are being persecuted unjustly may be
   easily angered and become hostile. Often, paranoid schizophrenics will
   come to the attention of mental health professionals only when there
   has been some major stress in their life that has caused an increase in
   their symptoms. At that point, sufferers may recognize the need for
   outside help or act in a fashion to bring attention to themselves.

   Since there may be no observable features, the evaluation requires
   sufferers to be somewhat open to discussing their thoughts. If there is
   a significant degree of suspiciousness or paranoia present, people may
   be very reluctant to discuss these issues with a stranger.

   There is a broad spectrum to the nature and severity of symptoms that
   may be present at any one time. When symptoms are in a phase of
   exacerbation or worsening, there may be some disorganization of the
   thought processes. At this time, people may have more trouble than
   usual remembering recent events, speaking coherently or generally
   behaving in an organized, rational manner. While these features are
   more characteristic of other subtypes, they can be present to differing
   degrees in people with the paranoid subtype, depending upon the current
   state of their illness. Supportive friends or family members often may
   be needed at such times to help the symptomatic person get professional
   help.

Schizophrenia: Disorganized Subtype

   As the name implies, this subtype’s predominant feature is
   disorganization of the thought processes. As a rule, hallucinations and
   delusions are less pronounced, although there may be some evidence of
   these symptoms. These people may have significant impairments in their
   ability to maintain the activities of daily living. Even the more
   routine tasks, such as dressing, bathing or brushing teeth, can be
   significantly impaired or lost.

   Often, there is impairment in the emotional processes of the
   individual. For example, these people may appear emotionally unstable,
   or their emotions may not seem appropriate to the context of the
   situation. They may fail to show ordinary emotional responses in
   situations that evoke such responses in healthy people. Mental health
   professionals refer to this particular symptom as blunted or flat
   affect. Additionally, these people may have an inappropriately jocular
   or giddy appearance, as in the case of a patient who chuckles
   inappropriately through a funeral service or other solemn occasion.

   People diagnosed with this subtype also may have significant impairment
   in their ability to communicate effectively. At times, their speech can
   become virtually incomprehensible, due to disorganized thinking. In
   such cases, speech is characterized by problems with the utilization
   and ordering of words in conversational sentences, rather than with
   difficulties of enunciation or articulation. In the past, the term
   hebephrenic has been used to describe this subtype.

   Pages: 1 2All


     *
     *
     *
     *

   APA Reference
   Bengston, M. (2006). Types of Schizophrenia. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/lib/types-of-schizophrenia/000714
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                           Types of Schizophrenia

                          By Michael Bengston, M.D.
                                ~ 5 min read

   Pages: 1 2All

Schizophrenia: Catatonic Subtype

   The predominant clinical features seen in the catatonic subtype involve
   disturbances in movement. Affected people may exhibit a dramatic
   reduction in activity, to the point that voluntary movement stops, as
   in catatonic stupor. Alternatively, activity can dramatically increase,
   a state known as catatonic excitement.

   Other disturbances of movement can be present with this subtype.
   Actions that appear relatively purposeless but are repetitively
   performed, also known as stereotypic behavior, may occur, often to the
   exclusion of involvement in any productive activity.

   Patients may exhibit an immobility or resistance to any attempt to
   change how they appear. They may maintain a pose in which someone
   places them, sometimes for extended periods of time. This symptom
   sometimes is referred to as waxy flexibility. Some patients show
   considerable physical strength in resistance to repositioning attempts,
   even though they appear to be uncomfortable to most people.

   Affected people may voluntarily assume unusual body positions, or
   manifest unusual facial contortions or limb movements. This set of
   symptoms sometimes is confused with another disorder called tardive
   dyskinesia, which mimics some of these same, odd behaviors. Other
   symptoms associated with the catatonic subtype include an almost
   parrot-like repeating of what another person is saying (echolalia) or
   mimicking the movements of another person (echopraxia). Echolalia and
   echopraxia also are seen in Tourette’s Syndrome.

Schizophrenia: Undifferentiated Subtype

   The undifferentiated subtype is diagnosed when people have symptoms of
   schizophrenia that are not sufficiently formed or specific enough to
   permit classification of the illness into one of the other subtypes.

   The symptoms of any one person can fluctuate at different points in
   time, resulting in uncertainty as to the correct subtype
   classification. Other people will exhibit symptoms that are remarkably
   stable over time but still may not fit one of the typical subtype
   pictures. In either instance, diagnosis of the undifferentiated subtype
   may best describe the mixed clinical syndrome.

Schizophrenia: Residual Subtype

   This subtype is diagnosed when the patient no longer displays prominent
   symptoms. In such cases, the schizophrenic symptoms generally have
   lessened in severity. Hallucinations, delusions or idiosyncratic
   behaviors may still be present, but their manifestations are
   significantly diminished in comparison to the acute phase of the
   illness.

   Just as the symptoms of schizophrenia are diverse, so are its
   ramifications. Different kinds of impairment affect each patient’s life
   to varying degrees. Some people require custodial care in state
   institutions, while others are gainfully employed and can maintain an
   active family life. However, the majority of patients are at neither of
   these extremes. Most will have a waxing and waning course marked with
   some hospitalizations and some assistance from outside support sources.

   People having a higher level of functioning before the start of their
   illness typically have a better outcome. In general, better outcomes
   are associated with brief episodes of symptoms worsening followed by a
   return to normal functioning. Women have a better prognosis for higher
   functioning than men, as do patients with no apparent structural
   abnormalities of the brain.

   In contrast, a poorer prognosis is indicated by a gradual or insidious
   onset, beginning in childhood or adolescence; structural brain
   abnormalities, as seen on imaging studies; and failure to return to
   prior levels of functioning after acute episodes.

                                                        » Next in Series:
                                                   Causes of Schizophrenia

   Schizophrenia Table of Contents
     * Introduction to Schizophrenia
     * Symptoms of Schizophrenia
     * Types of Schizophrenia
     * Causes of Schizophrenia
     * An Introduction to the Treatment of Schizophrenia
     * Treatment of Schizophrenia
     * Living with Schizophrenia
     * Helpful Hints About Schizophrenia for Family Members & Others

   Pages: 1 2All


     *
     *
     *
     *

   APA Reference
   Bengston, M. (2006). Types of Schizophrenia. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/lib/types-of-schizophrenia/000714
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     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 2 Sep 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

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                           Schizophrenia Symptoms

                           By Psych Central Staff

   Page:« 1 2View All»

   Schizophrenia is a mental disorder that is characterized by at least 2
   of the following  symptoms, for at least one month:
     * Delusions
     * Hallucinations
     * Disorganized speech (e.g., frequent derailment or incoherence)
     * Grossly disorganized or catatonic behavior
     * A set of three negative symptoms (a “flattening” of one’s
       emotions, alogia, avolition; see below)

   Only one of the above symptoms is required to make the diagnosis of
   schizophrenia if the person’s delusions are bizarre or if the
   hallucinations consist of a voice keeping up a running commentary
   on the person’s behavior or thoughts, or two or more voices conversing
   with each other.

                              Positive Symptoms
     * Delusions
     * Hallucinations
     * Disorganized thinking
     * Agitation

                              Negative Symptoms
     * Affective flattening- The person’s range of emotional expression is
       clearly diminished; poor eye contract; reduced body language
     * Alogia- A poverty of speech, such as brief, empty replies
     * Avolition – Inability to initiate and persist in goal-directed
       activities (such as school or work)

   Although the above symptoms must be present for at least one (1) month,
   there also needs to be continuous signs of the disturbance that persist
   for at least six (6) months.  During this period, the signs of the
   disorder may be present in a milder form, for instance as just odd
   beliefs or unusual perceptual experiences. During this 6 month period,
   at least two of the above criteria must be met, or only the criteria of
   Negative Symptoms must be present — if even just in milder form.

   Onset of schizophrenia prior to adolescence is rare. The peak age at
   onset for the first psychotic episode is in the early- to mid-20s for
   males and in the late-20s for females. Though active symptoms typically
   do not emerge until an individual is in their 20′s,
   oftentimes prodromal symptoms will precede the first psychotic episode,
   characterized by milder forms of hallucinations or delusions. For
   example, individuals may express a variety of unusual or odd beliefs
   that are not of delusional proportions (e.g., ideas of reference or
   magical thinking); they may have unusual perceptual experiences (e.g.,
   sensing the presence of an unseen person); their speech may be
   generally understandable but vague; and their behavior may be unusual
   but not grossly disorganized (e.g., mumbling in public).

   Individuals with schizophrenia evidence large distress and impairments
   in various life domains. Functioning in areas such as work,
   interpersonal relations, or self-care must be markedly below the level
   achieved prior to the onset of the symptoms to receive the diagnosis
   (or when the onset is in childhood or adolescence, failure to achieve
   expected level of interpersonal, academic, or occupational
   achievement).

   Schizoaffective Disorder and Mood Disorder With Psychotic Features must
   be considered as alternative explanations for the symptoms and have
   been ruled out. The disturbance must also not be due to the direct
   physiological effects of use or abuse of a substance (e.g., alcohol,
   drugs, medications) or a general medical condition.

   If there is a history of Autistic Disorder or another Pervasive
   Developmental Disorder, the additional diagnosis of Schizophrenia is
   made only if prominent delusions or hallucinations are also present for
   at least a month (or less if successfully treated).

   0.3%–0.7% of individuals appear to acquire schizophrenia. although
   there is reported variation by race/ethnicity, across countries, and by
   geographic origin for immigrants and children of immigrants. The sex
   ratio differs across samples and populationHostility and aggression can
   be associated with schizophrenia, although spontaneous or random
   assault is uncommon. Aggression is more frequent for younger males and
   for individuals with a past history of violence, non-adherence with
   treatment, substance abuse, and impulsivity. It should be noted that
   the vast majority of persons with schizophrenia are not aggressive and
   are more frequently victimized than are individuals in the general
   population.


Entry has been updated for DSM-5; diagnostic code 295.90.

The old criteria in the DSM-IV divided schizophrenia by different Types.
Though we not longer use such specifiers in the updated DSM-5, they remain
below for informational/historical purposes.

A brief list of types of schizophrenia, according to DSM-IV:

     * Paranoid schizophrenia– a person feels extremely suspicious,
       persecuted, grandiose, or experiences a combination of these
       emotions.
     * Disorganized schizophrenia  — a person is often incoherent but may
       not have delusions.
     * Catatonic schizophrenia– a person is withdrawn, mute, negative and
       often assumes very unusual postures.
     * Residual schizophrenia — a person is no longer delusion or
       hallucinating, but has no motivation or interest in life. These
       symptoms can be most devastating.


   Page: 1 2View All


   IFRAME:
   http://platform.twitter.com/widgets/tweet_button.html?url=http://psych.
   ly/12WOIxz&counturl=http://psychcentral.com/disorders/schizophrenia-sym
   ptoms/&text=Schizophrenia
   Symptoms&count=vertical&lang=en&via=psychcentral&related=

     *
     *
     *
     *

   « Mental Disorders Index


   APA Reference
   Psych Central. (2014). Schizophrenia Symptoms. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/disorders/schizophrenia-symptoms/

   Symptom criteria summarized from:
   American Psychiatric Association. (2013). Diagnostic and statistical
   manual of mental disorders, fifth edition. Washington, DC: American
   Psychiatric Association.
           or
   American Psychiatric Association. (1994). Diagnostic and statistical
   manual of mental disorders, fourth edition. Washington, DC: American
   Psychiatric Association.

     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 22 Jun 2014
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

     Long-Acting Treatments for Schizophrenia

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     Betrayal & Hearing Voices

     Art Therapy: Beneficial Schizophrenia Treatment?


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                   Illuminating 13 Myths of Schizophrenia

                       By Margarita Tartakovsky, M.S.
                                ~ 6 min read

   It’s safe to say that no mental disorder is more shrouded in mystery,
   misunderstanding and fear than schizophrenia. “The modern-day
   equivalent of leprosy” is how renowned research psychiatrist E. Fuller
   Torrey, M.D., refers to schizophrenia in his excellent book, Surviving
   Schizophrenia: A Manual for Families, Patients, and Providers.

   While 85 percent of Americans recognize that schizophrenia is a
   disorder, only 24 percent are actually familiar with it. And according
   to a 2008 survey by the National Alliance on Mental Illness (NAMI), 64
   percent can’t recognize its symptoms or think the symptoms include a
   “split” or multiple personalities. (They don’t.)

   Aside from ignorance, images of the aggressive, sadistic
   “schizophrenic” are plentiful in the media. Such stereotypes only
   further the stigma and quash any shred of sympathy for individuals with
   this illness, writes Dr. Torrey. Stigma has a slew of negative
   consequences. It’s been associated with reduced housing and employment
   opportunities, diminished quality of life, low self-esteem and more
   symptoms and stress (see Penn, Chamberlin & Mueser, 2003).

   So it’s bad enough that people with schizophrenia are afflicted with a
   terrible disease. But they also have to deal with the confusion, fear
   and disgust of others. Whether your loved one has schizophrenia or
   you’d like to learn more, gaining a better understanding of it helps
   demystify the disease and is a huge help to those who suffer from it.

   Below are some pervasive myths — followed by actual facts — regarding
   schizophrenia.

   1. Individuals with schizophrenia all have the same symptoms.

   For starters, there are different types of schizophrenia. Even
   individuals diagnosed with the same subtype of schizophrenia often look
   very different. Schizophrenia is “a huge, huge range of people and
   problems,” said Robert E. Drake, M.D., Ph.D, professor of psychiatry
   and of community and family medicine at Dartmouth Medical School.

   Part of the reason that schizophrenia is so mysterious is because we’re
   unable to put ourselves in the shoes of someone with the disorder. It’s
   simply hard to imagine what having schizophrenia would be like.
   Everyone experiences sadness, anxiety and anger, but schizophrenia
   seems so out of our realm of feeling and understanding. It may help to
   adjust our perspective. Dr. Torrey writes:

     Those of us who have not had this disease should ask ourselves, for
     example, how we would feel if our brain began playing tricks on us,
     if unseen voices shouted at us, if we lost the capacity to feel
     emotions, and if we lost the ability to reason logically.

   2. People with schizophrenia are dangerous, unpredictable and out of
   control.

   “When their illness is treated with medication and psychosocial
   interventions, individuals with schizophrenia are no more violent than
   the general population,” said Dawn I. Velligan, Ph.D, professor and
   co-director of the Division of Schizophrenia and Related Disorders at
   the Department of Psychiatry, UT Health Science Center at San Antonio.
   Also, “People with schizophrenia more often tend to be victims rather
   than perpetrators of violence although untreated mental illness and
   substance abuse often increase the risk of aggressive behavior,” said
   Irene S. Levine, Ph.D, psychologist and co-author of Schizophrenia for
   Dummies.

   3. Schizophrenia is a character flaw.

   Lazy, lacking in motivation, lethargic, easily confused…the list of
   “qualities” individuals with schizophrenia appear to have goes on and
   on. However, the idea that schizophrenia is a character defect “is no
   more realistic than suggesting that someone could prevent his epileptic
   seizures if he really wanted to or that someone could ‘decide’ not to
   have cancer if he ate the right foods. What often appears as character
   defects are symptoms of schizophrenia,” write Levine and co-author
   Jerome Levine, M.D., in Schizophrenia for Dummies.

   4. Cognitive decline is a major symptom of schizophrenia.

   Seemingly unmotivated individuals most likely experience cognitive
   difficulties with problem solving, attention, memory and processing.
   They may forget to take their medication. They may ramble and not make
   sense. They may have a tough time organizing their thoughts. Again,
   these are symptoms of schizophrenia, which have nothing to do with
   character or personality.

   5. There are psychotic and non-psychotic people.

   The public and clinicians alike view psychosis as categorical — you’re
   either psychotic or you’re not — instead of symptoms residing on a
   continuum, said Demian Rose, M.D., Ph.D, medical director of the
   University of California, San Francisco PART Program and director of
   the UCSF Early Psychosis Clinic. For instance, most people will agree
   that individuals aren’t simply depressed or happy. There are gradients
   of depression, from mild one-day melancholy to deep, crippling clinical
   depression. Similarly, schizophrenia symptoms are not fundamentally
   different brain processes, but lie on a continuum with normal cognitive
   processes, Dr. Rose said. Auditory hallucinations may seem
   extraordinarily different but how often have you had a song stuck in
   your head that you can hear pretty clearly?

   6. Schizophrenia develops quickly.

   “It’s quite rare to have a big drop in functioning,” Dr. Rose said.
   Schizophrenia tends to develop slowly. Initial signs often show during
   adolescence. These signs typically include school, social and work
   decline, difficulties managing relationships and problems with
   organizing information, he said. Again, symptoms lie on a continuum. In
   schizophrenia’s beginning stages, an individual may not hear voices.
   Instead, he may hear whispers, which he can’t make out. This
   “prodromal” period — before the onset of schizophrenia — is the perfect
   time to intervene and seek treatment.

   7. Schizophrenia is purely genetic.

   “Studies have shown that in pairs of identical twins (who share an
   identical genome) the prevalence of developing the illness is 48
   percent,” said Sandra De Silva, Ph.D, psychosocial treatment
   co-director and outreach director at the Staglin Music Festival Center
   for the Assessment and Prevention of Prodromal States (CAPPS) at UCLA,
   departments of psychology and psychiatry. Because other factors are
   involved, it’s possible to reduce the risk of developing the illness,
   she added. There are various prodromal programs that focus on helping
   at-risk adolescents and adults.

   Along with genetics, research has shown that stress and family
   environment can play a big role in increasing a person’s susceptibility
   to psychosis. “While we can’t change genetic vulnerability, we can
   reduce the amount of stress in someone’s life, build coping skills to
   improve the way we respond to stress, and create a protective low-key,
   calm family environment without a lot of conflict and tension in hopes
   of reducing the risk of illness progression,” De Sliva said.

   8. Schizophrenia is untreatable.

   “While schizophrenia is not curable, it is an eminently treatable and
   manageable chronic illness, just like diabetes or heart disease,”
   Levine said. The key is to get the right treatment for your needs. See
   Living with Schizophrenia here for details.

   9. Sufferers need to be hospitalized.

   Most individuals with schizophrenia “do well living in the community
   with outpatient treatment,” Velligan said. Again, the key is the right
   treatment and adhering to that treatment, especially taking medication
   as prescribed.

   10. People with schizophrenia can’t lead productive lives.

   “Many individuals can lead happy and productive lives,” Velligan said.
   In a 10-year study of 130 individuals with schizophrenia and substance
   abuse — which co-occurs in nearly 50 percent of patients — from the New
   Hampshire Dual Diagnosis Study, many gained control over both
   disorders, reducing their episodes of hospitalization and homelessness,
   living on their own and achieving a better quality of life (Drake,
   McHugo, Xie, Fox, Packard & Helmstetter, 2006). Specifically, “62.7
   percent were controlling symptoms of schizophrenia; 62.5 percent were
   actively attaining remissions from substance abuse; 56.8 percent were
   in independent living situations; 41.4 percent were competitively
   employed; 48.9 percent had regular social contacts with non–substance
   abusers; and 58.3 percent expressed overall life satisfaction.”

   11. Medications make sufferers zombies.

   When we think of antipsychotic medication for schizophrenia, we
   automatically think of adjectives like lethargic, listless,
   uninterested and vacant. Many believe medication causes these sorts of
   symptoms. However, most often these symptoms are either from
   schizophrenia itself or because of overmedication. Zombie-like
   reactions are “relatively minor, compared with the number of patients
   who have never been given an adequate trial of available medications,”
   according to Dr. Torrey in Surviving Schizophrenia.

   12. Antipsychotic medications are worse than the illness itself.

   Medication is the mainstay of schizophrenia treatment. Antipsychotic
   medications effectively reduce hallucinations, delusions, confusing
   thoughts and bizarre behaviors. These agents can have severe side
   effects and can be fatal, but this is rare. “Antipsychotic drugs, as a
   group, are one of the safest groups of drugs in common use and are the
   greatest advance in the treatment of schizophrenia that has occurred to
   date,” Dr. Torrey writes.

   13. Individuals with schizophrenia can never regain normal functioning.

   Unlike dementia, which worsens over time or doesn’t improve,
   schizophrenia seems to be a problem that’s reversible, Dr. Rose said.
   There’s no line that once it’s crossed signifies that there’s no hope
   for a person with schizophrenia, he added.

   References

   Drake, R.E., McHugo, G.J., Xie, H., Fox, M., Packard, J., &
   Helmstetter, B. (2006). Ten-Year Recovery Outcomes for Clients With
   Co-Occurring Schizophrenia and Substance Use Disorders>. Schizophrenia
   Bulletin, 32, 464-473.

   Penn, D.L., Chamberlin, C., & Mueser, K.T. (2003). The effects of a
   documentary film about schizophrenia on psychiatric stigma.
   Schizophrenia Bulletin, 29, 383-391.


     *
     *
     *
     *

   Margarita Tartakovsky, M.S. is an Associate Editor at Psych Central and
   blogs regularly about eating and self-image issues on her own blog,
   Weightless.
   APA Reference
   Tartakovsky, M. (2010). Illuminating 13 Myths of Schizophrenia. Psych
   Central. Retrieved on February 4, 2015, from
   http://psychcentral.com/lib/illuminating-13-myths-of-schizophrenia/0002
   709
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         Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
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     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
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                         What Causes Schizophrenia?

                             By Brian Smith, MS
                                ~ 3 min read

   What Causes Schizophrenia? The causes of schizophrenia, like all mental
   disorders, are not completely understood or known at this time.

   There is no known single cause of schizophrenia. Many diseases, such as
   heart disease, result from an interplay of genetic, behavioral and
   other factors, and this may be the case for schizophrenia as well.
   Scientists do not yet understand all of the factors necessary to
   produce, but all the tools of modern biomedical research are being used
   to search for genes, critical moments in brain development, and other
   factors that may lead to the illness.

Can Schizophrenia Be Inherited?

   It has been long understood that schizophrenia runs in families. People
   who have a close relative with schizophrenia are more likely to develop
   the disorder than are people who have no relatives with the illness. A
   child whose parent has schizophrenia has about a 10 percent chance of
   developing schizophrenia themselves. A monozygotic (identical) twin of
   a person with schizophrenia has the highest risk — a 40 to 65 percent
   chance of developing the illness. People who have second-degree
   relatives (aunts, uncles, grandparents, or cousins) with the disease
   also develop schizophrenia more often than the general population. By
   comparison, the risk of schizophrenia in the general population is
   about 1 percent.

   Scientists are continuing to study and better understand the genetic
   factors related to schizophrenia. We inherit our genes from both
   parents. Scientists believe several genes are associated with an
   increased risk of schizophrenia, but that no gene causes the disease by
   itself. In fact, recent research has found that people with
   schizophrenia tend to have higher rates of rare genetic mutations.
   These genetic differences involve hundreds of different genes and
   probably disrupt brain development.

   In addition, factors such as prenatal difficulties like intrauterine
   starvation or viral infections, perinatal complications, and various
   nonspecific stressors, seem to influence the development of
   schizophrenia. However, it is not yet understood how the genetic
   predisposition is transmitted, and it cannot yet be accurately
   predicted whether a given person will or will not develop the disorder.

   Other recent studies suggest that schizophrenia may result in part when
   a certain gene that is key to making important brain chemicals
   malfunctions. This problem may affect the part of the brain involved in
   developing higher functioning skills.Research into this gene is
   ongoing, so it is not yet possible to use the genetic information to
   predict who will develop the disease.

   In addition, it probably takes more than genes to cause the disorder.
   Scientists think interactions between genes and the environment are
   necessary for schizophrenia to develop. Many environmental factors may
   be involved, such as exposure to viruses or malnutrition before birth,
   problems during birth, and other not yet known psychosocial factors.

Is Schizophrenia Caused by a Chemical Defect in the Brain?

   Basic knowledge about brain chemistry and its link to schizophrenia is
   expanding rapidly. Neurotransmitters, substances that allow
   communication between nerve cells, have long been thought to be
   involved in the development of schizophrenia. It is likely, although
   not yet certain, that the disorder is associated with some imbalance of
   the complex, interrelated chemical systems of the brain, perhaps
   involving the neurotransmitters dopamine and glutamate.

Is Schizophrenia Caused by a Physical Abnormality in the Brain?

   There have been dramatic advances in neuroimaging technology that
   permit scientists to study brain structure and function in living
   individuals. Many studies of people with schizophrenia have found
   abnormalities in brain structure. In some small but potentially
   important ways, the brains of people with schizophrenia look different
   than those of healthy people. For example, fluid-filled cavities at the
   center of the brain, called ventricles, are larger in some people with
   schizophrenia. The brains of people with the illness also tend to have
   less gray matter, and some areas of the brain may have less or more
   activity.

   It should be emphasized that these abnormalities are quite subtle and
   are not characteristic of all people with schizophrenia, nor do they
   occur only in individuals with this illness. Microscopic studies of
   brain tissue after death have also shown small changes in distribution
   or number of brain cells in people with schizophrenia. It appears that
   many (but probably not all) of these changes are present before an
   individual becomes ill, and schizophrenia may be, in part, a disorder
   in development of the brain.

   Developmental neurobiologists have found that schizophrenia may be a
   developmental disorder resulting when neurons form inappropriate
   connections during fetal development. These errors may lie dormant
   until puberty, when changes in the brain that occur normally during
   this critical stage of maturation interact adversely with the faulty
   connections. This research has spurred efforts to identify prenatal
   factors that may have some bearing on the apparent developmental
   abnormality.

   In other studies, investigators using brain-imaging techniques have
   found evidence of early biochemical changes that may precede the onset
   of disease symptoms, prompting examination of the neural circuits that
   are most likely to be involved in producing those symptoms. Meanwhile,
   scientists working at the molecular level are exploring the genetic
   basis for abnormalities in brain development and in the
   neurotransmitter systems regulating brain function.

                                                        » Next in Series:
                         An Introduction to the Treatment of Schizophrenia

   Schizophrenia Table of Contents
     * Introduction to Schizophrenia
     * Symptoms of Schizophrenia
     * Types of Schizophrenia
     * Causes of Schizophrenia
     * An Introduction to the Treatment of Schizophrenia
     * Treatment of Schizophrenia
     * Living with Schizophrenia
     * Helpful Hints About Schizophrenia for Family Members & Others

   Based upon material from the National Institute of Mental Health.


     *
     *
     *
     *

   APA Reference
   Psych Central. (2006). What Causes Schizophrenia?. Psych Central.
   Retrieved on February 4, 2015, from
   http://psychcentral.com/lib/what-causes-schizophrenia/000715
     * Types of Schizophrenia
     * Helpful Hints about Schizophrenia for Family Members and Others
     * Long-Acting Treatments for Schizophrenia
     * Maximum Brainpower: Challenging the Brain for Health and Wisdom
     * Cannabis May Cause Schizophrenia-Like Brain Changes
     * Demons in the Age of Light: A Memoir of Psychosis and Recovery
     * Schizophrenia and Genetics: Research Update
     * The Dopamine Connection Between Schizophrenia and Creativity
     * Illuminating 13 Myths of Schizophrenia
     * Schizophrenia Fact Sheet

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     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

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     * Taking Medications for Schizophrenia
     * Side Effects of Medications
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Biological insights from 108 schizophrenia-associated genetic loci

     * Schizophrenia Working Group of the Psychiatric Genomics Consortium

     * Affiliations
     * Contributions
     * Corresponding author

   Journal name:
          Nature

   Volume:
          511,

   Pages:
          421–427

   Date published:
          (24 July 2014)

   DOI:
          doi:10.1038/nature13595

   Received
          06 March 2014

   Accepted
          18 June 2014

   Published online
          22 July 2014

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Abstract

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Schizophrenia is a highly heritable disorder. Genetic risk is conferred
   by a large number of alleles, including common alleles of small effect
   that might be detected by genome-wide association studies. Here we
   report a multi-stage schizophrenia genome-wide association study of up
   to 36,989 cases and 113,075 controls. We identify 128 independent
   associations spanning 108 conservatively defined loci that meet
   genome-wide significance, 83 of which have not been previously
   reported. Associations were enriched among genes expressed in brain,
   providing biological plausibility for the findings. Many findings have
   the potential to provide entirely new insights into aetiology, but
   associations at DRD2 and several genes involved in glutamatergic
   neurotransmission highlight molecules of known and potential
   therapeutic relevance to schizophrenia, and are consistent with leading
   pathophysiological hypotheses. Independent of genes expressed in brain,
   associations were enriched among genes expressed in tissues that have
   important roles in immunity, providing support for the speculated link
   between the immune system and schizophrenia.

Subject terms:

     * Genome-wide association studies

At a glance

Figures

   View all figures
    1. Manhattan plot showing schizophrenia associations. Figure 1:
       Manhattan plot showing schizophrenia associations.
       Manhattan plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). The x axis is chromosomal position and
       the y axis is the significance (–log[10] P; 2-tailed) of
       association derived by logistic regression. The red line shows the
       genome-wide significance level (5 × 10^−8). SNPs in green are in
       linkage disequilibrium with the index SNPs (diamonds) which
       represent independent genome-wide significant associations.
       Full size image
       View in article
    2. Enrichment in enhancers of credible SNPs. Figure 2: Enrichment in
       enhancers of credible SNPs.
       Cell and tissue type specific enhancers were identified using
       ChIP-seq data sets (H3K27ac signal) from 56 cell line and tissue
       samples (y axis). We defined cell and tissue type enhancers as the
       top 10% of enhancers with the highest ratio of reads in that cell
       or tissue type divided by the total number of reads. Enrichment of
       credible causal associated SNPs from the schizophrenia GWAS was
       compared with frequency matched sets of 1000 Genomes SNPs
       (Supplementary Methods). The x axis is the –log[10] P for
       enrichment. P values are uncorrected for the number of tissues or
       cells tested. A –log[10] P of roughly 3 can be considered
       significant after Bonferroni correction. Descriptions of cell and
       tissue types at the Roadmap Epigenome website
       (http://www.roadmapepigenomics.org).
       Full size image
       View in article
    3. Odds ratio by risk score profile. Figure 3: Odds ratio by risk
       score profile.
       Odds ratio for schizophrenia by risk score profile (RPS) decile in
       the Sweden (Sw1-6), Denmark (Aarhus), and Molecular Genetics of
       Schizophrenia studies (Supplementary Methods). Risk alleles and
       weights were derived from ‘leave one out’ analyses in which those
       samples were excluded from the GWAS meta-analysis (Supplementary
       Methods). The threshold for selecting risk alleles was P[T] < 0.05.
       The RPS were converted to deciles (1 = lowest, 10 = highest RPS),
       and nine dummy variables created to contrast deciles 2-10 to decile
       1 as the reference. Odds ratios and 95% confidence intervals (bars)
       were estimated using logistic regression with PCs to control for
       population stratification.
       Full size image
       View in article
    4. Homogeneity of effects across studies. Extended Data Fig. 1:
       Homogeneity of effects across studies.
       Plot of the first two principal components (PCs) from principal
       components analysis (PCA) of the logistic regression β coefficients
       for autosomal genome-wide significant associations. The input data
       were the β coefficients from 52 samples for 112 independent SNP
       associations (excluding 3 chrX SNPs and 13 SNPs with missing values
       in Asian samples). PCAs were weighted by the number of cases. Each
       circle shows the location of a study on PC1 and PC2. Circle size
       and colour are proportional to the number of cases in each sample
       (larger and darker red circles correspond to more cases). Most
       samples cluster. Outliers had either small numbers of cases
       (‘small’) or were genotyped on older arrays. Abbreviations: a500
       (Affymetrix 500K); a5 (Affymetrix 5.0). Studies that did not use
       conventional research interviews are in the central cluster
       (CLOZUK, Sweden, and Denmark-Aarhus studies, see Supplementary
       Methods for sample descriptions).
       Full size image
       View in article
    5. Quantile-quantile plot. Extended Data Fig. 2: Quantile-quantile
       plot.
       Quantile-quantile plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). Expected –log[10] P values are those
       expected under the null hypothesis. Observed are the GWAS
       association results derived by logistic regression (2-tailed) as in
       Fig. 1. For clarity, we avoided expansion of the y axis by setting
       the smallest association P values to 10^−12. The shaded area
       surrounded by a red line indicates the 95% confidence interval
       under the null. λ[GC] is the observed median χ^2 test statistic
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       View in article
    6. Linkage disequilibrium score regression consistent with polygenic
       inheritance. Extended Data Fig. 3: Linkage disequilibrium score
       regression consistent with polygenic inheritance.
       The relationship between marker χ^2 association statistics and
       linkage disequilibrium (LD) as measured by the linkage
       disequilibrium score. Linkage disequilibrium score is the sum of
       the r^2 values between a variant and all other known variants
       within a 1 cM window, and quantifies the amount of genetic
       variation tagged by that variant. Variants were grouped into 50
       equal-sized bins based on linkage disequilibrium score rank.
       Linkage disequilibrium score bin and mean χ^2 denotes mean linkage
       disequilibrium score and test statistic for markers each bin. a, b,
       We simulated (Supplementary Methods) test statistics under two
       scenarios: a, no true association, inflation due to population
       stratification; and b, polygenic inheritance (λ = 1.32), in which
       we assigned independent and identically distributed
       per-normalized-genotype effects to a randomly selected subset of
       variants. c, Results from the PGC schizophrenia GWAS (λ = 1.48).
       The real data are strikingly similar to the simulated data
       summarized in b but not a. The intercept estimates the inflation in
       the mean χ^2 that results from confounding biases, such as cryptic
       relatedness or population stratification. Thus, the intercept of
       1.066 for the schizophrenia GWAS suggests that ~90% of the
       inflation in the mean χ^2 results from polygenic signal. The
       results of the simulations are also consistent with theoretical
       expectation (see Supplementary Methods). λ is the median χ^2 test
       statistic from the simulations (a, b) or the observed data (c)
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       View in article
    7. Enrichment of associations in tissues and cells. Extended Data Fig.
       4: Enrichment of associations in tissues and cells.
       Genes whose transcriptional start is nearest to the most associated
       SNP at each schizophrenia-associated locus were tested for enriched
       expression in purified brain cell subsets obtained from mouse
       ribotagged lines^41 using enrichment analysis described in the
       Supplementary Methods. The red dotted line indicates P = 0.05.
       Full size image
       View in article
    8. MGS risk profile score analysis. Extended Data Fig. 5: MGS risk
       profile score analysis.
       Polygenic risk profile score (RPS) analyses using the MGS^18 sample
       as target, and deriving risk alleles from three published
       schizophrenia data sets (x axis): ISC (2,615 cases and 3,338
       controls)^10, PGC1 (excluding MGS, 9,320 cases and 10,228
       controls)^16, and the current meta-analysis (excluding MGS) with
       32,838 cases and 44,357 controls. Samples sizes differ slightly
       from the original publications due to different analytical
       procedures. This shows the increasing RPS prediction with
       increasing training data set size reflecting improved precision of
       estimates of the SNP effect sizes. The proportion of variance
       explained (y axis; Nagelkerke’s R^2) was computed by comparison of
       a full model (covariates + RPS) score to a reduced model
       (covariates only). Ten different P value thresholds (P[T]) for
       selecting risk alleles are denoted by the colour of each bar
       (legend above plot). For significance testing, see the bottom
       legend which denotes the P value for the test that R^2 is different
       from zero. All numerical data and methods used to generate these
       plots are available in Supplementary Table 6 and Supplementary
       Methods.
       Full size image
       View in article
    9. Risk profile score analysis. Extended Data Fig. 6: Risk profile
       score analysis.
       We defined 40 target subgroups of the primary GWAS data set and
       performed 40 leave-one-out GWAS analyses (see Supplementary Methods
       and Supplementary Table 7) from which we derived risk alleles for
       RPS analysis (x axis) for each target subgroup. a, The proportion
       of variance explained (y axis; Nagelkerke’s R^2) was computed for
       each target by comparison of a full model (covariates + RPS) score
       to a reduced model (covariates only). For clarity, 3 different P
       value thresholds (P[T]) are presented denoted by the colour of each
       bar (legend above plot) as for Extended Data Fig. 5, but for
       clarity we restrict to fewer P value thresholds (P[T] of 5 × 10^−8,
       1 × 10^−4 and 0.05) and removed the significance values. b, The
       proportion of variance on the liability scale from risk scores
       calculated at the P[T] 0.05 with 95% CI bar assuming baseline
       population disease risk of 1%. c, Area under the receiver operating
       curve (AUC). All numerical data and methods used to generate these
       plots are available in Supplementary Table 7 and Supplementary
       Methods.
       Full size image
       View in article
   10. Pairwise epistasis analysis of significant SNPs. Extended Data Fig.
       7: Pairwise epistasis analysis of significant SNPs.
       Quantile-quantile plot for all pair-wise (n = 7,750) combinations
       of the 125 independent autosomal genome-wide significant SNPs
       tested for non-additive effects on risk using case-control data
       sets of European ancestry (32,405 cases and 42,221 controls). We
       included as covariates the principal components from the main
       analysis as well as a study indicator. The interaction model is
       described by:
       and are genotypes at the two loci, is the interaction between the
       two genotypes modelled in a multiplicative fashion, is the vector
       of principal components, is the vector of study indicator
       variables. Each is the regression coefficient in the generalized
       linear model using logistic regression. The overall distribution of
       P values did not deviate from the null and the smallest P value
       (4.28 × 10^−4) did not surpass the Bonferroni correction threshold
       (P = 0.05/7750 = 6.45 × 10^−6). The line x = y indicates the
       expected null distribution with the grey area bounded by red lines
       indicating the expected 95% confidence interval for the null.
       Full size image
       View in article

Tables

   View all tables
    1. ALIGATOR and INRICH Extended Data Table 1: ALIGATOR and INRICH
       Full size image
       View in article
    2. de novo overlap Extended Data Table 2: de novo overlap
       Full size image
       View in article

Introduction

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Schizophrenia has a lifetime risk of around 1%, and is associated with
   substantial morbidity and mortality as well as personal and societal
   costs^1, 2, 3. Although pharmacological treatments are available for
   schizophrenia, their efficacy is poor for many patients^4. All
   available antipsychotic drugs are thought to exert their main
   therapeutic effects through blockade of the type 2 dopaminergic
   receptor^5, 6 but, since the discovery of this mechanism over 60 years
   ago, no new antipsychotic drug of proven efficacy has been developed
   based on other target molecules. Therapeutic stasis is in large part a
   consequence of the fact that the pathophysiology of schizophrenia is
   unknown. Identifying the causes of schizophrenia is therefore a
   critical step towards improving treatments and outcomes for those with
   the disorder.

   High heritability points to a major role for inherited genetic variants
   in the aetiology of schizophrenia^7, 8. Although risk variants range in
   frequency from common to extremely rare^9, estimates^10, 11 suggest
   half to a third of the genetic risk of schizophrenia is indexed by
   common alleles genotyped by current genome-wide association study
   (GWAS) arrays. Thus, GWAS is potentially an important tool for
   understanding the biological underpinnings of schizophrenia.

   To date, around 30 schizophrenia-associated loci^10, 11, 12, 13, 14,
   15, 16, 17, 18, 19, 20, 21, 22, 23 have been identified through GWAS.
   Postulating that sample size is one of the most important limiting
   factors in applying GWAS to schizophrenia, we created the Schizophrenia
   Working Group of the Psychiatric Genomics Consortium (PGC). Our primary
   aim was to combine all available schizophrenia samples with published
   or unpublished GWAS genotypes into a single, systematic analysis^24.
   Here we report the results of that analysis, including at least 108
   independent genomic loci that exceed genome-wide significance. Some of
   the findings support leading pathophysiological hypotheses of
   schizophrenia or targets of therapeutic relevance, but most of the
   findings provide new insights.

108 independent associated loci

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   We obtained genome-wide genotype data from which we constructed 49
   ancestry matched, non-overlapping case-control samples (46 of European
   and three of east Asian ancestry, 34,241 cases and 45,604 controls) and
   3 family-based samples of European ancestry (1,235 parent
   affected-offspring trios) (Supplementary Table 1 and Supplementary
   Methods). These comprise the primary PGC GWAS data set. We processed
   the genotypes from all studies using unified quality control procedures
   followed by imputation of SNPs and insertion-deletions using the 1000
   Genomes Project reference panel^25. In each sample, association testing
   was conducted using imputed marker dosages and principal components
   (PCs) to control for population stratification. The results were
   combined using an inverse-variance weighted fixed effects model^26.
   After quality control (imputation INFO score ≥ 0.6, MAF ≥ 0.01, and
   successfully imputed in ≥ 20 samples), we considered around 9.5 million
   variants. The results are summarized in Fig. 1. To enable acquisition
   of large samples, some groups ascertained cases via clinician diagnosis
   rather than a research-based assessment and provided evidence of the
   validity of this approach (Supplementary Information)^11, 13. Post hoc
   analyses revealed the pattern of effect sizes for associated loci was
   similar across different assessment methods and modes of ascertainment
   (Extended Data Fig. 1), supporting our a priori decision to include
   samples of this nature.
   Figure 1: Manhattan plot showing schizophrenia associations.
   Manhattan plot showing schizophrenia associations.

   Manhattan plot of the discovery genome-wide association meta-analysis
   of 49 case control samples (34,241 cases and 45,604 controls) and 3
   family based association studies (1,235 parent affected-offspring
   trios). The x axis is chromosomal position and the y axis is the
   significance (–log[10] P; 2-tailed) of association derived by logistic
   regression. The red line shows the genome-wide significance level (5 ×
   10^−8). SNPs in green are in linkage disequilibrium with the index SNPs
   (diamonds) which represent independent genome-wide significant
   associations.
     * Full size image (230 KB)
     * Download PowerPoint slide (376 KB)

     * Figures/tables index
     * Next

   For the subset of linkage-disequilibrium-independent single nucleotide
   polymorphisms (SNPs) with P < 1 × 10^−6 in the meta-analysis, we next
   obtained results from deCODE genetics (1,513 cases and 66,236 controls
   of European ancestry). We define linkage-disequilibrium-independent
   SNPs as those with low linkage disequilibrium (r^2 < 0.1) to a more
   significantly associated SNP within a 500-kb window. Given high linkage
   disequilibrium in the extended major histocompatibility complex (MHC)
   region spans ~8 Mb, we conservatively include only a single MHC SNP to
   represent this locus. The deCODE data were then combined with those
   from the primary GWAS to give a data set of 36,989 cases and 113,075
   controls. In this final analysis, 128
   linkage-disequilibrium-independent SNPs exceeded genome-wide
   significance (P ≤ 5 × 10^−8) (Supplementary Table 2).

   As in meta-analyses of other complex traits which identified large
   numbers of common risk variants^27, 28, the test statistic distribution
   from our GWAS deviates from the null (Extended Data Fig. 2). This is
   consistent with the previously documented polygenic contribution to
   schizophrenia^10, 11. The deviation in the test statistics from the
   null (λ[GC] = 1.47, λ[1000] = 1.01) is only slightly less than expected
   (λ[GC] = 1.56) under a polygenic model given fully informative
   genotypes, the current sample size, and the lifetime risk and
   heritability of schizophrenia^29.

   Additional lines of evidence allow us to conclude the deviation between
   the observed and null distributions in our primary GWAS indicates a
   true polygenic contribution to schizophrenia. First, applying a novel
   method^30 that uses linkage disequilibrium information to distinguish
   between the major potential sources of test statistic inflation, we
   found our results are consistent with polygenic architecture but not
   population stratification (Extended Data Fig. 3). Second, the
   schizophrenia-associated alleles at 78% of 234
   linkage-disequilibrium-independent SNPs exceeding P < 1 × 10^−6 in the
   case-control GWAS were again overrepresented in cases in the
   independent samples from deCODE. This degree of consistency between the
   case-control GWAS and the replication data is highly unlikely to occur
   by chance (P = 6 × 10^−19). The tested alleles surpassed the P < 10^−6
   threshold in our GWAS before we added either the trios or deCODE data
   to the meta-analysis. This trend test is therefore independent of the
   primary case-control GWAS. Third, analysing the 1,235 parent-proband
   trios, we again found excess transmission of the
   schizophrenia-associated allele at 69% of the 263
   linkage-disequilibrium-independent SNPs with P < 1 × 10^−6 in the
   case-control GWAS. This is again unlikely to occur by chance (P = 1 ×
   10^−9) and additionally excludes population stratification as fully
   explaining the associations reaching our threshold for seeking
   replication. Fourth, we used the trios trend data to estimate the
   expected proportion of true associations at P < 1 × 10^−6 in the
   discovery GWAS, allowing for the fact that half of the index SNPs are
   expected to show the same allelic trend in the trios by chance, and
   that some true associations will show opposite trends given the limited
   number of trio samples (Supplementary Methods). Given the observed
   trend test results, around 67% (95% confidence interval: 64–73%) or n =
   176 of the associations in the scan at P < 1 × 10^−6 are expected to be
   true, and therefore the number of associations that will ultimately be
   validated from this set of SNPs will be considerably more than those
   that now meet genome-wide significance. Taken together, these analyses
   indicate that the observed deviation of test statistics from the null
   primarily represents polygenic association signal and the considerable
   excess of associations at the tail of extreme significance largely
   correspond to true associations.

   Independently associated SNPs do not translate to well-bounded
   chromosomal regions. Nevertheless, it is useful to define physical
   boundaries for the SNP associations to identify candidate risk genes.
   We defined an associated locus as the physical region containing all
   SNPs correlated at r^2 > 0.6 with each of the 128 index SNPs.
   Associated loci within 250 kb of each other were merged. This resulted
   in 108 physically distinct associated loci, 83 of which have not been
   previously implicated in schizophrenia and therefore harbour potential
   new biological insights into disease aetiology (Supplementary Table 3;
   regional plots in Supplementary Fig. 1). The significant regions
   include all but 5 loci previously reported to be genome-wide
   significant in large samples (Supplementary Table 3).

Characterization of associated loci

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Of the 108 loci, 75% include protein-coding genes (40%, a single gene)
   and a further 8% are within 20 kb of a gene (Supplementary Table 3).
   Notable associations relevant to major hypotheses of the aetiology and
   treatment of schizophrenia include DRD2 (the target of all effective
   antipsychotic drugs) and many genes (for example, GRM3, GRIN2A, SRR,
   GRIA1) involved in glutamatergic neurotransmission and synaptic
   plasticity. In addition, associations at CACNA1C, CACNB2 and CACNA1I,
   which encode voltage-gated calcium channel subunits, extend previous
   findings implicating members of this family of proteins in
   schizophrenia and other psychiatric disorders^11, 13, 31, 32. Genes
   encoding calcium channels, and proteins involved in glutamatergic
   neurotransmission and synaptic plasticity have been independently
   implicated in schizophrenia by studies of rare genetic variation^33,
   34, 35, suggesting convergence at a broad functional level between
   studies of common and rare genetic variation. We highlight in the
   Supplementary Discussion genes of particular interest within associated
   loci with respect to current hypotheses of schizophrenia aetiology or
   treatment (although we do not imply that these genes are necessarily
   the causal elements).

   For each of the schizophrenia-associated loci, we identified a credible
   causal set of SNPs (for definition, see Supplementary Methods)^36. In
   only 10 instances (Supplementary Table 4) was the association signal
   credibly attributable to a known non-synonymous exonic polymorphism.
   The apparently limited role of protein-coding variants is consistent
   both with exome sequencing findings^33 and with the hypothesis that
   most associated variants detected by GWAS exert their effects through
   altering gene expression rather than protein structure^37, 38 and with
   the observation that schizophrenia risk loci are enriched for
   expression quantitative trait loci (eQTL)^39.

   To try to identify eQTLs that could explain associations with
   schizophrenia, we merged the credible causal set of SNPs defined above
   with eQTLs from a meta-analysis of human brain cortex eQTL studies (n =
   550) and an eQTL study of peripheral venous blood (n = 3,754)^40
   (Supplementary Methods). Multiple schizophrenia loci contained at least
   one eQTL for a gene within 1 Mb of the locus (Supplementary Table 4).
   However, in only 12 instances was the eQTL plausibly causal (two in
   brain, and nine in peripheral blood, one in both). This low proportion
   suggests that if most risk variants are regulatory, available eQTL
   catalogues do not yet provide power, cellular specificity, or
   developmental diversity to provide clear mechanistic hypotheses for
   follow-up experiments.

The brain and immunity

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   To further explore the regulatory nature of the schizophrenia
   associations, we mapped the credible sets (n = 108) of causal variants
   onto sequences with epigenetic markers characteristic of active
   enhancers in 56 different tissues and cell lines (Supplementary
   Methods). Schizophrenia associations were significantly enriched at
   enhancers active in brain (Fig. 2) but not in tissues unlikely to be
   relevant to schizophrenia (for example, bone, cartilage, kidney and
   fibroblasts). Brain tissues used to define enhancers consist of
   heterogeneous populations of cells. Seeking greater specificity, we
   contrasted genes enriched for expression in neurons and glia using
   mouse ribotagged lines^41. Genes with strong expression in multiple
   cortical and striatal neuronal lineages were enriched for associations,
   providing support for an important neuronal pathology in schizophrenia
   (Extended Data Fig. 4) but this is not statistically more significant
   than, or exclusionary of, contributions from other lineages^42.
   Figure 2: Enrichment in enhancers of credible SNPs.
   Enrichment in enhancers of credible SNPs.

   Cell and tissue type specific enhancers were identified using ChIP-seq
   data sets (H3K27ac signal) from 56 cell line and tissue samples (y
   axis). We defined cell and tissue type enhancers as the top 10% of
   enhancers with the highest ratio of reads in that cell or tissue type
   divided by the total number of reads. Enrichment of credible causal
   associated SNPs from the schizophrenia GWAS was compared with frequency
   matched sets of 1000 Genomes SNPs (Supplementary Methods). The x axis
   is the –log[10] P for enrichment. P values are uncorrected for the
   number of tissues or cells tested. A –log[10] P of roughly 3 can be
   considered significant after Bonferroni correction. Descriptions of
   cell and tissue types at the Roadmap Epigenome website
   (http://www.roadmapepigenomics.org).
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     * Figures/tables index
     * Next

   Schizophrenia associations were also strongly enriched at enhancers
   that are active in tissues with important immune functions,
   particularly B-lymphocyte lineages involved in acquired immunity (CD19
   and CD20 lines, Fig. 2). These enrichments remain significant even
   after excluding the extended MHC region and regions containing brain
   enhancers (enrichment P for CD20 < 10^−6), demonstrating that this
   finding is not an artefact of correlation between enhancer elements in
   different tissues and not driven by the strong and diffuse association
   at the extended MHC. Epidemiological studies have long hinted at a role
   for immune dysregulation in schizophrenia, the present findings provide
   genetic support for this hypothesis^43.

   To develop additional biological hypotheses beyond those that emerge
   from inspection of the individual loci, we further undertook a limited
   mining of the data through gene-set analysis. However, as there is no
   consensus methodology by which such analyses should be conducted, nor
   an established optimal significance threshold for including loci, we
   sought to be conservative, using only two of the many available
   approaches^44, 45 and restricting analyses to genes within genome-wide
   significant loci. Neither approach identified gene-sets that were
   significantly enriched for associations after correction for the number
   of pathways tested (Supplementary Table 5) although nominally
   significantly enrichments were observed among several predefined
   candidate pathways (Extended Data Table 1). A fuller exploratory
   analysis of the data will be presented elsewhere.

Overlap with rare mutations

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   CNVs associated with schizophrenia overlap with those associated with
   autism spectrum disorder (ASD) and intellectual disability^9, as do
   genes with deleterious de novo mutations^34. Here we find significant
   overlap between genes in the schizophrenia GWAS associated intervals
   and those with de novo non-synonymous mutations in schizophrenia (P =
   0.0061) (Extended Data Table 2), suggesting that mechanistic studies of
   rare genetic variation in schizophrenia will be informative for
   schizophrenia more widely. We also find evidence for overlap between
   genes in schizophrenia GWAS regions and those with de novo
   non-synonymous mutations in intellectual disability (P = 0.00024) and
   ASD (P = 0.035), providing further support for the hypothesis that
   these disorders have partly overlapping pathophysiologies^9, 34.

Polygenic risk score profiling

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Previous studies have shown that risk profile scores (RPS) constructed
   from alleles showing modest association with schizophrenia in a
   discovery GWAS can predict case-control status in independent samples,
   albeit with low sensitivity and specificity^10, 11, 16. This finding
   was robustly confirmed in the present study. The estimate of Nagelkerke
   R^2 (a measure of variance in case-control status explained) depends on
   the specific target data set and threshold (P[T]) for selecting risk
   alleles for RPS analysis (Extended Data Fig. 5 and 6a). However, using
   the same target sample as earlier studies and P[T] = 0.05, R^2 is now
   increased from 0.03 (ref. 10) to 0.184 (Extended Data Fig. 5). Assuming
   a liability-threshold model, a lifetime risk of 1%, independent SNP
   effects, and adjusting for case-control ascertainment, RPS now explains
   about 7% of variation on the liability scale^46 to schizophrenia across
   the samples (Extended Data Fig. 6b), about half of which (3.4%) is
   explained by genome-wide significant loci.

   We also evaluated the capacity of RPS to predict case-control status
   using a standard epidemiological approach to a continuous risk factor.
   We illustrate this in three samples, each with different ascertainment
   schemes (Fig. 3). The Danish sample is population-based (that is,
   inpatient and outpatient facilities), the Swedish sample is based on
   all cases hospitalized for schizophrenia in Sweden, and the Molecular
   Genetics of Schizophrenia (MGS) sample was ascertained specially for
   genetic studies from clinical sources in the US and Australia. We
   grouped individuals into RPS deciles and estimated the odds ratios for
   affected status for each decile with reference to the lowest risk
   decile. The odds ratios increased with greater number of schizophrenia
   risk alleles in each sample, maximizing for the tenth decile in all
   samples: Denmark 7.8 (95% confidence interval (CI): 4.4–13.9), Sweden
   15.0 (95% CI: 12.1–18.7) and MGS 20.3 (95% CI: 14.7–28.2). Given the
   need for measures that index liability to schizophrenia^47, 48, the
   ability to stratify individuals by RPS offers new opportunities for
   clinical and epidemiological research. Nevertheless, we stress that the
   sensitivity and specificity of RPS do not support its use as a
   predictive test. For example, in the Danish epidemiological sample, the
   area under the receiver operating curve is only 0.62 (Extended Data
   Fig. 6c, Supplementary Table 6).
   Figure 3: Odds ratio by risk score profile.
   Odds ratio by risk score profile.

   Odds ratio for schizophrenia by risk score profile (RPS) decile in the
   Sweden (Sw1-6), Denmark (Aarhus), and Molecular Genetics of
   Schizophrenia studies (Supplementary Methods). Risk alleles and weights
   were derived from ‘leave one out’ analyses in which those samples were
   excluded from the GWAS meta-analysis (Supplementary Methods). The
   threshold for selecting risk alleles was P[T] < 0.05. The RPS were
   converted to deciles (1 = lowest, 10 = highest RPS), and nine dummy
   variables created to contrast deciles 2-10 to decile 1 as the
   reference. Odds ratios and 95% confidence intervals (bars) were
   estimated using logistic regression with PCs to control for population
   stratification.
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   Finally, seeking evidence for non-additive effects on risk, we tested
   for statistical interaction between all pairs of 125 autosomal SNPs
   that reached genome-wide significance. P values for the interaction
   terms were distributed according to the null, and no interaction was
   significant after correction for multiple comparisons. Thus, we find no
   evidence for epistatic or non-additive effects between the significant
   loci (Extended Data Fig. 7). It is possible that such effects could be
   present between other loci, or occur in the form of higher-order
   interactions.

Discussion

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   In the largest (to our knowledge) molecular genetic study of
   schizophrenia, or indeed of any neuropsychiatric disorder, ever
   conducted, we demonstrate the power of GWAS to identify large numbers
   of risk loci. We show that the use of alternative ascertainment and
   diagnostic schemes designed to rapidly increase sample size does not
   inevitably introduce a crippling degree of heterogeneity. That this is
   true for a phenotype like schizophrenia, in which there are no
   biomarkers or supportive diagnostic tests, provides grounds to be
   optimistic that this approach can be successfully applied to GWAS of
   other clinically defined disorders.

   We further show that the associations are not randomly distributed
   across genes of all classes and function; rather they converge upon
   genes that are expressed in certain tissues and cellular types. The
   findings include molecules that are the current, or the most promising,
   targets for therapeutics, and point to systems that align with the
   predominant aetiological hypotheses of the disorder. This suggests that
   the many novel findings we report also provide an aetiologically
   relevant foundation for mechanistic and treatment development studies.
   We also find overlap between genes affected by rare variants in
   schizophrenia and those within GWAS loci, and broad convergence in the
   functions of some of the clusters of genes implicated by both sets of
   genetic variants, particularly genes related to abnormal glutamatergic
   synaptic and calcium channel function. How variation in these genes
   impact function to increase risk for schizophrenia cannot be answered
   by genetics, but the overlap strongly suggests that common and rare
   variant studies are complementary rather than antagonistic, and that
   mechanistic studies driven by rare genetic variation will be
   informative for schizophrenia.

References

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

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Acknowledgements

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

   Core funding for the Psychiatric Genomics Consortium is from the US
   National Institute of Mental Health (U01 MH094421). We thank T. Lehner
   (NIMH). The work of the contributing groups was supported by numerous
   grants from governmental and charitable bodies as well as philanthropic
   donation. Details are provided in the Supplementary Notes. Membership
   of the Wellcome Trust Case Control Consortium and of the Psychosis
   Endophenotype International Consortium are provided in the
   Supplementary Notes.

Author information

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

Affiliations

    1. Analytic and Translational Genetics Unit, Massachusetts General
       Hospital, Boston, Massachusetts 02114, USA.
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Kai-How Farh,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + Hailiang Huang,
          + Menachem Fromer,
          + Jacqueline I. Goldstein &
          + Mark J. Daly
    2. Stanley Center for Psychiatric Research, Broad Institute of MIT and
       Harvard, Cambridge, Massachusetts 02142, USA.
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + Richard A. Belliveau Jr,
          + Sarah E. Bergen,
          + Elizabeth Bevilacqua,
          + Kimberly D. Chambert,
          + Menachem Fromer,
          + Giulio Genovese,
          + Colm O’Dushlaine,
          + Edward M. Scolnick,
          + Jordan W. Smoller,
          + Steven A. McCarroll,
          + Jennifer L. Moran,
          + Aarno Palotie,
          + Tracey L. Petryshen &
          + Mark J. Daly
    3. Medical and Population Genetics Program, Broad Institute of MIT and
       Harvard, Cambridge, Massachusetts 02142, USA.
          + Benjamin M. Neale,
          + Hailiang Huang,
          + Tune H. Pers,
          + Jacqueline I. Goldstein,
          + Joel N. Hirschhorn,
          + Alkes Price,
          + Eli A. Stahl,
          + Tõnu Esko &
          + Mark J. Daly
    4. Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts
       General Hospital, Boston, Massachusetts 02114, USA.
          + Benjamin M. Neale,
          + Phil Lee,
          + Menachem Fromer,
          + Jordan W. Smoller &
          + Aarno Palotie
    5. Neuropsychiatric Genetics Research Group, Department of Psychiatry,
       Trinity College Dublin, Dublin 8, Ireland.
          + Aiden Corvin,
          + Paul Cormican,
          + Gary Donohoe,
          + Derek W. Morris &
          + Michael Gill
    6. MRC Centre for Neuropsychiatric Genetics and Genomics, Institute of
       Psychological Medicine and Clinical Neurosciences, School of
       Medicine, Cardiff University, Cardiff CF24 4HQ, UK.
          + James T. R. Walters,
          + Peter A. Holmans,
          + Noa Carrera,
          + Nick Craddock,
          + Valentina Escott-Price,
          + Lyudmila Georgieva,
          + Marian L. Hamshere,
          + David Kavanagh,
          + Sophie E. Legge,
          + Andrew J. Pocklington,
          + Alexander L. Richards,
          + Douglas M. Ruderfer,
          + Nigel M. Williams,
          + George Kirov,
          + Michael J. Owen &
          + Michael C. O’Donovan
    7. National Centre for Mental Health, Cardiff University, Cardiff CF24
       4HQ, UK.
          + Peter A. Holmans,
          + Nick Craddock,
          + Michael J. Owen &
          + Michael C. O’Donovan
    8. Eli Lilly and Company Limited, Erl Wood Manor, Sunninghill Road,
       Windlesham, Surrey GU20 6PH, UK.
          + David A. Collier &
          + Younes Mokrab
    9. Social, Genetic and Developmental Psychiatry Centre, Institute of
       Psychiatry, King’s College London, London SE5 8AF, UK.
          + David A. Collier
   10. Center for Biological Sequence Analysis, Department of Systems
       Biology, Technical University of Denmark, DK-2800, Denmark.
          + Tune H. Pers
   11. Division of Endocrinology and Center for Basic and Translational
       Obesity Research, Boston Children’s Hospital, Boston, Massachusetts
       02115, USA.
          + Tune H. Pers,
          + Joel N. Hirschhorn &
          + Tõnu Esko
   12. Department of Clinical Neuroscience, Psychiatry Section, Karolinska
       Institutet, SE-17176 Stockholm, Sweden.
          + Ingrid Agartz,
          + Erik Söderman &
          + Erik G. Jönsson
   13. Department of Psychiatry, Diakonhjemmet Hospital, 0319 Oslo,
       Norway.
          + Ingrid Agartz
   14. NORMENT, KG Jebsen Centre for Psychosis Research, Institute of
       Clinical Medicine, University of Oslo, 0424 Oslo, Norway.
          + Ingrid Agartz,
          + Srdjan Djurovic,
          + Morten Mattingsdal,
          + Ingrid Melle,
          + Ole A. Andreassen &
          + Erik G. Jönsson
   15. Centre for Integrative Register-based Research, CIRRAU, Aarhus
       University, DK-8210 Aarhus, Denmark.
          + Esben Agerbo &
          + Preben B. Mortensen
   16. National Centre for Register-based Research, Aarhus University,
       DK-8210 Aarhus, Denmark.
          + Esben Agerbo &
          + Preben B. Mortensen
   17. The Lundbeck Foundation Initiative for Integrative Psychiatric
       Research, iPSYCH, Denmark.
          + Esben Agerbo,
          + Ditte Demontis,
          + Thomas Hansen,
          + Manuel Mattheisen,
          + Ole Mors,
          + Line Olsen,
          + Henrik B. Rasmussen,
          + Anders D. Børglum,
          + Preben B. Mortensen &
          + Thomas Werge
   18. State Mental Hospital, 85540 Haar, Germany.
          + Margot Albus
   19. Department of Psychiatry and Behavioral Sciences, Stanford
       University, Stanford, California 94305, USA.
          + Madeline Alexander,
          + Claudine Laurent &
          + Douglas F. Levinson
   20. Department of Psychiatry and Behavioral Sciences, Atlanta Veterans
       Affairs Medical Center, Atlanta, Georgia 30033, USA.
          + Farooq Amin
   21. Department of Psychiatry and Behavioral Sciences, Emory University,
       Atlanta, Georgia 30322, USA.
          + Farooq Amin
   22. Virginia Institute for Psychiatric and Behavioral Genetics,
       Department of Psychiatry, Virginia Commonwealth University,
       Richmond, Virginia 23298, USA.
          + Silviu A. Bacanu,
          + Tim B. Bigdeli,
          + Bradley T. Webb &
          + Brandon K. Wormley
   23. Clinical Neuroscience, Max Planck Institute of Experimental
       Medicine, Göttingen 37075, Germany.
          + Martin Begemann,
          + Christian Hammer,
          + Sergi Papiol &
          + Hannelore Ehrenreich
   24. Department of Medical Genetics, University of Pécs, Pécs H-7624,
       Hungary.
          + Judit Bene &
          + Bela Melegh
   25. Szentagothai Research Center, University of Pécs, Pécs H-7624,
       Hungary.
          + Judit Bene &
          + Bela Melegh
   26. Department of Medical Epidemiology and Biostatistics, Karolinska
       Institutet, Stockholm SE-17177, Sweden.
          + Sarah E. Bergen,
          + Anna K. Kähler,
          + Patrik K. E. Magnusson,
          + Christina M. Hultman &
          + Patrick F. Sullivan
   27. Department of Psychiatry, University of Iowa Carver College of
       Medicine, Iowa City, Iowa 52242, USA.
          + Donald W. Black
   28. University Medical Center Groningen, Department of Psychiatry,
       University of Groningen NL-9700 RB, The Netherlands.
          + Richard Bruggeman
   29. School of Nursing, Louisiana State University Health Sciences
       Center, New Orleans, Louisiana 70112, USA.
          + Nancy G. Buccola
   30. Athinoula A. Martinos Center, Massachusetts General Hospital,
       Boston, Massachusetts 02129, USA.
          + Randy L. Buckner &
          + Joshua L. Roffman
   31. Center for Brain Science, Harvard University, Cambridge,
       Massachusetts 02138, USA.
          + Randy L. Buckner
   32. Department of Psychiatry, Massachusetts General Hospital, Boston,
       Massachusetts 02114, USA.
          + Randy L. Buckner &
          + Joshua L. Roffman
   33. Department of Psychiatry, University of California at San
       Francisco, San Francisco, California 94143, USA.
          + William Byerley
   34. University Medical Center Utrecht, Department of Psychiatry, Rudolf
       Magnus Institute of Neuroscience, 3584 Utrecht, The Netherlands.
          + Wiepke Cahn,
          + René S. Kahn,
          + Eric Strengman &
          + Roel A. Ophoff
   35. Department of Human Genetics, Icahn School of Medicine at Mount
       Sinai, New York, New York 10029, USA.
          + Guiqing Cai &
          + Joseph D. Buxbaum
   36. Department of Psychiatry, Icahn School of Medicine at Mount Sinai,
       New York, New York 10029, USA.
          + Guiqing Cai,
          + Kenneth L. Davis,
          + Elodie Drapeau,
          + Joseph I. Friedman,
          + Vahram Haroutunian,
          + Elena Parkhomenko,
          + Abraham Reichenberg,
          + Jeremy M. Silverman &
          + Joseph D. Buxbaum
   37. Centre Hospitalier du Rouvray and INSERM U1079 Faculty of Medicine,
       76301 Rouen, France.
          + Dominique Campion
   38. Department of Human Genetics, David Geffen School of Medicine,
       University of California, Los Angeles, California 90095, USA.
          + Rita M. Cantor &
          + Roel A. Ophoff
   39. Schizophrenia Research Institute, Sydney NSW 2010, Australia.
          + Vaughan J. Carr,
          + Stanley V. Catts,
          + Frans A. Henskens,
          + Carmel M. Loughland,
          + Patricia T. Michie,
          + Christos Pantelis,
          + Ulrich Schall,
          + Rodney J. Scott &
          + Assen V. Jablensky
   40. School of Psychiatry, University of New South Wales, Sydney NSW
       2031, Australia.
          + Vaughan J. Carr
   41. Royal Brisbane and Women’s Hospital, University of Queensland,
       Brisbane, St Lucia QLD 4072, Australia.
          + Stanley V. Catts
   42. Institute of Psychology, Chinese Academy of Science, Beijing
       100101, China.
          + Raymond C. K. Chan
   43. Department of Psychiatry, Li Ka Shing Faculty of Medicine, The
       University of Hong Kong, Hong Kong, China.
          + Ronald Y. L. Chen,
          + Eric Y. H. Chen,
          + Miaoxin Li,
          + Hon-Cheong So,
          + Emily H. M. Wong &
          + Pak C. Sham
   44. State Key Laboratory for Brain and Cognitive Sciences, Li Ka Shing
       Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
          + Eric Y. H. Chen,
          + Miaoxin Li &
          + Pak C. Sham
   45. Department of Computer Science, University of North Carolina,
       Chapel Hill, North Carolina 27514, USA.
          + Wei Cheng
   46. Castle Peak Hospital, Hong Kong, China.
          + Eric F. C. Cheung
   47. Institute of Mental Health, Singapore 539747, Singapore.
          + Siow Ann Chong,
          + Jimmy Lee Chee Keong,
          + Kang Sim &
          + Mythily Subramaniam
   48. Department of Psychiatry, Washington University, St. Louis,
       Missouri 63110, USA.
          + C. Robert Cloninger &
          + Dragan M. Svrakic
   49. Department of Child and Adolescent Psychiatry, Assistance Publique
       Hopitaux de Paris, Pierre and Marie Curie Faculty of Medicine and
       Institute for Intelligent Systems and Robotics, Paris 75013,
       France.
          + David Cohen
   50. Blue Note Biosciences, Princeton, New Jersey 08540, USA
          + Nadine Cohen
   51. Department of Genetics, University of North Carolina, Chapel Hill,
       North Carolina 27599-7264, USA.
          + James J. Crowley,
          + Martilias S. Farrell,
          + Paola Giusti-Rodríguez,
          + Yunjung Kim,
          + Jin P. Szatkiewicz,
          + Stephanie Williams &
          + Patrick F. Sullivan
   52. Department of Psychological Medicine, Queen Mary University of
       London, London E1 1BB, UK.
          + David Curtis
   53. Molecular Psychiatry Laboratory, Division of Psychiatry, University
       College London, London WC1E 6JJ, UK.
          + David Curtis,
          + Jonathan Pimm,
          + Hugh Gurling &
          + Andrew McQuillin
   54. Sheba Medical Center, Tel Hashomer 52621, Israel.
          + Michael Davidson &
          + Mark Weiser
   55. Department of Genomics, Life and Brain Center, D-53127 Bonn,
       Germany.
          + Franziska Degenhardt,
          + Stefan Herms,
          + Per Hoffmann,
          + Andrea Hofman,
          + Sven Cichon &
          + Markus M. Nöthen
   56. Institute of Human Genetics, University of Bonn, D-53127 Bonn,
       Germany.
          + Franziska Degenhardt,
          + Stefan Herms,
          + Per Hoffmann,
          + Andrea Hofman,
          + Sven Cichon &
          + Markus M. Nöthen
   57. Applied Molecular Genomics Unit, VIB Department of Molecular
       Genetics, University of Antwerp, B-2610 Antwerp, Belgium.
          + Jurgen Del Favero
   58. Centre for Integrative Sequencing, iSEQ, Aarhus University, DK-8000
       Aarhus C, Denmark.
          + Ditte Demontis,
          + Manuel Mattheisen,
          + Ole Mors &
          + Anders D. Børglum
   59. Department of Biomedicine, Aarhus University, DK-8000 Aarhus C,
       Denmark.
          + Ditte Demontis,
          + Manuel Mattheisen &
          + Anders D. Børglum
   60. First Department of Psychiatry, University of Athens Medical
       School, Athens 11528, Greece.
          + Dimitris Dikeos &
          + George N. Papadimitriou
   61. Department of Psychiatry, University College Cork, Co. Cork,
       Ireland.
          + Timothy Dinan
   62. Department of Medical Genetics, Oslo University Hospital, 0424
       Oslo, Norway.
          + Srdjan Djurovic
   63. Cognitive Genetics and Therapy Group, School of Psychology and
       Discipline of Biochemistry, National University of Ireland Galway,
       Co. Galway, Ireland.
          + Gary Donohoe &
          + Derek W. Morris
   64. Department of Psychiatry and Behavioral Neuroscience, University of
       Chicago, Chicago, Illinois 60637, USA.
          + Jubao Duan,
          + Alan R. Sanders &
          + Pablo V. Gejman
   65. Department of Psychiatry and Behavioral Sciences, NorthShore
       University HealthSystem, Evanston, Illinois 60201, USA.
          + Jubao Duan,
          + Alan R. Sanders &
          + Pablo V. Gejman
   66. Department of Non-Communicable Disease Epidemiology, London School
       of Hygiene and Tropical Medicine, London WC1E 7HT, UK.
          + Frank Dudbridge
   67. Department of Child and Adolescent Psychiatry, University Clinic of
       Psychiatry, Skopje 1000, Republic of Macedonia.
          + Naser Durmishi
   68. Department of Psychiatry, University of Regensburg, 93053
       Regensburg, Germany.
          + Peter Eichhammer
   69. Department of General Practice, Helsinki University Central
       Hospital, University of Helsinki P.O. Box 20, Tukholmankatu 8 B,
       FI-00014, Helsinki, Finland
          + Johan Eriksson
   70. Folkhälsan Research Center, Helsinki, Finland, Biomedicum Helsinki
       1, Haartmaninkatu 8, FI-00290, Helsinki, Finland.
          + Johan Eriksson
   71. National Institute for Health and Welfare, P.O. Box 30, FI-00271
       Helsinki, Finland.
          + Johan Eriksson &
          + Veikko Salomaa
   72. Translational Technologies and Bioinformatics, Pharma Research and
       Early Development, F. Hoffman-La Roche, CH-4070 Basel, Switzerland.
          + Laurent Essioux
   73. Department of Psychiatry, Georgetown University School of Medicine,
       Washington DC 20057, USA.
          + Ayman H. Fanous
   74. Department of Psychiatry, Keck School of Medicine of the University
       of Southern California, Los Angeles, California 90033, USA.
          + Ayman H. Fanous
   75. Departmentof Psychiatry, Virginia Commonwealth University School of
       Medicine, Richmond, Virginia 23298, USA.
          + Ayman H. Fanous
   76. Mental Health Service Line, Washington VA Medical Center,
       Washington DC 20422, USA.
          + Ayman H. Fanous
   77. Department of Genetic Epidemiology in Psychiatry, Central Institute
       of Mental Health, Medical Faculty Mannheim, University of
       Heidelberg, Heidelberg , D-68159 Mannheim, Germany.
          + Josef Frank,
          + Sandra Meier,
          + Thomas G. Schulze,
          + Jana Strohmaier,
          + Stephanie H. Witt &
          + Marcella Rietschel
   78. Department of Genetics, University of Groningen, University Medical
       Centre Groningen, 9700 RB Groningen, The Netherlands.
          + Lude Franke &
          + Juha Karjalainen
   79. Department of Psychiatry, University of Colorado Denver, Aurora,
       Colorado 80045, USA.
          + Robert Freedman &
          + Ann Olincy
   80. Center for Neurobehavioral Genetics, Semel Institute for
       Neuroscience and Human Behavior, University of California, Los
       Angeles, California 90095, USA.
          + Nelson B. Freimer &
          + Roel A. Ophoff
   81. Department of Psychiatry, University of Halle, 06112 Halle,
       Germany.
          + Marion Friedl,
          + Ina Giegling,
          + Annette M. Hartmann,
          + Bettina Konte &
          + Dan Rujescu
   82. Division of Psychiatric Genomics, Department of Psychiatry, Icahn
       School of Medicine at Mount Sinai, New York, New York, New York
       10029, USA.
          + Menachem Fromer,
          + Shaun M. Purcell,
          + Panos Roussos,
          + Douglas M. Ruderfer,
          + Eli A. Stahl &
          + Pamela Sklar
   83. Department of Psychiatry, University of Munich, 80336, Munich,
       Germany.
          + Ina Giegling &
          + Dan Rujescu
   84. Departments of Psychiatry and Human and Molecular Genetics, INSERM,
       Institut de Myologie, Hôpital de la Pitiè-Salpêtrière, Paris 75013,
       France.
          + Stephanie Godard
   85. Mental Health Research Centre, Russian Academy of Medical Sciences,
       115522 Moscow, Russia.
          + Vera Golimbet
   86. Neuroscience Therapeutic Area, Janssen Research and Development,
       Raritan, New Jersey 08869, USA.
          + Srihari Gopal,
          + Dai Wang &
          + Qingqin S. Li
   87. Queensland Brain Institute, The University of Queensland, Brisbane,
       Queensland, QLD 4072, Australia.
          + Jacob Gratten,
          + S. Hong Lee,
          + Naomi R. Wray,
          + Peter M. Visscher &
          + Bryan J. Mowry
   88. Academic Medical Centre University of Amsterdam, Department of
       Psychiatry, 1105 AZ Amsterdam, The Netherlands.
          + Lieuwe de Haan &
          + Carin J. Meijer
   89. Illumina, La Jolla, California, California 92122, USA.
          + Mark Hansen
   90. Institute of Biological Psychiatry, Mental Health Centre Sct. Hans,
       Mental Health Services Copenhagen, DK-4000, Denmark.
          + Thomas Hansen,
          + Line Olsen,
          + Henrik B. Rasmussen &
          + Thomas Werge
   91. Friedman Brain Institute, Icahn School ofMedicine at Mount Sinai,
       New York, New York 10029, USA.
          + Vahram Haroutunian,
          + Joseph D. Buxbaum &
          + Pamela Sklar
   92. J. J. Peters VA Medical Center, Bronx, New York, New York 10468,
       USA.
          + Vahram Haroutunian
   93. Priority Research Centre for Health Behaviour, University of
       Newcastle, Newcastle NSW 2308, Australia.
          + Frans A. Henskens
   94. School of Electrical Engineering and Computer Science, University
       of Newcastle, Newcastle NSW 2308, Australia.
          + Frans A. Henskens
   95. Division of Medical Genetics, Department of Biomedicine, University
       of Basel, Basel CH-4058, Switzerland.
          + Stefan Herms,
          + Per Hoffmann &
          + Sven Cichon
   96. Department of Genetics, Harvard Medical School, Boston,
       Massachusetts, Massachusetts 02115, USA.
          + Joel N. Hirschhorn,
          + Tõnu Esko &
          + Steven A. McCarroll
   97. Section of Neonatal Screening and Hormones, Department of Clinical
       Biochemistry, Immunology and Genetics, Statens Serum Institut,
       Copenhagen DK-2300, Denmark.
          + Mads V. Hollegaard &
          + David M. Hougaard
   98. Department of Psychiatry, Fujita Health University School of
       Medicine, Toyoake, Aichi,470-1192, Japan.
          + Masashi Ikeda &
          + Nakao Iwata
   99. Regional Centre for Clinical Research in Psychosis, Department of
       Psychiatry, Stavanger University Hospital, 4011 Stavanger, Norway.
          + Inge Joa
   100. Rheumatology Research Group, Vall d'Hebron Research Institute,
       Barcelona 08035, Spain.
          + Antonio Julià &
          + Sara Marsal
   101. Centre for Medical Research, The University of Western Australia,
       Perth WA6009, Australia.
          + Luba Kalaydjieva
   102. The Perkins Institute for Medical Research, The University of
       Western Australia, Perth WA6009, Australia.
          + Luba Kalaydjieva &
          + Assen V. Jablensky
   103. Department of Medical Genetics, Medical University, Sofia 1431,
       Bulgaria.
          + Sena Karachanak-Yankova &
          + Draga Toncheva
   104. Department of Psychology, University of Colorado Boulder, Boulder,
       Colorado 80309, USA.
          + Matthew C. Keller
   105. Campbell Family Mental Health Research Institute, Centre for
       Addiction and Mental Health, Toronto, Ontario M5T 1R8, Canada.
          + James L. Kennedy,
          + Clement C. Zai &
          + Jo Knight
   106. Department of Psychiatry, University of Toronto, Toronto, Ontario
       M5T 1R8, Canada.
          + James L. Kennedy,
          + Clement C. Zai &
          + Jo Knight
   107. Institute of Medical Science, University of Toronto, Toronto,
       Ontario M5S 1A8, Canada.
          + James L. Kennedy &
          + Jo Knight
   108. Institute of Molecular Genetics, Russian Academy of Sciences,
       Moscow 123182, Russia.
          + Andrey Khrunin,
          + Svetlana Limborska &
          + Petr Slominsky
   109. Latvian Biomedical Research and Study Centre, Riga, LV-1067,
       Latvia.
          + Janis Klovins &
          + Liene Nikitina-Zake
   110. Department of Psychiatry and Zilkha Neurogenetics Institute, Keck
       School of Medicine at University of Southern California, Los
       Angeles, California 90089, USA.
          + James A. Knowles,
          + Michele T. Pato &
          + Carlos N. Pato
   111. Faculty of Medicine, Vilnius University, LT-01513 Vilnius,
       Lithuania.
          + Vaidutis Kucinskas &
          + Zita Ausrele Kucinskiene
   112. Department of Biology and Medical Genetics, 2nd Faculty of
       Medicine and University Hospital Motol, 150 06 Prague, Czech
       Republic.
          + Hana Kuzelova-Ptackova &
          + Milan Macek Jr
   113. Department of Child and Adolescent Psychiatry, Pierre and Marie
       Curie Faculty of Medicine, Paris 75013, France.
          + Claudine Laurent
   114. Duke-NUS Graduate Medical School, Singapore 169857.
          + Jimmy Lee Chee Keong
   115. Department of Psychiatry, Hadassah-Hebrew University Medical
       Center, Jerusalem 91120, Israel.
          + Bernard Lerer
   116. Centre for Genomic Sciences, The University of Hong Kong, Hong
       Kong, China.
          + Miaoxin Li &
          + Pak C. Sham
   117. Mental Health Centre and Psychiatric Laboratory, West China
       Hospital, Sichuan University, Chengdu, 610041 Sichuan, China.
          + Tao Li &
          + Qiang Wang
   118. Department of Biostatistics, Johns Hopkins University Bloomberg
       School of Public Health, Baltimore, Maryland 21205, USA.
          + Kung-Yee Liang
   119. Department of Psychiatry, Columbia University, New York, New York
       10032, USA.
          + Jeffrey Lieberman &
          + T. Scott Stroup
   120. Priority Centre for Translational Neuroscience and Mental Health,
       University of Newcastle, Newcastle NSW 2300, Australia.
          + Carmel M. Loughland &
          + Ulrich Schall
   121. Department of Genetics and Pathology, International Hereditary
       Cancer Center, Pomeranian Medical University in Szczecin, 70-453
       Szczecin, Poland.
          + Jan Lubinski
   122. Department of Mental Health and Substance Abuse Services; National
       Institute for Health and Welfare, P.O. BOX 30, FI-00271 Helsinki,
       Finland.
          + Jouko Lönnqvist &
          + Jaana Suvisaari
   123. Department of Mental Health, Bloomberg School of Public Health,
       Johns Hopkins University, Baltimore, Maryland 21205, USA.
          + Brion S. Maher
   124. Department of Psychiatry, University of Bonn, D-53127 Bonn,
       Germany.
          + Wolfgang Maier
   125. Centre National de la Recherche Scientifique, Laboratoire de
       Génétique Moléculaire de la Neurotransmission et des Processus
       Neurodégénératifs, Hôpital de la Pitié Salpêtrière, 75013 Paris,
       France.
          + Jacques Mallet
   126. Department of Genomics Mathematics, University of Bonn, D-53127
       Bonn, Germany.
          + Manuel Mattheisen
   127. Research Unit, Sørlandet Hospital, 4604 Kristiansand, Norway.
          + Morten Mattingsdal
   128. Department of Psychiatry, Harvard Medical School, Boston,
       Massachusetts 02115, USA.
          + Robert W. McCarley,
          + Raquelle I. Mesholam-Gately,
          + Larry J. Seidman &
          + Tracey L. Petryshen
   129. VA Boston Health Care System, Brockton, Massachusetts 02301, USA.
          + Robert W. McCarley
   130. Department of Psychiatry, National University of Ireland Galway,
       Co. Galway, Ireland.
          + Colm McDonald
   131. Centre for Cognitive Ageing and Cognitive Epidemiology, University
       of Edinburgh, Edinburgh EH16 4SB, UK.
          + Andrew M. McIntosh
   132. Division of Psychiatry, University of Edinburgh, Edinburgh EH16
       4SB, UK.
          + Andrew M. McIntosh &
          + Douglas H. R. Blackwood
   133. Division of Mental Health and Addiction, Oslo University Hospital,
       0424 Oslo, Norway.
          + Ingrid Melle &
          + Ole A. Andreassen
   134. Massachusetts Mental Health Center Public Psychiatry Division of
       the Beth Israel Deaconess Medical Center, Boston, Massachusetts
       02114, USA.
          + Raquelle I. Mesholam-Gately &
          + Larry J. Seidman
   135. Estonian Genome Center, University of Tartu, Tartu 50090, Estonia.
          + Andres Metspalu,
          + Lili Milani,
          + Mari Nelis &
          + Tõnu Esko
   136. School of Psychology, University of Newcastle, Newcastle NSW 2308,
       Australia.
          + Patricia T. Michie
   137. First Psychiatric Clinic, Medical University, Sofia 1431,
       Bulgaria.
          + Vihra Milanova
   138. Department P, Aarhus University Hospital, DK-8240 Risskov,
       Denmark.
          + Ole Mors &
          + Anders D. Børglum
   139. Department of Psychiatry, Royal College of Surgeons in Ireland,
       Dublin 2, Ireland.
          + Kieran C. Murphy
   140. King’s College London, London SE5 8AF, UK.
          + Robin M. Murray &
          + John Powell
   141. Maastricht University Medical Centre, South Limburg Mental Health
       Research and Teaching Network, EURON, 6229 HX Maastricht, The
       Netherlands.
          + Inez Myin-Germeys &
          + Jim Van Os
   142. Institute of Translational Medicine, University of Liverpool,
       Liverpool L69 3BX, UK.
          + Bertram Müller-Myhsok
   143. Max Planck Institute of Psychiatry, 80336 Munich, Germany.
          + Bertram Müller-Myhsok
   144. Munich Cluster for Systems Neurology (SyNergy), 80336 Munich,
       Germany.
          + Bertram Müller-Myhsok
   145. Department of Psychiatry and Psychotherapy, Jena University
       Hospital, 07743 Jena, Germany.
          + Igor Nenadic
   146. Department of Psychiatry, Queensland Brain Institute and
       Queensland Centre for Mental Health Research, University of
       Queensland, Brisbane, Queensland, St Lucia QLD 4072, Australia.
          + Deborah A. Nertney
   147. Department of Psychiatry and Behavioral Sciences, Johns Hopkins
       University School of Medicine, Baltimore, Maryland 21205, USA.
          + Gerald Nestadt &
          + Ann E. Pulver
   148. Department of Psychiatry, Trinity College Dublin, Dublin 2,
       Ireland.
          + Kristin K. Nicodemus
   149. Eli Lilly and Company,Lilly Corporate Center, Indianapolis, 46285
       Indiana, USA.
          + Laura Nisenbaum
   150. Department of Clinical Sciences, Psychiatry, Umeå University,
       SE-901 87 Umeå, Sweden.
          + Annelie Nordin &
          + Rolf Adolfsson
   151. DETECT Early Intervention Service for Psychosis, Blackrock, Co.
       Dublin, Ireland.
          + Eadbhard O’Callaghan
   152. Centre for Public Health, Institute of Clinical Sciences, Queen’s
       University Belfast, Belfast BT12 6AB, UK.
          + F. Anthony O’Neill
   153. Lawrence Berkeley National Laboratory, University of California at
       Berkeley, Berkeley, California 94720, USA.
          + Sang-Yun Oh
   154. Institute of Psychiatry, King’s College London, London SE5 8AF,
       UK.
          + Jim Van Os
   155. A list of authors and affiliations appear in the Supplementary
       Information.
          + Psychosis Endophenotypes International Consortium
   156. Melbourne Neuropsychiatry Centre, University of Melbourne &
       Melbourne Health, Melbourne, Vic 3053, Australia.
          + Christos Pantelis
   157. Department of Psychiatry, University of Helsinki, P.O. Box 590,
       FI-00029 HUS, Helsinki, Finland.
          + Tiina Paunio
   158. Public Health Genomics Unit, National Institute for Health and
       Welfare, P.O. BOX 30, FI-00271 Helsinki, Finland
          + Tiina Paunio &
          + Olli Pietiläinen
   159. Medical Faculty, University of Belgrade, 11000 Belgrade, Serbia.
          + Milica Pejovic-Milovancevic
   160. Department of Psychiatry, University of North Carolina, Chapel
       Hill, North Carolina 27599-7160, USA.
          + Diana O. Perkins &
          + Patrick F. Sullivan
   161. Institute for Molecular Medicine Finland, FIMM, University of
       Helsinki, P.O. Box 20FI-00014, Helsinki, Finland
          + Olli Pietiläinen &
          + Aarno Palotie
   162. Department of Epidemiology, Harvard School of Public Health,
       Boston, Massachusetts 02115, USA.
          + Alkes Price
   163. Department of Psychiatry, University of Oxford, Oxford, OX3 7JX,
       UK.
          + Digby Quested
   164. Virginia Institute for Psychiatric and Behavioral Genetics,
       Virginia Commonwealth University, Richmond, Virginia 23298, USA.
          + Mark A. Reimers &
          + Aaron R. Wolen
   165. Institute for Multiscale Biology, Icahn School of Medicine at
       Mount Sinai, New York, New York 10029, USA.
          + Panos Roussos &
          + Pamela Sklar
   166. PharmaTherapeutics Clinical Research, Pfizer Worldwide Research
       and Development, Cambridge, Massachusetts 02139, USA.
          + Christian R. Schubert &
          + Jens R. Wendland
   167. Department of Psychiatry and Psychotherapy, University of
       Gottingen, 37073 Göttingen, Germany.
          + Thomas G. Schulze
   168. Psychiatry and Psychotherapy Clinic, University of Erlangen, 91054
       Erlangen, Germany.
          + Sibylle G. Schwab
   169. Hunter New England Health Service, Newcastle NSW 2308, Australia.
          + Rodney J. Scott
   170. School of Biomedical Sciences, University of Newcastle, Newcastle
       NSW 2308, Australia.
          + Rodney J. Scott
   171. Division of Cancer Epidemiology and Genetics, National Cancer
       Institute, Bethesda, Maryland 20892, USA.
          + Jianxin Shi
   172. University of Iceland, Landspitali, National University Hospital,
       101 Reykjavik, Iceland.
          + Engilbert Sigurdsson
   173. Department of Psychiatry and Drug Addiction, Tbilisi State Medical
       University (TSMU), N33, 0177 Tbilisi, Georgia.
          + Teimuraz Silagadze
   174. Research and Development, Bronx Veterans Affairs Medical Center,
       New York, New York 10468, USA.
          + Jeremy M. Silverman
   175. Wellcome Trust Centre for Human Genetics, Oxford OX3 7BN, UK.
          + ChrisC. A. Spencer
   176. deCODE Genetics, 101 Reykjavik, Iceland.
          + Hreinn Stefansson,
          + Stacy Steinberg &
          + Kari Stefansson
   177. Department of Clinical Neurology, Medical University of Vienna,
       1090 Wien, Austria.
          + Elisabeth Stogmann &
          + Fritz Zimprich
   178. Lieber Institute for Brain Development, Baltimore, Maryland 21205,
       USA.
          + Richard E. Straub &
          + Daniel R. Weinberger
   179. Department of Medical Genetics, University Medical Centre Utrecht,
       Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands.
          + Eric Strengman
   180. Berkshire Healthcare NHS Foundation Trust, Bracknell RG12 1BQ, UK.
          + Srinivas Thirumalai
   181. Section of Psychiatry, University of Verona, 37134 Verona, Italy.
          + Sarah Tosato
   182. Department of Psychiatry, University of Oulu, P.O. Box 5000,
       90014, Finland.
          + Juha Veijola
   183. University Hospital of Oulu, P.O. Box 20, 90029 OYS, Finland.
          + Juha Veijola
   184. Molecular and Cellular Therapeutics, Royal College of Surgeons in
       Ireland, Dublin 2, Ireland.
   185. Health Research Board, Dublin 2, Ireland.
          + Dermot Walsh
   186. School of Psychiatry and Clinical Neurosciences, The University of
       Western Australia, Perth WA6009, Australia.
          + Dieter B. Wildenauer &
          + Assen V. Jablensky
   187. Computational Sciences CoE, Pfizer Worldwide Research and
       Development, Cambridge, Massachusetts 02139, USA.
          + Hualin Simon Xi
   188. Human Genetics, Genome Institute of Singapore, A*STAR, Singapore
       138672.
          + Jianjun Liu
   189. A list of authors and affiliations appear in the Supplementary
       Information.
          + Wellcome Trust Case-Control Consortium
   190. University College London, London WC1E 6BT, UK.
   191. Department of Neuroscience, Icahn School of Medicine at Mount
       Sinai, New York, New York 10029, USA.
          + Joseph D. Buxbaum
   192. Institute of Neuroscience and Medicine (INM-1), Research Center
       Juelich, 52428 Juelich, Germany.
          + Sven Cichon
   193. Department of Genetics, The Hebrew University of Jerusalem, 91905
       Jerusalem, Israel.
          + Ariel Darvasi
   194. Neuroscience Discovery and Translational Area, Pharma Research and
       Early Development, F. Hoffman-La Roche, CH-4070 Basel, Switzerland.
          + Enrico Domenici
   195. Centre for Clinical Research in Neuropsychiatry, School of
       Psychiatry and Clinical Neurosciences, The University of Western
       Australia, Medical Research Foundation Building, Perth WA6000,
       Australia.
          + Assen V. Jablensky
   196. Virginia Institute for Psychiatric and Behavioral Genetics,
       Departments of Psychiatry and Human and Molecular Genetics,
       Virginia Commonwealth University, Richmond, Virginia 23298, USA.
          + Kenneth S. Kendler &
          + Brien P. Riley
   197. The Feinstein Institute for Medical Research, Manhasset, New York
       11030, USA.
          + Todd Lencz &
          + Anil K. Malhotra
   198. The Hofstra NS-LIJ School of Medicine, Hempstead, New York 11549,
       USA.
          + Todd Lencz &
          + Anil K. Malhotra
   199. The Zucker Hillside Hospital, Glen Oaks, New York 11004, USA.
          + Todd Lencz &
          + Anil K. Malhotra
   200. Saw Swee Hock School of Public Health, National University of
       Singapore, Singapore 117597, Singapore.
          + Jianjun Liu
   201. Queensland Centre for Mental Health Research, University of
       Queensland, Brisbane 4076, Queensland, Australia.
          + Bryan J. Mowry
   202. Center for Human Genetic Research and Department of Psychiatry,
       Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
          + Tracey L. Petryshen
   203. Department of Child and Adolescent Psychiatry, Erasmus University
       Medical Centre, Rotterdam 3000, The Netherlands.
          + Danielle Posthuma
   204. Department of Complex Trait Genetics, Neuroscience Campus
       Amsterdam, VU University Medical Center Amsterdam, Amsterdam 1081,
       The Netherlands.
          + Danielle Posthuma
   205. Department of Functional Genomics, Center for Neurogenomics and
       Cognitive Research, Neuroscience Campus Amsterdam, VU University,
       Amsterdam 1081, The Netherlands.
          + Danielle Posthuma
   206. University of Aberdeen, Institute of Medical Sciences, Aberdeen
       AB25 2ZD, UK.
          + David St Clair
   207. Departments of Psychiatry, Neurology, Neuroscience and Institute
       of Genetic Medicine, Johns Hopkins School of Medicine, Baltimore,
       Maryland 21205, USA.
          + Daniel R. Weinberger
   208. Department of Clinical Medicine, University of Copenhagen,
       Copenhagen 2200, Denmark.
          + Thomas Werge

Consortia

    1. Schizophrenia Working Group of the Psychiatric Genomics Consortium
          + Stephan Ripke,
          + Benjamin M. Neale,
          + Aiden Corvin,
          + James T. R. Walters,
          + Kai-How Farh,
          + Peter A. Holmans,
          + Phil Lee,
          + Brendan Bulik-Sullivan,
          + David A. Collier,
          + Hailiang Huang,
          + Tune H. Pers,
          + Ingrid Agartz,
          + Esben Agerbo,
          + Margot Albus,
          + Madeline Alexander,
          + Farooq Amin,
          + Silviu A. Bacanu,
          + Martin Begemann,
          + Richard A. Belliveau Jr,
          + Judit Bene,
          + Sarah E. Bergen,
          + Elizabeth Bevilacqua,
          + Tim B. Bigdeli,
          + Donald W. Black,
          + Richard Bruggeman,
          + Nancy G. Buccola,
          + Randy L. Buckner,
          + William Byerley,
          + Wiepke Cahn,
          + Guiqing Cai,
          + Dominique Campion,
          + Rita M. Cantor,
          + Vaughan J. Carr,
          + Noa Carrera,
          + Stanley V. Catts,
          + Kimberly D. Chambert,
          + Raymond C. K. Chan,
          + Ronald Y. L. Chen,
          + Eric Y. H. Chen,
          + Wei Cheng,
          + Eric F. C. Cheung,
          + Siow Ann Chong,
          + C. Robert Cloninger,
          + David Cohen,
          + Nadine Cohen,
          + Paul Cormican,
          + Nick Craddock,
          + James J. Crowley,
          + David Curtis,
          + Michael Davidson,
          + Kenneth L. Davis,
          + Franziska Degenhardt,
          + Jurgen Del Favero,
          + Ditte Demontis,
          + Dimitris Dikeos,
          + Timothy Dinan,
          + Srdjan Djurovic,
          + Gary Donohoe,
          + Elodie Drapeau,
          + Jubao Duan,
          + Frank Dudbridge,
          + Naser Durmishi,
          + Peter Eichhammer,
          + Johan Eriksson,
          + Valentina Escott-Price,
          + Laurent Essioux,
          + Ayman H. Fanous,
          + Martilias S. Farrell,
          + Josef Frank,
          + Lude Franke,
          + Robert Freedman,
          + Nelson B. Freimer,
          + Marion Friedl,
          + Joseph I. Friedman,
          + Menachem Fromer,
          + Giulio Genovese,
          + Lyudmila Georgieva,
          + Ina Giegling,
          + Paola Giusti-Rodríguez,
          + Stephanie Godard,
          + Jacqueline I. Goldstein,
          + Vera Golimbet,
          + Srihari Gopal,
          + Jacob Gratten,
          + Lieuwe de Haan,
          + Christian Hammer,
          + Marian L. Hamshere,
          + Mark Hansen,
          + Thomas Hansen,
          + Vahram Haroutunian,
          + Annette M. Hartmann,
          + Frans A. Henskens,
          + Stefan Herms,
          + Joel N. Hirschhorn,
          + Per Hoffmann,
          + Andrea Hofman,
          + Mads V. Hollegaard,
          + David M. Hougaard,
          + Masashi Ikeda,
          + Inge Joa,
          + Antonio Julià,
          + René S. Kahn,
          + Luba Kalaydjieva,
          + Sena Karachanak-Yankova,
          + Juha Karjalainen,
          + David Kavanagh,
          + Matthew C. Keller,
          + James L. Kennedy,
          + Andrey Khrunin,
          + Yunjung Kim,
          + Janis Klovins,
          + James A. Knowles,
          + Bettina Konte,
          + Vaidutis Kucinskas,
          + Zita Ausrele Kucinskiene,
          + Hana Kuzelova-Ptackova,
          + Anna K. Kähler,
          + Claudine Laurent,
          + Jimmy Lee Chee Keong,
          + S. Hong Lee,
          + Sophie E. Legge,
          + Bernard Lerer,
          + Miaoxin Li,
          + Tao Li,
          + Kung-Yee Liang,
          + Jeffrey Lieberman,
          + Svetlana Limborska,
          + Carmel M. Loughland,
          + Jan Lubinski,
          + Jouko Lönnqvist,
          + Milan Macek Jr,
          + Patrik K. E. Magnusson,
          + Brion S. Maher,
          + Wolfgang Maier,
          + Jacques Mallet,
          + Sara Marsal,
          + Manuel Mattheisen,
          + Morten Mattingsdal,
          + Robert W. McCarley,
          + Colm McDonald,
          + Andrew M. McIntosh,
          + Sandra Meier,
          + Carin J. Meijer,
          + Bela Melegh,
          + Ingrid Melle,
          + Raquelle I. Mesholam-Gately,
          + Andres Metspalu,
          + Patricia T. Michie,
          + Lili Milani,
          + Vihra Milanova,
          + Younes Mokrab,
          + Derek W. Morris,
          + Ole Mors,
          + Kieran C. Murphy,
          + Robin M. Murray,
          + Inez Myin-Germeys,
          + Bertram Müller-Myhsok,
          + Mari Nelis,
          + Igor Nenadic,
          + Deborah A. Nertney,
          + Gerald Nestadt,
          + Kristin K. Nicodemus,
          + Liene Nikitina-Zake,
          + Laura Nisenbaum,
          + Annelie Nordin,
          + Eadbhard O’Callaghan,
          + Colm O’Dushlaine,
          + F. Anthony O’Neill,
          + Sang-Yun Oh,
          + Ann Olincy,
          + Line Olsen,
          + Jim Van Os,
          + Psychosis Endophenotypes International Consortium,
          + Christos Pantelis,
          + George N. Papadimitriou,
          + Sergi Papiol,
          + Elena Parkhomenko,
          + Michele T. Pato,
          + Tiina Paunio,
          + Milica Pejovic-Milovancevic,
          + Diana O. Perkins,
          + Olli Pietiläinen,
          + Jonathan Pimm,
          + Andrew J. Pocklington,
          + John Powell,
          + Alkes Price,
          + Ann E. Pulver,
          + Shaun M. Purcell,
          + Digby Quested,
          + Henrik B. Rasmussen,
          + Abraham Reichenberg,
          + Mark A. Reimers,
          + Alexander L. Richards,
          + Joshua L. Roffman,
          + Panos Roussos,
          + Douglas M. Ruderfer,
          + Veikko Salomaa,
          + Alan R. Sanders,
          + Ulrich Schall,
          + Christian R. Schubert,
          + Thomas G. Schulze,
          + Sibylle G. Schwab,
          + Edward M. Scolnick,
          + Rodney J. Scott,
          + Larry J. Seidman,
          + Jianxin Shi,
          + Engilbert Sigurdsson,
          + Teimuraz Silagadze,
          + Jeremy M. Silverman,
          + Kang Sim,
          + Petr Slominsky,
          + Jordan W. Smoller,
          + Hon-Cheong So,
          + ChrisC. A. Spencer,
          + Eli A. Stahl,
          + Hreinn Stefansson,
          + Stacy Steinberg,
          + Elisabeth Stogmann,
          + Richard E. Straub,
          + Eric Strengman,
          + Jana Strohmaier,
          + T. Scott Stroup,
          + Mythily Subramaniam,
          + Jaana Suvisaari,
          + Dragan M. Svrakic,
          + Jin P. Szatkiewicz,
          + Erik Söderman,
          + Srinivas Thirumalai,
          + Draga Toncheva,
          + Sarah Tosato,
          + Juha Veijola,
          + John Waddington,
          + Dermot Walsh,
          + Dai Wang,
          + Qiang Wang,
          + Bradley T. Webb,
          + Mark Weiser,
          + Dieter B. Wildenauer,
          + Nigel M. Williams,
          + Stephanie Williams,
          + Stephanie H. Witt,
          + Aaron R. Wolen,
          + Emily H. M. Wong,
          + Brandon K. Wormley,
          + Hualin Simon Xi,
          + Clement C. Zai,
          + Xuebin Zheng,
          + Fritz Zimprich,
          + Naomi R. Wray,
          + Kari Stefansson,
          + Peter M. Visscher,
          + Wellcome Trust Case-Control Consortium,
          + Rolf Adolfsson,
          + Ole A. Andreassen,
          + Douglas H. R. Blackwood,
          + Elvira Bramon,
          + Joseph D. Buxbaum,
          + Anders D. Børglum,
          + Sven Cichon,
          + Ariel Darvasi,
          + Enrico Domenici,
          + Hannelore Ehrenreich,
          + Tõnu Esko,
          + Pablo V. Gejman,
          + Michael Gill,
          + Hugh Gurling,
          + Christina M. Hultman,
          + Nakao Iwata,
          + Assen V. Jablensky,
          + Erik G. Jönsson,
          + Kenneth S. Kendler,
          + George Kirov,
          + Jo Knight,
          + Todd Lencz,
          + Douglas F. Levinson,
          + Qingqin S. Li,
          + Jianjun Liu,
          + Anil K. Malhotra,
          + Steven A. McCarroll,
          + Andrew McQuillin,
          + Jennifer L. Moran,
          + Preben B. Mortensen,
          + Bryan J. Mowry,
          + Markus M. Nöthen,
          + Roel A. Ophoff,
          + Michael J. Owen,
          + Aarno Palotie,
          + Carlos N. Pato,
          + Tracey L. Petryshen,
          + Danielle Posthuma,
          + Marcella Rietschel,
          + Brien P. Riley,
          + Dan Rujescu,
          + Pak C. Sham,
          + Pamela Sklar,
          + David St Clair,
          + Daniel R. Weinberger,
          + Jens R. Wendland,
          + Thomas Werge,
          + Mark J. Daly,
          + Patrick F. Sullivan &
          + Michael C. O’Donovan
    2.

Contributions

   The individual studies or consortia contributing to the GWAS
   meta-analysis were led by R.A., O.A.A., D.H.R.B., A.D.B., E. Bramon,
   J.D.B., A.C., D.A.C., S.C., A.D., E. Domenici, H.E., T.E., P.V.G.,
   M.G., H.G., C.M.H., N.I., A.V.J., E.G.J., K.S.K., G.K., J. Knight, T.
   Lencz, D.F.L., Q.S.L., J. Liu, A.K.M., S.A.M., A. McQuillin, J.L.M.,
   P.B.M., B.J.M., M.M.N., M.C.O’D., R.A.O., M.J.O., A. Palotie, C.N.P.,
   T.L.P., M.R., B.P.R., D.R., P.C.S, P. Sklar. D.St.C., P.F.S., D.R.W.,
   J.R.W., J.T.R.W. and T.W. Together with the core statistical analysis
   group led by M.J.D. comprising S.R., B.M.N. and P.A.H., this group
   comprised the management group led by M.C.O’D. who were responsible for
   the management of the study and the overall content of the manuscript.
   Additional analyses and interpretations were contributed by E.A.,
   B.B.-S., D.K., K.-H.F., M. Fromer, H.H., P.L., P.B.M., S.M.P., T.H.P.,
   N.R.W. and P.M.V. The phenotype supervisory group comprised A.C.,
   A.H.F., P.V.G., K.K.K. and B.J.M. D.A.C. led the candidate selected
   genes subgroup comprised of M.J.D., E. Dominici, J.A.K., A.M.H.,
   M.C.O’D, B.P.R., D.R., E.M.S. and P. Sklar. Replication results were
   provided by S.S., H.S. and K.S. The remaining authors contributed to
   the recruitment, genotyping, or data processing for the contributing
   components of the meta-analysis. A.C., M.J.D., B.M.N., S.R., P.F.S. and
   M.C.O’D. took responsibility for the primary drafting of the manuscript
   which was shaped by the management group. All other authors saw, had
   the opportunity to comment on, and approved the final draft.

Competing financial interests

   CFI statement–Several of the authors are employees of the following
   pharmaceutical companies; Pfizer (C.R.S., J.R.W., H.S.X.), F.Hoffman-La
   Roche (E.D., L.E.), Eli Lilly (D.A.C., Y.M., L.N.) and Janssen (S.G.,
   D.W., Q.S.L.; also N.C. an ex-employee). Others are employees of deCODE
   genetics (S.S, H.S., K.S.). None of these companies influenced the
   design of the study, the interpretation of the data, or the amount of
   data reported, or financially profit by publication of the results
   which are pre-competitive. The other authors declare no competing
   interests.

Corresponding author

   Correspondence to:
     * Michael C. O’Donovan

   Results can be downloaded from the Psychiatric Genomics Consortium
   website (http://pgc.unc.edu) and visualized using Ricopili
   (http://www.broadinstitute.org/mpg/ricopili). Genotype data for the
   samples where the ethics permit deposition are available upon
   application from the NIMH Genetics Repository
   (https://www.nimhgenetics.org).

Author details

Extended data figures and tables

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

Extended Data Figures

    1.

        Extended Data Figure 1: Homogeneity of effects across studies. (87
                KB)
                Plot of the first two principal components (PCs) from
                principal components analysis (PCA) of the logistic
                regression β coefficients for autosomal genome-wide
                significant associations. The input data were the β
                coefficients from 52 samples for 112 independent SNP
                associations (excluding 3 chrX SNPs and 13 SNPs with
                missing values in Asian samples). PCAs were weighted by
                the number of cases. Each circle shows the location of a
                study on PC1 and PC2. Circle size and colour are
                proportional to the number of cases in each sample (larger
                and darker red circles correspond to more cases). Most
                samples cluster. Outliers had either small numbers of
                cases (‘small’) or were genotyped on older arrays.
                Abbreviations: a500 (Affymetrix 500K); a5 (Affymetrix
                5.0). Studies that did not use conventional research
                interviews are in the central cluster (CLOZUK, Sweden, and
                Denmark-Aarhus studies, see Supplementary Methods for
                sample descriptions).

    2.

        Extended Data Figure 2: Quantile-quantile plot. (111 KB)
                Quantile-quantile plot of the discovery genome-wide
                association meta-analysis of 49 case control samples
                (34,241 cases and 45,604 controls) and 3 family based
                association studies (1,235 parent affected-offspring
                trios). Expected –log[10] P values are those expected
                under the null hypothesis. Observed are the GWAS
                association results derived by logistic regression
                (2-tailed) as in Fig. 1. For clarity, we avoided expansion
                of the y axis by setting the smallest association P values
                to 10^−12. The shaded area surrounded by a red line
                indicates the 95% confidence interval under the null.
                λ[GC]is the observed median χ^2 test statistic divided by
                the median expected χ^2 test statistic under the null
                hypothesis.

    3.

        Extended Data Figure 3: Linkage disequilibrium score regression
                consistent with polygenic inheritance. (273 KB)
                The relationship between marker χ^2 association statistics
                and linkage disequilibrium (LD) as measured by the linkage
                disequilibrium score. Linkage disequilibrium score is the
                sum of the r^2 values between a variant and all other
                known variants within a 1 cM window, and quantifies the
                amount of genetic variation tagged by that variant.
                Variants were grouped into 50 equal-sized bins based on
                linkage disequilibrium score rank. Linkage disequilibrium
                score bin and mean χ^2 denotes mean linkage disequilibrium
                score and test statistic for markers each bin. a, b, We
                simulated (Supplementary Methods) test statistics under
                two scenarios: a, no true association, inflation due to
                population stratification; and b, polygenic inheritance (λ
                = 1.32), in which we assigned independent and identically
                distributed per-normalized-genotype effects to a randomly
                selected subset of variants. c, Results from the PGC
                schizophrenia GWAS (λ = 1.48). The real data are
                strikingly similar to the simulated data summarized in b
                but not a. The intercept estimates the inflation in the
                mean χ^2 that results from confounding biases, such as
                cryptic relatedness or population stratification. Thus,
                the intercept of 1.066 for the schizophrenia GWAS suggests
                that ~90% of the inflation in the mean χ^2 results from
                polygenic signal. The results of the simulations are also
                consistent with theoretical expectation (see Supplementary
                Methods). λ is the median χ^2 test statistic from the
                simulations (a, b) or the observed data (c) divided by the
                median expected χ^2 test statistic under the null
                hypothesis.

    4.

        Extended Data Figure 4: Enrichment of associations in tissues and
                cells. (259 KB)
                Genes whose transcriptional start is nearest to the most
                associated SNP at each schizophrenia-associated locus were
                tested for enriched expression in purified brain cell
                subsets obtained from mouse ribotagged lines^41 using
                enrichment analysis described in the Supplementary
                Methods. The red dotted line indicates P = 0.05.

    5.

        Extended Data Figure 5: MGS risk profile score analysis. (110 KB)
                Polygenic risk profile score (RPS) analyses using the
                MGS^18 sample as target, and deriving risk alleles from
                three published schizophrenia data sets (x axis): ISC
                (2,615 cases and 3,338 controls)^10, PGC1 (excluding MGS,
                9,320 cases and 10,228 controls)^16, and the current
                meta-analysis (excluding MGS) with 32,838 cases and 44,357
                controls. Samples sizes differ slightly from the original
                publications due to different analytical procedures. This
                shows the increasing RPS prediction with increasing
                training data set size reflecting improved precision of
                estimates of the SNP effect sizes. The proportion of
                variance explained (y axis; Nagelkerke’s R^2) was computed
                by comparison of a full model (covariates + RPS) score to
                a reduced model (covariates only). Ten different P value
                thresholds (P[T]) for selecting risk alleles are denoted
                by the colour of each bar (legend above plot). For
                significance testing, see the bottom legend which denotes
                the P value for the test that R^2 is different from zero.
                All numerical data and methods used to generate these
                plots are available in Supplementary Table 6 and
                Supplementary Methods.

    6.

        Extended Data Figure 6: Risk profile score analysis. (448 KB)
                We defined 40 target subgroups of the primary GWAS data
                set and performed 40 leave-one-out GWAS analyses (see
                Supplementary Methods and Supplementary Table 7) from
                which we derived risk alleles for RPS analysis (x axis)
                for each target subgroup. a, The proportion of variance
                explained (y axis; Nagelkerke’s R^2) was computed for each
                target by comparison of a full model (covariates + RPS)
                score to a reduced model (covariates only). For clarity, 3
                different P value thresholds (P[T]) are presented denoted
                by the colour of each bar (legend above plot) as for
                Extended Data Fig. 5, but for clarity we restrict to fewer
                P value thresholds (P[T] of 5 × 10^−8, 1 × 10^−4 and 0.05)
                and removed the significance values. b, The proportion of
                variance on the liability scale from risk scores
                calculated at the P[T] 0.05 with 95% CI bar assuming
                baseline population disease risk of 1%. c, Area under the
                receiver operating curve (AUC). All numerical data and
                methods used to generate these plots are available in
                Supplementary Table 7 and Supplementary Methods.

    7.

        Extended Data Figure 7: Pairwise epistasis analysis of significant
                SNPs. (106 KB)
                Quantile-quantile plot for all pair-wise (n = 7,750)
                combinations of the 125 independent autosomal genome-wide
                significant SNPs tested for non-additive effects on risk
                using case-control data sets of European ancestry (32,405
                cases and 42,221 controls). We included as covariates the
                principal components from the main analysis as well as a
                study indicator. The interaction model is described by:

                and are genotypes at the two loci, is the interaction
                between the two genotypes modelled in a multiplicative
                fashion, is the vector of principal components, is the
                vector of study indicator variables. Each is the
                regression coefficient in the generalized linear model
                using logistic regression. The overall distribution of P
                values did not deviate from the null and the smallest P
                value (4.28 × 10^−4) did not surpass the Bonferroni
                correction threshold (P = 0.05/7750 = 6.45 × 10^−6). The
                line x = y indicates the expected null distribution with
                the grey area bounded by red lines indicating the expected
                95% confidence interval for the null.

Extended Data Tables

    1.

        Extended Data Table 1: ALIGATOR and INRICH (182 KB)

    2.

        Extended Data Table 2: de novo overlap (213 KB)

Supplementary information

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

PDF files

    1.

        Supplementary Information (1.7 MB)
                This file contains Supplementary Text, Supplementary
                Tables 1-3, Supplementary References and Supplementary
                Notes (including a list of consortium members and
                acknowledgements) – see contents page for details.

    2.

        Supplementary Figure (2.1 MB)
                This file contains Supplementary Figure 1.

Excel files

    1.

        Supplementary Table 4 (106 KB)
                Credible causal schizophrenia SNPs, coding variants, and
                eQTLs. Worksheet 1: Coding variants: Index SNP is the
                schizophrenia associated SNP defining the schizophrenia
                associated region. Coding variant, R2, and gene denotes a
                coding credible SNP and the R2 with the index SNP, and the
                gene containing the coding variant. CHR (chromosome), BP
                (base position), A1A2 (alleles 1 and 2), frequencies of
                allele 1 (FRQ_A1), INFO (imputation quality) and P
                (P-value) refer to the index SNP in the discovery GWAS. P
                (incl rep) refers to replication P value for index SNP.
                Worksheets 2 and 3: Brain and blood eQTL: Credible SNP
                denotes a SNP within the schizophrenia credible set
                (defined in supplementary material) that is also a cis
                eQTL (transcript within 1Mb, PeQTL<1x10-4). P(cSCZ) is the
                schizophrenia (discovery) GWAS association P-value for the
                credible SNP. The Prob(cSCZ) is the normalized probability
                of the credible variant being causal for schizophrenia.
                N(cSCZ) is the number of variants in the credible set of
                schizophrenia variants within a region spanned by eQTLs at
                P<10-4. eQTL SNP is the most significant expression
                associated SNP in the region for the gene in next column
                (N.B., many regions have an eQTL for more than 1 gene).
                eQTLgene is the gene that is linked to the eQTL SNP.
                P(eQTL) is the association P-value between the eQTL SNP
                and the eQTLgene in the previous two columns. Prob(eQTL)
                is the normalized probability that the eQTL SNP is also
                the causal SNP for schizophrenia (high values mean higher
                probability of being causal). eQTLcumsum is the cumulative
                sum of the probability of all SNPs into the region, up to
                the inclusion of the max eQTL in locus ordered by
                probability of being the functional SNP. PeQTL(SCZ) is the
                schizophrenia association P-value for the eQTL SNP. R2
                (cSCZ/ eQTL) is the R2 between the credibleSNP and eQTL
                SNP. Associations to schizophrenia that are plausibly
                explained by an eQTL are in bold. Separate worksheets
                provide information on brain and blood eQTL analyses.
                Distinct loci are alternately shaded/unshaded.

    2.

        Supplementary Table 5 (173 KB)
                Pathway analyses by ALIGATOR and INRICH. Enrichment
                analyses using ALIGATOR and INRICH were performed as
                described in Supplementary Text. Pathway ID denotes the
                pathway source: GO (Gene ontology;
                http://www.geneontology.org), KEGG (Kyoto Encyclopaedia of
                Genes and Genomes; http://www.genome.jp/kegg), PAN-PW
                (PANTHER; http://www.pantherdb.org/pathway), Reactome
                (http://www.reactome.org/download), BioCarta (downloaded
                from the Molecular Signatures Database v4.0
                http://www.broadinstitute.org/gsea/msigdb/index.jsp), MGI
                (Mouse Genome Informatics;
                http://www.informatics.jax.org), and NCI pathways (NCI:
                http://pid.nci.nih.gov).

    3.

        Supplementary Table 7 (96 KB)
                Risk Profile Score Analyses. Risk Profile Score (RPS)
                analysis was performed as described in supplementary text.
                RPS datasets tab provides the name given for sample in
                which RPS was performed (target label) and the datasets
                included (defined in Supplementary Table 1). The GWAS data
                used to define the risk alleles for RPS analysis
                represents the remaining GWAS samples. For various GWAS
                P-value thresholds (denoted PT), we calculated: 1) the
                significance of the case-control score difference was
                analyzed (P tab), 2) the proportion of variance explained
                (Nagelkerke’s R2, R2 tab), 3) the proportion of variance
                on the liability scale explained by RPS (h2I tab) with
                standard error in brackets, 4) area under the receiver
                operator characteristic curve (AUC tab), and 5) odds ratio
                for the 10th RPS decile group compared with lowest decile
                with confidence interval in brackets. Ncases tab denotes
                number of cases in each target set.

    4.

        Supplementary Table 6 (32 KB)
                RPS analysis of MGS sample. Risk Profile Score (RPS)
                analyses was performed using the MGS dataset as target,
                using three distinct published results for SCZ GWAS, from
                the (1) ISC (2009) study of 2615 cases and 3338 controls11
                (denoted ISC columns) (2) PGC1 (excluding MGS, denoted
                PGC1 columns) with 9320 cases and 10228 controls22, (3)
                current meta analysis (excluding MGS, denoted Current
                columns) with 32838 cases and 44357 controls. For various
                GWAS P value thresholds (denoted PT), we calculated 1) the
                significance of the case-control score difference was
                analyzed (P tab) 2) The proportion of variance explained
                (Nagelkerke’s R2, R2 tab) 3) The proportion of variance on
                the liability scale explained by RPS (h2I tab) with
                standard error in brackets 4) Area under the receiver
                operator characteristic curve (AUC tab) and 5) Odds ratio
                for 10th RPS decile group compared with lowest decile with
                confidence interval in brackets. Ncases tab denotes number
                of cases in each target set.

Comments

     * Abstract•
     * Introduction•
     * 108 independent associated loci•
     * Characterization of associated loci•
     * The brain and immunity•
     * Overlap with rare mutations•
     * Polygenic risk score profiling•
     * Discussion•
     * References•
     * Acknowledgements•
     * Author information•
     * Extended data figures and tables•
     * Supplementary information•
     * Comments

    1. 2014-08-09 06:42 AM
       Report this comment #63705

        Hugh Fletcher said:
                This suggests two things: 1/ That studies of
                neurotransmission are easier than studies of the immune
                system, and the known involvement of the immune system in
                autism, OCD and schizophrenia has been largely ignored,
                just as APOE was neglected for amyloid precursor in
                studies of Alzheimer's. Stoner shows evidence of focal
                damage to layers of the cortex of brains of children with
                autism (N Engl J Med 2014; 370:1209-1219 March 27, 2014).
                These look similar to viral plaques and could easily
                involve the immune system, either failing to prevent
                infection or locally causing autoimune damage to specific
                cell types. Overgrowth could be a response to specific
                deficiencies. 2/ That mental health is subject to chaos
                theory. None of these alleles are necessary or sufficient.
                Particular combinations of tiny factors, many
                unpredictable, produce deviations from the norm. When
                these exceed a threshold they can be described as illness.
                If you think of human brains distributed as a pile of
                sand, most are in the central heap and are in the normal
                range. Near the edge is a line around which the difference
                from normal becomes noticable and diagnosis of a disorder
                becomes more likely. The line is nearer the centre in
                countries with a well developed health system and poor
                support for individuals. The designation of the disorder
                depends on where on the rim of the mound it falls; the
                exact location and severity of the lesions. This huge
                collection of data may be distracting. In type II
                diabetes, any loci affecting the immune system, insulin
                production or response, or glucose metabolism are risk
                factors. When a system approaches a state of failure any
                little thing that agrevates the situation may appear as a
                cause of collapse. Hopefully a unified picture of the
                primary system failure will emerge. It may be cell loss,
                rather than synaptic problems.

    2. 2014-08-20 08:23 AM
       Report this comment #63843

        Michael Lerman said:
                The CALL/CHL1 gene on 3p26 (first gene on 3p discovered by
                MH Wei and myself) was found strongly associated with
                schizophrenia in Japanese (Sakurai et al Mol Psychiatry,
                7,412, 2002) and Chinese populations (Chen QY et al,
                Schizophrenia Research, 73, 269, 2005). However a brief
                survey of Table 3 of the Supplementary Information did not
                show the CALL/CHL1 gene. Does this mean this gene is
                specific for the Chinese and Japanese populations? Michael
                Lerman, Ph.D., M.D.

   Subscribe to comments

Additional data

     * Extended Data Figure 1: Homogeneity of effects across studies.
       Hover over figure to zoom
       Plot of the first two principal components (PCs) from principal
       components analysis (PCA) of the logistic regression β coefficients
       for autosomal genome-wide significant associations. The input data
       were the β coefficients from 52 samples for 112 independent SNP
       associations (excluding 3 chrX SNPs and 13 SNPs with missing values
       in Asian samples). PCAs were weighted by the number of cases. Each
       circle shows the location of a study on PC1 and PC2. Circle size
       and colour are proportional to the number of cases in each sample
       (larger and darker red circles correspond to more cases). Most
       samples cluster. Outliers had either small numbers of cases
       (‘small’) or were genotyped on older arrays. Abbreviations: a500
       (Affymetrix 500K); a5 (Affymetrix 5.0). Studies that did not use
       conventional research interviews are in the central cluster
       (CLOZUK, Sweden, and Denmark-Aarhus studies, see Supplementary
       Methods for sample descriptions).
       Full size image
       Enable zoom
     * Extended Data Figure 2: Quantile-quantile plot.
       Hover over figure to zoom
       Quantile-quantile plot of the discovery genome-wide association
       meta-analysis of 49 case control samples (34,241 cases and 45,604
       controls) and 3 family based association studies (1,235 parent
       affected-offspring trios). Expected –log[10] P values are those
       expected under the null hypothesis. Observed are the GWAS
       association results derived by logistic regression (2-tailed) as in
       Fig. 1. For clarity, we avoided expansion of the y axis by setting
       the smallest association P values to 10^−12. The shaded area
       surrounded by a red line indicates the 95% confidence interval
       under the null. λ[GC] is the observed median χ^2 test statistic
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       Enable zoom
     * Extended Data Figure 3: Linkage disequilibrium score regression
       consistent with polygenic inheritance.
       Hover over figure to zoom
       The relationship between marker χ^2 association statistics and
       linkage disequilibrium (LD) as measured by the linkage
       disequilibrium score. Linkage disequilibrium score is the sum of
       the r^2 values between a variant and all other known variants
       within a 1 cM window, and quantifies the amount of genetic
       variation tagged by that variant. Variants were grouped into 50
       equal-sized bins based on linkage disequilibrium score rank.
       Linkage disequilibrium score bin and mean χ^2 denotes mean linkage
       disequilibrium score and test statistic for markers each bin. a, b,
       We simulated (Supplementary Methods) test statistics under two
       scenarios: a, no true association, inflation due to population
       stratification; and b, polygenic inheritance (λ = 1.32), in which
       we assigned independent and identically distributed
       per-normalized-genotype effects to a randomly selected subset of
       variants. c, Results from the PGC schizophrenia GWAS (λ = 1.48).
       The real data are strikingly similar to the simulated data
       summarized in b but not a. The intercept estimates the inflation in
       the mean χ^2 that results from confounding biases, such as cryptic
       relatedness or population stratification. Thus, the intercept of
       1.066 for the schizophrenia GWAS suggests that ~90% of the
       inflation in the mean χ^2 results from polygenic signal. The
       results of the simulations are also consistent with theoretical
       expectation (see Supplementary Methods). λ is the median χ^2 test
       statistic from the simulations (a, b) or the observed data (c)
       divided by the median expected χ^2 test statistic under the null
       hypothesis.
       Full size image
       Enable zoom
     * Extended Data Figure 4: Enrichment of associations in tissues and
       cells.
       Hover over figure to zoom
       Genes whose transcriptional start is nearest to the most associated
       SNP at each schizophrenia-associated locus were tested for enriched
       expression in purified brain cell subsets obtained from mouse
       ribotagged lines^41 using enrichment analysis described in the
       Supplementary Methods. The red dotted line indicates P = 0.05.
       Full size image
       Enable zoom
     * Extended Data Figure 5: MGS risk profile score analysis.
       Hover over figure to zoom
       Polygenic risk profile score (RPS) analyses using the MGS^18 sample
       as target, and deriving risk alleles from three published
       schizophrenia data sets (x axis): ISC (2,615 cases and 3,338
       controls)^10, PGC1 (excluding MGS, 9,320 cases and 10,228
       controls)^16, and the current meta-analysis (excluding MGS) with
       32,838 cases and 44,357 controls. Samples sizes differ slightly
       from the original publications due to different analytical
       procedures. This shows the increasing RPS prediction with
       increasing training data set size reflecting improved precision of
       estimates of the SNP effect sizes. The proportion of variance
       explained (y axis; Nagelkerke’s R^2) was computed by comparison of
       a full model (covariates + RPS) score to a reduced model
       (covariates only). Ten different P value thresholds (P[T]) for
       selecting risk alleles are denoted by the colour of each bar
       (legend above plot). For significance testing, see the bottom
       legend which denotes the P value for the test that R^2 is different
       from zero. All numerical data and methods used to generate these
       plots are available in Supplementary Table 6 and Supplementary
       Methods.
       Full size image
       Enable zoom
     * Extended Data Figure 6: Risk profile score analysis.
       Hover over figure to zoom
       We defined 40 target subgroups of the primary GWAS data set and
       performed 40 leave-one-out GWAS analyses (see Supplementary Methods
       and Supplementary Table 7) from which we derived risk alleles for
       RPS analysis (x axis) for each target subgroup. a, The proportion
       of variance explained (y axis; Nagelkerke’s R^2) was computed for
       each target by comparison of a full model (covariates + RPS) score
       to a reduced model (covariates only). For clarity, 3 different P
       value thresholds (P[T]) are presented denoted by the colour of each
       bar (legend above plot) as for Extended Data Fig. 5, but for
       clarity we restrict to fewer P value thresholds (P[T] of 5 × 10^−8,
       1 × 10^−4 and 0.05) and removed the significance values. b, The
       proportion of variance on the liability scale from risk scores
       calculated at the P[T] 0.05 with 95% CI bar assuming baseline
       population disease risk of 1%. c, Area under the receiver operating
       curve (AUC). All numerical data and methods used to generate these
       plots are available in Supplementary Table 7 and Supplementary
       Methods.
       Full size image
       Enable zoom
     * Extended Data Figure 7: Pairwise epistasis analysis of significant
       SNPs.
       Hover over figure to zoom
       Quantile-quantile plot for all pair-wise (n = 7,750) combinations
       of the 125 independent autosomal genome-wide significant SNPs
       tested for non-additive effects on risk using case-control data
       sets of European ancestry (32,405 cases and 42,221 controls). We
       included as covariates the principal components from the main
       analysis as well as a study indicator. The interaction model is
       described by:
       and are genotypes at the two loci, is the interaction between the
       two genotypes modelled in a multiplicative fashion, is the vector
       of principal components, is the vector of study indicator
       variables. Each is the regression coefficient in the generalized
       linear model using logistic regression. The overall distribution of
       P values did not deviate from the null and the smallest P value
       (4.28 × 10^−4) did not surpass the Bonferroni correction threshold
       (P = 0.05/7750 = 6.45 × 10^−6). The line x = y indicates the
       expected null distribution with the grey area bounded by red lines
       indicating the expected 95% confidence interval for the null.
       Full size image
       Enable zoom

     * Extended Data Table 1: ALIGATOR and INRICH
       Hover over figure to zoom
       Gene sets that have been reported to be enriched for schizophrenia
       associations and or rare mutations were tested for enrichment for
       genome-wide significant associations using ALIGATOR^44 and
       INRICH^45. Specifically, we tested the glutamatergic postsynaptic
       proteins comprising activity-regulated cytoskeleton-associated
       protein (ARC) and N-methyl-d-aspartate receptor (NMDAR)
       complexes^33, 34, 35, other curated synaptic gene-sets^14, 49,
       targets of fragile X mental retardation protein (FMRP)^33, 34, 35,
       calcium channels^11, 33, and TargetScan predicted MIR137 sets^11,
       16. The MIR137 TargetScan sets contain computationally predicted
       conserved miRNA target sites in 3′ UTRs of human genes^50. The
       current version is v6, but the version used in the prior PGC SCZ
       report^16 was based on v5 (filtered for a probability of conserved
       targeting > 0.9). We report the results of both analyses for
       consistency with previous work. The association at the extended MHC
       complex was not included given the extensive linkage disequilibrium
       at this region spans large numbers of genes. NA means that the
       pathway in question contained fewer than 2 significant genes (for
       ALIGATOR) or regions (INRICH).
       Full size table
       Enable zoom
     * Extended Data Table 2: de novo overlap
       Hover over figure to zoom
       Test of overlap between genes mapping to schizophrenia-associated
       loci in the present study and genes affected by non-synonymous (NS)
       de novo mutations. Enrichment was calculated using the dnenrich
       permutation framework as described^34. Genes within the GWS loci
       (Supplementary Table 3) were weighted by 1/N, where N is the number
       of coding genes within each associated locus. The observed test
       statistic (stat) is the sum of weights of genes impacted by de novo
       mutations. The expected test statistics are calculated by averaging
       over 50,000 permuted de novo mutation sets. Genes within
       schizophrenia-associated loci affected by de novo mutations are
       listed (multiple hits listed in parentheses). Cohorts: SCZ,
       schizophrenia; ID, intellectual disability; ASD, autism spectrum
       disorder. All mutations analysed annotated according to a unified
       system (see Supplementary Tables 1 and 2 of ref. 34). Genes with
       loss-of-function de novo mutations are underlined and in italics.
       Full size table
       Enable zoom

Editor's summary in العربية

   Although schizophrenia is a highly heritable disorder, its complex
   polygenic nature has impeded attempts to establish its genetic basis.
   This paper reports a genome-wide association study of more than 36,000
   schizophrenia patients and 100,000 controls. The study identifies 128
   independent associations in 108 loci, 83 of them new. Among them are
   many genes involved in glutamatergic neurotransmission, highlighting a
   potential therapeutic avenue. In addition, the results provide support
   for the hypothesized link between the immune system and schizophrenia.

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   Home > Health & Education > Mental Health Information

Schizophrenia

     * What Is Schizophrenia?
     * Causes
     * Who Is At Risk?
     * Signs & Symptoms
     * Treatments
     * Living With
     * Clinical Trials

   More
     * What Is Schizophrenia?
     * Causes
     * Who Is At Risk?
     * Signs & Symptoms
     * Treatments
     * Living With
     * Clinical Trials

What Is Schizophrenia?

   Schizophrenia is a chronic, severe, and disabling brain disorder that
   has affected people throughout history.

   People with the disorder may hear voices other people don't hear. They
   may believe other people are reading their minds, controlling their
   thoughts, or plotting to harm them. This can terrify people with the
   illness and make them withdrawn or extremely agitated.

   People with schizophrenia may not make sense when they talk. They may
   sit for hours without moving or talking. Sometimes people with
   schizophrenia seem perfectly fine until they talk about what they are
   really thinking.

   Families and society are affected by schizophrenia too. Many people
   with schizophrenia have difficulty holding a job or caring for
   themselves, so they rely on others for help.

   Treatment helps relieve many symptoms of schizophrenia, but most people
   who have the disorder cope with symptoms throughout their lives.
   However, many people with schizophrenia can lead rewarding and
   meaningful lives in their communities. Researchers are developing more
   effective medications and using new research tools to understand the
   causes of schizophrenia. In the years to come, this work may help
   prevent and better treat the illness.

Causes

   Experts think schizophrenia is caused by several factors.

   Genes and environment. Scientists have long known that schizophrenia
   runs in families. The illness occurs in 1 percent of the general
   population, but it occurs in 10 percent of people who have a
   first-degree relative with the disorder, such as a parent, brother, or
   sister. People who have second-degree relatives (aunts, uncles,
   grandparents, or cousins) with the disease also develop schizophrenia
   more often than the general population. The risk is highest for an
   identical twin of a person with schizophrenia. He or she has a 40 to 65
   percent chance of developing the disorder.

   We inherit our genes from both parents. Scientists believe several
   genes are associated with an increased risk of schizophrenia, but that
   no gene causes the disease by itself. In fact, recent research has
   found that people with schizophrenia tend to have higher rates of rare
   genetic mutations. These genetic differences involve hundreds of
   different genes and probably disrupt brain development.

   Other recent studies suggest that schizophrenia may result in part when
   a certain gene that is key to making important brain chemicals
   malfunctions. This problem may affect the part of the brain involved in
   developing higher functioning skills. Research into this gene is
   ongoing, so it is not yet possible to use the genetic information to
   predict who will develop the disease.

   Despite this, tests that scan a person's genes can be bought without a
   prescription or a health professional's advice. Ads for the tests
   suggest that with a saliva sample, a company can determine if a client
   is at risk for developing specific diseases, including schizophrenia.
   However, scientists don't yet know all of the gene variations that
   contribute to schizophrenia. Those that are known raise the risk only
   by very small amounts. Therefore, these "genome scans" are unlikely to
   provide a complete picture of a person's risk for developing a mental
   disorder like schizophrenia.

   In addition, it probably takes more than genes to cause the disorder.
   Scientists think interactions between genes and the environment are
   necessary for schizophrenia to develop. Many environmental factors may
   be involved, such as exposure to viruses or malnutrition before birth,
   problems during birth, and other not yet known psychosocial factors.

   Different brain chemistry and structure. Scientists think that an
   imbalance in the complex, interrelated chemical reactions of the brain
   involving the neurotransmitters dopamine and glutamate, and possibly
   others, plays a role in schizophrenia. Neurotransmitters are substances
   that allow brain cells to communicate with each other. Scientists are
   learning more about brain chemistry and its link to schizophrenia.

   Also, in small ways the brains of people with schizophrenia look
   different than those of healthy people. For example, fluid-filled
   cavities at the center of the brain, called ventricles, are larger in
   some people with schizophrenia. The brains of people with the illness
   also tend to have less gray matter, and some areas of the brain may
   have less or more activity.

   Studies of brain tissue after death also have revealed differences in
   the brains of people with schizophrenia. Scientists found small changes
   in the distribution or characteristics of brain cells that likely
   occurred before birth. Some experts think problems during brain
   development before birth may lead to faulty connections. The problem
   may not show up in a person until puberty. The brain undergoes major
   changes during puberty, and these changes could trigger psychotic
   symptoms. Scientists have learned a lot about schizophrenia, but more
   research is needed to help explain how it develops.

Who Is At Risk?

   About 1% of Americans have this illness.

   Schizophrenia affects men and women equally. It occurs at similar rates
   in all ethnic groups around the world. Symptoms such as hallucinations
   and delusions usually start between ages 16 and 30. Men tend to
   experience symptoms a little earlier than women. Most of the time,
   people do not get schizophrenia after age 45. Schizophrenia rarely
   occurs in children, but awareness of childhood-onset schizophrenia is
   increasing.

   It can be difficult to diagnose schizophrenia in teens. This is because
   the first signs can include a change of friends, a drop in grades,
   sleep problems, and irritability—behaviors that are common among teens.
   A combination of factors can predict schizophrenia in up to 80% of
   youth who are at high risk of developing the illness. These factors
   include isolating oneself and withdrawing from others, an increase in
   unusual thoughts and suspicions, and a family history of psychosis. In
   young people who develop the disease, this stage of the disorder is
   called the "prodromal" period.

Signs & Symptoms

   The symptoms of schizophrenia fall into three broad categories:
   positive symptoms, negative symptoms, and cognitive symptoms.

   Positive symptoms

   Positive symptoms are psychotic behaviors not seen in healthy people.
   People with positive symptoms often "lose touch" with reality. These
   symptoms can come and go. Sometimes they are severe and at other times
   hardly noticeable, depending on whether the individual is receiving
   treatment. They include the following:

   Hallucinations are things a person sees, hears, smells, or feels that
   no one else can see, hear, smell, or feel. "Voices" are the most common
   type of hallucination in schizophrenia. Many people with the disorder
   hear voices. The voices may talk to the person about his or her
   behavior, order the person to do things, or warn the person of danger.
   Sometimes the voices talk to each other. People with schizophrenia may
   hear voices for a long time before family and friends notice the
   problem.

   Other types of hallucinations include seeing people or objects that are
   not there, smelling odors that no one else detects, and feeling things
   like invisible fingers touching their bodies when no one is near.

   Delusions are false beliefs that are not part of the person's culture
   and do not change. The person believes delusions even after other
   people prove that the beliefs are not true or logical. People with
   schizophrenia can have delusions that seem bizarre, such as believing
   that neighbors can control their behavior with magnetic waves. They may
   also believe that people on television are directing special messages
   to them, or that radio stations are broadcasting their thoughts aloud
   to others. Sometimes they believe they are someone else, such as a
   famous historical figure. They may have paranoid delusions and believe
   that others are trying to harm them, such as by cheating, harassing,
   poisoning, spying on, or plotting against them or the people they care
   about. These beliefs are called "delusions of persecution."

   Thought disorders are unusual or dysfunctional ways of thinking. One
   form of thought disorder is called "disorganized thinking." This is
   when a person has trouble organizing his or her thoughts or connecting
   them logically. They may talk in a garbled way that is hard to
   understand. Another form is called "thought blocking." This is when a
   person stops speaking abruptly in the middle of a thought. When asked
   why he or she stopped talking, the person may say that it felt as if
   the thought had been taken out of his or her head. Finally, a person
   with a thought disorder might make up meaningless words, or
   "neologisms."

   Movement disorders may appear as agitated body movements. A person with
   a movement disorder may repeat certain motions over and over. In the
   other extreme, a person may become catatonic. Catatonia is a state in
   which a person does not move and does not respond to others. Catatonia
   is rare today, but it was more common when treatment for schizophrenia
   was not available.

   Negative symptoms

   Negative symptoms are associated with disruptions to normal emotions
   and behaviors. These symptoms are harder to recognize as part of the
   disorder and can be mistaken for depression or other conditions. These
   symptoms include the following:
     * "Flat affect" (a person's face does not move or he or she talks in
       a dull or monotonous voice)
     * Lack of pleasure in everyday life
     * Lack of ability to begin and sustain planned activities
     * Speaking little, even when forced to interact.

   People with negative symptoms need help with everyday tasks. They often
   neglect basic personal hygiene. This may make them seem lazy or
   unwilling to help themselves, but the problems are symptoms caused by
   the schizophrenia.

   Cognitive symptoms

   Cognitive symptoms are subtle. Like negative symptoms, cognitive
   symptoms may be difficult to recognize as part of the disorder. Often,
   they are detected only when other tests are performed. Cognitive
   symptoms include the following:
     * Poor "executive functioning" (the ability to understand information
       and use it to make decisions)
     * Trouble focusing or paying attention
     * Problems with "working memory" (the ability to use information
       immediately after learning it).

   Cognitive symptoms often make it hard to lead a normal life and earn a
   living. They can cause great emotional distress.

Treatments

   Because the causes of schizophrenia are still unknown, treatments focus
   on eliminating the symptoms of the disease. Treatments include
   antipsychotic medications and various psychosocial treatments.

   Antipsychotic medications

   Antipsychotic medications have been available since the mid-1950's. The
   older types are called conventional or "typical" antipsychotics. Some
   of the more commonly used typical medications include:
     * Chlorpromazine (Thorazine)
     * Haloperidol (Haldol)
     * Perphenazine (Etrafon, Trilafon)
     * Fluphenazine (Prolixin).

   In the 1990's, new antipsychotic medications were developed. These new
   medications are called second generation, or "atypical" antipsychotics.

   One of these medications, clozapine (Clozaril) is an effective
   medication that treats psychotic symptoms, hallucinations, and breaks
   with reality. But clozapine can sometimes cause a serious problem
   called agranulocytosis, which is a loss of the white blood cells that
   help a person fight infection. People who take clozapine must get their
   white blood cell counts checked every week or two. This problem and the
   cost of blood tests make treatment with clozapine difficult for many
   people. But clozapine is potentially helpful for people who do not
   respond to other antipsychotic medications.

   Other atypical antipsychotics were also developed. None cause
   agranulocytosis. Examples include:
     * Risperidone (Risperdal)
     * Olanzapine (Zyprexa)
     * Quetiapine (Seroquel)
     * Ziprasidone (Geodon)
     * Aripiprazole (Abilify)
     * Paliperidone (Invega).

   What are the side effects?

   Some people have side effects when they start taking these medications.
   Most side effects go away after a few days and often can be managed
   successfully. People who are taking antipsychotics should not drive
   until they adjust to their new medication. Side effects of many
   antipsychotics include:
     * Drowsiness
     * Dizziness when changing positions
     * Blurred vision
     * Rapid heartbeat
     * Sensitivity to the sun
     * Skin rashes
     * Menstrual problems for women.

   Atypical antipsychotic medications can cause major weight gain and
   changes in a person's metabolism. This may increase a person's risk of
   getting diabetes and high cholesterol. A person's weight, glucose
   levels, and lipid levels should be monitored regularly by a doctor
   while taking an atypical antipsychotic medication.

   Typical antipsychotic medications can cause side effects related to
   physical movement, such as:
     * Rigidity
     * Persistent muscle spasms
     * Tremors
     * Restlessness.

   Long-term use of typical antipsychotic medications may lead to a
   condition called tardive dyskinesia (TD). TD causes muscle movements a
   person can't control. The movements commonly happen around the mouth.
   TD can range from mild to severe, and in some people the problem cannot
   be cured. Sometimes people with TD recover partially or fully after
   they stop taking the medication.

   TD happens to fewer people who take the atypical antipsychotics, but
   some people may still get TD. People who think that they might have TD
   should check with their doctor before stopping their medication.

   How are antipsychotics taken and how do people respond to them?

   Antipsychotics are usually in pill or liquid form. Some anti-psychotics
   are shots that are given once or twice a month.

   Symptoms of schizophrenia, such as feeling agitated and having
   hallucinations, usually go away within days. Symptoms like delusions
   usually go away within a few weeks. After about six weeks, many people
   will see a lot of improvement.

   However, people respond in different ways to antipsychotic medications,
   and no one can tell beforehand how a person will respond. Sometimes a
   person needs to try several medications before finding the right one.
   Doctors and patients can work together to find the best medication or
   medication combination, as well as the right dose.

   Some people may have a relapse-their symptoms come back or get worse.
   Usually, relapses happen when people stop taking their medication, or
   when they only take it sometimes. Some people stop taking the
   medication because they feel better or they may feel they don't need it
   anymore. But no one should stop taking an antipsychotic medication
   without talking to his or her doctor. When a doctor says it is okay to
   stop taking a medication, it should be gradually tapered off, never
   stopped suddenly.

   How do antipsychotics interact with other medications?

   Antipsychotics can produce unpleasant or dangerous side effects when
   taken with certain medications. For this reason, all doctors treating a
   patient need to be aware of all the medications that person is taking.
   Doctors need to know about prescription and over-the-counter medicine,
   vitamins, minerals, and herbal supplements. People also need to discuss
   any alcohol or other drug use with their doctor.

   To find out more about how antipsychotics work, the National Institute
   of Mental Health (NIMH) funded a study called CATIE (Clinical
   Antipsychotic Trials of Intervention Effectiveness). This study
   compared the effectiveness and side effects of five antipsychotics used
   to treat people with schizophrenia. In general, the study found that
   the older typical antipsychotic perphenazine (Trilafon) worked as well
   as the newer, atypical medications. But because people respond
   differently to different medications, it is important that treatments
   be designed carefully for each person. More information about CATIE is
   on the NIMH website.

   Psychosocial treatments

   Psychosocial treatments can help people with schizophrenia who are
   already stabilized on antipsychotic medication. Psychosocial treatments
   help these patients deal with the everyday challenges of the illness,
   such as difficulty with communication, self-care, work, and forming and
   keeping relationships. Learning and using coping mechanisms to address
   these problems allow people with schizophrenia to socialize and attend
   school and work.

   Patients who receive regular psychosocial treatment also are more
   likely to keep taking their medication, and they are less likely to
   have relapses or be hospitalized. A therapist can help patients better
   understand and adjust to living with schizophrenia. The therapist can
   provide education about the disorder, common symptoms or problems
   patients may experience, and the importance of staying on medications.
   For more information on psychosocial treatments, see the
   psychotherapies section on the NIMH website.

   Illness management skills. People with schizophrenia can take an active
   role in managing their own illness. Once patients learn basic facts
   about schizophrenia and its treatment, they can make informed decisions
   about their care. If they know how to watch for the early warning signs
   of relapse and make a plan to respond, patients can learn to prevent
   relapses. Patients can also use coping skills to deal with persistent
   symptoms.

   Integrated treatment for co-occurring substance abuse. Substance abuse
   is the most common co-occurring disorder in people with schizophrenia.
   But ordinary substance abuse treatment programs usually do not address
   this population's special needs. When schizophrenia treatment programs
   and drug treatment programs are used together, patients get better
   results.

   Rehabilitation. Rehabilitation emphasizes social and vocational
   training to help people with schizophrenia function better in their
   communities. Because schizophrenia usually develops in people during
   the critical career-forming years of life (ages 18 to 35), and because
   the disease makes normal thinking and functioning difficult, most
   patients do not receive training in the skills needed for a job.

   Rehabilitation programs can include job counseling and training, money
   management counseling, help in learning to use public transportation,
   and opportunities to practice communication skills. Rehabilitation
   programs work well when they include both job training and specific
   therapy designed to improve cognitive or thinking skills. Programs like
   this help patients hold jobs, remember important details, and improve
   their functioning.

   Family education. People with schizophrenia are often discharged from
   the hospital into the care of their families. So it is important that
   family members know as much as possible about the disease. With the
   help of a therapist, family members can learn coping strategies and
   problem-solving skills. In this way the family can help make sure their
   loved one sticks with treatment and stays on his or her medication.
   Families should learn where to find outpatient and family services.

   Cognitive behavioral therapy. Cognitive behavioral therapy (CBT) is a
   type of psychotherapy that focuses on thinking and behavior. CBT helps
   patients with symptoms that do not go away even when they take
   medication. The therapist teaches people with schizophrenia how to test
   the reality of their thoughts and perceptions, how to "not listen" to
   their voices, and how to manage their symptoms overall. CBT can help
   reduce the severity of symptoms and reduce the risk of relapse.

   Self-help groups. Self-help groups for people with schizophrenia and
   their families are becoming more common. Professional therapists
   usually are not involved, but group members support and comfort each
   other. People in self-help groups know that others are facing the same
   problems, which can help everyone feel less isolated. The networking
   that takes place in self-help groups can also prompt families to work
   together to advocate for research and more hospital and community
   treatment programs. Also, groups may be able to draw public attention
   to the discrimination many people with mental illnesses face.

Living With

   How can you help a person with schizophrenia?

   People with schizophrenia can get help from professional case managers
   and caregivers at residential or day programs. However, family members
   usually are a patient's primary caregivers.

   People with schizophrenia often resist treatment. They may not think
   they need help because they believe their delusions or hallucinations
   are real. In these cases, family and friends may need to take action to
   keep their loved one safe. Laws vary from state to state, and it can be
   difficult to force a person with a mental disorder into treatment or
   hospitalization. But when a person becomes dangerous to himself or
   herself, or to others, family members or friends may have to call the
   police to take their loved one to the hospital.

   Treatment at the hospital. In the emergency room, a mental health
   professional will assess the patient and determine whether a voluntary
   or involuntary admission is needed. For a person to be admitted
   involuntarily, the law states that the professional must witness
   psychotic behavior and hear the person voice delusional thoughts.
   Family and friends can provide needed information to help a mental
   health professional make a decision.

   After a loved one leaves the hospital. Family and friends can help
   their loved ones get treatment and take their medication once they go
   home. If patients stop taking their medication or stop going to
   follow-up appointments, their symptoms likely will return. Sometimes
   symptoms become severe for people who stop their medication and
   treatment. This is dangerous, since they may become unable to care for
   themselves. Some people end up on the street or in jail, where they
   rarely receive the kind of help they need.

   Family and friends can also help patients set realistic goals and learn
   to function in the world. Each step toward these goals should be small
   and taken one at a time. The patient will need support during this
   time. When people with a mental illness are pressured and criticized,
   they usually do not get well. Often, their symptoms may get worse.
   Telling them when they are doing something right is the best way to
   help them move forward.

   It can be difficult to know how to respond to someone with
   schizophrenia who makes strange or clearly false statements. Remember
   that these beliefs or hallucinations seem very real to the person. It
   is not helpful to say they are wrong or imaginary. But going along with
   the delusions is not helpful, either. Instead, calmly say that you see
   things differently. Tell them that you acknowledge that everyone has
   the right to see things his or her own way. In addition, it is
   important to understand that schizophrenia is a biological illness.
   Being respectful, supportive, and kind without tolerating dangerous or
   inappropriate behavior is the best way to approach people with this
   disorder.

   Are people with schizophrenia violent?

   People with schizophrenia are not usually violent. In fact, most
   violent crimes are not committed by people with schizophrenia. However,
   some symptoms are associated with violence, such as delusions of
   persecution. Substance abuse may also increase the chance a person will
   become violent. If a person with schizophrenia becomes violent, the
   violence is usually directed at family members and tends to take place
   at home.

   The risk of violence among people with schizophrenia is small. But
   people with the illness attempt suicide much more often than others.
   About 10 percent (especially young adult males) die by suicide. It is
   hard to predict which people with schizophrenia are prone to suicide.
   If you know someone who talks about or attempts suicide, help him or
   her find professional help right away.

   What about substance abuse?

   Some people who abuse drugs show symptoms similar to those of
   schizophrenia. Therefore, people with schizophrenia may be mistaken for
   people who are affected by drugs. Most researchers do not believe that
   substance abuse causes schizophrenia. However, people who have
   schizophrenia are much more likely to have a substance or alcohol abuse
   problem than the general population.

   Substance abuse can make treatment for schizophrenia less effective.
   Some drugs, like marijuana and stimulants such as amphetamines or
   cocaine, may make symptoms worse. In fact, research has found
   increasing evidence of a link between marijuana and schizophrenia
   symptoms. In addition, people who abuse drugs are less likely to follow
   their treatment plan.

   Schizophrenia and smoking

   Addiction to nicotine is the most common form of substance abuse in
   people with schizophrenia. They are addicted to nicotine at three times
   the rate of the general population (75 to 90 percent vs. 25 to 30
   percent).

   The relationship between smoking and schizophrenia is complex. People
   with schizophrenia seem to be driven to smoke, and researchers are
   exploring whether there is a biological basis for this need. In
   addition to its known health hazards, several studies have found that
   smoking may make antipsychotic drugs less effective.

   Quitting smoking may be very difficult for people with schizophrenia
   because nicotine withdrawal may cause their psychotic symptoms to get
   worse for a while. Quitting strategies that include nicotine
   replacement methods may be easier for patients to handle. Doctors who
   treat people with schizophrenia should watch their patients' response
   to antipsychotic medication carefully if the patient decides to start
   or stop smoking.

Clinical Trials

   NIMH supports research studies on mental health and disorders. See
   also: A Participant's Guide to Mental Health Clinical Research.

   Participate, refer a patient or learn about results of studies in
   ClinicalTrials.gov , the NIH/National Library of Medicine's registry of
   federally and privately funded clinical trials for all disease.

   Find NIH-funded studies currently recruiting participants with
   schizophrenia.

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                           Types of Schizophrenia

                          By Michael Bengston, M.D.
                                ~ 5 min read

   Pages: 1 2All

   The kinds of symptoms that are utilized to make a diagnosis of
   schizophrenia differ between affected people and may change from one
   year to the next within the same person as the disease progresses.
   Different subtypes of schizophrenia are defined according to the most
   significant and predominant characteristics present in each person at
   each point in time. The result is that one person may be diagnosed with
   different subtypes over the course of his illness.

Schizophrenia: Paranoid Subtype

   The defining feature of the paranoid subtype (also known as paranoid
   schizophrenia) is the presence of auditory hallucinations or prominent
   delusional thoughts about persecution or conspiracy. However, people
   with this subtype may be more functional in their ability to work and
   engage in relationships than people with other subtypes of
   schizophrenia. The reasons are not entirely clear, but may partly
   reflect that people suffering from this subtype often do not exhibit
   symptoms until later in life and have achieved a higher level of
   functioning before the onset of their illness. People with the paranoid
   subtype may appear to lead fairly normal lives by successful management
   of their disorder.

   Paranoid schizophrenia is the most common subtype.

   People diagnosed with the paranoid subtype may not appear odd or
   unusual and may not readily discuss the symptoms of their illness.
   Typically, the hallucinations and delusions revolve around some
   characteristic theme, and this theme often remains fairly consistent
   over time. A person’s temperaments and general behaviors often are
   related to the content of the disturbance of thought. For example,
   people who believe that they are being persecuted unjustly may be
   easily angered and become hostile. Often, paranoid schizophrenics will
   come to the attention of mental health professionals only when there
   has been some major stress in their life that has caused an increase in
   their symptoms. At that point, sufferers may recognize the need for
   outside help or act in a fashion to bring attention to themselves.

   Since there may be no observable features, the evaluation requires
   sufferers to be somewhat open to discussing their thoughts. If there is
   a significant degree of suspiciousness or paranoia present, people may
   be very reluctant to discuss these issues with a stranger.

   There is a broad spectrum to the nature and severity of symptoms that
   may be present at any one time. When symptoms are in a phase of
   exacerbation or worsening, there may be some disorganization of the
   thought processes. At this time, people may have more trouble than
   usual remembering recent events, speaking coherently or generally
   behaving in an organized, rational manner. While these features are
   more characteristic of other subtypes, they can be present to differing
   degrees in people with the paranoid subtype, depending upon the current
   state of their illness. Supportive friends or family members often may
   be needed at such times to help the symptomatic person get professional
   help.

Schizophrenia: Disorganized Subtype

   As the name implies, this subtype’s predominant feature is
   disorganization of the thought processes. As a rule, hallucinations and
   delusions are less pronounced, although there may be some evidence of
   these symptoms. These people may have significant impairments in their
   ability to maintain the activities of daily living. Even the more
   routine tasks, such as dressing, bathing or brushing teeth, can be
   significantly impaired or lost.

   Often, there is impairment in the emotional processes of the
   individual. For example, these people may appear emotionally unstable,
   or their emotions may not seem appropriate to the context of the
   situation. They may fail to show ordinary emotional responses in
   situations that evoke such responses in healthy people. Mental health
   professionals refer to this particular symptom as blunted or flat
   affect. Additionally, these people may have an inappropriately jocular
   or giddy appearance, as in the case of a patient who chuckles
   inappropriately through a funeral service or other solemn occasion.

   People diagnosed with this subtype also may have significant impairment
   in their ability to communicate effectively. At times, their speech can
   become virtually incomprehensible, due to disorganized thinking. In
   such cases, speech is characterized by problems with the utilization
   and ordering of words in conversational sentences, rather than with
   difficulties of enunciation or articulation. In the past, the term
   hebephrenic has been used to describe this subtype.

   Pages: 1 2All


     *
     *
     *
     *

   APA Reference
   Bengston, M. (2006). Types of Schizophrenia. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/lib/types-of-schizophrenia/000714
     * Ben Behind His Voices: One Family’s Journey from the Chaos of
       Schizophrenia to Hope
     * The Dopamine Connection Between Schizophrenia and Creativity
     * Living with Schizoaffective Disorder
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       Illness
     * Therapists Spill: How to End Therapy
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     * When You Can’t Afford Psychotherapy

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     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 2 Sep 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
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     * Books
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     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

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   Schizophrenia

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                           Types of Schizophrenia

                          By Michael Bengston, M.D.
                                ~ 5 min read

   Pages: 1 2All

Schizophrenia: Catatonic Subtype

   The predominant clinical features seen in the catatonic subtype involve
   disturbances in movement. Affected people may exhibit a dramatic
   reduction in activity, to the point that voluntary movement stops, as
   in catatonic stupor. Alternatively, activity can dramatically increase,
   a state known as catatonic excitement.

   Other disturbances of movement can be present with this subtype.
   Actions that appear relatively purposeless but are repetitively
   performed, also known as stereotypic behavior, may occur, often to the
   exclusion of involvement in any productive activity.

   Patients may exhibit an immobility or resistance to any attempt to
   change how they appear. They may maintain a pose in which someone
   places them, sometimes for extended periods of time. This symptom
   sometimes is referred to as waxy flexibility. Some patients show
   considerable physical strength in resistance to repositioning attempts,
   even though they appear to be uncomfortable to most people.

   Affected people may voluntarily assume unusual body positions, or
   manifest unusual facial contortions or limb movements. This set of
   symptoms sometimes is confused with another disorder called tardive
   dyskinesia, which mimics some of these same, odd behaviors. Other
   symptoms associated with the catatonic subtype include an almost
   parrot-like repeating of what another person is saying (echolalia) or
   mimicking the movements of another person (echopraxia). Echolalia and
   echopraxia also are seen in Tourette’s Syndrome.

Schizophrenia: Undifferentiated Subtype

   The undifferentiated subtype is diagnosed when people have symptoms of
   schizophrenia that are not sufficiently formed or specific enough to
   permit classification of the illness into one of the other subtypes.

   The symptoms of any one person can fluctuate at different points in
   time, resulting in uncertainty as to the correct subtype
   classification. Other people will exhibit symptoms that are remarkably
   stable over time but still may not fit one of the typical subtype
   pictures. In either instance, diagnosis of the undifferentiated subtype
   may best describe the mixed clinical syndrome.

Schizophrenia: Residual Subtype

   This subtype is diagnosed when the patient no longer displays prominent
   symptoms. In such cases, the schizophrenic symptoms generally have
   lessened in severity. Hallucinations, delusions or idiosyncratic
   behaviors may still be present, but their manifestations are
   significantly diminished in comparison to the acute phase of the
   illness.

   Just as the symptoms of schizophrenia are diverse, so are its
   ramifications. Different kinds of impairment affect each patient’s life
   to varying degrees. Some people require custodial care in state
   institutions, while others are gainfully employed and can maintain an
   active family life. However, the majority of patients are at neither of
   these extremes. Most will have a waxing and waning course marked with
   some hospitalizations and some assistance from outside support sources.

   People having a higher level of functioning before the start of their
   illness typically have a better outcome. In general, better outcomes
   are associated with brief episodes of symptoms worsening followed by a
   return to normal functioning. Women have a better prognosis for higher
   functioning than men, as do patients with no apparent structural
   abnormalities of the brain.

   In contrast, a poorer prognosis is indicated by a gradual or insidious
   onset, beginning in childhood or adolescence; structural brain
   abnormalities, as seen on imaging studies; and failure to return to
   prior levels of functioning after acute episodes.

                                                        » Next in Series:
                                                   Causes of Schizophrenia

   Schizophrenia Table of Contents
     * Introduction to Schizophrenia
     * Symptoms of Schizophrenia
     * Types of Schizophrenia
     * Causes of Schizophrenia
     * An Introduction to the Treatment of Schizophrenia
     * Treatment of Schizophrenia
     * Living with Schizophrenia
     * Helpful Hints About Schizophrenia for Family Members & Others

   Pages: 1 2All


     *
     *
     *
     *

   APA Reference
   Bengston, M. (2006). Types of Schizophrenia. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/lib/types-of-schizophrenia/000714
     * Ben Behind His Voices: One Family’s Journey from the Chaos of
       Schizophrenia to Hope
     * The Dopamine Connection Between Schizophrenia and Creativity
     * Living with Schizoaffective Disorder
     * What Causes Schizophrenia?
     * Bipolar Disorder: 6 Ways To Distinguish Between Yourself & Your
       Illness
     * Therapists Spill: How to End Therapy
     * Helping Parents Understand OCD
     * Grief and Mourning in Schizophrenia: A Safety Plan
     * How to Get Going When the Going Gets Tough
     * When You Can’t Afford Psychotherapy

   Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

     Long-Acting Treatments for Schizophrenia

     Treating Schizophrenia Successfully

     Book Review: Leave of Absence

     Betrayal & Hearing Voices

     Art Therapy: Beneficial Schizophrenia Treatment?

     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 2 Sep 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

     Long-Acting Treatments for Schizophrenia

     Treating Schizophrenia Successfully

     Book Review: Leave of Absence

     Betrayal & Hearing Voices

     Art Therapy: Beneficial Schizophrenia Treatment?


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                           Schizophrenia Symptoms

                           By Psych Central Staff

   Page:« 1 2View All»

   Schizophrenia is a mental disorder that is characterized by at least 2
   of the following  symptoms, for at least one month:
     * Delusions
     * Hallucinations
     * Disorganized speech (e.g., frequent derailment or incoherence)
     * Grossly disorganized or catatonic behavior
     * A set of three negative symptoms (a “flattening” of one’s
       emotions, alogia, avolition; see below)

   Only one of the above symptoms is required to make the diagnosis of
   schizophrenia if the person’s delusions are bizarre or if the
   hallucinations consist of a voice keeping up a running commentary
   on the person’s behavior or thoughts, or two or more voices conversing
   with each other.

                              Positive Symptoms
     * Delusions
     * Hallucinations
     * Disorganized thinking
     * Agitation

                              Negative Symptoms
     * Affective flattening- The person’s range of emotional expression is
       clearly diminished; poor eye contract; reduced body language
     * Alogia- A poverty of speech, such as brief, empty replies
     * Avolition – Inability to initiate and persist in goal-directed
       activities (such as school or work)

   Although the above symptoms must be present for at least one (1) month,
   there also needs to be continuous signs of the disturbance that persist
   for at least six (6) months.  During this period, the signs of the
   disorder may be present in a milder form, for instance as just odd
   beliefs or unusual perceptual experiences. During this 6 month period,
   at least two of the above criteria must be met, or only the criteria of
   Negative Symptoms must be present — if even just in milder form.

   Onset of schizophrenia prior to adolescence is rare. The peak age at
   onset for the first psychotic episode is in the early- to mid-20s for
   males and in the late-20s for females. Though active symptoms typically
   do not emerge until an individual is in their 20′s,
   oftentimes prodromal symptoms will precede the first psychotic episode,
   characterized by milder forms of hallucinations or delusions. For
   example, individuals may express a variety of unusual or odd beliefs
   that are not of delusional proportions (e.g., ideas of reference or
   magical thinking); they may have unusual perceptual experiences (e.g.,
   sensing the presence of an unseen person); their speech may be
   generally understandable but vague; and their behavior may be unusual
   but not grossly disorganized (e.g., mumbling in public).

   Individuals with schizophrenia evidence large distress and impairments
   in various life domains. Functioning in areas such as work,
   interpersonal relations, or self-care must be markedly below the level
   achieved prior to the onset of the symptoms to receive the diagnosis
   (or when the onset is in childhood or adolescence, failure to achieve
   expected level of interpersonal, academic, or occupational
   achievement).

   Schizoaffective Disorder and Mood Disorder With Psychotic Features must
   be considered as alternative explanations for the symptoms and have
   been ruled out. The disturbance must also not be due to the direct
   physiological effects of use or abuse of a substance (e.g., alcohol,
   drugs, medications) or a general medical condition.

   If there is a history of Autistic Disorder or another Pervasive
   Developmental Disorder, the additional diagnosis of Schizophrenia is
   made only if prominent delusions or hallucinations are also present for
   at least a month (or less if successfully treated).

   0.3%–0.7% of individuals appear to acquire schizophrenia. although
   there is reported variation by race/ethnicity, across countries, and by
   geographic origin for immigrants and children of immigrants. The sex
   ratio differs across samples and populationHostility and aggression can
   be associated with schizophrenia, although spontaneous or random
   assault is uncommon. Aggression is more frequent for younger males and
   for individuals with a past history of violence, non-adherence with
   treatment, substance abuse, and impulsivity. It should be noted that
   the vast majority of persons with schizophrenia are not aggressive and
   are more frequently victimized than are individuals in the general
   population.


Entry has been updated for DSM-5; diagnostic code 295.90.

The old criteria in the DSM-IV divided schizophrenia by different Types.
Though we not longer use such specifiers in the updated DSM-5, they remain
below for informational/historical purposes.

A brief list of types of schizophrenia, according to DSM-IV:

     * Paranoid schizophrenia– a person feels extremely suspicious,
       persecuted, grandiose, or experiences a combination of these
       emotions.
     * Disorganized schizophrenia  — a person is often incoherent but may
       not have delusions.
     * Catatonic schizophrenia– a person is withdrawn, mute, negative and
       often assumes very unusual postures.
     * Residual schizophrenia — a person is no longer delusion or
       hallucinating, but has no motivation or interest in life. These
       symptoms can be most devastating.


   Page: 1 2View All


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     *
     *
     *
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   « Mental Disorders Index


   APA Reference
   Psych Central. (2014). Schizophrenia Symptoms. Psych Central. Retrieved
   on February 4, 2015, from
   http://psychcentral.com/disorders/schizophrenia-symptoms/

   Symptom criteria summarized from:
   American Psychiatric Association. (2013). Diagnostic and statistical
   manual of mental disorders, fifth edition. Washington, DC: American
   Psychiatric Association.
           or
   American Psychiatric Association. (1994). Diagnostic and statistical
   manual of mental disorders, fourth edition. Washington, DC: American
   Psychiatric Association.

     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 22 Jun 2014
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

     Long-Acting Treatments for Schizophrenia

     Treating Schizophrenia Successfully

     Book Review: Leave of Absence

     Betrayal & Hearing Voices

     Art Therapy: Beneficial Schizophrenia Treatment?


   From Our News Bureau
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     * Insomnia Therapy Can Reduce Suicidal Thoughts in Veterans
     * Smartphones Tied to Poor Sleep In Teens

   Just Published...
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     * The Chemistry Of ADHD
     * 20 Mental Health Symptoms of Food-Borne Metal Toxicity

   What's Hot
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     * The Funny Thing About Self-Care
     * 10 Nutritional Deficiencies that May Cause Depression

   advertisement
     *
     *
     *
     *

Most Popular News

     * Diet, Nutrition Closely Linked to Mental Health
     * Fermented Food Linked to Mental Health
     * Musical Training in Youth Can Protect Brain in Old Age
     * Depression and Loneliness = Extreme Television Viewing
     * Insomnia Therapy Can Reduce Suicidal Thoughts in Veterans
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                   Illuminating 13 Myths of Schizophrenia

                       By Margarita Tartakovsky, M.S.
                                ~ 6 min read

   It’s safe to say that no mental disorder is more shrouded in mystery,
   misunderstanding and fear than schizophrenia. “The modern-day
   equivalent of leprosy” is how renowned research psychiatrist E. Fuller
   Torrey, M.D., refers to schizophrenia in his excellent book, Surviving
   Schizophrenia: A Manual for Families, Patients, and Providers.

   While 85 percent of Americans recognize that schizophrenia is a
   disorder, only 24 percent are actually familiar with it. And according
   to a 2008 survey by the National Alliance on Mental Illness (NAMI), 64
   percent can’t recognize its symptoms or think the symptoms include a
   “split” or multiple personalities. (They don’t.)

   Aside from ignorance, images of the aggressive, sadistic
   “schizophrenic” are plentiful in the media. Such stereotypes only
   further the stigma and quash any shred of sympathy for individuals with
   this illness, writes Dr. Torrey. Stigma has a slew of negative
   consequences. It’s been associated with reduced housing and employment
   opportunities, diminished quality of life, low self-esteem and more
   symptoms and stress (see Penn, Chamberlin & Mueser, 2003).

   So it’s bad enough that people with schizophrenia are afflicted with a
   terrible disease. But they also have to deal with the confusion, fear
   and disgust of others. Whether your loved one has schizophrenia or
   you’d like to learn more, gaining a better understanding of it helps
   demystify the disease and is a huge help to those who suffer from it.

   Below are some pervasive myths — followed by actual facts — regarding
   schizophrenia.

   1. Individuals with schizophrenia all have the same symptoms.

   For starters, there are different types of schizophrenia. Even
   individuals diagnosed with the same subtype of schizophrenia often look
   very different. Schizophrenia is “a huge, huge range of people and
   problems,” said Robert E. Drake, M.D., Ph.D, professor of psychiatry
   and of community and family medicine at Dartmouth Medical School.

   Part of the reason that schizophrenia is so mysterious is because we’re
   unable to put ourselves in the shoes of someone with the disorder. It’s
   simply hard to imagine what having schizophrenia would be like.
   Everyone experiences sadness, anxiety and anger, but schizophrenia
   seems so out of our realm of feeling and understanding. It may help to
   adjust our perspective. Dr. Torrey writes:

     Those of us who have not had this disease should ask ourselves, for
     example, how we would feel if our brain began playing tricks on us,
     if unseen voices shouted at us, if we lost the capacity to feel
     emotions, and if we lost the ability to reason logically.

   2. People with schizophrenia are dangerous, unpredictable and out of
   control.

   “When their illness is treated with medication and psychosocial
   interventions, individuals with schizophrenia are no more violent than
   the general population,” said Dawn I. Velligan, Ph.D, professor and
   co-director of the Division of Schizophrenia and Related Disorders at
   the Department of Psychiatry, UT Health Science Center at San Antonio.
   Also, “People with schizophrenia more often tend to be victims rather
   than perpetrators of violence although untreated mental illness and
   substance abuse often increase the risk of aggressive behavior,” said
   Irene S. Levine, Ph.D, psychologist and co-author of Schizophrenia for
   Dummies.

   3. Schizophrenia is a character flaw.

   Lazy, lacking in motivation, lethargic, easily confused…the list of
   “qualities” individuals with schizophrenia appear to have goes on and
   on. However, the idea that schizophrenia is a character defect “is no
   more realistic than suggesting that someone could prevent his epileptic
   seizures if he really wanted to or that someone could ‘decide’ not to
   have cancer if he ate the right foods. What often appears as character
   defects are symptoms of schizophrenia,” write Levine and co-author
   Jerome Levine, M.D., in Schizophrenia for Dummies.

   4. Cognitive decline is a major symptom of schizophrenia.

   Seemingly unmotivated individuals most likely experience cognitive
   difficulties with problem solving, attention, memory and processing.
   They may forget to take their medication. They may ramble and not make
   sense. They may have a tough time organizing their thoughts. Again,
   these are symptoms of schizophrenia, which have nothing to do with
   character or personality.

   5. There are psychotic and non-psychotic people.

   The public and clinicians alike view psychosis as categorical — you’re
   either psychotic or you’re not — instead of symptoms residing on a
   continuum, said Demian Rose, M.D., Ph.D, medical director of the
   University of California, San Francisco PART Program and director of
   the UCSF Early Psychosis Clinic. For instance, most people will agree
   that individuals aren’t simply depressed or happy. There are gradients
   of depression, from mild one-day melancholy to deep, crippling clinical
   depression. Similarly, schizophrenia symptoms are not fundamentally
   different brain processes, but lie on a continuum with normal cognitive
   processes, Dr. Rose said. Auditory hallucinations may seem
   extraordinarily different but how often have you had a song stuck in
   your head that you can hear pretty clearly?

   6. Schizophrenia develops quickly.

   “It’s quite rare to have a big drop in functioning,” Dr. Rose said.
   Schizophrenia tends to develop slowly. Initial signs often show during
   adolescence. These signs typically include school, social and work
   decline, difficulties managing relationships and problems with
   organizing information, he said. Again, symptoms lie on a continuum. In
   schizophrenia’s beginning stages, an individual may not hear voices.
   Instead, he may hear whispers, which he can’t make out. This
   “prodromal” period — before the onset of schizophrenia — is the perfect
   time to intervene and seek treatment.

   7. Schizophrenia is purely genetic.

   “Studies have shown that in pairs of identical twins (who share an
   identical genome) the prevalence of developing the illness is 48
   percent,” said Sandra De Silva, Ph.D, psychosocial treatment
   co-director and outreach director at the Staglin Music Festival Center
   for the Assessment and Prevention of Prodromal States (CAPPS) at UCLA,
   departments of psychology and psychiatry. Because other factors are
   involved, it’s possible to reduce the risk of developing the illness,
   she added. There are various prodromal programs that focus on helping
   at-risk adolescents and adults.

   Along with genetics, research has shown that stress and family
   environment can play a big role in increasing a person’s susceptibility
   to psychosis. “While we can’t change genetic vulnerability, we can
   reduce the amount of stress in someone’s life, build coping skills to
   improve the way we respond to stress, and create a protective low-key,
   calm family environment without a lot of conflict and tension in hopes
   of reducing the risk of illness progression,” De Sliva said.

   8. Schizophrenia is untreatable.

   “While schizophrenia is not curable, it is an eminently treatable and
   manageable chronic illness, just like diabetes or heart disease,”
   Levine said. The key is to get the right treatment for your needs. See
   Living with Schizophrenia here for details.

   9. Sufferers need to be hospitalized.

   Most individuals with schizophrenia “do well living in the community
   with outpatient treatment,” Velligan said. Again, the key is the right
   treatment and adhering to that treatment, especially taking medication
   as prescribed.

   10. People with schizophrenia can’t lead productive lives.

   “Many individuals can lead happy and productive lives,” Velligan said.
   In a 10-year study of 130 individuals with schizophrenia and substance
   abuse — which co-occurs in nearly 50 percent of patients — from the New
   Hampshire Dual Diagnosis Study, many gained control over both
   disorders, reducing their episodes of hospitalization and homelessness,
   living on their own and achieving a better quality of life (Drake,
   McHugo, Xie, Fox, Packard & Helmstetter, 2006). Specifically, “62.7
   percent were controlling symptoms of schizophrenia; 62.5 percent were
   actively attaining remissions from substance abuse; 56.8 percent were
   in independent living situations; 41.4 percent were competitively
   employed; 48.9 percent had regular social contacts with non–substance
   abusers; and 58.3 percent expressed overall life satisfaction.”

   11. Medications make sufferers zombies.

   When we think of antipsychotic medication for schizophrenia, we
   automatically think of adjectives like lethargic, listless,
   uninterested and vacant. Many believe medication causes these sorts of
   symptoms. However, most often these symptoms are either from
   schizophrenia itself or because of overmedication. Zombie-like
   reactions are “relatively minor, compared with the number of patients
   who have never been given an adequate trial of available medications,”
   according to Dr. Torrey in Surviving Schizophrenia.

   12. Antipsychotic medications are worse than the illness itself.

   Medication is the mainstay of schizophrenia treatment. Antipsychotic
   medications effectively reduce hallucinations, delusions, confusing
   thoughts and bizarre behaviors. These agents can have severe side
   effects and can be fatal, but this is rare. “Antipsychotic drugs, as a
   group, are one of the safest groups of drugs in common use and are the
   greatest advance in the treatment of schizophrenia that has occurred to
   date,” Dr. Torrey writes.

   13. Individuals with schizophrenia can never regain normal functioning.

   Unlike dementia, which worsens over time or doesn’t improve,
   schizophrenia seems to be a problem that’s reversible, Dr. Rose said.
   There’s no line that once it’s crossed signifies that there’s no hope
   for a person with schizophrenia, he added.

   References

   Drake, R.E., McHugo, G.J., Xie, H., Fox, M., Packard, J., &
   Helmstetter, B. (2006). Ten-Year Recovery Outcomes for Clients With
   Co-Occurring Schizophrenia and Substance Use Disorders>. Schizophrenia
   Bulletin, 32, 464-473.

   Penn, D.L., Chamberlin, C., & Mueser, K.T. (2003). The effects of a
   documentary film about schizophrenia on psychiatric stigma.
   Schizophrenia Bulletin, 29, 383-391.


     *
     *
     *
     *

   Margarita Tartakovsky, M.S. is an Associate Editor at Psych Central and
   blogs regularly about eating and self-image issues on her own blog,
   Weightless.
   APA Reference
   Tartakovsky, M. (2010). Illuminating 13 Myths of Schizophrenia. Psych
   Central. Retrieved on February 4, 2015, from
   http://psychcentral.com/lib/illuminating-13-myths-of-schizophrenia/0002
   709
     * After Schizophrenia
     * Clinicians on the Couch: 10 Questions with Therapist Claire
       Dorotik-Nana
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     * Treating Schizophrenia Successfully
     * Increasing Treatment Adherence in Schizophrenia
     * A Current Look at Chronic Depression
     * Recovering from Mental Illness? Be Your Own Best Friend
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     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

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                         What Causes Schizophrenia?

                             By Brian Smith, MS
                                ~ 3 min read

   What Causes Schizophrenia? The causes of schizophrenia, like all mental
   disorders, are not completely understood or known at this time.

   There is no known single cause of schizophrenia. Many diseases, such as
   heart disease, result from an interplay of genetic, behavioral and
   other factors, and this may be the case for schizophrenia as well.
   Scientists do not yet understand all of the factors necessary to
   produce, but all the tools of modern biomedical research are being used
   to search for genes, critical moments in brain development, and other
   factors that may lead to the illness.

Can Schizophrenia Be Inherited?

   It has been long understood that schizophrenia runs in families. People
   who have a close relative with schizophrenia are more likely to develop
   the disorder than are people who have no relatives with the illness. A
   child whose parent has schizophrenia has about a 10 percent chance of
   developing schizophrenia themselves. A monozygotic (identical) twin of
   a person with schizophrenia has the highest risk — a 40 to 65 percent
   chance of developing the illness. People who have second-degree
   relatives (aunts, uncles, grandparents, or cousins) with the disease
   also develop schizophrenia more often than the general population. By
   comparison, the risk of schizophrenia in the general population is
   about 1 percent.

   Scientists are continuing to study and better understand the genetic
   factors related to schizophrenia. We inherit our genes from both
   parents. Scientists believe several genes are associated with an
   increased risk of schizophrenia, but that no gene causes the disease by
   itself. In fact, recent research has found that people with
   schizophrenia tend to have higher rates of rare genetic mutations.
   These genetic differences involve hundreds of different genes and
   probably disrupt brain development.

   In addition, factors such as prenatal difficulties like intrauterine
   starvation or viral infections, perinatal complications, and various
   nonspecific stressors, seem to influence the development of
   schizophrenia. However, it is not yet understood how the genetic
   predisposition is transmitted, and it cannot yet be accurately
   predicted whether a given person will or will not develop the disorder.

   Other recent studies suggest that schizophrenia may result in part when
   a certain gene that is key to making important brain chemicals
   malfunctions. This problem may affect the part of the brain involved in
   developing higher functioning skills.Research into this gene is
   ongoing, so it is not yet possible to use the genetic information to
   predict who will develop the disease.

   In addition, it probably takes more than genes to cause the disorder.
   Scientists think interactions between genes and the environment are
   necessary for schizophrenia to develop. Many environmental factors may
   be involved, such as exposure to viruses or malnutrition before birth,
   problems during birth, and other not yet known psychosocial factors.

Is Schizophrenia Caused by a Chemical Defect in the Brain?

   Basic knowledge about brain chemistry and its link to schizophrenia is
   expanding rapidly. Neurotransmitters, substances that allow
   communication between nerve cells, have long been thought to be
   involved in the development of schizophrenia. It is likely, although
   not yet certain, that the disorder is associated with some imbalance of
   the complex, interrelated chemical systems of the brain, perhaps
   involving the neurotransmitters dopamine and glutamate.

Is Schizophrenia Caused by a Physical Abnormality in the Brain?

   There have been dramatic advances in neuroimaging technology that
   permit scientists to study brain structure and function in living
   individuals. Many studies of people with schizophrenia have found
   abnormalities in brain structure. In some small but potentially
   important ways, the brains of people with schizophrenia look different
   than those of healthy people. For example, fluid-filled cavities at the
   center of the brain, called ventricles, are larger in some people with
   schizophrenia. The brains of people with the illness also tend to have
   less gray matter, and some areas of the brain may have less or more
   activity.

   It should be emphasized that these abnormalities are quite subtle and
   are not characteristic of all people with schizophrenia, nor do they
   occur only in individuals with this illness. Microscopic studies of
   brain tissue after death have also shown small changes in distribution
   or number of brain cells in people with schizophrenia. It appears that
   many (but probably not all) of these changes are present before an
   individual becomes ill, and schizophrenia may be, in part, a disorder
   in development of the brain.

   Developmental neurobiologists have found that schizophrenia may be a
   developmental disorder resulting when neurons form inappropriate
   connections during fetal development. These errors may lie dormant
   until puberty, when changes in the brain that occur normally during
   this critical stage of maturation interact adversely with the faulty
   connections. This research has spurred efforts to identify prenatal
   factors that may have some bearing on the apparent developmental
   abnormality.

   In other studies, investigators using brain-imaging techniques have
   found evidence of early biochemical changes that may precede the onset
   of disease symptoms, prompting examination of the neural circuits that
   are most likely to be involved in producing those symptoms. Meanwhile,
   scientists working at the molecular level are exploring the genetic
   basis for abnormalities in brain development and in the
   neurotransmitter systems regulating brain function.

                                                        » Next in Series:
                         An Introduction to the Treatment of Schizophrenia

   Schizophrenia Table of Contents
     * Introduction to Schizophrenia
     * Symptoms of Schizophrenia
     * Types of Schizophrenia
     * Causes of Schizophrenia
     * An Introduction to the Treatment of Schizophrenia
     * Treatment of Schizophrenia
     * Living with Schizophrenia
     * Helpful Hints About Schizophrenia for Family Members & Others

   Based upon material from the National Institute of Mental Health.


     *
     *
     *
     *

   APA Reference
   Psych Central. (2006). What Causes Schizophrenia?. Psych Central.
   Retrieved on February 4, 2015, from
   http://psychcentral.com/lib/what-causes-schizophrenia/000715
     * Types of Schizophrenia
     * Helpful Hints about Schizophrenia for Family Members and Others
     * Long-Acting Treatments for Schizophrenia
     * Maximum Brainpower: Challenging the Brain for Health and Wisdom
     * Cannabis May Cause Schizophrenia-Like Brain Changes
     * Demons in the Age of Light: A Memoir of Psychosis and Recovery
     * Schizophrenia and Genetics: Research Update
     * The Dopamine Connection Between Schizophrenia and Creativity
     * Illuminating 13 Myths of Schizophrenia
     * Schizophrenia Fact Sheet

   Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

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     Art Therapy: Beneficial Schizophrenia Treatment?

     Scientifically Reviewed
         Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
         Published on PsychCentral.com. All rights reserved.


Schizophrenia

     * Overview of Schizophrenia
     * Schizophrenia Quick Fact Sheet
     *
     * Schizophrenia Screening Quiz
     *
     * An Introduction to Schizophrenia
     * Schizophrenia Symptoms
     * Types of Schizophrenia
     * Treatment Overview
     * Schizophrenia Treatment
     * Living with Schizophrenia
     * Schizophrenia & Genetics: Research Update
     *
     * 13 Schizophrenia Myths
     * Taking Medications for Schizophrenia
     * Side Effects of Medications
     * Helpful Hints About Schizophrenia for Family Members
     * Schizophrenia and Substance Abuse
     * Schizophrenia and Violence
     * What Causes Schizophrenia?
     * When Someone Has Schizophrenia
     *
     * Related Topics
     * Schizophrenia News
     * Clinical Trials
     * Research
     * DSM Codes for Schizophrenia
     *
     * Recommended Resources
     * Books
     * Websites & Organizations
     *
     * Connect with Others
     * Join Our Support Group
     * Rate 'n Review Schizophrenia Medications

Latest Articles

     The Fog of Paranoia: A Sister’s Journey through Her Brother’s
   Schizophrenia

     Long-Acting Treatments for Schizophrenia

     Treating Schizophrenia Successfully

     Book Review: Leave of Absence

     Betrayal & Hearing Voices

     Art Therapy: Beneficial Schizophrenia Treatment?


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                           Schizophrenia Treatment

                          By John M. Grohol, Psy.D.

   Table of Contents
     * Introduction
     * Psychotherapy
     * Medications
     * Coping Guidelines For The Family
     * Self-Help
       _______________________________________________________________

Introduction

   Schizophrenia usually first appears in a person during their late teens
   or throughout their twenties. It affects more men than women, and is
   considered a life-long condition which rarely is "cured," but rather
   treated. The primary treatment for schizophrenia and similar thought
   disorders is medication. Unfortunately, compliance with a medication
   regimen is often one of the largest problems associated with the
   ongoing treatment of schizophrenia. Because people who live with this
   disorder often go off of their medication during periods throughout
   their lives, the repercussions of this loss of treatment are acutely
   felt not only by the individual, but by their family and friends as
   well.

   Successful treatment of schizophrenia, therefore, depends upon a
   life-long regimen of both drug and psychosocial, support therapies.
   While the medication helps control the psychosis associated with
   schizophrenia (e.g., the delusions and hallucinations), it cannot help
   the person find a job, learn to be effective in social relationships,
   increase the individual's coping skills, and help them learn to
   communicate and work well with others. Poverty, homelessness, and
   unemployment are often associated with this disorder, but they don't
   have to be. If the individual finds appropriate treatment and sticks
   with it, a person with schizophrenia can lead a happy and successful
   life. But the initial recovery from the first symptoms of schizophrenia
   can be an extremely lonely experience. Individuals coping with the
   onset of schizophrenia for the first time in their lives require all
   the support that their families, friends, and communities can provide.

   With such support, determination, and understanding, someone who has
   schizophrenia can learn to cope and live with it for their entire life.
   But stability with this disorder means complying with the treatment
   plan set up between the person and their therapist or doctor, and
   maintaining the balance provided for by the medication and therapy. A
   sudden stopping of treatment will most often lead to a relapse of the
   symptoms associated with schizophrenia and then a gradual recovery as
   treatment is reinstated.

Psychotherapy

   Psychotherapy is not the treatment of choice for someone with
   schizophrenia. Used as an adjunct to a good medication plan, however,
   psychotherapy can help maintain the individual on their medication,
   learn needed social skills, and support the person's weekly goals and
   activities in their community. This may include advice, reassurance,
   education, modeling, limit setting, and reality testing with the
   therapist. Encouragement in setting small goals and reaching them can
   often be helpful.

   People with schizophrenia often have a difficult time performing
   ordinary life skills such as cooking and personal grooming as well as
   communicating with others in the family and at work. Therapy or
   rehabilitation therapy can help a person regain the confidence to take
   care of themselves and live a fuller life.

   Group therapy, combined with drugs, produces somewhat better results
   than drug treatment alone, particularly with schizophrenic outpatients.
   Positive results are more likely to be obtained when group therapy
   focuses on real-life plans, problems, and relationships; on social and
   work roles and interaction; on cooperation with drug therapy and
   discussion of its side effects; or on some practical recreational or
   work activity. This supportive group therapy can be especially helpful
   in decreasing social isolation and increasing reality testing (Long,
   1996).

   Family therapy can significantly decrease relapse rates for the
   schizophrenic family member. In high-stress families, schizophrenic
   patients given standard aftercare relapse 50-60% of the time in the
   first year out of hospital. Supportive family therapy can reduce this
   relapse rate to below 10 percent. This therapy encourages the family to
   convene a family meeting whenever an issue arises, in order to discuss
   and specify the exact nature of the problem, to list and consider
   alternative solutions, and to select and implement the consensual best
   solution. (Long, 1996).

Medications

   Schizophrenia appears to be a combination of a thought disorder, mood
   disorder, and anxiety disorder. The medical management of schizophrenia
   often requires a combination of antipsychotic, antidepressant, and
   antianxiety medication. One of the biggest challenges of treatment is
   that many people don't keep taking the medications prescribed for the
   disorder. After the first year of treatment, most people will
   discontinue their use of medications, especially ones where the side
   effects are difficult to tolerate.

   As a recent National Institute of Mental Health Study indicated,
   regardless of the drug, three-quarters of all patients stop taking
   their medications. They stopped the schizophrenia medications either
   because they did not make them better or they had intolerable side
   effects. The discontinuation rates remained high when they were
   switched to a new drug, but patients stayed on clozapine about 11
   months, compared with only three months for Seroquel, Risperdal or
   Zyprexa, which are far more heavily marketed -- and dominate sales.
   Because of findings such as this, it's generally recommended that
   someone with schizophrenia begin their treatment with a drug such as
   clozapine (clozapine is often significantly cheaper than other
   antipsychotic medications). Clozapine (also known as clozaril) has been
   shown to be more effective than many newer antipsychotics as well.

   Antipsychotic medications help to normalize the biochemical imbalances
   that cause schizophrenia. They are also important in reducing the
   likelihood of relapse. There are two major types of antipsychotics,
   traditional and new antipsychotics.

   Traditional antipsychotics effectively control the hallucinations,
   delusions, and confusion of schizophrenia. This type of antipsychotic
   drug, such as haloperidol, chlorpromazine, and fluphenazine, has been
   available since the mid-1950s. These drugs primarily block dopamine
   receptors and are effective in treating the "positive" symptoms of
   schizophrenia.

   Side effects for antipsychotics may cause a patient to stop taking
   them. However, it is important to talk with your doctor before making
   any changes in medication since many side effects can be controlled. Be
   sure to weigh the risks against the potential benefits that
   antipsychotic drugs can provide.

   Mild side effects: dry mouth, blurred vision, constipation, drowsiness
   and dizziness. These side affects usually disappear a few weeks after
   the person starts treatment.

   More serious side effects: trouble with muscle control, muscle spasms
   or cramps in the head and neck, fidgeting or pacing, tremors and
   shuffling of the feet (much like those affecting people with
   Parkinson's disease).

   Side effects due to prolonged use of traditional antipsychotic
   medications: facial ticks, thrusting and rolling of the tongue, lip
   licking, panting and grimacing.

   There are many newer antipsychotic medications available since the
   1990's, including Seroquel, Risperdal, Zyprexa and Clozaril. Some of
   these medications may work on both the serotonin and dopamine
   receptors, thereby treating both the "positive" and "negative" symptoms
   of schizophrenia. Other newer antipsychotics are referred to as
   atypical antipsychotics, because of how they affect the dopamine
   receptors in the brain. These newer medications may be more effective
   in treating a broader range of symptoms of schizophrenia, and some have
   fewer side effects than traditional antipsychotics. Learn more about
   the atypical antipsychotics used to help treat schizophrenia.

Coping Guidelines For The Family

    1. Establish a daily routine for the patient to follow.
    2. Help the patient stay on the medication.
    3. Keep the lines of communication open about problems or fears the
       patient may have.
    4. Understand that caring for the patient can be emotionally and
       physically exhausting. Take time for yourself.
    5. Keep your communications simple and brief when speaking with the
       patient.
    6. Be patient and calm.
    7. Ask for help if you need it; join a support group.

Self-Help

   Self-help methods for the treatment of this disorder are often
   overlooked by the medical profession because very few professionals are
   involved in them. Adjunctive community support groups in concurrence
   with psychotherapy is usually beneficial to most people who suffer from
   schizophrenia. Caution should be utilized, however, if the person's
   symptoms aren't under control of a medication. People with this
   disorder often have a difficult time in social situations, therefore a
   support group should not be considered as an initial treatment option.
   As the person progresses in treatment, a support group may be a useful
   option to help the person make the transition back into daily social
   life.

   Another use of self-help is for the family members of someone who lives
   with schizophrenia. The stress and hardships causes of having a loved
   one with this disorder are often overwhelming and difficult to cope
   with for a family. Family members should use a support group within
   their community to share common experiences and learn about ways to
   best deal with their frustrations, feelings of helplessness, and anger.

                                                        » Next in Series:
                                                 Living with Schizophrenia

   Schizophrenia Table of Contents
     * Introduction to Schizophrenia
     * Symptoms of Schizophrenia
     * Types of Schizophrenia
     * Causes of Schizophrenia
     * An Introduction to the Treatment of Schizophrenia
     * Treatment of Schizophrenia
     * Living with Schizophrenia
     * Helpful Hints About Schizophrenia for Family Members & Others

   References: Psych Central, National Mental Health Association,
   National Institute for Mental Health, National Alliance for the
   Mentally Ill,
   Internet Mental Health

     Last reviewed:
       On 9 Oct 2013
       By John M. Grohol, Psy.D.


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Cannabis-Derivative a Potential New Schizophrenia Treatment

   by Nina Flanagan on April 8, 2014
   medicine.image

   There have been many research studies suggesting that marijuana may
   increase risk of schizophrenia (see here). But there is also a recent
   study at Harvard Medical School, led by Ashley C. Proal, that has
   suggested this may not be the case. This recent comparison between
   families with a history of schizophrenia and those without, found no
   connection to marijuana as a cause for the disorder.

   There are over 400 different chemicals in the marijuana plant, so the
   issue is more complex than it might seem at first and it appears that
   there may be some chemicals from the plant that may actually be helpful
   for people who have schizophrenia.

   In fact, GW Pharmaceuticals (www.gwpharm.com), which has several
   cannabinoid-based drugs in the research pipeline, is now gearing up for
   a human trial of one of its CBDs to treat schizophrenia. Steve Schultz,
   VP, investor relations, says the company wants to differentiate itself
   from medical marijuana. “We grow all our plants in a controlled
   environment and extract various chemicals that undergo rigorous
   testing. This is completely different from medical marijuana, which is
   not regulated.”

   Studies have shown that CBDs block, or counteract the effects of THC
   (terahydrocannabinol) which is the psychotogenic part of cannabis, and
   are anti-psychotic in humans.

   The company will be enrolling 80 patients in Europe this year for a
   Phase IIa trial that will examine the safety and efficacy of a purified
   CBD agent the company has titled GWP-42003. Preclinical data verified
   that it has anti-psychotic effects in pre-clinical models of
   schizophrenia, as well as demonstrating a reduction in movement
   disorders often induced by current anti-psychotic drugs. What sets this
   compound apart from current anti-psychotics is that cannabinoids do not
   work via the dopamine D2 receptor and may have the potential to target
   both positive and negative symptoms of the disease. This may, in turn,
   improve patient compliance.

   Additional in-house research indicates that cannabinoids show potential
   to treat additional mental health disorders, such as: anxiety, bipolar
   affective disorder, depression, treating disorders, insomnia and
   post-traumatic stress disorder.

   There have been a number of published papers on the topic of
   cannabinoids and Schizophrenia. Some of these are listed on the company
   website: www.gwpharm.com.

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                     Treating Schizophrenia Successfully

                       By Margarita Tartakovsky, M.S.
                                ~ 5 min read

   Treating Schizophrenia Successfully Schizophrenia is a complex and
   often chronic illness that requires long-term treatment. Medication is
   the bedrock of managing schizophrenia, said Peter Buckley, MD, a
   psychiatrist and expert in schizophrenia, and dean of the Medical
   College of Georgia at Georgia Regents University.

   But a comprehensive plan, which includes familial support and
   education, and considers the person’s individual psychological needs,
   is key, he said.

   The specifics of treatment depend on the stage of the illness and the
   person’s age, said Robert Buchanan, MD, director of the Maryland
   Psychiatric Research Center and a leading expert in schizophrenia.
   “Someone who is having a first episode of psychosis might have a
   different treatment plan than someone who is 45 and has been ill for
   many years.”

Taking an Active Role in Treatment

   “The most effective way to treat the illness is for the person to learn
   about the disorder and its symptoms, and to take an active role in
   their treatment,” said Susan Gingerich, MSW, a clinician based in
   Philadelphia with over 30 years of experience working with individuals
   with schizophrenia and their families.

   That includes focusing on life goals that are important to you, such as
   working, going to school or having close relationships, she said.

   It also includes other key elements: taking medication as prescribed;
   learning to manage stress and symptoms; avoiding drugs and alcohol;
   developing and using a relapse prevention plan; sticking with
   treatment; and building a social support network, she said.

Taking Medication

   Because schizophrenia tends to be a lifelong illness, it requires
   lifelong management with medication. Finding the right medication is a
   trial-and-error process. “There are no predicators for which drug will
   be most effective for a particular individual,” Buchanan said. That’s
   why having a collaborative relationship with the prescribing physician
   is so important.

   Medication adherence is a big challenge. In the Clinical Antipsychotic
   Trials of Intervention Effectiveness (CATIE), 74 percent of patients
   stopped taking their medication within the first 18 months of
   treatment. Not taking medication increases the risk for relapse,
   hospitalization and suicidal behavior.

   “Adherence seems very simple, but it’s actually remarkably
   complicated,” Buckley said. The reasons people don’t take their
   medication differ with each individual, he said. The most common reason
   is lack of awareness of being ill. As Buckley said, if you don’t
   consider yourself psychotic, why would you take an antipsychotic
   medication?

   There are gradients of insight, and insight may fluctuate, Buchanan
   said. For instance, “a person may not have insight into their illness,
   per say, but they may know that they’re having trouble going outside of
   their house and feeling comfortable.” In supportive therapy, the
   therapist and patient may talk about how medication can help them
   achieve their goal of feeling comfortable with leaving their house, he
   said.

   Individuals also might not take medication because it doesn’t work or
   has bothersome side effects. Substance abuse is common, and may
   contribute to non-adherence, as well.

   Other factors include the disapproving opinions of family members and
   others’ bad experiences with medication, Buckley said.

   Plus, “lots of people don’t take their medicines exactly as
   prescribed.” For instance, individuals who’ve been taking blood
   pressure medication for many years also slip up, he said.

   According to Buchanan, a collaborative relationship between the
   psychiatrist and patient is critical in enhancing adherence. In fact,
   another reason people don’t take medication is because they feel
   pressured or “ordered” to take it “without having been involved in
   shared decision-making,” said Gingerich, also co-author of The Complete
   Family Guide to Schizophrenia, Social Skills Training for
   Schizophrenia, and Illness Management and Recovery: Personalized Skills
   and Strategies for Those with Mental Illness.

   It’s important to have open discussions around what the patient finds
   helpful about the medication and what they don’t like, Buchanan said.
   This way they can make adjustments and try different medications, he
   said.

   Sometimes, people don’t like taking pills or because of their cognitive
   impairment, they have a hard time remembering to take their medication,
   Buchanan said. One strategy is to incorporate medication into the
   person’s daily routine, Gingerich said.

   For instance, this can include “putting one’s pill bottle next to their
   tooth brush so they are reminded to take their medication when they
   brush their teeth,” along with using pill organizers and setting up
   cues “such as using a calendar, or programming one’s cell phone.”

   Another strategy is “offering the option of long-acting injectable
   medication. Instead of taking a pill every day, [patients] can receive
   a shot once every two weeks or four weeks,” Buchanan said.

Psychosocial Interventions

   “Psychosocial interventions are a cornerstone of the comprehensive
   treatment of patients with schizophrenia, and when used in combination
   with medication, they are more effective than antipsychotics alone,”
   write Buckley and Brian Miller, MD, PhD, in the 2013 edition of Conn’s
   Current Therapy.

   This can include educating families about schizophrenia and the best
   ways to offer support. Having loved ones involved in treatment can
   increase medication adherence and decrease relapse rates.

   Other interventions include social skills training, which teaches
   individuals with schizophrenia to be assertive, resolve conflict and
   navigate work issues.

   Supported employment helps people find and keep jobs in the community
   based on their abilities and preferences. It includes “individually
   tailored job development, rapid job search, availability of ongoing job
   supports, and integration of vocational and mental health services,”
   according to this 2009 research-based summary of psychosocial
   treatments. Supported employment helps in building self-esteem and
   self-image, Buchanan said.

   Cognitive-behavioral therapy (CBT) aims to treat the positive symptoms
   of schizophrenia, such as hallucinations and delusions, and negative
   symptoms, such as lack of motivation. It also helps individuals
   identify their recovery goals and work toward them. And it helps with
   any co-occurring disorders such as depression and anxiety.

Treating Substance Use

   Substance abuse is the most common co-occurring disorder for people
   with schizophrenia. When a person has both schizophrenia and issues
   with substance use, “it is important to get treatment from
   professionals who treat the disorders concurrently and in an integrated
   way,” Gingerich said.

   This treatment is typically called “Integrated Treatment for Dual
   Disorders” or “Co-Occurring Disorder Treatment.”

   According to Gingerich, it usually includes these areas: helping the
   person identify why they are using substances (for instance, it might
   be to cope with symptoms); talking about how they can get these same
   needs met without turning to drugs or alcohol; helping them identify
   the harmful consequences of their use, such as relapse or legal or
   relationship problems; “helping the person weigh the pros and cons of
   sobriety”; and “identifying high-risk situations and ways to avoid them
   or cope with them.”

   It also includes helping the person make a plan for reducing their use
   or stopping it altogether, when they’re ready, she said. And it
   includes gathering support, “from groups such as Dual Recovery
   Anonymous and from sober friends and family.”

Other Interventions

   Peer counseling can be very helpful and take various forms. It tends to
   be similar to Alcoholics Anonymous, as individuals who are living
   successfully with schizophrenia are trained to help others with the
   illness. They may help with everything from sharing insight into
   navigating the mental healthcare system to providing information on
   managing stress and symptoms.

   You can learn more about peer services and support at the National
   Alliance on Mental Illness.

   Antipsychotic medication doesn’t help with the debilitating cognitive
   deficits schizophrenia causes, which affect nearly all patients. That’s
   why researchers also are exploring the efficacy of cognitive
   remediation.

   This is a behavioral training-based intervention that aims to improve
   cognitive processes, such as attention, memory and executive function.
   Most cognitive remediation programs use computers and target one or
   several cognitive skills.

   Often, it’s the cognitive symptoms that are most damaging to a person’s
   ability to work, study and even live independently. Cognitive deficits
   make it harder to remember and process information. Individuals may
   have a difficult time with everything from remembering their
   supervisor’s instructions to maintaining a budget to navigating public
   transportation.

   As this piece points out, “Sometimes patients are labeled as
   unmotivated and uncooperative when, in fact, they want to remember but
   simply are not able to.”

   Again, successful treatment for schizophrenia is comprehensive and
   includes both pharmacological and psychosocial interventions. Family
   education is especially critical.

   It’s also important to have faith in your loved one and “help them keep
   hope alive,” Gingerich said. “Focus on their strengths and talents and
   how they can accomplish their goals and contribute to the world.”

   And, if you have schizophrenia, have faith in yourself. “People with
   schizophrenia can lead productive, rewarding lives.”


     *
     *
     *
     *

   Margarita Tartakovsky, M.S. is an Associate Editor at Psych Central and
   blogs regularly about eating and self-image issues on her own blog,
   Weightless.
   APA Reference
   Tartakovsky, M. (2014). Treating Schizophrenia Successfully. Psych
   Central. Retrieved on February 4, 2015, from
   http://psychcentral.com/lib/treating-schizophrenia-successfully/0001892
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   Home » Schizophrenia

Schizophrenia

     * Schizophrenia: What You Need to Know
     * Schizoaffective Disorder
     * Schizophrenia in Children
     * Staying Well When You Have a Mental Illness PDF

En Espanol:

     * Esquizofrenia: Lo Que Usted Necesita Saber

Clinical Trials:

     * National Institute of Mental Health —Project Among African
       Americans to Explore Risks for Schizophrenia (PAARTNERS)
     * National Institute of Mental Health -- NIMH Schizophrenia Research
       Program
     * National Institute of Mental Health -- Evaluating Genetic Risk
       Factors for Childhood-Onset Schizophrenia
     * National Institute of Mental Health -- Schizophrenia Trials

Schizophrenia: What You Need to Know

   Schizophrenia is a serious disorder which affects how a person thinks,
   feels and acts. Someone with schizophrenia may have difficulty
   distinguishing between what is real and what is imaginary; may
   be unresponsive or withdrawn; and may have difficulty expressing normal
   emotions in social situations.

   Contrary to public perception, schizophrenia is not split personality
   or multiple personality. The vast majority of people with schizophrenia
   are not violent and do not pose a danger to others. Schizophrenia
   is not caused by childhood experiences, poor parenting or lack of
   willpower, nor are the symptoms identical for each person.

What causes schizophrenia?

   The cause of schizophrenia is still unclear. Some theories about the
   cause of this disease include: genetics (heredity), biology (the
   imbalance in the brain’s chemistry); and/or possible viral infections
   and immune disorders.

   Genetics (Heredity). Scientists recognize that the disorder tends to
   run in families and that a person inherits a tendency to develop the
   disease. Schizophrenia may also be triggered by environmental events,
   such as viral infections or highly stressful situations or a
   combination of both.

   Similar to some other genetically-related illnesses, schizophrenia
   appears when the body undergoes hormonal and physical changes, like
   those that occur during puberty in the teen and young adult years.

   Chemistry. Genetics help to determine how the brain uses certain
   chemicals. People with schizophrenia have a chemical imbalance of brain
   chemicals (serotonin and dopamine) which are neurotransmitters. These
   neurotransmitters allow nerve cells in the brain to send messages to
   each other. The imbalance of these chemicals affects the way a person’s
   brain reacts to stimuli--which explains why a person with schizophrenia
   may be overwhelmed by sensory information (loud music or bright lights)
   which other people can easily handle. This problem in processing
   different sounds, sights, smells and tastes can also lead to
   hallucinations or delusions.

What are the early warning signs of schizophrenia?

   The signs of schizophrenia are different for everyone. Symptoms may
   develop slowly over months or years, or may appear very abruptly. The
   disease may come and go in cycles of relapse and remission.

   Behaviors that are early warning signs of schizophrenia include:
     * Hearing or seeing something that isn’t there
     * A constant feeling of being watched
     * Peculiar or nonsensical way of speaking or writing
     * Strange body positioning
     * Feeling indifferent to very important situations
     * Deterioration of academic or work performance
     * A change in personal hygiene and appearance
     * A change in personality
     * Increasing withdrawal from social situations
     * Irrational, angry or fearful response to loved ones
     * Inability to sleep or concentrate
     * Inappropriate or bizarre behavior
     * Extreme preoccupation with religion or the occult

   Schizophrenia affects about 1% of the world population. In the United
   States one in a hundred people, about 2.5 million, have this disease.
   It knows no racial, cultural or economic boundaries. Symptoms usually
   appear between the ages of 13 and 25, but often appear earlier in males
   than females.

   If you or a loved one experience several of these symptoms for more
   than two weeks, seek help immediately.

What are the symptoms of schizophrenia?

   A medical or mental health professional may use the following terms
   when discussing the symptoms of schizophrenia.

   Positive symptoms are disturbances that are “added” to the person’s
   personality.
     * Delusions -- false ideas--individuals may believe that someone is
       spying on him or her, or that they are someone famous.
     * Hallucinations –seeing, feeling, tasting, hearing or smelling
       something that doesn’t really exist. The most common experience is
       hearing imaginary voices that give commands or comments to the
       individual.
     * Disordered thinking and speech -- moving from one topic to another,
       in a nonsensical fashion. Individuals may make up their own words
       or sounds.

   Negative symptoms are capabilities that are “lost” from the person’s
   personality.
     * Social withdrawal
     * Extreme apathy
     * Lack of drive or initiative
     * Emotional unresponsiveness

What are the different types of schizophrenia?

     * Paranoid schizophrenia -- a person feels extremely suspicious,
       persecuted, or grandiose, or experiences a combination of these
       emotions.
     * Disorganized schizophrenia -- a person is often incoherent in
       speech and thought, but may not have delusions.
     * Catatonic schizophrenia -- a person is withdrawn, mute, negative
       and often assumes very unusual body positions.
     * Residual schizophrenia -- a person is no longer experiencing
       delusions or hallucinations, but has no motivation or interest in
       life.
     * Schizoaffective disorder--a person has symptoms of both
       schizophrenia and a major mood disorder such as depression.

   No cure for schizophrenia has been discovered, but with proper
   treatment, many people with this illness can lead productive and
   fulfilling lives.

What treatments are available for schizophrenia?

   If you suspect someone you know is experiencing symptoms of
   schizophrenia, encourage them to see a medical or mental health
   professional immediately. Early treatment--even as early as the first
   episode--can mean a better long-term outcome.

   Recovery and Rehabilitation

   While no cure for schizophrenia exists, many people with this illness
   can lead productive and fulfilling lives with the proper treatment.
   Recovery is possible through a variety of services, including
   medication and rehabilitation programs. Rehabilitation can help a
   person recover the confidence and skills needed to live a productive
   and independent life in the community. Types of services that help a
   person with schizophrenia include:
     * Case management helps people access services, financial assistance,
       treatment and other resources.
     * Psychosocial Rehabilitation Programs are programs that help people
       regain skills such as: employment, cooking, cleaning, budgeting,
       shopping, socializing, problem solving, and stress management.
     * Self-help groups provide on-going support and information to
       persons with serious mental illness by individuals who experience
       mental illness themselves.
     * Drop-in centers are places where individuals with mental illness
       can socialize and/or receive informal support and services on an
       as-needed basis.
     * Housing programs offer a range of support and supervision from 24
       hour supervised living to drop-in support as needed.
     * Employment programs assist individuals in finding employment and/or
       gaining the skills necessary to re-enter the workforce.
     * Therapy/Counseling includes different forms of “talk”therapy, both
       individual and group, that can help both the patient and family
       members to better understand the illness and share their concerns.
     * Crisis Services include 24 hour hotlines, after hours counseling,
       residential placement and in-patient hospitalization.

ANTIPSYCHOTIC MEDICATION

   The new generation of antipsychotic medications help people with
   schizophrenia to live fulfilling lives. They help to reduce the
   biochemical imbalances that cause schizophrenia and decrease the
   likelihood of relapse. Like all medications, however, anti-psychotic
   medications should be taken only under the supervision of a mental
   health professional.

   There are two major types of antipsychotic medication:
     * Conventional antipsychotics effectively control the
       “positive”symptoms such as hallucinations, delusions, and confusion
       of schizophrenia.
     * New Generation (also called atypical) antipsychotics treat both the
       positive and negative symptoms of schizophrenia, often with fewer
       side effects.

   Side effects are common with antipsychotic drugs. They range from mild
   side effects such as dry mouth, blurred vision, constipation,
   drowsiness and dizziness which usually disappear after a few weeks to
   more serious side effects such as trouble with muscle control, pacing,
   tremors and facial ticks. The newer generation of drugs have fewer side
   effects. However, it is important to talk with your mental health
   professional before making any changes in medication since many side
   effects can be controlled.

Other Resources

   National Alliance for the Mentally Ill (NAMI)
   1-800-950-NAM
   Iwww.nami.org

   National Alliance for Research on Schizophrenia and Depression (NARSAD)
     [numbers_button_skype_logo.png] 1-800-829-8289
   www.narsad.org

   National Institute of Mental Health
     [numbers_button_skype_logo.png] 301-443-4513
   www.nimh.nih.gov

   Family members or caregivers of a person with schizophrenia can refer
   to Mental Health America’s “Mental Illness in the Family”brochure
   series, available through Mental Health America’s Resource Center.
   phone icon
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   Call 1-800-273-TALK

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Schizophrenia Health Center

Tools & Resources

     * Schizophrenia Symptoms
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Schizophrenia Types and Symptoms

In this article

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   Usually with schizophrenia, the person's inner world and behavior
   change notably. Behavior changes might include the following:
     * Social withdrawal
     * Depersonalization (a sense of being unreal, hazy and in a dreamlike
       state), sometimes accompanied by intense anxiety
     * Loss of appetite
     * Loss of hygiene
     * Delusions
     * Hallucinations (hearing or seeing things that aren't there)
     * The sense of being controlled by outside forces
     * Disorganized speech

   A person with schizophrenia may not have any outward appearance of
   being ill. In other cases, the illness may be more apparent, causing
   bizarre behaviors. For example, a person with schizophrenia may wear
   aluminum foil in the belief that it will stop one's thoughts from being
   broadcast and protect against malicious waves entering the brain.

Recommended Related to Schizophrenia

   Helping Your Loved One Get Schizophrenia Treatment

   If your friend or relative with schizophrenia won't get treatment,
   there are steps you can take to help.

   Read the Helping Your Loved One Get Schizophrenia Treatment article > >

   People with schizophrenia vary widely in their behavior as they
   struggle with an illness beyond their control. In active stages, those
   affected may ramble in illogical sentences or react with uncontrolled
   anger or violence to a perceived threat. People with schizophrenia may
   also experience relatively passive phases of the illness in which they
   seem to lack personality, movement, and emotion (also called a flat
   affect). People with schizophrenia may alternate in these extremes.
   Their behavior may or may not be predictable.

   In order to better understand schizophrenia, the concept of clusters of
   symptoms is often used. Thus, people with schizophrenia can experience
   symptoms that may be grouped under the following categories:
     * Positive symptoms: Hearing voices, suspiciousness, feeling as
       though they are under constant surveillance, delusions, or making
       up words without a meaning (neologisms).
     * Negative (or deficit) symptoms: Social withdrawal, difficulty in
       expressing emotions (in extreme cases called blunted affect),
       difficulty in taking care of themselves, inability to feel
       pleasure. These symptoms cause severe impairment and are often
       mistaken for laziness.
     * Cognitive symptoms: Difficulties attending to and processing of
       information, understanding the environment, and remembering simple
       tasks.
     * Affective (or mood) symptoms: Most notably depression, accounting
       for a very high rate of attempted suicide in people suffering from
       schizophrenia. Anxiety can also be present and may be a direct
       result of the psychosis or come and go during a psychotic episode.

   1|2
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guide icon Schizophrenia Guide

   1
   Overview & Facts
   2
   Symptoms & Types
   3
   Diagnosis & Tests
   4
   Treatment & Care
   5
   Living & Managing
   6
   Support & Resources
   Continue reading below...

Top Picks

     * 8 Suicide Warning Signs
     * Mental Illness Rights: Protect Yourself
     * Ease Schizophrenia Symptoms With Art Therapy
     * What Causes Tardive Dyskinesia?
     * Is It Schizophrenia or Bipolar Disorder?
     * Schizophrenia: 10 Questions to Ask Your M.D.

Further Reading:

     * Schizophrenia Myths and Facts
     * Is It Possible to Prevent Schizophrenia?
     * Antipsychotics for Treating Schizophrenia
     * Schizophrenia-Frequently Asked Questions
     * Schizophrenia-Medicines
     * Schizophrenia-Recovery
     * Schizophrenia-Treatment Overview
     * See All Psychosis Topics

     * Schizophrenia Health Home
     * News
     * Reference
     * Slideshows
     * Videos
     * Medications
     * Community
     * Crisis Assistance
     * Find a Psychiatrist

   Guide
   Schizophrenia Guide
   1
   Overview & Facts
   2
   Symptoms & Types
   3
   Diagnosis & Tests
   4
   Treatment & Care
   5
   Living & Managing
   6
   Support & Resources

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Schizophrenia Health Center

Tools & Resources

     * Schizophrenia Symptoms
     * Tests for Schizophrenia
     * Can You Prevent Schizophrenia?
     * Schizophrenia Myths & Facts
     * Causes of Schizophrenia
     * Art Therapy for Schizophrenia

   Select An Article [All Subchapter Articles:....................] Go
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Schizophrenia Myths and Facts

In this article

     * Myth: People with schizophrenia have multiple personalities.
     * Myth: Most people with schizophrenia are violent or dangerous.
     * Myth: Schizophrenia is caused by bad parenting.
     * Myth: If your parent has schizophrenia, you'll get it too.
     * Myth: People with schizophrenia are stupid.
     * Myth: If you have schizophrenia, you belong in a mental hospital.
     * Myth: You can't hold a job if you have schizophrenia.
     * Myth: Schizophrenia makes people lazy.
     * Myth: You can never recover from schizophrenia.

   Font Size
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   A

   There's a lot of incorrect info out there about schizophrenia. Some of
   it is spread by movies or TV shows. Or sometimes people use stereotypes
   when talking about schizophrenia.

   Get the real story behind some common myths.

Recommended Related to Schizophrenia

   Schizophrenia: Symptoms

   Positive symptoms can come and go. Know what to look for, so you can
   take action. Positive Symptoms of Schizophrenia

   Read the Schizophrenia: Symptoms article > >

Myth: People with schizophrenia have multiple personalities.

   This is one of the biggest misunderstandings about schizophrenia. One
   poll found that 64% of Americans believe schizophrenia involves a split
   personality -- which means someone acts like they are two separate
   people.

   A person with schizophrenia doesn't have two different personalities.
   Instead, he or she has false ideas or has lost touch with reality.
   Schizophrenia and multiple personality disorder are two different and
   unrelated conditions.

Myth: Most people with schizophrenia are violent or dangerous.

   In movies and TV shows, who is the crazed killer? Often it's the
   character with schizophrenia. That's not the case in real life.

   Even though people with schizophrenia can act unpredictably at times,
   most aren't violent, especially if they're getting treated.

   When people with schizophrenia do commit violent acts, they usually
   have another condition, like childhood conduct problems or substance
   abuse.

Myth: Schizophrenia is caused by bad parenting.

   Some people mistakenly think that schizophrenia is due to bad
   parenting, especially by the mother.

   Schizophrenia is a mental illness. It has many causes, including genes,
   trauma, and drug abuse. Mistakes you've made as a parent won't give
   your child schizophrenia.

Myth: If your parent has schizophrenia, you'll get it too.

   Genes do play a role in schizophrenia. But just because one of your
   parents has the condition doesn't mean you're destined to get it.

   If one parent has schizophrenia, your risk of the condition is about
   10%. Having more than one family member with schizophrenia raises your
   risk further.

Myth: People with schizophrenia are stupid.

   There have been studies that found people with schizophrenia have more
   trouble on tests of mental function, including attention, learning, and
   memory. Yet that doesn't mean they're not intelligent.

   Many creative and smart people throughout history have had
   schizophrenia, such as Russian ballet dancer Vaslav Nijinsky and Nobel
   Prize-winning mathematician John Nash. Scientists have even discovered
   a gene linking mental disorders like schizophrenia to creativity and
   intellect.
   1|2
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   Next Article: [What Is Schizophrenia?......................] Go

guide icon Schizophrenia Guide

   1
   Overview & Facts
   2
   Symptoms & Types
   3
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   4
   Treatment & Care
   5
   Living & Managing
   6
   Support & Resources
   Continue reading below...

Top Picks

     * 8 Suicide Warning Signs
     * Mental Illness Rights: Protect Yourself
     * Ease Schizophrenia Symptoms With Art Therapy
     * What Causes Tardive Dyskinesia?
     * Is It Schizophrenia or Bipolar Disorder?
     * Schizophrenia: 10 Questions to Ask Your M.D.

Further Reading:

     * Is It Possible to Prevent Schizophrenia?
     * Antipsychotics for Treating Schizophrenia
     * Schizophrenia-Frequently Asked Questions
     * Schizophrenia-Medicines
     * Schizophrenia-Recovery
     * Schizophrenia-Treatment Overview
     * Schizophrenia-When to Call a Doctor
     * See All Psychosis Topics

Psychosis Home

     * Medical Reference
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     * Schizophrenia Health Home
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     * Reference
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     * Medications
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   Guide
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   3
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   4
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   Mental Health Psychotic Disorders
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   9 Types of Psychotic Disorder

   Schizophrenia Medications
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   10 Questions to Ask Doctor About Schizophrenia
   Article
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   Slideshow
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   Schizophrenia What Increases Your Risk
   Article
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   male patient with doctor
   Article
   Schizophrenia: Find the Right Doctors
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   Article
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Schizophrenia and Electroconvulsive Therapy (ECT)

In this article

     * Why Is ECT Used?
     * How Is ECT Performed?
     * Controversy Surrounding ECT
     * Making an Informed Decision About ECT

   Font Size
   A
   A
   A

   Electroconvulsive therapy (ECT) is typically used to treat severe
   depression, but it occasionally is used for other mental illnesses such
   as schizophrenia. During ECT, an electric current is briefly applied
   through the scalp to the brain while the patient is asleep under
   general anesthesia, inducing a seizure.


Recommended Related to Schizophrenia

   Schizophrenia: Choosing a Doctor and Therapist

   Types of Mental Health Specialists Choosing the right doctor and/or
   therapist to treat schizophrenia and other mental health issues may
   seem like a daunting task. But, finding the right doctor is an
   important step towards getting the right treatment. A number of
   different types of doctors can treat mental illnesses, including the
   following: Psychiatrists: These professionals diagnose and specialize
   in the treatment of schizophrenia and other mental, emotional, or
   behavioral problems...

   Read the Schizophrenia: Choosing a Doctor and Therapist article > >

Why Is ECT Used?

   ECT is one of the fastest and most effective ways to relieve symptoms
   in severely depressed or suicidal patients or patients who suffer from
   mania or other mental illnesses. ECT is generally used when severe
   depression is unresponsive to several or more medications or other
   forms of therapy, or when these patients pose a severe threat to
   themselves or others and it is dangerous to wait until medications take
   effect.  ECT is also often considered the safest and most effective
   treatment for mood disorders in women who are pregnant.

   In schizophrenia, ECT is often extremely effective for a subtype of
   illness called catatonia, where the patient may not speak, have periods
   of excitement, or appear motionless and have repetitive, unusual or
   rigid muscle movements.  ECT is also sometimes used for other core
   symptoms of schizophrenia, such as delusions, hallucinations, or
   disorganized thinking, but its use is less well-established than for
   the treatment of mood symptoms.


How Is ECT Performed?

   Prior to ECT treatment, a patient is put to sleep using general
   anesthesia and given a muscle relaxant. Electrodes are placed on the
   patient's scalp and a finely controlled electric current is momentarily
   applied, which causes a brief seizure in the brain.

   Because the muscles are relaxed, the seizure will usually be limited to
   slight movement of the hands and feet. Patients are carefully monitored
   during the treatment and awaken minutes later, not remembering the
   treatment or events surrounding it. The patient is often confused for a
   short period after treatment. ECT is usually given up to three times a
   week for two to four weeks.

   A course of ECT is usually followed by psychotherapy and medicine under
   a psychiatrist's care.

Controversy Surrounding ECT

   ECT remains misunderstood by the general public even though it has been
   used since the 1940s. Many of the risks and side effects have been
   related to the misuse of equipment, incorrect administration, and
   improperly trained staff. There is also a misconception that ECT is
   used as a "quick fix" instead of long-term therapy or hospitalization.
   Unfavorable portrayals in movies or television shows and
   misrepresentation in media coverage have added to the controversy
   surrounding this treatment. In fact, ECT is safe and among the most
   effective treatments available for depression.
   1|2
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guide icon Schizophrenia Guide

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   2
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   3
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   4
   Treatment & Care
   5
   Living & Managing
   6
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   Continue reading below...

Top Picks

     * 8 Suicide Warning Signs
     * Mental Illness Rights: Protect Yourself
     * Ease Schizophrenia Symptoms With Art Therapy
     * What Causes Tardive Dyskinesia?
     * Is It Schizophrenia or Bipolar Disorder?
     * Schizophrenia: 10 Questions to Ask Your M.D.

Further Reading:

     * Electroconvulsive Therapy (ECT) for Depression
     * Electroconvulsive Therapy and Other Depression Treatments
     * Bipolar Disorder and Electroconvulsive Therapy
     * Electroconvulsive Therapy (ECT)
     * Treatments for Mania in Bipolar Disorder
     * Depression Treatment Options
     * The Diagnosis & Treatment of Depression
     * See All Electroconvulsive Therapy (ECT) Topics

Electroconvulsive Therapy (ECT) Home

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   Guide
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   3
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Today on WebMD

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Causes of Schizophrenia

In this article

     * What causes schizophrenia?
     * Genes and environment
     * Different brain chemistry and structure

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What causes schizophrenia?

   Experts think schizophrenia is caused by several factors.

Genes and environment

   Scientists have long known that schizophrenia runs in families. The
   illness occurs in 1 percent of the general population, but it occurs in
   10 percent of people who have a first-degree relative with the
   disorder, such as a parent, brother, or sister. People who have
   second-degree relatives (aunts, uncles, grandparents, or cousins) with
   the disease also develop schizophrenia more often than the general
   population. The risk is highest for an identical twin of a person with
   schizophrenia. He or she has a 40 to 65 percent chance of developing
   the disorder.

   We inherit our genes from both parents. Scientists believe several
   genes are associated with an increased risk of schizophrenia, but that
   no gene causes the disease by itself. In fact, recent research has
   found that people with schizophrenia tend to have higher rates of rare
   genetic mutations. These genetic differences involve hundreds of
   different genes and probably disrupt brain development.

   Other recent studies suggest that schizophrenia may result in part when
   a certain gene that is key to making important brain chemicals
   malfunctions. This problem may affect the part of the brain involved in
   developing higher functioning skills. Research into this gene is
   ongoing, so it is not yet possible to use the genetic information to
   predict who will develop the disease.

   Despite this, tests that scan a person's genes can be bought without a
   prescription or a health professional's advice. Ads for the tests
   suggest that with a saliva sample, a company can determine if a client
   is at risk for developing specific diseases, including schizophrenia.
   However, scientists don't yet know all of the gene variations that
   contribute to schizophrenia. Those that are known raise the risk only
   by very small amounts. Therefore, these "genome scans" are unlikely to
   provide a complete picture of a person's risk for developing a mental
   disorder like schizophrenia.

   In addition, it probably takes more than genes to cause the disorder.
   Scientists think interactions between genes and the environment are
   necessary for schizophrenia to develop. Many environmental factors may
   be involved, such as exposure to viruses or malnutrition before birth,
   problems during birth, heavy adolescent marijuana use, and other not
   yet known psychosocial factors.
   1|2
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Therapy for Schizophrenia

In this article

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   In spite of successful antipsychotic drug treatment, many people with
   schizophrenia have difficulty with thinking, motivation, activities of
   daily living, relationships, and communication. Also, since the illness
   typically begins during the years critical to education and
   professional training, people with schizophrenia often lack social and
   work skills and experience. In these cases, the psychosocial treatments
   can be especially important. Many useful therapies have been developed
   to assist people suffering from schizophrenia and include:
     * Individual psychotherapy: This involves regular sessions between
       the patient and a therapist focused on past or current problems,
       thoughts, feelings, or relationships. Thus, via contact with a
       trained professional, people with schizophrenia become able to
       understand more about the illness, to learn about themselves and to
       better handle the problems of their daily lives. They become better
       able to differentiate between what is real and, by contrast, what
       is not and can acquire beneficial problem-solving skills.
     * Rehabilitation: Rehabilitation may include job and vocational
       counseling, problem solving support, social skills training, and
       education in money management.
     * Cognitive Remediation: This is a form of behavioral treatment often
       using paper-and-pencil exercises and drills or a computer-based
       series of exercises that aims to help people with schizophrenia
       strengthen and develop existing cognitive skills and develop new,
       more effective strategies for managing problems with attention,
       memory, planning, and organization.
     * Family education: Research has consistently shown that people with
       schizophrenia who have involved families fare better than those who
       battle the condition alone. Insofar as possible, all family members
       should be involved in the care of a loved one. with schizophrenia.
     * Self-help groups: Community care and outreach programs are very
       helpful in avoiding relapse, non-compliance, legal problems, and
       repeat hospitalizations.The National Alliance on Mental Illness
       (NAMI) is an outreach organization that offers information on
       treatments and support for people with schizophrenia and their
       families.


Recommended Related to Schizophrenia

   Is It Possible to Prevent Schizophrenia?

   Schizophrenia is a complex illness that may partly involve your genes.
   But other events in your life may also play a role. Scientists are
   edging closer to figuring out if there are ways to lower the risk of
   schizophrenia.

   Read the Is It Possible to Prevent Schizophrenia? article > >

   WebMD Medical Reference
   View Article Sources Sources

   SOURCES:

   National Institute of Mental Health: "How Is Schizophrenia Treated?"

   National Alliance on Mental Illness: "Treatment, Services and Support."


   Reviewed by Joseph Goldberg, MD on May 11, 2014
   © 2014 WebMD, LLC. All rights reserved.
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Schizophrenia - Medicines

   Schizophrenia Guide
     * Topic Overview
     * Frequently Asked Questions
     * Cause
     * Symptoms
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   Medicines are the treatment that works best for schizophrenia, and you
   may be taking more than one at a time. They may be used for positive or
   negative symptoms, but they don't work as well for negative symptoms as
   they do for positive symptoms.

   It may take time to find which medicines are best for you. This may be
   frustrating. Getting support from your family, your friends, and a
   community-based rehabilitation program is helpful, especially while you
   and your doctor are trying to find the best medicines. It also may help
   to speak with and get support from others who have had trouble finding
   the right medicines.

Recommended Related to Schizophrenia

   When Schizophrenia Appears

   People with schizophrenia can have a hard time telling what’s real and
   what’s not. They may see things that aren’t there or hold firm beliefs
   that fly in the face of fact. Understanding schizophrenia’s nature can
   help patients and their loved ones regain a sense of control.

   Read the When Schizophrenia Appears article > >

   If you stop taking your medicines, you may have a relapse. Don't stop
   taking your medicines until you talk with your doctor. If you and your
   health care team decide you should stop using medicine, you will need
   to be checked on a regular basis.

Medicine choices

   Medicines used most often to treat schizophrenia include:
     * Antipsychotic medicines, such as aripiprazole, clozapine, and
       haloperidol.

   These medicines often are used along with the medicines listed above:
     * Mood-stabilizing medicine such as carbamazepine, lithium, and
       valproate.
     * Antianxiety medicines, such as clonazepam and diazepam.
     * Selective serotonin reuptake inhibitors (SSRIs) for depression,
       such as citalopram, escitalopram, and fluoxetine.
     * Tricyclic antidepressants such as amitriptyline, desipramine, and
       doxepin.

Side effects

   Because of side effects or the risk of side effects, you may be tempted
   to stop using your medicine. But if you stop using medicine, the
   symptoms of schizophrenia may come back or get worse.

   If you have any concerns about side effects, talk to your doctor. He or
   she will work with you. Your doctor may give you a smaller dose of the
   antipsychotic medicine, have you try another antipsychotic medicine, or
   give you another medicine to treat the side effect.

   Some side effects of antipsychotic medicines can be serious.
     * Neuroleptic malignant syndrome is a rare but life-threatening side
       effect of antipsychotics. The first signs usually include a fever
       between 102 °F (38.9 °C) and 103 °F (39.4 °C), a fast or irregular
       heartbeat, rapid breathing, and severe sweating.
     * Tardive dyskinesia is body movement that you can't control.
     * Type 2 diabetes might develop as a result of weight gain caused by
       some antipsychotics. Some antipsychotics may also increase insulin
       resistance.

   You may need regular blood tests to check for side effects. Children,
   teens, and older adults may need to have blood tests more often than
   other people.

In this article

   This information is produced and provided by the National Cancer
   Institute (NCI). The information in this topic may have changed since
   it was written. For the most current information, contact the National
   Cancer Institute via the Internet web site at http:// cancer .gov or
   call 1-800-4-CANCER.

   WebMD Medical Reference from Healthwise
   Last Updated: August 31, 2012
   This information is not intended to replace the advice of a doctor.
   Healthwise disclaims any liability for the decisions you make based on
   this information.
   © 1995-2014 Healthwise, Incorporated. Healthwise, Healthwise for every
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Understanding Schizophrenia

Symptoms, Types, Causes, and Early Warning Signs

   Schizophrenia: Signs, Types & Causes In This Article

   Schizophrenia is a challenging disorder that makes it difficult to
   distinguish between what is real and unreal, think clearly, manage
   emotions, relate to others, and function normally. But that doesn't
   mean there isn't hope. Schizophrenia can be successfully managed. The
   first step is to identify the signs and symptoms. The second step is to
   seek help without delay and the third is to stick with the treatment.
   With the right treatment and support, a person with schizophrenia can
   lead a happy, fulfilling life.

What is schizophrenia?

   Schizophrenia is a brain disorder that affects the way a person acts,
   thinks, and sees the world. People with schizophrenia have an altered
   perception of reality, often a significant loss of contact with
   reality. They may see or hear things that don’t exist, speak in strange
   or confusing ways, believe that others are trying to harm them, or feel
   like they’re being constantly watched. With such a blurred line between
   the real and the imaginary, schizophrenia makes it difficult—even
   frightening—to negotiate the activities of daily life. In response,
   people with schizophrenia may withdraw from the outside world or act
   out in confusion and fear.

   Most cases of schizophrenia appear in the late teens or early
   adulthood. However, schizophrenia can appear for the first time in
   middle age or even later. In rare cases, schizophrenia can even affect
   young children and adolescents, although the symptoms are slightly
   different. In general, the earlier schizophrenia develops, the more
   severe it is. Schizophrenia also tends to be more severe in men than in
   women.

   Although schizophrenia is a chronic disorder, there is help available.
   With support, medication, and therapy, many people with schizophrenia
   are able to function independently and live satisfying lives. However,
   the outlook is best when schizophrenia is diagnosed and treated right
   away. If you spot the signs and symptoms of schizophrenia and seek help
   without delay, you or your loved one can take advantage of the many
   treatments available and improve the chances of recovery.

Common misconceptions about schizophrenia

   MYTH: Schizophrenia refers to a "split personality" or multiple
   personalities.

   FACT: Multiple personality disorder is a different and much less common
   disorder than schizophrenia. People with schizophrenia do not have
   split personalities. Rather, they are “split off” from reality.

   MYTH: Schizophrenia is a rare condition.

   FACT: Schizophrenia is not rare; the lifetime risk of developing
   schizophrenia is widely accepted to be around 1 in 100.

   MYTH: People with schizophrenia are dangerous.

   FACT: Although the delusional thoughts and hallucinations of
   schizophrenia sometimes lead to violent behavior, most people with
   schizophrenia are neither violent nor a danger to others.

   MYTH: People with schizophrenia can’t be helped.

   FACT: While long-term treatment may be required, the outlook for
   schizophrenia is not hopeless. When treated properly, many people with
   schizophrenia are able to enjoy life and function within their families
   and communities.

Early warning signs of schizophrenia

   In some people, schizophrenia appears suddenly and without warning. But
   for most, it comes on slowly, with subtle warning signs and a gradual
   decline in functioning long before the first severe episode. Many
   friends and family members of people with schizophrenia report knowing
   early on that something was wrong with their loved one, they just
   didn’t know what.

   In this early phase, people with schizophrenia often seem eccentric,
   unmotivated, emotionless, and reclusive. They isolate themselves, start
   neglecting their appearance, say peculiar things, and show a general
   indifference to life. They may abandon hobbies and activities, and
   their performance at work or school deteriorates.

The most common early warning signs of schizophrenia include:

     * Social withdrawal
     * Hostility or suspiciousness
     * Deterioration of personal hygiene
     * Flat, expressionless gaze
     * Inability to cry or express joy
     * Inappropriate laughter or crying
     * Depression
     * Oversleeping or insomnia
     * Odd or irrational statements
     * Forgetful; unable to concentrate
     * Extreme reaction to criticism
     * Strange use of words or way of speaking

   While these warning signs can result from a number of problems—not just
   schizophrenia—they are cause for concern. When out-of-the-ordinary
   behavior is causing problems in your life or the life of a loved one,
   seek medical advice. If schizophrenia or another mental problem is the
   cause, treatment will help.

Daniel’s story

   Daniel is 21 years old. Six months ago, he was doing well in college
   and holding down a part-time job in the stockroom of a local
   electronics store. But then he began to change, becoming increasingly
   paranoid and acting out in bizarre ways. First, he became convinced
   that his professors were “out to get him” since they didn’t appreciate
   his confusing, off-topic classroom rants. Then he told his roommate
   that the other students were “in on the conspiracy.” Soon after, he
   dropped out of school.

   From there, things just got worse. Daniel stopped bathing, shaving, and
   washing his clothes. At work, he became convinced that his boss was
   watching him through surveillance bugs planted in the store’s
   television sets. Then he started hearing voices telling him to find the
   bugs and deactivate them. Things came to a head when he acted on the
   voices, smashing several TVs and screaming that he wasn’t going to put
   up with the “illegal spying” any more. His frightened boss called the
   police, and Daniel was hospitalized.

Signs and symptoms of schizophrenia

   There are five types of symptoms characteristic of schizophrenia:
   delusions, hallucinations, disorganized speech, disorganized behavior,
   and the so-called “negative” symptoms. However, the signs and symptoms
   of schizophrenia vary dramatically from person to person, both in
   pattern and severity. Not every person with schizophrenia will have all
   symptoms, and the symptoms of schizophrenia may also change over time.

Delusions

   A delusion is a firmly-held idea that a person has despite clear and
   obvious evidence that it isn’t true. Delusions are extremely common in
   schizophrenia, occurring in more than 90% of those who have the
   disorder. Often, these delusions involve illogical or bizarre ideas or
   fantasies. Common schizophrenic delusions include:
     * Delusions of persecution – Belief that others, often a vague
       “they,” are out to get him or her. These persecutory delusions
       often involve bizarre ideas and plots (e.g. “Martians are trying to
       poison me with radioactive particles delivered through my tap
       water”).
     * Delusions of reference – A neutral environmental event is believed
       to have a special and personal meaning. For example, a person with
       schizophrenia might believe a billboard or a person on TV is
       sending a message meant specifically for them.
     * Delusions of grandeur – Belief that one is a famous or important
       figure, such as Jesus Christ or Napolean. Alternately, delusions of
       grandeur may involve the belief that one has unusual powers that no
       one else has (e.g. the ability to fly).
     * Delusions of control – Belief that one’s thoughts or actions are
       being controlled by outside, alien forces. Common delusions of
       control include thought broadcasting (“My private thoughts are
       being transmitted to others”), thought insertion (“Someone is
       planting thoughts in my head”), and thought withdrawal (“The CIA is
       robbing me of my thoughts”).

Hallucinations

   Hallucinations are sounds or other sensations experienced as real when
   they exist only in the person's mind. While hallucinations can involve
   any of the five senses, auditory hallucinations (e.g. hearing voices or
   some other sound) are most common in schizophrenia. Visual
   hallucinations are also relatively common. Research suggests that
   auditory hallucinations occur when people misinterpret their own inner
   self-talk as coming from an outside source.

   Schizophrenic hallucinations are usually meaningful to the person
   experiencing them. Many times, the voices are those of someone they
   know. Most commonly, the voices are critical, vulgar, or abusive.
   Hallucinations also tend to be worse when the person is alone.

Disorganized speech

   Fragmented thinking is characteristic of schizophrenia. Externally, it
   can be observed in the way a person speaks. People with schizophrenia
   tend to have trouble concentrating and maintaining a train of thought.
   They may respond to queries with an unrelated answer, start sentences
   with one topic and end somewhere completely different, speak
   incoherently, or say illogical things.

   Common signs of disorganized speech in schizophrenia include:
     * Loose associations – Rapidly shifting from topic to topic, with no
       connection between one thought and the next.
     * Neologisms – Made-up words or phrases that only have meaning to the
       patient.
     * Perseveration – Repetition of words and statements; saying the same
       thing over and over.
     * Clang – Meaningless use of rhyming words (“I said the bread and
       read the shed and fed Ned at the head").

Disorganized behavior

   Schizophrenia disrupts goal-directed activity, causing impairments in a
   person’s ability to take care of him or herself, work, and interact
   with others. Disorganized behavior appears as:
     * A decline in overall daily functioning
     * Unpredictable or inappropriate emotional responses
     * Behaviors that appear bizarre and have no purpose
     * Lack of inhibition and impulse control

Negative symptoms (absence of normal behaviors)

   The so-called “negative” symptoms of schizophrenia refer to the absence
   of normal behaviors found in healthy individuals. Common negative
   symptoms of schizophrenia include:
     * Lack of emotional expression – Inexpressive face, including a flat
       voice, lack of eye contact, and blank or restricted facial
       expressions.
     * Lack of interest or enthusiasm – Problems with motivation; lack of
       self-care.
     * Seeming lack of interest in the world – Apparent unawareness of the
       environment; social withdrawal.
     * Speech difficulties and abnormalities – Inability to carry a
       conversation; short and sometimes disconnected replies to
       questions; speaking in monotone.

Causes of schizophrenia

   The causes of schizophrenia are not fully known. However, it appears
   that schizophrenia usually results from a complex interaction between
   genetic and environmental factors.

Genetic causes of schizophrenia

   Schizophrenia has a strong hereditary component. Individuals with a
   first-degree relative (parent or sibling) who has schizophrenia have a
   10 percent chance of developing the disorder, as opposed to the 1
   percent chance of the general population.

   But schizophrenia is only influenced by genetics, not determined by it.
   While schizophrenia runs in families, about 60% of schizophrenics have
   no family members with the disorder. Furthermore, individuals who are
   genetically predisposed to schizophrenia don’t always develop the
   disease, which shows that biology is not destiny.

Environmental causes of schizophrenia

   Twin and adoption studies suggest that inherited genes make a person
   vulnerable to schizophrenia and then environmental factors act on this
   vulnerability to trigger the disorder.

   As for the environmental factors involved, more and more research is
   pointing to stress, either during pregnancy or at a later stage of
   development. High levels of stress are believed to trigger
   schizophrenia by increasing the body’s production of the hormone
   cortisol.

   Research points to several stress-inducing environmental factors that
   may be involved in schizophrenia, including:
     * Prenatal exposure to a viral infection
     * Low oxygen levels during birth (from prolonged labor or premature
       birth)
     * Exposure to a virus during infancy
     * Early parental loss or separation
     * Physical or sexual abuse in childhood

Abnormal brain structure

   In addition to abnormal brain chemistry, abnormalities in brain
   structure may also play a role in schizophrenia. Enlarged brain
   ventricles are seen in some schizophrenics, indicating a deficit in the
   volume of brain tissue. There is also evidence of abnormally low
   activity in the frontal lobe, the area of the brain responsible for
   planning, reasoning, and decision-making.

   Some studies also suggest that abnormalities in the temporal lobes,
   hippocampus, and amygdala are connected to schizophrenia’s positive
   symptoms. But despite the evidence of brain abnormalities, it is highly
   unlikely that schizophrenia is the result of any one problem in any one
   region of the brain.

Effects of schizophrenia

   When the signs and symptoms of schizophrenia are ignored or improperly
   treated, the effects can be devastating both to the individual with the
   disorder and those around him or her.  Some of the possible effects of
   schizophrenia are:
     * Relationship problems. Relationships suffer because people with
       schizophrenia often withdraw and isolate themselves. Paranoia can
       also cause a person with schizophrenia to be suspicious of friends
       and family.
     * Disruption to normal daily activities. Schizophrenia causes
       significant disruptions to daily functioning, both because of
       social difficulties and because everyday tasks become hard, if not
       impossible to do. A schizophrenic person’s delusions,
       hallucinations, and disorganized thoughts typically prevent him or
       her from doing normal things like bathing, eating, or running
       errands.
     * Alcohol and drug abuse. People with schizophrenia frequently
       develop problems with alcohol or drugs, which are often used in an
       attempt to self-medicate, or relieve symptoms. In addition, they
       may also be heavy smokers, a complicating situation as cigarette
       smoke can interfere with the effectiveness of medications
       prescribed for the disorder.
     * Increased suicide risk. People with schizophrenia have a high risk
       of attempting suicide. Any suicidal talk, threats, or gestures
       should be taken very seriously. People with schizophrenia are
       especially likely to commit suicide during psychotic episodes,
       during periods of depression, and in the first six months after
       they’ve started treatment.

Diagnosing schizophrenia

   A diagnosis of schizophrenia is made based on a full psychiatric
   evaluation, medical history, physical exam, and lab tests.
     * Psychiatric evaluation – The doctor or psychiatrist will ask a
       series of questions about you or your loved one's symptoms,
       psychiatric history, and family history of mental health problems.
     * Medical history and exam – Your doctor will ask about your personal
       and family health history. He or she will also perform a complete
       physical examination to check for medical issues that could be
       causing or contributing to the problem.
     * Laboratory tests – While there are no laboratory tests that can
       diagnose schizophrenia, simple blood and urine tests can rule out
       other medical causes of symptoms. The doctor may also order
       brain-imaging studies, such as an MRI or a CT scan, in order to
       look for brain abnormalities associated with schizophrenia.

Mental health professionals use the following criteria to diagnose
schizophrenia:

     * The presence of two or more of the following symptoms for at least
       30 days:
         1. Hallucinations
         2. Delusions
         3. Disorganized speech
         4. Disorganized or catatonic behavior
         5. Negative symptoms (emotional flatness, apathy, lack of speech)
     * Significant problems functioning at work or school, relating to
       other people, and taking care of oneself.
     * Continuous signs of schizophrenia for at least 6 months, with
       active symptoms (hallucinations, delusions, etc.) for at least 1
       month.
     * No other mental health disorder, medical issue, or substance abuse
       problem is causing the symptoms.

Conditions that can look like schizophrenia

   The medical and psychological conditions the doctor must rule out
   before diagnosing schizophrenia include:
     * Other psychotic disorders – Schizophrenia is a type of psychotic
       disorder, meaning it involves a significant loss of contact with
       reality. But there are other psychotic disorders that cause similar
       symptoms of psychosis, including schizoaffective disorder,
       schizophreniform disorder, and brief psychotic disorder. Because of
       the difficulty in differentiating between the psychotic disorders,
       it may take six months or longer to arrive at a correct diagnosis.
     * Substance abuse – Psychotic symptoms can be triggered by many
       drugs, including alcohol, PCP, heroin, amphetamines, and cocaine.
       Some over-the-counter and prescription drugs can also trigger
       psychotic reactions. A toxicology screen can rule out drug-induced
       psychosis. If substance abuse is involved, the physician will
       determine whether the drug is the source of the symptoms or merely
       an aggravating factor.
     * Medical conditions – Schizophrenia-like symptoms can also result
       from certain neurological disorders (such as epilepsy, brain
       tumors, and encephalitis), endocrine and metabolic disturbances,
       and autoimmune conditions involving the central nervous system.
     * Mood disorders – Schizophrenia often involves changes in mood,
       including mania and depression. While these mood changes are
       typically less severe than those seen in bipolar disorder and major
       depressive disorder, they can make diagnosis tricky. Schizophrenia
       is particularly difficult to distinguish from bipolar disorder. The
       positive symptoms of schizophrenia (delusions, hallucinations, and
       disorganized speech) can look like a manic episode of bipolar
       disorder, while the negative symptoms of schizophrenia (apathy,
       social withdrawal, and low energy) can look like a depressive
       episode.
     * Post-traumatic stress disorder (PTSD) – PTSD is an anxiety disorder
       that can develop after exposure to a traumatic event, such as
       military combat, an accident, or a violent assault. People with
       PTSD experience symptoms that are similar to schizophrenia. The
       images, sounds, and smells of PTSD flashbacks can look like
       psychotic hallucinations. The PTSD symptoms of emotional numbness
       and avoidance can look like the negative symptoms of schizophrenia.

Hope for schizophrenia

   Treatment options for schizophrenia are good, and the outlook for the
   disorder continues to improve. With medication, therapy, and a strong
   support network, many people with schizophrenia are able to control
   their symptoms, gain greater independence, and lead fulfilling lives.

   If you think that someone close to you has schizophrenia, you can make
   a difference by showing your love and support and helping that person
   get properly evaluated and treated. To learn more, see the related
   articles below.

More help for schizophrenia

     * Helping a Person with Schizophrenia: Overcoming Challenges While
       Taking Care of Yourself
     * Schizophrenia Treatment and Recovery: Getting the Help and Support
       You Need
     * Substance Abuse and Mental Health: Substance Abuse and Co-Occurring
       Disorders
     * Suicide Help: Dealing with Suicidal Thoughts and Feelings
     * Suicide Prevention: How to Help Someone who is Suicidal
     * Caregiver Stress and Burnout: Tips for Recharging and Finding
       Balance

Resources and references

Understanding schizophrenia

   Schizophrenia – Provides a comprehensive overview discussing causes,
   symptoms, diagnosis, treatment and current research on schizophrenia.
   (National Institute of Mental Health)

   Learn More About Schizophrenia – A guide to the symptoms, causes,
   diagnosis, and treatment of schizophrenia. (Schizophrenia Society of
   Canada)

   Basic Facts About Schizophrenia (PDF) – This 40-page booklet covers the
   most frequently asked questions about schizophrenia, including what
   it’s like and how families can help. (British Columbia Schizophrenia
   Society)

   Understanding Schizophrenia and Recovery (PDF) – Covers what people
   with schizophrenia and their families need to know about schizophrenia
   and its treatment. (National Alliance on Mental Illness)

Symptoms and early warning signs of schizophrenia

   Schizophrenia in Children – Describes symptoms in children, which may
   be different from those in adults. (American Academy of Child and
   Adolescent Psychiatry)

   The First Signs of Schizophrenia – Read through personal stories,
   offered by both people with schizophrenia and their loved ones,
   describing the early signs and symptoms they observed.
   (Schizophrenia.com)

Types of schizophrenia

   Paranoid Schizophrenia – Learn about the most common subtype of
   schizophrenia, including typical signs and symptoms such as paranoid
   delusions. (PsychCentral)

   Catatonic Schizophrenia – Overview of the signs and symptoms of
   catatonic schizophrenia, as well as its causes and effects.
   (PsychCentral)

   Disorganized Schizophrenia – Guide to disorganized schizophrenia’s
   signs and symptoms, such as disorganized thinking, disorganized
   behavior, and flat affect. (MedlinePluse)

Causes of schizophrenia

   Possible Causes of Schizophrenia – Reviews the possible causes of
   schizophrenia, including biological, psychological, and social factors.
   (Schizophrenia Fellowship of NSW)

   What Causes Schizophrenia? – Covers the combination of causes involved
   in schizophrenia, including genes, brain chemistry, and brain
   structure. (National Institute of Mental Health)

   Authors: Melinda Smith, M.A., and Jeanne Segal, Ph.D.  Last updated:
   December 2014.

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What is schizophrenia?

   Last updated: 28 November 2014
   Last updated: 28 Nov 2014
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   Schizophrenia is a mental disorder that generally appears in late
   adolescence or early adulthood - however, it can emerge at any time in
   life. It is one of many brain diseases that may include delusions, loss
   of personality (flat affect), confusion, agitation, social withdrawal,
   psychosis, and bizarre behavior.

   Contents of this article:

    1. What is schizophrenia?
    2. The brain
    3. Signs and symptoms
    4. What causes schizophrenia?
    5. Tests and diagnosis
    6. Treatment options
    7. How common is schizophrenia?
    8. Video: a case study

   There are also quotes from Medical News Today news articles at the end
   of some sections.

What is schizophrenia?

   Individuals with schizophrenia may hear voices that are not there. Some
   may be convinced that others are reading their minds, controlling how
   they think, or plotting against them. This can distress patients
   severely and persistently, making them withdrawn and frantic.

   Others may find it hard to make sense of what a person with
   schizophrenia is talking about. In some cases, the individual may spend
   hours completely still, without talking. On other occasions he or she
   may seem fine, until they start explaining what they are truly
   thinking.

   The effects of schizophrenia reach far beyond the patient -
   schizophrenia does not only affect the person with the disorder.
   Families, friends and society are affected too. A sizable proportion of
   people with schizophrenia have to rely on others, because they are
   unable to hold a job or care for themselves.

   With proper treatment, patients can lead productive lives - according
   to the National Institute of Mental Health^1 (NIMN), treatment can help
   relieve many of the symptoms of schizophrenia. However, the majority of
   patients with the disorder have to cope with the symptoms for life.
   This does not mean that a person with schizophrenia who receives
   treatment cannot lead a rewarding, productive and meaningful life in
   his or her community.

   Schizophrenia most commonly strikes between the ages of 15 to 25 among
   men, and about 25 to 35 in women. In many cases the disorder develops
   so slowly that the sufferer does not know he/she has it for a long
   time. While, with other people it can strike suddenly and develop fast.

   Schizophrenia, possibly many illnesses combined - it is a complex,
   chronic, severe, and disabling brain disorder and affects approximately
   1% of all adults globally. Experts say schizophrenia is probably many
   illnesses masquerading as one. Research indicates that schizophrenia is
   likely to be the result of faulty neuronal development in the brain of
   the fetus, which later in life emerges as a full-blown illness.

   According to the University of Maryland Medical Center^2, schizophrenia
   affects males and females equally. However, an article in the BMJ^8
   says that schizophrenia affects 1.4 males for every 1 female.

   The Schizophrenic Disorders Clinic^3 at the Stanford School of Medicine
   describes schizophrenia as "a thought disorder: a brain disorder that
   interferes with a person's ability to think clearly, manage emotions,
   make decisions, and relate to others."
   John Forbes Nash, Jr. by Peter Badge
   John Forbes Nash Jr. (born June 13, 1928) has lived
   with paranoid schizophrenia.

   John Nash, an American mathematician who worked at Princeton
   University, won the Nobel Prize in Economics and lived with paranoid
   schizophrenia most of his life. He eventually managed to live without
   medication. A film was made of his life "A Beautiful Mind", which Nash
   says was "loosely accurate".

   A study published in The Lancet^7 found that schizophrenia with active
   psychosis is the third most disabling condition after quadriplegia and
   dementia, and ahead of blindness and paraplegia.

   The word schizophrenia comes from the Greek word skhizein meaning "to
   split" and the Greek word Phrenos (phren) meaning "diaphragm, heart,
   mind". In 1910, the Swiss psychiatrist, Eugen Bleuler (1857-1939)
   coined the term Schizophrenie in a lecture in Berlin on April 24th,
   1908.

The brain

   Our brain consists of billions of nerve cells. Each nerve cell has
   branches that give out and receive messages from other nerve cells.

   The ending of these nerve cells release neurotransmitters - types of
   chemicals. These neurotransmitters carry messages from the endings of
   one nerve cell to the nerve cell body of another. In the brain of a
   person who has schizophrenia, this messaging system does not work
   properly.

Signs and symptoms

   Other interesting related articles:

   What is Catatonic Schizophrenia?

   What is Schizoaffective Disorder?

   What is Childhood Schizophrenia?

   What is Disorganized Schizophrenia (Hebephrenia)?

   What is Paranoid Schizophrenia?

   What are the Different Types of Schizophrenia?

   There is, to date, no physical or laboratory test that can absolutely
   diagnose schizophrenia. The doctor, a psychiatrist, will make a
   diagnosis based on the patient's clinical symptoms. However, physical
   testing can rule out some other disorders and conditions which
   sometimes have similar symptoms, such as seizure disorders, thyroid
   dysfunction, brain tumor, drug use, and metabolic disorders.

   Symptoms and signs of schizophrenia will vary, depending on the
   individual. The symptoms are classified into four categories:
     * Positive symptoms - also known as psychotic symptoms. These are
       symptoms that appear, which people without schizophrenia do not
       have. For example, delusion.
     * Negative symptoms - these refer to elements that are taken away
       from the individual; loss or absence of normal traits or abilities
       that people without schizophrenia normally have. For example,
       blunted emotion.
     * Cognitive symptoms - these are symptoms within the person's thought
       processes. They may be positive or negative symptoms, for example,
       poor concentration is a negative symptom.
     * Emotional symptoms - these are symptoms within the person's
       feelings. They are usually negative symptoms, such as blunted
       emotions.

   Below is a list of the major symptoms:
     * Delusions - The patient has false beliefs of persecution, guilt of
       grandeur. He/she may feel things are being controlled from outside.
       It is not uncommon for people with schizophrenia to describe plots
       against them. They may think they have extraordinary powers and
       gifts. Some patients with schizophrenia may hide in order to
       protect themselves from an imagined persecution.
     * Hallucinations - hearing voices is much more common than seeing,
       feeling, tasting, or smelling things which are not there, but seem
       very real to the patient.
     * Thought disorder - the person may jump from one subject to another
       for no logical reason. The speaker may be hard to follow. The
       patient's speech might be muddled and incoherent. In some cases the
       patient may believe that somebody is messing with his/her mind.

   Other symptoms schizophrenia patients may experience include:
     * Lack of motivation (avolition) - the patient loses his/her drive.
       Everyday automatic actions, such as washing and cooking are
       abandoned. It is important that those close to the patient
       understand that this loss of drive is due to the illness, and has
       nothing to do with slothfulness.
     * Poor expression of emotions - responses to happy or sad occasions
       may be lacking, or inappropriate.
     * Social withdrawal - when a patient with schizophrenia withdraws
       socially it is often because he/she believes somebody is going to
       harm them. Other reasons could be a fear of interacting with other
       humans because of poor social skills.
     * Unaware of illness - as the hallucinations and delusions seem so
       real for the patients, many of them may not believe they are ill.
       They may refuse to take medications which could help them
       enormously for fear of side-effects, for example.
     * Cognitive difficulties - the patient's ability to concentrate,
       remember things, plan ahead, and to organize himself/herself are
       affected. Communication becomes more difficult.

   Recent developments on the symptoms of schizophrenia from MNT news

   Impaired eye movements linked to schizophrenia - researchers from the
   University of British Columbia explained in the Journal of Neuroscience
   that people with schizophrenia find it harder to follow a moving dot on
   a computer screen.

What causes schizophrenia?

   Nobody has been able to pinpoint one single cause. Experts believe
   several factors are generally involved in contributing to the onset of
   schizophrenia.

   The likely factors do not work in isolation, either. Evidence does
   suggest that genetic and environmental factors generally act together
   to bring about schizophrenia. Evidence indicated that the diagnosis of
   schizophrenia has an inherited element, but it is also significantly
   influenced by environmental triggers. In other words, imagine your body
   is full of buttons, and some of those buttons result in schizophrenia
   if somebody comes and presses them enough times and in the right
   sequences.

   The buttons would be your genetic susceptibility, while the person
   pressing them would be the environmental factors.

   Below is a list of the factors that are thought to contribute towards
   the onset of schizophrenia:
     * Your genes
       If there is no history of schizophrenia in your family your chances
       of developing it are less than 1%. However, that risk rises to 10%
       if one of your parents was/is a sufferer.
       A gene that is probably the most studied "schizophrenia gene" plays
       a surprising role in the brain: It controls the birth of new
       neurons in addition to their integration into existing brain
       circuitry, according to an article published by Cell.
       A Swedish study found that schizophrenia and bipolar disorder have
       the same genetic causes.
       Thirteen locations in the human genetic code may help explain the
       cause of schizophrenia - a study involving 59,000 people, 5,001 of
       whom had been diagnosed with schizophrenia, identified 22 genome
       locations, with 13 new ones that are thought to be involved in the
       development of schizophrenia.
       The scientists added that of particular importance to schizophrenia
       were two genetically-determined processes - the "micro-RNA 137"
       pathway and the "calcium channel pathway".
       Principal investigator, Professor Patrick Sullivan, of the Center
       for Psychiatric Genomics at the University of North Carolina School
       of Medicine, said "This study gives us the clearest picture to date
       of two different pathways that might be going wrong in people with
       schizophrenia. Now we need to concentrate our research very
       urgently on these two pathways in our quest to understand what
       causes this disabling mental illness."
     * Chemical imbalance in the brain
       Experts believe that an imbalance of dopamine, a neurotransmitter,
       is involved in the onset of schizophrenia. They also believe that
       this imbalance is most likely caused by your genes making you
       susceptible to the illness. Some researchers say other the levels
       of other neurotransmitters, such as serotonin, may also be
       involved.
       Changes in key brain functions, such as perception, emotion and
       behavior lead experts to conclude that the brain is the biological
       site of schizophrenia.
       Schizophrenia could be caused by faulty signaling in the brain,
       according to research published in the journal Molecular
       Psychiatry.
     * Family relationships
       Although there is no evidence to prove or even indicate that family
       relationships might cause schizophrenia, some patients with the
       illness believe family tension may trigger relapses.
     * Environment
       Although there is yet no definite proof, many suspect that prenatal
       or perinatal trauma, and viral infections may contribute to the
       development of the disease. Perinatal means "occurring about 5
       months before and up to one month after birth".
       Stressful experiences often precede the emergence of schizophrenia.
       Before any acute symptoms are apparent, people with schizophrenia
       habitually become bad-tempered, anxious, and unfocussed. This can
       trigger relationship problems, divorce and unemployment. These
       factors are often blamed for the onset of the disease, when really
       it was the other way round - the disease caused the crisis.
       Therefore, it is extremely difficult to know whether schizophrenia
       caused certain stresses or occurred as a result of them.
     * Some drugs
       Cannabis and LSD are known to cause schizophrenia relapses.
       According to the State Government of Victoria^6 in Australia, for
       people with a predisposition to a psychotic illness such as
       schizophrenia, usage of cannabis may trigger the first episode in
       what can be a disabling condition that lasts for the rest of their
       lives.
       The National Library of Medicine^9 says that some prescription
       drugs, such as steroids and stimulants, can cause psychosis.

Tests and diagnosis

   A schizophrenia diagnosis is carried out by observing the actions of
   the patient. If the doctor suspects possible schizophrenia, they will
   need to know about the patient's medical and psychiatric history.

   Certain tests will be ordered to rule out other illnesses and
   conditions that may trigger schizophrenia-like symptoms. Examples of
   some of the tests may include:
     * Blood tests - to determine CBC (complete blood count) as well as
       some other blood tests.
     * Imaging studies - to rule out tumors, problems in the structure of
       the brain, and other conditions/illnesses
     * Psychological evaluation - a specialist will assess the patient's
       mental state by asking about thoughts, moods, hallucinations,
       suicidal traits, violent tendencies or potential for violence, as
       well as observing their demeanor and appearance.

   Schizophrenia - Diagnostic Criteria

   Patients must meet the criteria laid down in the DSM (Diagnostic and
   Statistical Manual of Mental Disorders). It is an American Psychiatric
   Association manual that is used by health care professionals to
   diagnose mental illnesses and conditions.

   The health care professional needs to exclude other possible mental
   health disorders, such as bipolar disorder or schizoaffective disorder.

   It is also important to establish that the signs and symptoms have not
   been caused by, for example, a prescribed medication, a medical
   condition, or substance abuse.

   Also, the patient must:
     * Have at least two of the following typical symptoms of
       schizophrenia -
       - Delusions
       - Disorganized or catatonic behavior
       - Disorganized speech
       - Hallucinations
       - Negative symptoms that are present for much of the time during
       the last four weeks.
     * Experience considerable impairment in the ability to attend school,
       carry out their work duties, or carry out every day tasks
     * Have symptoms which persist for six months or more

   Sometimes, the person with schizophrenia may find their symptoms
   frightening, and conceal them from others. If there is severe paranoia,
   they may be suspicious of family or friends who try to help. There are
   many elements in disease that make it difficult to confirm a
   schizophrenia diagnosis.

   Recent developments on schizophrenia from MNT news

   Collecting neurons from the nose to diagnose schizophrenia -
   researchers from Tel Aviv University, Israel, reported in Neurobiology
   of Disease that collecting neurons from the nose of the patient may be
   a rapid way to test for schizophrenia.

   Noam Shomron of TAU's Sackler Faculty of Medicine, and team describe
   how they devised a potential way of diagnosing schizophrenia by testing
   microRNA molecules found in the neurons inside the patient's nose. A
   sample can be taken via a simple biopsy.

   Shomron believes this could become a "more sure-fire" way of diagnosing
   schizophrenia than ever before. It may also be a way of detecting the
   devastating disease earlier on. Schizophrenia treatment is usually much
   more effective if it can start during the early stages.

   Are autism and schizophrenia related? - when seen at first glance,
   autism and schizophrenia appear to be completely different disorders.
   However, a discovery made by researchers at Tel Aviv University's
   Sackler Faculty of Medicine and the Sheba Medical Center showed that
   the two disorders have similar roots, and are linked to other mental
   conditions, such as bipolar disorder.

   Both schizophrenia and autism share come traits, including a limited
   ability to lead a normal life function in the real world, as well as
   cognitive and social dysfunction.

   The scientists found a genetic link between the two disorders, which
   causes a higher risk within families. Dr. Mark Weiser and team found
   that people with a sibling with schizophrenia had a twelve-fold higher
   chance of having autism than those without schizophrenia in the family.

   Schizophrenia genetically linked to four other mental illnesses or
   disorders - researchers the Cross Disorders Group of the Psychiatric
   Genomic Consortium reported that schizophrenia, major depressive
   disorder, bipolar disorder, autism spectrum disorders, and ADHD
   (attention-deficit hyperactivity disorder) share the same common
   inherited genetic faults.

   Does schizophrenia begin in the womb? Stem cell study says yes -
   researchers from the Salk Institute in California have demonstrated
   that neurons from skin cells of patients with schizophrenia behave
   oddly in early stages of development, supporting the theory that
   schizophrenia begins in the womb.

   The researchers, who published their results in the journal Molecular
   Psychiatry, say their findings could provide clues for how to detect
   and treat the disease early.

   Researchers identify genetic mutations that may cause schizophrenia -
   Schizophrenia affects around 2.4 million adults in the US. The exact
   cause of the condition is unknown, but past research has suggested that
   genetics may play a part. Now, investigators from the Columbia
   University Medical Center in New York, NY, have uncovered clues that
   may build on this concept. The research team published their findings
   in the journal Neuron.

   Schizophrenia and cannabis use may have genetic link - There is growing
   evidence that cannabis use is a cause of schizophrenia and now a new
   study led by King's College London, UK, also finds increased cannabis
   use and schizophrenia may have genes in common.

   How a genetic variation 'may increase schizophrenia risk' - The exact
   causes of schizophrenia are unknown, but past research has suggested
   that some individuals with the condition possess certain genetic
   variations. Now, researchers at Johns Hopkins University School of
   Medicine in Baltimore, MD, say they have begun to understand how one
   schizophrenia-related genetic variation influences brain cell
   development.

   Researchers identify more than 80 new genes linked to schizophrenia -
   What causes schizophrenia has long baffled scientists. But in what is
   deemed the largest ever molecular genetic study of schizophrenia, a
   team of international researchers has pinpointed 108 genes linked to
   the condition - 83 of which are newly discovered - that may help
   identify its causes and pave the way for new treatments.

   Schizophrenia 'made up of eight specific genetic disorders' - Past
   studies have indicated that rather than being a single disease,
   schizophrenia is a collection of different disorders. Now, a new study
   by researchers at Washington University in St. Louis, MO, claims the
   condition consists of eight distinct genetic disorders, all of which
   present their own specific symptoms.

   Brain network vulnerable to Alzheimer's and schizophrenia identified -
   New research has emerged that reveals a specific brain network - that
   is the last to develop and the first to show signs of neurodegeneration
   - is more vulnerable to unhealthy aging as well as to disorders that
   emerge in young people, shedding light on conditions such as
   Alzheimer's disease and schizophrenia.

Treatment options

   The UK's National Health Service^4 says it is important that
   schizophrenia is diagnosed as early as possible, because the chances of
   a recovery are much greater the earlier it is treated.

   Psychiatrists say the most effective treatment for schizophrenia
   patients is usually a combination of medication, psychological
   counseling, and self-help resources.

   Anti-psychosis drugs have transformed schizophrenia treatment. Thanks
   to them, the majority of patients are able to live in the community,
   rather than stay in hospital. In many parts of the world care is
   delivered in the community, rather than in hospital.

   The primary schizophrenia treatment is medication. Sadly, compliance is
   a major problem. Compliance, in medicine, means following the
   medication regimen. People with schizophrenia often go off their
   medication for long periods during their lives, at huge personal costs
   to themselves and often to those around them as well.

   The Cleveland Clinic^5 says that the patient must continue taking
   medication even when symptoms are gone, otherwise they will come back.

   The majority of patients go off their medication within the first year
   of treatment. In order to address this, successful schizophrenia
   treatment needs to consist of a life-long regimen of both drug and
   psychosocial, support therapies. The medication can help control the
   patient's hallucinations and delusions, but it cannot help them learn
   to communicate with others, get a job, and thrive in society.

   Although a significant number of people with schizophrenia live in
   poverty, this does not have to be the case. A person with schizophrenia
   who complies with the treatment regimen long-term will be able to lead
   a happy and productive life.

   The first time a person experiences schizophrenia symptoms can be very
   unpleasant. He/she may take a long time to recover, and that recovery
   can be a lonely experience. It is crucial that a schizophrenia sufferer
   receives the full support of his/her family, friends, and community
   services when onset appears for the first time.

   Medications

   The medical management of schizophrenia generally involves drugs for
   psychosis, depression and anxiety. This is because schizophrenia is a
   combination of thought disorder, mood disorder and anxiety disorder.

   The most common antipsychotic drugs are Risperidone (Risperdal),
   Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), and
   Clozapine (Clozaril):
     * Risperidone (Risperdal) - introduced in America in 1994. This drug
       is less sedating than other atypical antipsychotics. There is a
       higher probability, compared to other atypical antipsychotics, of
       extrapyramidal symptoms (affecting the extrapyramidal motor system,
       a neural network located in the brain that is involved in the
       coordination of movement). Although weight gain and diabetes are
       possible risks, they are less likely to happen, compared with
       Clozapine or Olanzapine.
     * Olanzapine (Zyprexa) - approved in the USA in 1996. A typical dose
       is 10 to 20 mg per day. Risk of extrapyramidal symptoms is low,
       compared to Risperidone. This drug may also improve negative
       symptoms. However, the risks of serious weight gain and the
       development of diabetes are significant.
     * Quetiapine (Seroquel) - came onto the market in America in 1997.
       Typical dose is between 400 to 800 mg per day. If the patient is
       resistant to treatment the dose may be higher. The risk of
       extrapyramidal symptoms is low, compared to Risperidone. There is a
       risk of weight gain and diabetes, however the risk is lower than
       Clozapine or Olanzapine.
     * Ziprasidone (Geodon) - became available in the USA in 2001. Typical
       doses range from 80 to 160 mg per day. This drug can be given
       orally or by intramuscular administration. The risk of
       extrapyramidal symptoms is low. The risk of weight gain and
       diabetes is lower than other atypical antipsychotics. However, it
       might contribute to cardiac arrhythmia, and must not be taken
       together with other drugs that also have this side effect.
     * Clozapine (Clozaril) - has been available in the USA since 1990. A
       typical dose ranges from 300 to 700 mg per day. It is very
       effective for patients who have been resistant to treatment. It is
       known to lower suicidal behaviors. Patients must have their blood
       regularly monitored as it can affect the white blood cell count.
       The risk of weight gain and diabetes is significant.

   Recent developments on schizophrenia treatment from MNT news

   Researchers at the University of Iowa found that higher dosages of
   anti-psychotic medications resulted in the loss of more brain tissue.
   They also found that brain scans after patients' first psychotic
   episode revealed that they had less brain tissue than healthy people
   without schizophrenia.

   Head investigator, Professor Nancy Andreasen, said "This was a very
   upsetting finding. We spent a couple of years analyzing the data more
   or less hoping we had made a mistake. But in the end, it was a solid
   finding that wasn't going to go away, so we decided to go ahead and
   publish it. The impact is painful because psychiatrists, patients, and
   family members don't know how to interpret this finding. 'Should we
   stop using antipsychotic medication? Should we be using less?'"

How common is schizophrenia?

   The prevalence of schizophrenia globally varies slightly, depending on
   which report you look at, from about 0.7% to 1.2% of the adult
   population in general. Most of these percentages refer to people
   suffering from schizophrenia "at some time during their lives".

   An Australian study found that schizophrenia is more common in
   developed nations than developing ones. It also found that the illness
   is less widespread than previously thought. Estimates of 10 per 1,000
   people should be changed to 7 or 8 per 1,000 people, the study
   concluded.

   In the USA about 2.2 million adults, or about 1.1% of the population
   age 18 and older in a given year have schizophrenia.

   Schizophrenia is not a 'very' common disease. Approximately 1% of
   people throughout the globe suffer from schizophrenia (or perhaps a
   little less than 1% in developing countries) at some point in their
   lives. It is estimated that about 1.2% of Americans, a total of 3.2
   million people, have the disorder at some point in their lives.
   Globally, about 1.5 million people each year are diagnosed with
   schizophrenia. In the UK it is estimated that about 600,000 people have
   schizophrenia.

Video: A Case Study

   The video below contains a summary of current understanding of this
   psychological disorder.
   [EMBED]

Related articles:

     * Blocked Enzyme Reverses Schizophrenia-like Symptoms - MIT Study Of
       Mice Could Lead To Drug Treatments For The Brain Disorder
     * Schizophrenia-Linked Gene Controls The Birth Of New Neurons
     * Common Causes Of Schizophrenia And Bipolar Disorder
     * Optimism For Bipolar Disorder And Schizophrenia If Psychiatrists
       Abandon 19th Century Dogma, UK
     * Hollow Mask Illusion Fails To Fool Schizophrenia Patients
     * Hearing Could Hold Key To Unlocking Schizophrenia Mystery

   Written by Christian Nordqvist

   Copyright: Medical News Today
   Not to be reproduced without permission.
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     * References
     * Additional information
     * Citations

   These tabs require JavaScript to be enabled.

    1. "What Is Schizophrenia?", National Institute of Mental Health.
    2. "Schizophrenia", University of Maryland Medical Center.
    3. "What is Schizophrenic Disorder?", the Schizophrenic Disorders
       Clinic at the Stanford School of Medicine.
    4. "Schizophrenia", National Health Service.
    5. "Schizophrenia Overview", The Cleveland Clinic.
    6. ”Cannabis (marijuana)”, State Government of Victoria, Australia.
    7. "Multiple-informant ranking of the disabling effects of different
       health conditions in 14 countries", Jerome Bickenbach PhD et al,
       The Lancet, Volume 354, Issue 9173, Pages 111 - 115, 10 July 1999.
       doi:10.1016/S0140-6736(98)07507-2.
    8. "Clinical Review - Schizophrenia", Marco M Picchioni and Robin M
       Murray, BMJ. BMJ 2007;335:91. doi:
       http://dx.doi.org/10.1136/bmj.39227.616447.BE.
    9. ”Psychosis”, National Library of Medicine.

       This article originally appeared on Medical News Today on 14 May
       2009.
       Visit our Schizophrenia category page for the latest news on this
       subject.

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         ______________________________________________________________

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Schizophrenia

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Symptoms

   By Mayo Clinic Staff

   In men, schizophrenia symptoms typically start in the early to mid-20s.
   In women, symptoms typically begin in the late 20s. It's uncommon for
   children to be diagnosed with schizophrenia and rare for those older
   than 45.

   Schizophrenia involves a range of problems with thinking (cognitive),
   behavior or emotions. Signs and symptoms may vary, but they reflect an
   impaired ability to function. Symptoms may include:
     * Delusions. These are false beliefs that are not based in reality.
       For example, you're being harmed or harassed; certain gestures or
       comments are directed at you; you have exceptional ability or fame;
       another person is in love with you; a major catastrophe is about to
       occur; or your body is not functioning properly. Delusions occur in
       as many as 4 out of 5 people with schizophrenia.
     * Hallucinations. These usually involve seeing or hearing things that
       don't exist. Yet for the person with schizophrenia, they have the
       full force and impact of a normal experience. Hallucinations can be
       in any of the senses, but hearing voices is the most common
       hallucination.
     * Disorganized thinking (speech). Disorganized thinking is inferred
       from disorganized speech. Effective communication can be impaired,
       and answers to questions may be partially or completely unrelated.
       Rarely, speech may include putting together meaningless words that
       can't be understood, sometimes known as word salad.
     * Extremely disorganized or abnormal motor behavior. This may show in
       a number of ways, ranging from childlike silliness to unpredictable
       agitation. Behavior is not focused on a goal, which makes it hard
       to perform tasks. Abnormal motor behavior can include resistance to
       instructions, inappropriate and bizarre posture, a complete lack of
       response, or useless and excessive movement.
     * Negative symptoms. This refers to reduced ability or lack of
       ability to function normally. For example, the person appears to
       lack emotion, such as not making eye contact, not changing facial
       expressions, speaking without inflection or monotone, or not adding
       hand or head movements that normally provide the emotional emphasis
       in speech. Also, the person may have a reduced ability to plan or
       carry out activities, such as decreased talking and neglect of
       personal hygiene, or have a loss of interest in everyday
       activities, social withdrawal or a lack of ability to experience
       pleasure.

Symptoms in teenagers

   Schizophrenia symptoms in teenagers are similar to those in adults, but
   the condition may be more difficult to recognize in this age group.
   This may be in part because some of the early symptoms of schizophrenia
   in teenagers are common for typical development during teen years, such
   as:
     * Withdrawal from friends and family
     * A drop in performance at school
     * Trouble sleeping
     * Irritability or depressed mood
     * Lack of motivation

   Compared with schizophrenia symptoms in adults, teens may be:
     * Less likely to have delusions
     * More likely to have visual hallucinations

When to see a doctor

   People with schizophrenia often lack awareness that their difficulties
   stem from a mental illness that requires medical attention. So it often
   falls to family or friends to get them help.

Helping someone who may have schizophrenia

   If you think someone you know may have symptoms of schizophrenia, talk
   to him or her about your concerns. Although you can't force someone to
   seek professional help, you can offer encouragement and support and
   help your loved one find a qualified doctor or mental health provider.

   If your loved one poses a danger to self or others or can't provide his
   or her own food, clothing or shelter, you may need to call 911 or other
   emergency responders for help so that your loved one might be evaluated
   by a mental health provider. In some cases, emergency hospitalization
   may be needed. Laws on involuntary commitment for mental health
   treatment vary by state. You can contact community mental health
   agencies or police departments in your area for details.

Suicidal thoughts and behavior

   Suicidal thoughts and behavior are common among people with
   schizophrenia. If you have a loved one who is in danger of committing
   suicide or has made a suicide attempt, make sure someone stays with
   that person. Call 911 or your local emergency number immediately. Or,
   if you think you can do so safely, take the person to the nearest
   hospital emergency room.
     * Definition
     * Causes

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   Jan. 24, 2014

References

    1. Schizophrenia spectrum and other psychotic disorders. In:
       Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th
       ed. Arlington, Va.: American Psychiatric Association; 2013.
       http://www.psychiatryonline.org. Accessed July 12, 2013.
    2. Hales RE, et al. The American Psychiatric Publishing Textbook of
       Psychiatry. 5th ed. Washington, D.C.: American Psychiatric
       Publishing; 2008.
       http://www.psychiatryonline.com/resourceToc.aspx?resourceID=5.
       Accessed May 8, 2013.
    3. Schizophrenia. National Institute of Mental Health.
       http://www.nimh.nih.gov/health/publications/schizophrenia/complete-
       index.shtml. Accessed May 8, 2013.
    4. Fischer BA, et al. Schizophrenia: Clinical manifestations, course,
       assessment, and diagnosis. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    5. Fischer BA, et al. Schizophrenia: Epidemiology and pathogenesis.
       http://www.uptodate.com/home. Accessed May 8, 2013.
    6. Stroup TS, et al. Pharmacotherapy for schizophrenia: Acute and
       maintenance phase treatment. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    7. Mental illness and the family: Recognizing warning signs and how to
       cope. Mental Health America.
       http://www.nmha.org/go/information/get-info/mi-and-the-family/recog
       nizing-warning-signs-and-how-to-cope. Accessed May 16, 2013.
    8. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric
       Association. http://www.dsm5.org/Pages/Default.aspx. Accessed May
       17, 2013.
    9. Schak KM (expert opinion). Mayo Clinic, Rochester, Minn. Aug. 13,
       2013.
   10. Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Aug.
       18, 2013.

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Causes

   By Mayo Clinic Staff

   It's not known what causes schizophrenia, but researchers believe that
   a combination of genetics and environment contributes to development of
   the disorder.

   Problems with certain naturally occurring brain chemicals, including
   neurotransmitters called dopamine and glutamate, also may contribute to
   schizophrenia. Neuroimaging studies show differences in the brain
   structure and central nervous system of people with schizophrenia.
   While researchers aren't certain about the significance of these
   changes, they support evidence that schizophrenia is a brain disease.
     * Symptoms
     * Risk factors

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   Jan. 24, 2014

References

    1. Schizophrenia spectrum and other psychotic disorders. In:
       Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th
       ed. Arlington, Va.: American Psychiatric Association; 2013.
       http://www.psychiatryonline.org. Accessed July 12, 2013.
    2. Hales RE, et al. The American Psychiatric Publishing Textbook of
       Psychiatry. 5th ed. Washington, D.C.: American Psychiatric
       Publishing; 2008.
       http://www.psychiatryonline.com/resourceToc.aspx?resourceID=5.
       Accessed May 8, 2013.
    3. Schizophrenia. National Institute of Mental Health.
       http://www.nimh.nih.gov/health/publications/schizophrenia/complete-
       index.shtml. Accessed May 8, 2013.
    4. Fischer BA, et al. Schizophrenia: Clinical manifestations, course,
       assessment, and diagnosis. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    5. Fischer BA, et al. Schizophrenia: Epidemiology and pathogenesis.
       http://www.uptodate.com/home. Accessed May 8, 2013.
    6. Stroup TS, et al. Pharmacotherapy for schizophrenia: Acute and
       maintenance phase treatment. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    7. Mental illness and the family: Recognizing warning signs and how to
       cope. Mental Health America.
       http://www.nmha.org/go/information/get-info/mi-and-the-family/recog
       nizing-warning-signs-and-how-to-cope. Accessed May 16, 2013.
    8. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric
       Association. http://www.dsm5.org/Pages/Default.aspx. Accessed May
       17, 2013.
    9. Schak KM (expert opinion). Mayo Clinic, Rochester, Minn. Aug. 13,
       2013.
   10. Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Aug.
       18, 2013.

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    2. Paternal age
    3. Family therapy
    4. Blood Basics
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    6. CT scan
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    9. MRI
   10. MRI
   11. Seeing Inside the Heart with MRI

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Risk factors

   By Mayo Clinic Staff

   Although the precise cause of schizophrenia isn't known, certain
   factors seem to increase the risk of developing or triggering
   schizophrenia, including:
     * Having a family history of schizophrenia
     * Exposure to viruses, toxins or malnutrition while in the womb,
       particularly in the first and second trimesters
     * Increased immune system activation, such as from inflammation or
       autoimmune diseases
     * Older age of the father
     * Taking mind-altering (psychoactive or psychotropic) drugs during
       teen years and young adulthood

     * Causes
     * Complications

          + Share
          + Tweet

   Jan. 24, 2014

References

    1. Schizophrenia spectrum and other psychotic disorders. In:
       Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th
       ed. Arlington, Va.: American Psychiatric Association; 2013.
       http://www.psychiatryonline.org. Accessed July 12, 2013.
    2. Hales RE, et al. The American Psychiatric Publishing Textbook of
       Psychiatry. 5th ed. Washington, D.C.: American Psychiatric
       Publishing; 2008.
       http://www.psychiatryonline.com/resourceToc.aspx?resourceID=5.
       Accessed May 8, 2013.
    3. Schizophrenia. National Institute of Mental Health.
       http://www.nimh.nih.gov/health/publications/schizophrenia/complete-
       index.shtml. Accessed May 8, 2013.
    4. Fischer BA, et al. Schizophrenia: Clinical manifestations, course,
       assessment, and diagnosis. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    5. Fischer BA, et al. Schizophrenia: Epidemiology and pathogenesis.
       http://www.uptodate.com/home. Accessed May 8, 2013.
    6. Stroup TS, et al. Pharmacotherapy for schizophrenia: Acute and
       maintenance phase treatment. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    7. Mental illness and the family: Recognizing warning signs and how to
       cope. Mental Health America.
       http://www.nmha.org/go/information/get-info/mi-and-the-family/recog
       nizing-warning-signs-and-how-to-cope. Accessed May 16, 2013.
    8. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric
       Association. http://www.dsm5.org/Pages/Default.aspx. Accessed May
       17, 2013.
    9. Schak KM (expert opinion). Mayo Clinic, Rochester, Minn. Aug. 13,
       2013.
   10. Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Aug.
       18, 2013.

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     * Learn more
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See also

    1. Phantosmia: What causes olfactory hallucinations?
    2. Paternal age
    3. Family therapy
    4. Blood Basics
    5. Complete blood count
    6. CT scan
    7. CT scan
    8. CT scans: Are they safe?
    9. MRI
   10. MRI
   11. Seeing Inside the Heart with MRI

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     * An authoritative and approachable guide to going gluten-free
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     * Reduce the impact of stress on your health
     * The Mayo Clinic Diet Online — Eat well. Enjoy life. Lose weight.

Other Topics in Patient Care & Health Info

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     * Symptoms A-Z
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    3. Basics
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   Print
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         1. Definition
         2. Symptoms
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         4. Risk factors
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Treatments and drugs

   By Mayo Clinic Staff

Appointments & care

   At Mayo Clinic, we take the time to listen, to find answers and to
   provide you the best care.
   Learn more. Request an appointment.

   Schizophrenia requires lifelong treatment, even when symptoms have
   subsided. Treatment with medications and psychosocial therapy can help
   manage the condition. During crisis periods or times of severe
   symptoms, hospitalization may be necessary to ensure safety, proper
   nutrition, adequate sleep and basic hygiene.

   A psychiatrist experienced in treating schizophrenia usually guides
   treatment. The treatment team also may include a psychologist, social
   worker, psychiatric nurse and possibly a case manager to coordinate
   care. The full-team approach may be available in clinics with expertise
   in schizophrenia treatment.

Medications

   Medications are the cornerstone of schizophrenia treatment. However,
   because medications for schizophrenia can cause serious but rare side
   effects, people with schizophrenia may be reluctant to take them.

   Antipsychotic medications are the most commonly prescribed drugs to
   treat schizophrenia. They're thought to control symptoms by affecting
   the brain neurotransmitters dopamine and serotonin.

   Willingness to cooperate with treatment may affect medication choice.
   Someone who is resistant to taking medication consistently may need to
   be given injections instead of taking a pill. Someone who is agitated
   may need to be calmed initially with a benzodiazepine such as lorazepam
   (Ativan), which may be combined with an antipsychotic.

Atypical antipsychotics

   These newer, second-generation medications are generally preferred
   because they pose a lower risk of serious side effects than do
   conventional medications. They include:
     * Aripiprazole (Abilify)
     * Asenapine (Saphris)
     * Clozapine (Clozaril)
     * Iloperidone (Fanapt)
     * Lurasidone (Latuda)
     * Olanzapine (Zyprexa)
     * Paliperidone (Invega)
     * Quetiapine (Seroquel)
     * Risperidone (Risperdal)
     * Ziprasidone (Geodon)

   Ask your doctor about the benefits and side effects of any medication
   that's prescribed.

Conventional, or typical, antipsychotics

   These first-generation medications have frequent and potentially
   significant neurological side effects, including the possibility of
   developing a movement disorder (tardive dyskinesia) that may or may not
   be reversible. This group of medications includes:
     * Chlorpromazine
     * Fluphenazine
     * Haloperidol (Haldol)
     * Perphenazine

   These antipsychotics are often cheaper than newer counterparts,
   especially the generic versions, which can be an important
   consideration when long-term treatment is necessary.

   It can take several weeks after first starting a medication to notice
   an improvement in symptoms. In general, the goal of treatment with
   antipsychotic medications is to effectively control signs and symptoms
   at the lowest possible dosage. The psychiatrist may try different
   medications, different dosages or combinations over time to achieve the
   desired result. Other medications also may help, such as
   antidepressants or anti-anxiety medications.

Psychosocial interventions

   Once psychosis recedes, psychological and social (psychosocial)
   interventions are important — in addition to continuing on medication.
   These may include:
     * Individual therapy. Learning to cope with stress and identify early
       warning signs of relapse can help people with schizophrenia manage
       their illness.
     * Social skills training. This focuses on improving communication and
       social interactions.
     * Family therapy. This provides support and education to families
       dealing with schizophrenia.
     * Vocational rehabilitation and supported employment. This focuses on
       helping people with schizophrenia prepare for, find and keep jobs.

   Most individuals with schizophrenia require some form of daily living
   support. Many communities have programs to help people with
   schizophrenia with jobs, housing, self-help groups and crisis
   situations. A case manager or someone on the treatment team can help
   find resources. With appropriate treatment, most people with
   schizophrenia can manage their condition.
     * Tests and diagnosis
     * Coping and support

          + Share
          + Tweet

   Jan. 24, 2014

References

    1. Schizophrenia spectrum and other psychotic disorders. In:
       Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th
       ed. Arlington, Va.: American Psychiatric Association; 2013.
       http://www.psychiatryonline.org. Accessed July 12, 2013.
    2. Hales RE, et al. The American Psychiatric Publishing Textbook of
       Psychiatry. 5th ed. Washington, D.C.: American Psychiatric
       Publishing; 2008.
       http://www.psychiatryonline.com/resourceToc.aspx?resourceID=5.
       Accessed May 8, 2013.
    3. Schizophrenia. National Institute of Mental Health.
       http://www.nimh.nih.gov/health/publications/schizophrenia/complete-
       index.shtml. Accessed May 8, 2013.
    4. Fischer BA, et al. Schizophrenia: Clinical manifestations, course,
       assessment, and diagnosis. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    5. Fischer BA, et al. Schizophrenia: Epidemiology and pathogenesis.
       http://www.uptodate.com/home. Accessed May 8, 2013.
    6. Stroup TS, et al. Pharmacotherapy for schizophrenia: Acute and
       maintenance phase treatment. http://www.uptodate.com/home. Accessed
       May 8, 2013.
    7. Mental illness and the family: Recognizing warning signs and how to
       cope. Mental Health America.
       http://www.nmha.org/go/information/get-info/mi-and-the-family/recog
       nizing-warning-signs-and-how-to-cope. Accessed May 16, 2013.
    8. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric
       Association. http://www.dsm5.org/Pages/Default.aspx. Accessed May
       17, 2013.
    9. Schak KM (expert opinion). Mayo Clinic, Rochester, Minn. Aug. 13,
       2013.
   10. Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Aug.
       18, 2013.

You Are ... The Campaign for Mayo Clinic

   Mayo Clinic is a not-for-profit organization. Make a difference today.
     * Learn more
     * Give now

Products and Services

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See also

    1. Phantosmia: What causes olfactory hallucinations?
    2. Paternal age
    3. Family therapy
    4. Blood Basics
    5. Complete blood count
    6. CT scan
    7. CT scan
    8. CT scans: Are they safe?
    9. MRI
   10. MRI
   11. Seeing Inside the Heart with MRI

   Show moreShow less

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   advertising help support our mission. Mayo Clinic does not endorse
   non-Mayo products and services.
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   Check out these best-sellers and special offers on books and
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     * Try Mayo Clinic Health Letter FREE!
     * An authoritative and approachable guide to going gluten-free
     * Get a better night's sleep with this three-step action plan
     * Reduce the impact of stress on your health
     * The Mayo Clinic Diet Online — Eat well. Enjoy life. Lose weight.

Other Topics in Patient Care & Health Info

     * Healthy Lifestyle
     * Symptoms A-Z
     * Diseases and Conditions A-Z
     * Tests and Procedures A-Z
     * Drugs and Supplements A-Z
     * Appointments
     * Patient and Visitor Guide
     * Patient Online Services

   .
   CON-20021077
    1. Home
    2. Schizophrenia
    3. Basics
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   personal use only. "Mayo," "Mayo Clinic," "MayoClinic.com,"
   "EmbodyHealth," "Enhance your life," and the triple-shield Mayo Clinic
   logo are trademarks of Mayo Foundation for Medical Education and
   Research.

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   We comply with the HONcode standard for trustworthy health information:
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                             Schizophrenia Logo

      Home   |  About   |  Donate/Volunteer   |  Contact   |   New!gif
   Schizophrenia Diagnosis and Treatment Centers new! Gif

   Schizophrenia Information > Facts
   Schizophrenia Facts and Statistics
     * Schizophrenia is a serious disorder of the mind and brain but it is
       also highly treatable. Although there is no cure (as of 2007) for
       schizophrenia, the treatment success rate with antipsychotic
       medications and psycho-social therapies can be high. If the
       appropriate level of investment is made in research, it has been
       estimated that a cure for schizophrenia could be found within 10
       years (by the year 2013). Traditionally, however, schizophrenia has
       only received a small fraction of the amount of medical research
       dollars that go into other serious diseases and disorders (see
       below - Schizophrenia Research - for more information).
     * New Treatments: There are over 15 new medications for the treatment
       of schizophrenia currently in development by different biotech and
       pharmaceuticals companies (source: Special report on New
       Schizophrenia Medications). Additionally, there are many new and
       improving psycho-social treatments and cognitive therapies for
       schizophrenia that are being rolled out with significant success.
       Together these new treatments hold significant promise of a better
       life in the future for people who have schizophrenia. Check here
       for the latest news coverage of these new therapies.
     * Schizophrenia is a devastating disorder for most people who are
       afflicted, and very costly for families and society. The overall
       U.S. 2002 cost of schizophrenia was estimated to be $62.7 billion,
       with $22.7 billion excess direct health care cost ($7.0 billion
       outpatient, $5.0 billion drugs, $2.8 billion inpatient, $8.0
       billion long-term care). (source: Analysis Group, Inc.)
     * Today the leading theory of why people get schizophrenia is that it
       is a result of a genetic predisposition combined with an
       environmental exposures and / or stresses during pregnancy or
       childhood that contribute to, or trigger, the disorder. Already
       researchers have identified several of the key genes - that when
       damaged - seem to create a predisposition, or increased risk, for
       schizophrenia. The genes, in combination with suspected
       environmental factors - are believed to be the factors that result
       in schizophrenia. These genes that seem to cause increased risk of
       schizophrenia include the DISC1, Dysbindin, Neuregulin and G72
       genes, but it has been estimated that up a dozen or more genes
       could be involved in schizophrenia risk. See our Schizophrenia
       Genetics news for the latest information in this fast-moving area.
     * One of the most positive areas of schizophrenia research today is
       in the area of identification of early risk factors for development
       of schizophrenia, and prevention of schizophrenia in those people
       who are predisposed to the disease. (source: Neuropsychiatry
       Review). For more information see Schizophrenia Causes and
       Prevention. One of the most easily avoided factors linked to
       development of schizophrenia are brain-altering street drugs like
       marijuana and cannabis.
     * Schizophrenia is a disease that typically begins in early
       adulthood; between the ages of 15 and 25. Men tend to get develop
       schizophrenia slightly earlier than women; whereas most males
       become ill between 16 and 25 years old, most females develop
       symptoms several years later, and the incidence in women is
       noticably higher in women after age 30. The average age of onset is
       18 in men and 25 in women. Schizophrenia onset is quite rare for
       people under 10 years of age, or over 40 years of age. The diagram
       below demonstrates the general "age of onset" trends for
       schizophrenia in men and women, from a representative study on the
       topic.
       [szage.onset.gif]
       Source: A typological model of schizophrenia based on age at onset,
       sex an familial morbidity. Acta Psych8atr. Scand. 89, 135-141
       (1994).
       The diagram below represents the differences in needs for
       hospitalizations, at different ages, for men and women who have
       schizophrenia. As shown in the diagram, schizophrenia tends to hit
       younger males hardest, with a much higher rate of hospitalization
       required between the ages of 15 and 40. (source: Hospital data from
       Canada).
       [schiz.age.impact.3-1_e.gif]
     * The earlier that schizophrenia is diagnosed and treated, the better
       the outcome of the person and the better the recovery. (Source:
       Yale University Medical School)
     * Schizophrenia occurs in all societies regardless of class, colour,
       religion, culture - however there are some variations in terms of
       incidence and outcomes for different groups of people. (Source: Dr.
       Robin Murray )
     * Schizophrenia Ranks among the top 10 causes of disability in
       developed countries worldwide (source: The global burden of
       disease: a comprehensive assessment of mortality and disability
       from diseases, injuries, and risk factors in 1990 and projected to
       2020. Cambridge, MA: Published by the Harvard School of Public
       Health on behalf of the World Health Organization and the World
       Bank, Harvard University Press, 1996.
       http://www.who.int/msa/mnh/ems/dalys/intro.htm ) For additional
       information See the World Health Organization's mental health
       publications.
       The Prevalance Rate for schizophrenia is approximately 1.1% of the
       population over the age of 18 (source: NIMH) or, in other words, at
       any one time as many as 51 million people worldwide suffer from
       schizophrenia, including;
          + 6 to 12 million people in China (a rough estimate based on the
            population)
          + 4.3 to 8.7 million people in India (a rough estimate based on
            the population)
          + 2.2 million people in USA
          + 285,000 people in Australia
          + Over 280,000 people in Canada
          + Over 250,000 diagnosed cases in Britain
     * Rates of schizophrenia are generally similar from country to
       country—about .5% to 1 percent of the population (there are
       variations - but the variance is difficult to track due to
       differing measuring standards in many countries, etc.). Source: Dr.
       Robin Murray.
       Another way to express the prevalence of schizophrenia at any give
       time is the number of individuals affected per 1,000 total
       population. In the United States that figure is 7.2 per 1,000. This
       means that a city of 3 million people will have over 21,000
       individuals suffering from schizophrenia.
       Incidence: The number of people who will be diagnosed as having
       schizophrenia in a year is about one in 4,000. So about 1.5 million
       people will be diagnosed with schizophrenia this year, worldwide.
       About 100,000 people in the United States will be diagnosed with
       schizophrenia this year.
       [Note: The term 'prevalence' of Schizophrenia usually refers to the
       estimated population of people who are living with Schizophrenia at
       any given time. The term 'incidence' of Schizophrenia refers to the
       annual diagnosis rate, or the number of new cases of Schizophrenia
       diagnosed each year. ]
       Prevalence of schizophrenia compared to other well-known diseases
       [schiz.prev.gif]
       Source: BCSS
       Therefore, the approximate number of people in the United States
       suffering from:
          + Schizophrenia: Over 2.2 million people
          + Multiple Sclerosis: 400,000 people
          + Insulin-dependent Diabetes: 350,000 people
          + Muscular Dystrophy: 35,000 people
       The Course of Schizophrenia
          + Early intervention and early use of new medications lead to
            better medical outcomes for the individual
          + The earlier someone with schizophrenia is diagnosed and
            stabilized on treatment, the better the long-term prognosis
            for their illness
          + Teen suicide is a growing problem -- and teens with
            schizophrenia have approximately a 50% risk of attempted
            suicide
          + In rare instances, children as young as five can develop
            schizophrenia.
       Anti-psychotic medications are the generally recommended treatment
       for schizophrenia. If medication for schizophrenia is discontinued,
       the relapse rate is about 80 percent within 2 years. With continued
       drug treatment, only about 40 percent of recovered patients will
       suffer relapses.( Source: NIMH)
       Wide variation occurs in the course of schizophrenia. Some people
       have psychotic episodes of illness lasting weeks or months with
       full remission of their symptoms between each episode; others have
       a fluctuating course in which symptoms are continuous but rise and
       fall in intensity; others have relatively little variation in the
       symptoms of their illness over time. At one end of the spectrum,
       the person has a single psychotic episode of schizophrenia followed
       by complete recovery; at the other end of the spectrum is a course
       in which the illness never abates and debilitating effects
       increase. (source: Openthedoors). Recent research increasingly
       shows that the disease process of schizophrenia gradually and
       significantly damages the brain of the person, and that earlier
       treatments (medications and other therapies) seem to result in less
       damage over time (source: UCLA NeuroImaging Lab , Other info - see
       "Early Treatment" section of this page).
       [sz.episodes.gif]
       After 10 years, of the people diagnosed with schizophrenia:
          + 25% Completely Recover
          + 25% Much Improved, relatively independent
          + 25% Improved, but require extensive support network
          + 15% Hospitalized, unimproved
          + 10% Dead (Mostly Suicide)
       After 30 years, of the people diagnosed with schizophrenia:
          + 25% Completely Recover
          + 35% Much Improved, relatively independent
          + 15% Improved, but require extensive support network
          + 10% Hospitalized, unimproved
          + 15% Dead (Mostly Suicide)
       (Source: Surviving Schizophrenia)
       Where are the People with Schizophrenia?
       Approximately:
          + 6% are homeless or live in shelters
          + 6% live in jails or prisons
          + 5% to 6% live in Hospitals
          + 10% live in Nursing homes
          + 25% live with a family member
          + 28% are living independently
          + 20% live in Supervised Housing (group homes, etc.)
       (Source: Surviving Schizophrenia)

   Homelessness and Schizophrenia
     * Approximately 200,000 individuals with schizophrenia or
       manic-depressive illness are homeless, constituting one-third of
       the approximately 600,000 homeless population (total homeless
       population statistic based on data from Department of Health and
       Human Services). These 200,000 individuals comprise more than the
       entire population of many U.S. cities, such as Hartford,
       Connecticut; Charleston, South Carolina; Reno, Nevada; Boise,
       Idaho; Scottsdale, Arizona; Orlando, Florida; Winston Salem, North
       Carolina; Ann Arbor, Michigan; Abilene, Texas or Topeka, Kansas.
     * At any given time, there are more people with untreated severe
       psychiatric illnesses living on America’s streets than are
       receiving care in hospitals. Approximately 90,000 individuals with
       schizophrenia or manic-depressive illness are in hospitals
       receiving treatment for their disease.
       Source: Treatment Advocacy Center

   The Cost of Schizophrenia to Society:

     Schizophrenia, long considered the most chronic, debilitating and
     costly mental illness, now consumes a total of about $63 billion a
     year for direct treatment, societal and family costs. Richard Wyatt,
     M.D., chief of neuropsychiatry, National Institutes of Mental
     Health, has said that nearly 30 percent ($19 billion) of
     schizophrenia's cost involves direct treatment and the rest is
     absorbed by other factors -- lost timefrom work for patients and
     care givers, social services and criminal justice resources.

     Wyatt said schizophrenia affects one percent of the population,
     accounts for a fourth of all mental health costs and takes up one in
     three psychiatric hospital beds. Since most schizophrenia patients
     are never able to work, they must be supported for life by Medicaid
     and other forms of public assistance. Source: NIMH

     A more recent estimate of the cost of schizophrenia and other
     serious mental illnesses (biplar disorder, serious depression, etc)
     from Dr, E. Fuller Torrey in Q1, 2004 was that federal costs for the
     care of seriously mentally ill individuals now total $41 billion
     yearly and are rocketing upward at a rate of $2.6 billion a year.

     More hospital beds in Canada (8%) are occupied by people with
     schizophrenia than by sufferers of any other medical condition
     (Source: BCSS)

     In the UK, in economic terms: some 80 million working days are lost
     each year at a cost of £3.7 billion; the NHS spends around £1
     billion on treatment and personal social services another £400
     million.

     The greatest cost of schizophrenia , however, is the non-economic
     costs to those who have it and their families.

     Schizophrenia Ranks among the top 10 causes of disability in
     developed countries worldwide (source: The global burden of disease:
     a comprehensive assessment of mortality and disability from
     diseases, injuries, and risk factors in 1990 and projected to 2020.
     Cambridge, MA: Published by the Harvard School of Public Health on
     behalf of the World Health Organization and the World Bank, Harvard
     University Press, 1996.
     http://www.who.int/msa/mnh/ems/dalys/intro.htm ) For additional
     information See the World Health Organization's mental health
     publications.

     Schizophrenia Research Expenditures:

     Research expenditures on schizophrenia still lag far behind those on
     other serious illnesses. US Government spending on research per
     person - Comparison (For More information: A Federal Failure in
     Psychiatric Research, November, 2003)

NIH Research Expenditure by Disease, 1999

   Disease
   FY 1999 NIH research expenditures
   Prevalence: Individuals with this disease
   NIH research dollars per person affected
   HIV (including AIDS)
     $1,792,700,000
           800,000
   $2,240.88
   lung cancer
        $163,100,000
           342,457
   $476.26
   cervical cancer
          $75,200,000
           231,064
   $325.45
   multiple sclerosis
          $96,300,000
           350,000
   $275.14
   breast cancer
        $474,700,000
         2,197,504
   $216.02
   colorectal cancer
        $175,900,000
         1,041,499
   $168.89
   Parkinson’s disease
        $132,300,000
         1,000,000
   $132.30
   prostate cancer
        $177,500,000
         1,637,208
   $108.42
   Alzheimer’s disease
        $406,500,000
         4,000,000
   $101.62
   schizophrenia
        $196,515,000
         2,632,396
   $74.65
   bipolar disorder
          $57,805,000
         2,227,412
   $25.95
   depression
        $199,600,000
       10,732,076
   $18.60
   panic disorder
          $19,049,000
         3,239,872
   $5.88
   obsessive-compulsive disorder
          $12,693,000
         4,859,808
   $2.61
    Sources of data:
          + The 1999 NIMH expenditures by disease were provided by the
            NIMH budget office, July 24, 2000. There are suggestions that
            some of these expenditures are inflated. The $196.5 million
            estimate for schizophrenia research in 1999, for example, is
            more than 50 percent higher than the $124.3 million estimate
            for 2002, recently made public by NIMH. The number of persons
            affected with serious mental illness was derived by using the
            “best estimate” one-year prevalence figures from the 1999
            Report of the Surgeon General (op. cit., p. 47) and
            multiplying by the 1999 U.S. population figures for all
            individuals 18 and over (202,492,000). The figure for
            schizophrenia and bipolar disorder is consistent with other
            prevalence figures for these disorders. However, the figures
            for depression (unipolar major depression), panic disorder,
            and obsessive-compulsive disorder clearly include individuals
            with non-severe forms of these disorders. The authors are not
            aware of reliable prevalence data that include only severe
            forms of these disorders.
          + The 1999 NIH expenditures for other diseases were obtained
            from NIH’s annual report “Research Initiatives/Programs of
            Interest ” for 1999,
            http://www4.od.nih.gov/ofm/diseases/index.stm. The number of
            individuals with various cancers was obtained from the
            National Cancer Institute,
            http://seer.cancer.gov/faststats/html/pre_all.html (click on
            “Prevalence” on the left, under “Available Statistics”) and
            represents complete prevalence, i.e., anyone who has ever had
            that cancer who is still alive. The number of individuals with
            other diseases was taken from the websites of the various
            advocacy organizations


   Suicide Risk

     People with the condition have a 50 times higher risk of attempting
     suicide than the general population; the risk of suicide is very
     serious in people with schizophrenia. Suicide is the number one
     cause of premature death among people with schizophrenia, with an
     estimated 10 percent to 13 percent killing themselves and
     approximately 40% attempting suicide at least once (and as much as
     60% of males attempting suicide). The extreme depression and
     psychoses that can result due to lack of treatment are the usual
     causes. These suicides rates can be compared to the general
     population, which is somewhere around 0.01%. (source: Treatment
     Advocacy Center and other sources)

     Schizophrenia and Violence

     People with schizophrenia are far more likely to harm themselves
     than be violent toward the public. Violence is not a symptom of
     schizophrenia.

     News and entertainment media tend to link mental illnesses including
     schizophrenia to criminal violence. Most people with schizophrenia,
     however, are not violent toward others but are withdrawn and prefer
     to be left alone. Drug or alcohol abuse raises the risk of violence
     in people with schizophrenia, particularly if the illness is
     untreated, but also in people who have no mental illness.

     Schizophrenia and Jail

     The vast majority of people with schizophrenia who are in jail have
     been charged with misdemeanors such as trespassing.

     As many as one in five (20%) of the 2.1 million Americans in jail
     and prison are seriously mentally ill, far outnumbering the number
     of mentally ill who are in mental hospitals, according to a
     comprehensive study. Source: Human Rights Watch

     The American Psychiatric Association estimated in 2000 that one in
     five prisoners were seriously mentally ill, with up to 5 percent
     actively psychotic at any given moment.

     In 1999, the statistical arm of the Justice Department estimated
     that 16 percent of state and federal prisoners and inmates in jails
     were suffering from mental illness. These illnesses included
     schizophrenia, manic depression (or bipolar disorder) and major
     depression.

     The figures are higher for female inmates, the report says. The
     Justice Department study found that 29 percent of white female
     inmates, 22 percent of Hispanic female inmates and 20 percent of
     black female inmates were identified as mentally ill.

     Many individuals with schizophrenia revolve between hospitals, jails
     and shelters. In Illinois 30% of patiants discharged from state
     psychiatric hospitals are rehospitalized within 30 days. In New York
     60% of discharged patients are rehospitalized within a year. Source:
     Surviving Schizophrenia

     What Percentage of Individuals with sever mental illnesses are
     untreated, and why?

     Recent American studies report that approximately half of all
     individuals with severe mental illnesses have received no treatment
     for their illnesses in the previous 12 months. These findings are
     consistent with other studies of medication compliance for
     individuals with schizophrenia and manic-depressive illness (bipolar
     disorder). The majority (55 percent) of those not receiving
     treatment have no awareness of their illness (anosognosia) and thus
     do not seek treatment. Stigma and dissatisfaction with services are
     relatively unimportant reasons why individuals with severe mental
     illnesses do not seek treatment.

     The 45 percent who acknowledged that they needed treatment (and thus
     had awareness of their illness) but still were not receiving
     treatment cited many reasons for this. These included (respondent
     could check several reasons):

     32% "wanted to solve problem on own"
     27% "thought the problem would get better by itself"
     20% "too expensive"
     18% "unsure about where to go for help"
     17% "help probably would not do any good"
     16% "health insurance would not cover treatment"

     Source: Treatment Advocacy Center

     The Risks of Getting Schizophrenia

     [schiz.risk.gif]

     After a person has been diagnosed with schizophrenia in a family,
     the chance for a sibling to also be diagnosed with schizophrenia is
     7 to 9 percent. If a parent has schizophrenia, the chance for a
     child to have the disorder is 10 to 15 percent. Risks increase with
     multiple affected family members.


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Schizophrenia is eight different diseases, not one

   New research shows that schizophrenia is not a single disease, but a
   group of eight distinct disorders, each caused by changes in clusters
   of genes that lead to different sets of symptoms.
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Schizophrenia is eight different diseases, not one

   [Szabo_Liz.png] Liz Szabo, USA TODAY 1:06 p.m. EDT September 15, 2014
   XXX_XXX_DNA

   Researchers found that certain genetic profiles matched particular
   symptoms in people with schizophrenia.(Photo: PhotoDisc)
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   New research shows that schizophrenia is not a single disease, but a
   group of eight distinct disorders, each caused by changes in clusters
   of genes that lead to different sets of symptoms.

   The finding sets the stage for scientists to develop better ways to
   diagnose and treat schizophrenia, a mental illness that can be
   devastating when not adequately managed, says C. Robert Cloninger,
   co-author of the study published Monday in the American Journal of
   Psychiatry.

   "We are really opening a new era of psychiatric diagnosis," says
   Cloninger, professor of psychiatry and genetics at the Washington
   University School of Medicine in St. Louis. Cloninger says he hopes his
   work will "allow for the development of a personalized diagnosis,
   opening the door to treating the cause, rather than just the symptoms,
   of schizophrenia."

   Clonginger and colleagues found that certain genetic profiles matched
   particular symptoms. While people with one genetic cluster have odd and
   disorganized speech – what is sometimes called "word salad" – people
   with another genetic profile hear voices, according to the study,
   funded by the National Institutes of Health.
   XXX_schizophrenia02

   Dr. C. Robert Cloninger, Washington University School of Medicine, and
   colleagues found that certain genetic profiles matched particular
   symptoms of schizophrenia.
    (Photo: Robert Boston, Washington University)

   Some genetic clusters gave people higher risks of the disease than
   others, according to the study, which compared the DNA of 4,200 people
   with schizophrenia to that of 3,800 healthy people.

   One set of genetic changes, for example, confers a 95% chance of
   developing schizophrenia. In the new study, researchers describe a
   woman with this genetic profile who developed signs of the disorder by
   age 5, when she taped over the mouths of her dolls to make them stop
   whispering to her and calling her name. Another patient – whose genetic
   profile gave her a 71% risk of schizophrenia – experienced a more
   typical disease course and began hearing voices at age 17.

   The average person has less than a 1% risk of developing schizophrenia,
   Cloninger says.

   Psychiatrists such as Stephen Marder describe the the study as a step
   forward. Today, doctors diagnose patients with mental illness with a
   process akin to a survey, asking about the person's family history and
   symptoms, says Marder, a professor at the David Geffen School of
   Medicine at the University of California-Los Angeles.

   "It underlines that the way we diagnose schizophrenia is relatively
   primitive," Marder says.

   Patients may wait years for an accurate diagnosis, and even longer to
   find treatments that help them without causing intolerable side
   effects.

   Doctors have long known that schizophrenia can run in families, says
   Robert Freedman, editor in chief of the American Journal of Psychiatry
   and chair of psychiatry at the University of Colorado Anschutz Medical
   Campus. If one identical twin has schizophrenia, for example, there is
   an 80% chance that the other twin has the disease, as well.

   In the past, doctors looked for single genes that might cause
   schizophrenia, without real success, Freedman says.

   The new paper suggests that genes work together like a winning or
   losing combination of cards in poker, Freedman says. "This shows us
   that there are some very bad hands out there," Freedman says.

   XXX_schizophrenia01

   Doctors have known for years that breast cancer is not one disease, but
   at least half a dozen diseases driven by different genes, says study
   co-author Igor Zwir, research associate in psychiatry at Washington
   University.
    (Photo: Robert Boston, Washington University)

   In some cases – in which a genetic profile conveys close to a 100% risk
   of schizophrenia – people may not be able to escape the disease,
   Cloninger says. But if doctors could predict who is at high risk, they
   might also be able to tailor an early intervention to help a patient
   better manage their condition, such as by managing stress.

   Doctors don't yet know why one person with a 70% risk of schizophrenia
   develops the disease and others don't, Clonginger says. It's possible
   that environment plays a key role, so that child with a supportive
   family and good nutrition might escape the diagnosis, while someone who
   experiences great trauma or deprivation might become very ill.

   The study also reflects how much has changed in the way that scientists
   think about the genetic causes of common diseases, Marder says. He
   notes that diseases caused by a single gene – such as sickle-cell
   anemia and cystic fibrosis – affect very few people. Most common
   diseases, such as cancer, are caused by combinations of genes. Even
   something as apparently simple as height is caused by combinations of
   genes, he says.

   Doctors have known for years that breast cancer is not one disease, for
   example, but at least half a dozen diseases driven by different genes,
   says study co-author Igor Zwir, research associate in psychiatry at
   Washington University. Doctors today have tests to predict a woman's
   risk of some types of breast cancer, and other tests that help them
   select the most effective drugs.

   Those sorts of tests could be extremely helpful for people with
   schizophrenia, who often try two or three drugs before finding one
   that's effective, Cloninger says.

   "Most treatment today is trial and error," Cloninger says.

   If doctors could pinpoint which drugs could be the most effective, they
   might be able to use lower doses, producing fewer of the bothersome
   side effects that lead many patients to stop taking their medication,
   Cloninger says.

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     * Causes
     * History
     * Childhood Schizophrenia
     * Statistics

Symptoms

     * Hallucinations
     * Hearing Voices
     * Managing Symptoms
     * Movement Disorders
     * Delusions
     * Schizophrenia and Suicide

Treatment

     * Support Groups
     * Psychotherapy
     * Self Help
     * ECT

Drugs for Treatment

     * Conventional Antipsychotics
          + Fluphenazine
          + Haldol
          + Lithium
          + Perphenazine
          + Thioridazine
     * Atypical Antipsychotics
          + Aripiprazole
          + Asenapine
          + Clozapine
          + Olanzapine
          + Palperidone
          + Quetiapine
          + Risperidone
          + Ziprasidone
     * Supplements
          + Choline
          + Creatine
          + DHEA

Types

     * Residual
     * Hebephrenic
     * Disorganized
     * Paranoid
     * Undifferentiated
     * Catatonic

Related Conditions

     * Split Personality
     * Anxiety and Schizophrenia
     * Depression and Schizophrenia
     * Bipolar Disorder
     * Brief Psychotic Disorder
     * Shared Psychotic Disorder
     * Schizotypal Personality Disorder
     * Schizophreniform Disorder
     * Schizoid Personality
     * Delusional Disorder
     * Substance Abuse
     * Schizoaffective Disorder
     * Schizophrenia and Self Injury

Living With Schizophrenia

     * Family Relationships
     * Homelessness
     * At Work
     * Violence
     * Hallucinations

Schizophrenic Symptoms

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   Schizophrenia is classified as a “psychotic disorder” in the DSM-IV,
   which is the diagnostic manual used by mental health professionals.
   When a person is “psychotic,” it means he is unable to distinguish
   between what is real and what is imagined.

   In more clinical terms, his “reality testing” is severely impaired. An
   individual with schizophrenia is not necessarily always psychotic, but
   may have periods of psychosis which are often referred to as “psychotic
   episodes.” These episodes make it impossible to function normally while
   they are occurring.

   Psychotic symptoms primarily involve hallucinations or delusions, but
   there are also many other types of symptoms associated with
   schizophrenia. Following is a brief overview of schizophrenic symptoms,
   broken down into two categories: positive symptoms, and negative
   symptoms.

Positive Symptoms

   Hallucinations
          A hallucination involves one of the five senses (sound, sight,
          taste, touch, or smell), but occurs when there is nothing in the
          environment to stimulate the sense organ. In other words, a
          hallucination is an imagined (or unreal) sound, vision, etc. For
          example, a person who is having auditory hallucinations may be
          hearing voices or music playing, but these voices or sounds are
          only in his mind.
          The most common type of hallucination that schizophrenics
          experience is an auditory hallucination. Many schizophrenics
          report hearing a voice or several voices. The voices may be
          telling the person to do something, such as harm himself or
          someone else. They may also be commenting on his actions or
          behavior. These voices can be very troubling and even
          frightening for the individual.

   Delusions
          A delusion is essentially a strongly held, but false belief that
          something which is not real is actually real, even when there is
          obvious proof or evidence to the contrary. Two examples of
          delusions would be a young man believing he is God, or that he
          is pregnant.
          While delusions may involve many different themes, the most
          common type of delusion experienced by schizophrenics is a
          paranoid delusion. This often involves a belief that the person
          is being followed or spied upon by someone, such as the FBI. The
          person may believe that his phone is tapped and that there are
          video cameras hidden in his home. Paranoid delusions can be very
          frightening when they occur, causing the person to try to hide,
          protect himself, or run to somewhere safe. Other types of
          delusions may be grandiose, persecutory, jealous, erotomanic
          (sexual), or somatic (having to do with his body) in nature.

   Disorganized speech
          When a person’s speech is disorganized, he may often quickly go
          off the topic and talk about a variety of unrelated things. His
          speech may also be incoherent, making no sense to anyone who is
          listening. When someone’s speech is incoherent, his words or
          phrases are not connected in a way which is logical or
          meaningful. Sometimes this is referred to as “word salad” or
          gibberish.

   Grossly disorganized behavior
          Grossly disorganized behavior can show up in a variety of ways.
          For example, the person may dress in a bizarre or grossly
          inappropriate way, such as wearing multiple layers of clothing
          on a very hot day. He may be unkempt, completely neglecting his
          hygiene. He may become easily agitated without any provocation
          or trigger, or act very silly and childlike.

   Catatonic behavior
          Catatonic behavior involves the person’s movement, posture and
          responsiveness. For example, he may be completely unresponsive
          to his surroundings, as in a catatonic stupor. He may stand or
          sit in a rigid and / or bizarre position. When someone is
          catatonic, he may be very resistant to any attempt to move or
          reposition him. Catatonia may also involve excessive, excited
          movement that has no purpose and no trigger.

Negative Symptoms

   The negative symptoms of schizophrenia are passive in nature. They
   affect the person’s thinking, emotion and behavior and can be the most
   devastating of all the symptoms. Three of the most common are flat
   affect, alogia, and avolition.

   Flat affect
          Flat affect is a common characteristic which means that the
          person shows little or no emotional expression or response.

   Alogia
          Alogia, which refers to impoverished thinking, occurs when the
          person’s speech is very limited in terms of content and lacks
          spontaneity.

   Avolition
          Avolition refers to the person’s inability to initiate and
          participate in any activity or task which is goal-oriented, such
          as dressing himself, performing a work-related function, or
          preparing a meal.

The Necessity of Treatment

   Because the symptoms of schizophrenia are both severe and chronic, they
   generally severely impact the individual with this disorder. Treatment,
   particularly anti-psychotic medication, can play a significant role in
   helping the patient function more normally and alleviate or reduce the
   psychotic episodes. While there is no cure at this time, ongoing
   treatment is crucial for any individual diagnosed with schizophrenia.

   by Dr. C. Lane, Psy.D.

Related Articles

   Schizophrenic Tendencies

   Catatonic Schizophrenia Symptoms

   Residual Schizophrenia Symptoms

   Schizophrenic Prayer

   Schizophrenia's Cognitive Symptoms

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   privacy policy. The information provided on schizophrenic.com is
   designed to support, not replace, the relationship that exists between
   a patient/site visitor and his/her health professional(s). This
   information is solely for informational and educational purposes. The
   publication and maintenance of this site does not constitute the
   practice of any type of medicine, and this information does not replace
   the advice of your physician or other health care provider. Neither the
   owners or employees of schizophrenic.com nor the author(s) of site
   content take responsibility for any possible consequences from any
   treatment, procedure, exercise, dietary modification, action or
   application of medication which results from reading this site. Always
   speak with your primary health care provider before engaging in any
   form of self treatment. Please see our Legal Statement for further
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   schizophrenia

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Community

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About Schizophrenia

     * Introduction
     * Diagnosing
     * Prognosis
     * Effects and Complications
     * Can Schizophrenia be Prevented?
     * Risk Factors
     * Causes
     * History
     * Childhood Schizophrenia
     * Statistics

Symptoms

     * Hallucinations
     * Hearing Voices
     * Managing Symptoms
     * Movement Disorders
     * Delusions
     * Schizophrenia and Suicide

Treatment

     * Support Groups
     * Psychotherapy
     * Self Help
     * ECT

Drugs for Treatment

     * Conventional Antipsychotics
          + Fluphenazine
          + Haldol
          + Lithium
          + Perphenazine
          + Thioridazine
     * Atypical Antipsychotics
          + Aripiprazole
          + Asenapine
          + Clozapine
          + Olanzapine
          + Palperidone
          + Quetiapine
          + Risperidone
          + Ziprasidone
     * Supplements
          + Choline
          + Creatine
          + DHEA

Types

     * Residual
     * Hebephrenic
     * Disorganized
     * Paranoid
     * Undifferentiated
     * Catatonic

Related Conditions

     * Split Personality
     * Anxiety and Schizophrenia
     * Depression and Schizophrenia
     * Bipolar Disorder
     * Brief Psychotic Disorder
     * Shared Psychotic Disorder
     * Schizotypal Personality Disorder
     * Schizophreniform Disorder
     * Schizoid Personality
     * Delusional Disorder
     * Substance Abuse
     * Schizoaffective Disorder
     * Schizophrenia and Self Injury

Living With Schizophrenia

     * Family Relationships
     * Homelessness
     * At Work
     * Violence
     * Hallucinations

Drugs for Schizophrenia Treatment

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   Schizophrenia is considered the most serious of all psychiatric
   disorders. The symptoms, which include hallucinations, delusions, and
   grossly disorganized or catatonic behavior can render a person
   significantly disabled until or unless stabilized. Sadly, there is
   currently no cure for this challenging and complex disorder. It is
   considered a life long disorder, so the symptoms typically reappear
   throughout one’s lifetime if not treated, and in many cases even if
   treated.

   Over the years, various drugs have been developed for the treatment of
   schizophrenia. While they all come with many side effects, it is often
   a matter of choosing the lesser of two evils – coping with and managing
   side effects or not being able to function at all on a fairly regular
   basis due to severe symptoms. For many, taking medication is the
   preferred option. It helps control symptoms and minimize their
   recurrence.

First generation antipsychotics

   Back in the early 1950s, one of the first drugs used to treat
   schizophrenia was introduced to the U.S. market. This drug, Thorazine,
   was the first in a long line of medications often referred to as first
   generation antipsychotics. They are also called conventional
   antipsychotics, major tranquilizers, or typical antipsychotics. Haldol,
   Trilafon, and Mellaril are a few of the medications in this group.

   These medications allowed individuals with schizophrenia to have more
   normal lives, and function better in society. Unfortunately, because of
   multiple problematic side effects, not to mention the very nature of
   the disorder, many schizophrenics didn’t (and still don’t) stay on
   their medication. Two side effects in particular which are closely
   associated with the typical antipsychotics are tardive dyskinesia (TD)
   and neuroleptic malignant syndrome (NMS).

   TD is often permanent and causes involuntary, uncontrollable and random
   movements of the face and body. NMS can be fatal, and includes symptoms
   like muscle stiffness, difficulty breathing, altered mental status,
   sudden renal failure, fluctuations in blood pressure or heartbeat,
   tremors, dehydration, racing heartbeat, and very high fever.

Atypical antipsychotics

   Since the early 1990s, a second group of medications, referred to as
   atypical antipsychotics or second generation antipsychotics (or “third
   generation antipsychotics” for the most recent), started to become
   available. These medications were initially well received because there
   was less risk of some of the problematic side effects of the older
   medications, particularly TD and NMS.

   Medications which fall into this group include Zyprexa, Seroquel,
   Risperdal and Abilify, to name a few. The newest atypical antipsychotic
   to be FDA-approved for schizophrenia is Asenapine (brand name Saphris).
   It was FDA-approved in late 2009 ^1. The atypical antipsychotics still
   come with many side effects, and just as with the older medications,
   many people with schizophrenia discontinue them as a result.

   Until a cure is found for schizophrenia, if that ever happens, drugs
   will likely be one of the core treatments for this disorder. Research
   is ongoing to find ways to better treat schizophrenia.

   written by Dr. Cheryl Lane, PsyD

Links to Additional Schizophrenia Drug Articles

     * Atypical Antipsychotics
     * Aripiprazole
     * Asenapine
     * Clozapine
     * Choline
     * Creatine
     * DHEA
     * Fluphenazine
     * Haldol
     * Lithium
     * Palperidone
     * Perphenazine
     * Quetiapine
     * Thioridazine
     * Ziprasidone

References

    1. Asenapine for Schizophrenia and Bipolar I Disorder

   Company Information

   Legal Statement | Privacy Policy | Contact

   ©2015 Schizophrenic.com. All rights reserved. Use of this site
   constitutes acceptance of Schizophrenic.com's terms of service and
   privacy policy. The information provided on schizophrenic.com is
   designed to support, not replace, the relationship that exists between
   a patient/site visitor and his/her health professional(s). This
   information is solely for informational and educational purposes. The
   publication and maintenance of this site does not constitute the
   practice of any type of medicine, and this information does not replace
   the advice of your physician or other health care provider. Neither the
   owners or employees of schizophrenic.com nor the author(s) of site
   content take responsibility for any possible consequences from any
   treatment, procedure, exercise, dietary modification, action or
   application of medication which results from reading this site. Always
   speak with your primary health care provider before engaging in any
   form of self treatment. Please see our Legal Statement for further
   information.

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   Home
   _______________ Search
     * Home
     * News
     * Videos
     * Articles
     * Schizophrenia Types
     * Schizophrenia Treatment
     * Find Treatment

Community

     * Ask a Question

About Schizophrenia

     * Introduction
     * Diagnosing
     * Prognosis
     * Effects and Complications
     * Can Schizophrenia be Prevented?
     * Risk Factors
     * Causes
     * History
     * Childhood Schizophrenia
     * Statistics

Symptoms

     * Hallucinations
     * Hearing Voices
     * Managing Symptoms
     * Movement Disorders
     * Delusions
     * Schizophrenia and Suicide

Treatment

     * Support Groups
     * Psychotherapy
     * Self Help
     * ECT

Drugs for Treatment

     * Conventional Antipsychotics
          + Fluphenazine
          + Haldol
          + Lithium
          + Perphenazine
          + Thioridazine
     * Atypical Antipsychotics
          + Aripiprazole
          + Asenapine
          + Clozapine
          + Olanzapine
          + Palperidone
          + Quetiapine
          + Risperidone
          + Ziprasidone
     * Supplements
          + Choline
          + Creatine
          + DHEA

Types

     * Residual
     * Hebephrenic
     * Disorganized
     * Paranoid
     * Undifferentiated
     * Catatonic

Related Conditions

     * Split Personality
     * Anxiety and Schizophrenia
     * Depression and Schizophrenia
     * Bipolar Disorder
     * Brief Psychotic Disorder
     * Shared Psychotic Disorder
     * Schizotypal Personality Disorder
     * Schizophreniform Disorder
     * Schizoid Personality
     * Delusional Disorder
     * Substance Abuse
     * Schizoaffective Disorder
     * Schizophrenia and Self Injury

Living With Schizophrenia

     * Family Relationships
     * Homelessness
     * At Work
     * Violence
     * Hallucinations

Introduction to Schizophrenia

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   While depression is often referred to by mental health professionals as
   the “common cold” of mental illness, schizophrenia is considered the
   “cancer”. This is because it is probably the most serious and
   debilitating psychiatric disorder that exists. Just over one out of
   every 100 people aged 18 or older has schizophrenia in the U.S. ^1.
   That’s nearly two and a half million Americans ^1.

   Unlike depression and anxiety, which sometimes occur only during a
   short period of a person’s life, schizophrenia is a lifelong disorder.
   And at this time, there is no known cure. The symptoms of schizophrenia
   typically first appear in a person’s late teens or early twenties,
   although they can begin at any age. Generally speaking, males exhibit
   the first signs of schizophrenia earlier then females. Unlike some
   disorders, schizophrenia does not favor one gender over another.

What Causes Schizophrenia?

   Despite much research, the specific cause of schizophrenia is
   essentially still a mystery. However, we do know that brain scans of
   individuals with the disorder show some differences from a brain scan
   of a normal person. Also, we’ve known for a long time that
   schizophrenia runs in families, which indicates a likely genetic
   factor. NIMH researchers recently discovered that schizophrenia may
   develop due to the absence of some key genes ^2. Various other factors
   may also play a role in its development in an individual.
   Unfortunately, it may be a long time before we learn the exact cause or
   causes of this disabling disorder.

What Does Schizophrenia Look Like?

   While the symptoms may vary depending on several factors, some of the
   most common symptoms of schizophrenia include hallucinations (such as
   hearing voices or seeing things which aren’t really there), delusions
   (believing something imagined is actually real), paranoia, lack of
   emotional expression, bizarre behavior, odd ways of thinking or
   speaking, and extremely disorganization behavior.

   There are actually five different types of schizophrenia, as classified
   in the DSM-IV. These types are: paranoid, disorganized,
   undifferentiated, catatonic, and residual. The diagnosis depends on the
   symptoms. Also, there are two related disorders: schizoaffective
   disorder, and schizophreniform disorder.

How is Schizophrenia Treated?

   Schizophrenia is typically treated with antipsychotic medications.
   There are many different types of antipsychotic medications available,
   and the effectiveness of each kind varies from individual to
   individual. May schizophrenics are hospitalized in psychiatric
   hospitals at some point, if not several times, in their life, due to
   the severity of their symptoms.

   Many mental health clinics and hospitals offer residential and day
   treatment programs, which may be for a period of time or ongoing. These
   programs are less intensive than hospitalization. Individual or family
   therapy may be part of the treatment, as well as some type of
   vocational training.

   Schizophrenia is a challenging disorder. However, many individuals with
   schizophrenia are able to have productive and happy lives. As research
   continues, there is always hope that we can either learn how to prevent
   it from developing, or cure it once it does.

   written by Dr. Cheryl Lane, PsyD

References

     * ^1 The Numbers Count: Mental Disorders in America
     * ^2 Science Update February 20, 2008 Scans Reveal Faulty Brain
       Wiring Caused by Missing Genes

Related Articles

   Am I schizophrenic?

   Schizophrenic Children

   What does schizophrenic mean?

   Do schizophrenics know they are schizophrenic?

   Schizophrenic Break

   Prevalence of Schizophrenia

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   a patient/site visitor and his/her health professional(s). This
   information is solely for informational and educational purposes. The
   publication and maintenance of this site does not constitute the
   practice of any type of medicine, and this information does not replace
   the advice of your physician or other health care provider. Neither the
   owners or employees of schizophrenic.com nor the author(s) of site
   content take responsibility for any possible consequences from any
   treatment, procedure, exercise, dietary modification, action or
   application of medication which results from reading this site. Always
   speak with your primary health care provider before engaging in any
   form of self treatment. Please see our Legal Statement for further
   information.

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Schizophrenia Treatment & Management

     * Author: Frances R Frankenburg, MD; Chief Editor: Eduardo
       Dunayevich, MD   more...


     * Overview
     * Presentation
     * DDx
     * Workup
     * Treatment
     * Medication
     *

   Updated: Dec 22, 2014
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     * Approach Considerations
     * Antipsychotic Pharmacotherapy
     * Other Pharmacotherapy
     * Psychosocial Interventions
     * Diet and Activity
     * Prevention
     * Other Treatments
     * Show All

   Multimedia Library
   References

Approach Considerations

   Treatment of schizophrenia requires integration of medical,
   psychological, and psychosocial inputs. The bulk of care occurs in an
   outpatient setting and probably is best carried out by a
   multidisciplinary team, including some combination of the following: a
   psychopharmacologist, a counselor or therapist, a social worker, a
   nurse, a vocational counselor, and a case manager. Clinical pharmacists
   and internists can be valuable members of the team.

   It is important not to neglect the medical care of the person with
   schizophrenia. Obesity, diabetes, cardiovascular disease, and lung
   diseases are prevalent in schizophrenia, and the person with
   schizophrenia often does not receive adequate medical care for such
   conditions.^[78]

   Antipsychotic medications (also known as neuroleptic medications or
   major tranquilizers) diminish the positive symptoms of schizophrenia
   and prevent relapses. Approximately 80% of patients relapse within 1
   year if antipsychotic medications are stopped, whereas only 20% relapse
   if treated. Children, pregnant or breastfeeding women, and elderly
   patients present special challenges. In all of these cases, medications
   must be used with particular caution.

   The choice of which drug to use for treatment of a patient with
   schizophrenia depends on many issues, including effectiveness, cost,
   side-effect burden, method of delivery, availability, and tolerability.
   Many studies have compared antipsychotic drugs with one another, but no
   broad consensus has been reached. In the absence of clinical or
   pharmacogenetic predictors of treatment response, the current treatment
   approach is largely one of trial and error across sequential medication
   choices.

   Although treatment is primarily provided on an outpatient basis,
   patients with schizophrenia may require hospitalization for
   exacerbation of symptoms caused by noncompliance with pharmacotherapy,
   substance abuse, adverse effects or toxicity of medications, medical
   illness, psychosocial stress, or the waxing and waning of the illness
   itself. Hospitalizations are usually brief and are typically oriented
   towards crisis management or symptom stabilization.

   Treatment of patients with schizophrenia, particularly during a
   psychotic episode, may raise the issue of informed consent. Consent is
   a legal term and should be used with respect to specific tasks. A
   person who is delusional in some but not all areas of life may still
   have the capacity to make medical and financial decisions.

Insurance concerns

   In the United States, patients with schizophrenia who are unable to
   work may be eligible for governmental programs, such as Medicare and
   Medicaid. These programs pay the cost of medical care. Unfortunately,
   if individuals begin to work and earn a sufficient salary, they may
   lose these benefits—an especially problematic occurrence when, as is
   often the case, their job provides minimal or no health benefits. This
   situation is complicated and must be monitored closely by professionals
   with a good understanding of health benefits.

   The impact of the American Affordable Care Act (ACA) on the care of
   schizophrenia has yet to be determined. Some parts of the ACA, such as
   the removal of exclusion of preexisting conditions as a barrier to
   getting insurance, and the removal of annual and lifetime benefit
   limits, will be helpful. The ACA mandates parity between care for
   medical and psychiatric illnesses.

   However, health plans in the new exchanges might not provide all of the
   services that are mentioned here, such as supported employment. As
   well, in the states that have chosen not to expand their Medicaid
   programs, patients with Medicaid as their insurer may continue to have
   difficulty in accessing care.[#Antipsychotic]
   Next

Antipsychotic Pharmacotherapy

   Before beginning antipsychotic medications, clinicians should warn
   patients and their families of adverse effects, and the slowness of
   response. The patient may be calmer and less agitated almost
   immediately, but alleviation of the psychosis itself often takes
   several weeks. Some clinicians routinely perform electrocardiography
   (ECG) before beginning treatment with antipsychotic medications and
   then as often as seems appropriate, for example if doses are increased
   or agents change. Because suicide is not uncommon in patients with
   psychotic illnesses, clinicians should write prescriptions for the
   lowest dosage that is consistent with good clinical care. Patients
   should be urged to avoid substance abuse. All medications should be
   given at lower dosages in children and elderly patients and used with
   great caution in women who are pregnant or breastfeeding.

   The first antipsychotic medications, chlorpromazine and haloperidol,
   were dopamine D2 antagonists. These and similar medications are known
   as first-generation, typical, or conventional antipsychotics. Other
   antipsychotics, beginning with clozapine, are known as
   second-generation, atypical, or novel antipsychotics.

   The conventional antipsychotic agents are available in generic forms
   and are less expensive than the newer agents. They are available in a
   variety of vehicles, including liquid and intramuscular (IM)
   preparations. Some of these agents (haloperidol and fluphenazine) are
   also available as depot preparations, meaning that a person can be
   given an injection of a medication every 2-4 weeks. Of the
   second-generation agents, risperidone is available as a long-acting
   injection that uses biodegradable polymers; olanzapine, paliperidone,
   and aripiprazole are also now available in long-acting injectable
   forms.^[79, 80, 81, 82]

   The first-generation antipsychotic drugs tend to cause extrapyramidal
   adverse effects and elevated prolactin levels. The second-generation
   drugs are more likely to cause weight gain and abnormalities in glucose
   and lipid control; in addition, they are often more expensive than the
   first-generation drugs.

Comparative efficacy of agents

   For some years, it was believed that the newer antipsychotic drugs were
   more effective, but there is now some uncertainty about that. An
   exception is clozapine, which consistently outperforms the other
   antipsychotic drugs.

   Phase 1 of the CATIE (Clinical Antipsychotic Trials of Intervention
   Effectiveness) study, a large nationwide trial that compared the
   first-generation antipsychotic perphenazine with the second-generation
   drugs olanzapine, risperidone, quetiapine, and ziprasidone, found that
   olanzapine was slightly better than the other drugs in terms of the
   patients choosing to stay on it, and number of hospitalizations, but
   also was associated with significant weight gain. Surprisingly,
   perphenazine performed about as well as the other 3 second-generation
   agents.^[83]

   In this and other studies the primary outcome, stopping the drug, may
   seem to be unusual. It is used because it reflects the “real-world”
   decision of the clinician and patient that the agent is either no
   longer tolerable or effective.

   In CUtLASS (Cost Utility of the Latest Antipsychotic drugs in
   Schizophrenia Study), a study from the United Kingdom, more than 200
   patients who were about to change antipsychotic medication were
   randomly assigned to either a first-generation or a second-generation
   agent. In this study, the first-generation drugs seemed to perform
   slightly better than the newer ones, as measured by the Quality-of-Life
   Scale.^[84]

   First-episode schizophrenia

   EUFEST (European First Episode Schizophrenia Trial) was a year-long
   open-label study conducted in nearly 500 patients in 13 European
   countries and Israel that, as did CATIE, used treatment discontinuance
   as the main outcome measure. The study found that patients were more
   likely to stop low-dose haloperidol than to stop olanzapine,
   quetiapine, ziprasidone, or amisulpride (not available in the United
   States); however, all medications were associated with similar
   decreases in symptoms.^[85]

   Similarly, the randomized, double-blind CAFE (Comparison of Atypicals
   for First Episode) study found few differences between olanzapine,
   quetiapine, and risperidone in 400 patients experiencing a first
   episode of psychosis, with all-cause treatment discontinuance rates in
   the vicinity of 70% by week 52. Drowsiness and weight gain were along
   the most common adverse events with all 3 drugs; in addition, insomnia
   was seen with olanzapine, a longer sleep time with quetiapine, and
   menstrual irregularities in women with risperidone.^[86]

   The Schizophrenia Patient Outcomes Research Team (PORT) of the
   University of Maryland recommended that any antipsychotic medication,
   with the exceptions of clozapine and olanzapine, can be used as
   first-line treatment for patients with schizophrenia who are
   experiencing their first episode of acute positive symptoms.^[87]

   According to a comprehensive review carried out by the Schizophrenia
   Patient Outcomes Research Team (PORT) of the University of Maryland,
   early treatment with any antipsychotic medication is associated with
   significant symptom reduction; first- and second-generation
   antipsychotics may have equivalent significant short-term efficacy.
   However, because of the adverse adverse-effect profile of clozapine and
   the significant metabolic risks associated with olanzapine, PORT
   advised that neither drug should be considered as a first-line
   treatment for first-episode schizophrenia.^[87]

   Noting that both responsiveness to treatment and sensitivity to adverse
   effects are greater in patients with first-episode schizophrenia than
   in those who have had multiple episodes, PORT recommended starting
   antipsychotic treatment for the former at doses lower than those
   recommended for the latter. An exception is quetiapine, which may not
   be effective in lower doses; in addition, low doses of aripiprazole or
   ziprasidone have not been evaluated in first-episode
   schizophrenia.^[87]

   Wunderink and colleagues followed just over 100 subjects participating
   in a study of first episode psychosis. Subjects were randomly assigned
   to antipsychotic medication dose reduction or dose maintenance. At 7
   years follow-up, they found that those treated with lower doses or no
   antipsychotics had more relapses and hospitalizations. This was not an
   unexpected finding. However, they also found that these lightly
   medicated patients overall were functioning better. They concluded that
   it seems that there are different responses of symptoms and functioning
   to medication.^[88]

   The National Institute of Mental Health (NIMH) has initiated a research
   project, Recovery After an Initial Schizophrenia Episode (RAISE), to
   determine whether coordinated and aggressive treatment in the earliest
   stages of illness can prevent long-term disability from schizophrenia.
   The RAISE Early Treatment Program (ETP), an integrated program
   delivered in community clinics, will be compared with the RAISE
   Connection program, a program offered in Baltimore and Manhattan in
   partnership with state mental health programs.

Choice of agent

   There is no clear antipsychotic drug of choice for schizophrenia.
   Clozapine is the most effective medication but is not recommended as
   first-line therapy because it has a high burden of adverse effects,
   requires regular blood work, and has not outperformed other medications
   in first-episode patients.^[89, 90]

   Numerous guidelines or algorithms for the treatment of schizophrenia
   are available. Treatment guidelines are recommendations that require
   clinical judgment in their application and must be regularly updated on
   the basis of new evidence.^[91]

   Few studies have examined the outcome of treatment using these
   algorithms. In a study from Canada, Agid et al described the outcome of
   treatment among 244 patients with first-episode schizophrenia who were
   treated according to a 2003 algorithm.^[92] If no response to the first
   antipsychotic was observed, a second antipsychotic was used. Most
   patients were treated with olanzapine or risperidone.

   Response rates fell from about 75% in the first trial to less than 20%
   in the second trial.^[92] The patients who did not respond to either
   trial were offered clozapine, and 75% responded. Unanswered questions
   from this study include the respective roles of first-generation and
   second-generation antipsychotic medications and when clozapine should
   be used.

   If the patient has not responded to a medication, physicians can switch
   medications or add another one. Using 2 or even 3 different
   antipsychotic agents together is common, though this practice lacks a
   compelling evidence base and does increase the complexity of the
   medication regimen.

   Nonetheless, in one large study, discontinuance of 1 of 2
   antipsychotics was followed by treatment discontinuance more often and
   more quickly than continuation of both antipsychotics were
   continued.^[93] A meta-analysis of 19 studies involving more than 1200
   subjects found a modest advantage for antipsychotic polypharmacy.^[94]

   Physicians sometimes choose what seems to be a simpler option than
   switching or adding medication, which is to increase the dose of the
   original medication. For example, quetiapine is sometimes prescribed at
   higher than approved doses for patients with schizophrenia or
   schizoaffective disorder. Honer et al found that dosages higher than
   800 mg/day did not show any advantage over dosages in the approved
   range.^[95]

   In a recent Cochrane review, authors studied quetiapine compared with
   other antipsychotics.^[96] Quetiapine seemed slightly less effective,
   but overall to have a slightly lower burden of adverse effects. Sixty
   percent of the patients started on quetiapine stopped taking it within
   a few weeks. The authors also noted that the clinical meaning of these
   many findings, many of them quite modest, remains unclear.

   PORT provided a detailed review addressing the choice of antipsychotic
   medications, including recommendations and discussions regarding acute,
   maintenance, first-episode, and targeted intermittent treatment, as
   well as treatment of individual symptoms.^[87]

Maximization of compliance

   Noncompliance with or nonadherence to pharmacologic therapy is
   difficult to estimate but is known to be common, and it is one of the
   reasons for the use of intramuscular (IM) preparations of antipsychotic
   medications. A regular routine of IM medication, such as every 2-4
   weeks, is preferred by some patients since it obviates the need to take
   medication every day. As well, it permits easier monitoring of
   medication adherence by the clinician. IM medication is less widely
   used in the United States than in Europe.

   Whether IM medication is superior to oral medication is not clear.

   A large trial that compared long-acting injectable risperidone with the
   psychiatrist’s choice of oral antipsychotic agent found, somewhat to
   the surprise of many, that injectable risperidone was not superior to
   the oral form and was associated with more side effects.^[97]

   In a meta-analysis of 21 randomized, controlled studies involving more
   than 5000 patients, the long-acting injectable agents were similar to
   the oral antipsychotics with regard to relapse prevention.^[98]
   However, in 10 studies using first-generation long-acting injectables,
   as well as studies published in or before 1991 (8 fluphenazine or
   long-acting injectable studies), the primary outcome with the
   long-acting injectable agents was superior to that with oral
   antipsychotics.

   Adherence is usually overestimated by both patient and physician.
   Nonadherence can be partial or complete, but even partial adherence is
   associated with relapse.^[99] In the past, nonadherence was thought to
   be due at least in part to the side effects of the conventional
   antipsychotic agents, such as akathisia. Nevertheless, nonadherence
   remains a major clinical problem, even with second-generation
   antipsychotic agents.

   Family members of people with schizophrenia, as well as clinicians
   providing care for them, should encourage them to take their
   medication, while at the same time respecting their autonomy. This is a
   difficult balance to achieve.

Adverse effects

   Patients tend not to be very adherent to antipsychotic medications, and
   this may, in part, be due to their adverse effects. Patients sometimes
   report they feel less like themselves, or less alert, when taking these
   medications. One troubling possibility is that while they are used to
   combat psychosis and in that sense to preserve brain functioning, these
   medications can actually interfere with the usual processes of the
   brain. Indeed, some practitioners have gone so far as to call
   haloperidol “neurotoxic” and suggest that it not be used. However,
   there may be adverse neurological effects with all of the antipsychotic
   medications, not just the conventional ones.

   For example, in an open-label 6-month pilot study in Canada, the
   reduction of risperidone or olanzapine dose by 50% improved cognitive
   function for stable patients with schizophrenia and did not lead to
   worsening of psychotic symptoms.^[100]

   The following are adverse effects typically associated with
   conventional antipsychotic agents and with the atypical antipsychotic
   risperidone at dosages higher than 6 mg/day:
     * Akathisia
     * Dystonia
     * Hyperprolactinemia
     * Neuroleptic malignant syndrome (NMS)
     * Parkinsonism
     * Tardive dyskinesia (TD)

   Akathisia is a subjective sense of inner restlessness, mental unease,
   irritability, and dysphoria. It can be difficult to distinguish from
   anxiety or an exacerbation of psychosis.

   Dystonia consists of painful and frightening muscle cramps, which
   affect the head and neck but may extend to the trunk and limbs.
   Dystonia usually occurs within 12-48 hours of the beginning of
   treatment or an increase in dose. Muscular young men are typically
   affected.

   Hyperprolactinemia is an elevation of the hormone prolactin in the
   blood, caused by the lowering of dopamine. (Dopamine inhibits the
   release of prolactin from the pituitary.) It is associated with
   galactorrhea, gynecomastia, and osteoporosis. In women it is associated
   with amenorrhea, and in men it is associated with impotence.

   NMS is marked by fever, muscular rigidity, altered mental state, and
   autonomic instability. Laboratory findings include increased creatine
   kinase levels and myoglobinuria. Acute kidney injury may result.
   Mortality is significant. NMS is thought to be less common in patients
   taking clozapine or other atypical antipsychotic agents.

   Parkinsonism consists of some combination of tremor, bradykinesia,
   akinesia, and rigidity.

   Tardive dyskinesia (TD) consists of involuntary and repetitive (but not
   rhythmic) movements of the mouth and face. Chewing, sucking, grimacing,
   or pouting movements of the facial muscles may occur. People may rock
   back and forth or tap their feet. Occasionally, diaphragmatic
   dyskinesia exists, which leads to loud and irregular gasping or “jerky”
   speech. The patient is often not aware of these movements. The
   incidence of TD is as high as 70% in elderly patients treated with
   antipsychotic agents. Risk factors for TD include older age, female
   sex, and negative symptoms.

   Physicians should warn patients, especially those being treated with
   conventional antipsychotic agents, about the risk of TD. Regular
   examinations, using the abnormal involuntary movement scale (AIMS),
   should be performed to document the presence or absence of TD.

   Anticholinergic effects

   Anticholinergic side effects occur with most antipsychotics (though
   risperidone, aripiprazole, and ziprasidone are relatively free of
   them). Such effects include the following:
     * Dry mouth
     * Acute exacerbation of narrow- or closed-angle glaucoma (if
       undiagnosed or untreated)
     * Confusion
     * Decreased memory
     * Agitation
     * Visual hallucinations
     * Constipation

   QT interval prolongation

   The QT interval is the interval between the beginning of the QRS
   complex and the end of the T wave on ECG. It reflects the time required
   for the ventricles to depolarize and repolarize. The QT interval
   corrected for heart rate is called the QTc. A prolonged QTc interval
   puts a person at risk for torsades de pointes, a malignant arrhythmia
   associated with syncope and sudden death.

   QTc intervals are lengthened by the conventional antipsychotic agents
   thioridazine, pimozide, and mesoridazine and, to a lesser extent, by
   the novel antipsychotic agent ziprasidone. (Mesoridazine is no longer
   available in the United States.) Risk is increased by individual
   susceptibility, heart failure, bradycardias, electrolyte imbalance
   (especially hypokalemia), hypomagnesemia, and female gender.^[101]

   No cases of torsades de pointes were reported in a large trial of more
   than 18,000 patients in 18 countries who were randomly assigned to
   receive either ziprasidone or olanzapine, though the event is so rare
   that this finding is not entirely surprising.^[102] No increase in
   nonsuicide mortality was reported. In particular, no increase in
   cardiac mortality was found, which is somewhat reassuring with respect
   to the cardiac safety of ziprasidone.

   Haloperidol has only a small influence on the ECG. Nevertheless, this
   agent has been implicated, albeit very rarely, in causing torsades de
   pointes.^[103]

   Clinicians should be alert to the ability of antipsychotic medications
   to cause ECG changes in patients with any of the above risk factors or
   in patients taking other medications that can lengthen the QTc
   interval. Particular caution is advised with regard to using these
   medications in patients who are elderly or medically ill.

   Altered glucose and lipid metabolism and weight gain

   Altered glucose and lipid metabolism, with or without weight gain, may
   occur with most antipsychotic agents, as can weight gain itself.^[104]
   Aripiprazole and ziprasidone are the antipsychotic drugs least likely
   to lead to these adverse effects, whereas olanzapine and clozapine are
   the drugs most likely to do so. The newer agents, asenapine,
   iloperidone, and lurasidone, may also share a lower liability for
   weight gain and metabolic disturbances.

   The mechanism of weight gain associated with psychotropic drugs is not
   understood. Sensitivity to insulin may be increased, or increased
   leptin levels may be present.

   A Danish study of the risk for diabetes with antipsychotics compared
   nearly 346,000 individuals who purchased antipsychotics and nearly 1.5
   million unexposed individuals and concluded that the rate ratio (RR)
   for risk with first-generation antipsychotics was 1.53, whereas the RR
   varied widely for second-generation antipsychotics (1.32; range,
   1.17-1.57).^[105]

   Stroup et al studied 215 patients whose psychotic symptoms were
   stabilized on olanzapine, quetiapine, or risperidone.^[106] After 24
   weeks, those who switched to aripiprazole had improved cholesterol
   levels and other metabolic factors, and they lost more weight than
   those who stayed on their original medication. Relapse or worsening of
   psychotic symptoms occurred no more frequently in patients who switched
   medications than in those who stayed on their original medication.
   However, patients who switched to aripiprazole were more likely to
   discontinue the assigned medication: 43.9% of those who switched
   discontinued their medication, whereas 24.5% of those who stayed on
   their original medication discontinued it. They concluded patients
   experiencing cardiovascular or metabolic adverse effects of an
   antipsychotic medication may fare better if they switch to a different
   agent, provided they are closely monitored.

   Weight gain is associated both with psychological problems (eg,
   decreased self-esteem) and with medical problems (eg, diabetes,
   coronary artery disease, and arthritis). Education about nutrition and
   exercise should be provided. Cognitive-behavioral therapy can be tried.

   It is unclear whether weight-reducing drugs should be added to
   antipsychotic therapy. In one randomized, placebo-controlled study
   conducted in 72 patients with first-episode schizophrenia who gained
   more than 7% of their predrug weight, metformin (1000 mg/day) was
   effective and safe in attenuating antipsychotic-induced weight gain and
   insulin resistance.^[107]

   Miscellaneous adverse effects

   All antipsychotic agents may be associated with esophageal dysmotility,
   thus increasing the risks of aspiration, choking, and the subsequent
   risk of pneumonia. Orthostatic hypotension can be problematic at the
   beginning of therapy, with dose increases, and in elderly patients.
   This problem is related to alpha[1] -blockade and seems to be
   particularly severe with risperidone and clozapine.

   Venous thromboembolism may be associated with the use of antipsychotic
   drugs. Patients treated with clozapine may be at particular risk for
   this complication; however, the reasons for this possible association
   are not understood.^[108, 109]

   Results from a prospective study indicated that in children and
   adolescents, long-term use of risperidone can negatively affect bone
   mass.^[110]

   Neurotoxic effects

   Some studies have explored the potential neurotoxic effects of
   antipsychotic medications; however, no clear conclusions have been
   reached. For example, Ho et al performed structural brain imaging in
   more than 200 patients with schizophrenia over 7 years and found that
   whereas patients treated with higher doses of antipsychotic medications
   seemed to lose gray matter throughout their brain (except the
   cerebellum), those treated with lower doses seemed to have a small
   increase in white matter.^[111]

   The clinical significance of these findings is unclear. It is not known
   whether these changes are directly associated with any clinical
   symptoms and whether they are reversible. It also is not known whether
   the higher medication doses were in response to the gray-matter loss or
   whether it was the other way around.

Monitoring of blood levels

   Regular measurement of blood medication levels in the blood would be
   helpful in schizophrenia, for the following reasons:
     * Patients may not always take their medications, and checking drug
       levels can detect this noncompliance
     * Patients may not always be the best reporters of side effects, and
       monitoring medication levels can occasionally help the clinician
       detect toxicity
     * Smoking tobacco products induces the liver enzyme CYP1A2 (though
       nicotine patches, nicotine inhalers, and chewing tobacco do not);
       this enzyme metabolizes a number of antipsychotic drugs, so that,
       for example, patients who stop smoking while being treated with
       clozapine or olanzapine often experience increased antipsychotic
       levels; a patient who has stopped smoking may have a variety of
       complaints, and checking drug levels can help determine their
       etiology

   For most antipsychotic medications, however, clear dose-response curves
   have not been established, and in clinical practice, drug levels are
   rarely monitored.

   There are 2 exceptions to this general statement. Plasma concentrations
   of haloperidol are correlated to some degree with clinical effects, and
   levels in the range of 15-25 ng/mL are thought to be optimal. Plasma
   concentrations of clozapine in the range of 300-400 ng/mL may be
   optimal.
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Other Pharmacotherapy

   Anticholinergic agents (eg, benztropine, trihexyphenidyl, and
   diphenhydramine) and amantadine are often used in conjunction with the
   conventional antipsychotic agents to prevent dystonic movements or to
   treat extrapyramidal symptoms. Akathisia is particularly difficult to
   treat, but it occasionally responds to an anticholinergic agent, a
   benzodiazepine, or a beta blocker.

   Many patients with schizophrenia are treated with other psychotropic
   medications in addition to antipsychotic agents. Polypharmacy in
   schizophrenia is supported by little rigorous evidence but is widely
   practiced nonetheless. Medications often used include antidepressants,
   mood stabilizers, and anxiolytic agents. Carbamazepine and clozapine
   should not be used together.

   Benzodiazepines are often used and are perceived as being quite safe.
   Nevertheless, they can be addictive and can lead to falls, especially
   in the elderly. There has long been a concern that they might increase
   mortality.^[70]
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Psychosocial Interventions

   Psychosocial treatment is essential for people with schizophrenia and
   includes a number of approaches, such as social skills training,
   cognitive-behavioral therapy, cognitive remediation, and social
   cognition training.^[112] PORT (see Antipsychotic Pharmacotherapy) also
   provides a detailed review of psychosocial interventions.^[113]

   Psychosocial treatments are currently oriented according to the
   recovery model. According to this model, the goals of treatment for a
   person with schizophrenia are as follows:
     * To have few or stable symptoms
     * To avoid hospitalization
     * To manage his or her own funds and medications
     * To be either working or in school at least half-time

   Hope, empowerment, choice, and community integration are emphasized in
   this treatment approach.

   A large study from China demonstrated the advantages of medication plus
   psychosocial intervention over medication alone.^[114] In the
   psychosocial intervention arm, each month patients and their families
   received 1 day of 4 types of evidence-based interventions:
   psychoeducation, family intervention, skills training, and
   cognitive-behavioral therapy. After 1 year, the patients in the group
   receiving the extra interventions were more compliant with their
   medications, had fewer rehospitalizations, and experienced better
   quality of life.

   Cognitive remediation, vocational rehabilitation, assertive community
   treatment, and family intervention are reviewed.

Cognitive remediation

   Cognitive impairment, a core feature of schizophrenia, is less dramatic
   than other symptoms of the disease (eg, hallucinations and delusions)
   but interferes with work, social relationships, and independent living.
   Cognitive impairment is not improved by medication.

   Cognitive remediation is a treatment modality derived from principles
   of neuropsychological rehabilitation and is based, in part, on the
   ideas that the brain has some plasticity and that brain exercises can
   encourage neurons to grow and can develop the neurocircuitry underlying
   many mental activities.

   Numerous different models of cognitive remediation are available. Some
   models use drill-based practicing of isolated cognitive skills with the
   aid of computers, whereas others help people develop strategies for
   overcoming areas of weakness. Other forms of this therapy are known as
   cognitive rehabilitation, cognitive enhancement, or metacognitive
   therapy.

   Cognitive remediation works best when patients are stable. Improvement
   occurs across numerous cognitive functions, and changes are found on
   brain imaging that reflect these changes in brain functioning.

   Cognitive remediation techniques are time-intensive and
   labor-intensive. Because cognitive deficits are multiple and vary from
   person to person, such techniques seem to work best when specifically
   tailored to each patient. When combined with other therapies, such as
   supported employment, cognitive remediation leads to clinically
   relevant improvements.^[115] These effects are durable, lasting even
   after the training has stopped.^[116]

   In a study by Grant et al, low-functioning patients with prominent
   negative symptoms were assigned to either recovery-oriented
   cognitive-behavioral therapy plus standard treatment or standard
   treatment; after 18 months, the authors found that both negative and
   positive symptoms had decreased in the group receiving the add-on
   cognitive therapy.^[117] The study was not blinded, and the treatment
   was delivered by enthusiastic doctoral level therapists; thus, the
   findings may not be widely generalizable.

   A study by Puig and colleagues also found cognitive remediation therapy
   to be effective. In the study, 50 patients between the ages of 12 and
   18 years with early onset schizophrenia were randomized to either
   cognitive remediation therapy plus usual treatment or usual treatment
   alone. Patients in the cognitive remediation group showed significantly
   greater improvements than patients in the usual treatment group in
   verbal memory, working memory, executive function, and cognitive
   composite scores, at the end of treatment and at 3-month follow-up. The
   cognitive remediation group also had greater improvements in daily
   living skills, global adaptive functioning, and self-perceived family
   burden.^[118]

   Cognitive therapy may be effective as a standalone treatment for
   schizophrenia.^[119, 120] For schizophrenic patients who cannot or will
   not take antipsychotic medication, cognitive therapy may be the most
   viable option. According to data from the first randomized trial of
   cognitive therapy as a standalone therapy for schizophrenia, structured
   treatment with a therapist significantly reduced the severity of
   psychiatric symptoms and improved personal and social functioning and
   some dimensions of delusional beliefs and voice hearing.^[119, 120]

   The study involved 74 individuals aged 16 to 65 years with
   schizophrenia spectrum disorders who had decided not to take or had
   stopped taking antipsychotics for at least 6 months.^[119, 120] Half
   were randomly assigned to cognitive therapy (26 sessions during a
   9-month period) plus treatment as usual and half to treatment as usual
   alone. After 18 months, 7 (41%) of 17 study participants receiving
   cognitive therapy had an improvement of more than 50% in the Positive
   and Negative Syndrome Scale (PANSS) total score compared with 3 (18%)
   of 17 receiving treatment as usual.^[119, 120]

   None of the antipsychotic medications currently available is
   particularly effective at addressing cognitive symptoms. A new
   initiative from NIMH, known as Measurement and Treatment Research to
   Improve Cognition in Schizophrenia (MATRICS), is a collaboration
   between various programs to develop tools for measuring cognition in
   clinical trials and aiding development of drugs that target these
   symptoms.

Vocational rehabilitation

   Most patients with schizophrenia would like to work; employment can
   improve income, self-esteem, and social status. However, few people
   with the disorder are able to maintain competitive employment.^[121]
   Supported employment programs currently thought to be most effective
   are those that offer individualized, supported, and rapid job
   assignments and that are integrated with other services. These programs
   are associated with higher rates of employment, but gains in other
   domains are surprisingly difficult to discern.^[122]

Assertive community treatment

   Assertive community treatment is a form of case management that is
   typically used for patients who have had multiple hospitalizations. The
   treatment involves active outreach to patients. Case managers usually
   have a fairly small outpatient load (about 10 patients) and are able to
   go into the community to work with their clients. The managers
   coordinate and integrate care by doing the following: they identify
   indications for treatment, make referrals to appropriate services, and
   promote engagement with interventions. This form of treatment is
   expensive but may be associated with better clinical and social
   outcomes and lower hospitalization rates.

Family intervention

   Schizophrenia affects the person’s whole family, and the family’s
   responses can affect the trajectory of the person’s illness. Familial
   “high expressed emotion” (hostile overinvolvement and intrusiveness)
   leads to more frequent relapses. Some studies have found that family
   therapy or family interventions may prevent relapse, reduce hospital
   admission, and improve medication compliance.^[123]

   The National Alliance for the Mentally Ill (NAMI) is a helpful advocacy
   group that is supportive for family members. NAMI also advocates
   funding and research.

Smoking cessation

   Most patients with schizophrenia smoke. This may be a result of
   previous conventional antipsychotic treatment, in that nicotine may
   ameliorate some of the adverse effects of these drugs. Smoking may also
   be related to the boredom associated with hospitalizations, the peer
   pressure from other patients to smoke, or the anomie associated with
   unemployment.

   Whatever the cause of the high incidence of smoking, the health risks
   from smoking are well known, and all schizophrenic patients should be
   encouraged to stop smoking.
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Diet and Activity

   Many psychotropic medications can cause weight gain and changes in
   glucose or lipid metabolism. Occasionally, a person with schizophrenia
   develops odd food preferences. Finally, many persons with schizophrenia
   have limited funds, do not cook for themselves, and live in areas where
   fast food outlets are abundant. Therefore, nutritional counseling is
   difficult but important.

   Because many psychotropic medications are associated with weight gain,
   and because of the many beneficial effects of exercise, persons with
   schizophrenia should be encouraged to be as physically active as
   possible.
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Prevention

   Many have wondered whether patients with schizophrenia would have a
   better prognosis if treatment could be started as early as possible. A
   study from Scandinavia found that early detection and intervention in
   first-episode psychosis led to higher recovery and employment rates at
   10-year follow-up.^[124]

   The North American Prodrome Longitudinal Study is exploring whether the
   incorporation of biologic measures into prediction algorithms can
   provide more accurate identification of young people who are at
   greatest risk for developing a psychotic disorder. The goal of this
   study is to establish objective criteria that can be used to develop
   preventive approaches.

   There are several studies of prodromal schizophrenia under way to
   inform early intervention strategies. In the absence of highly reliable
   methods of predicting schizophrenia, however, intervention during the
   prodromal stage could result in the unnecessary administration of
   antipsychotic medication to young people who are mistakenly identified
   as being at risk for schizophrenia.^[125]

   One approach to this problem is to use psychological therapies rather
   than pharmacotherapy. A German study of young people at risk for
   schizophrenia showed that the use of a psychological intervention
   involving cognitive-behavioral therapy, group skills training,
   cognitive remediation and multifamily psychoeducation delayed the onset
   of psychosis for at least 2 years.^[126]
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Other Treatments

   An entirely different kind of treatment for schizophrenia, still in its
   early stages, is transcranial magnetic stimulation (TMS). TMS involves
   the electromagnetic induction of an electric field in the brain.
   Standard TMS affects neurons within 1.5-2 cm from the scalp, and deep
   TMS can affect cells to a depth of 6 cm. The electric field changes the
   “excitability” of the neurons and seems to be safe with few adverse
   effects. TMS is mostly used for depression. However, early work
   suggests that TMS, in some cases, may decrease auditory
   hallucinations^[127] and negative symptoms^[128] in schizophrenia.
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   Proceed to Medication


   Contributor Information and Disclosures
   Author

   Frances R Frankenburg, MD  Professor, Department of Psychiatry, Boston
   University School of Medicine; Chief of Inpatient Psychiatry and
   Consulting Psychiatrist, Edith Nourse Rogers Memorial Veterans
   Administration Medical Center; Associate Psychiatrist, McLean Hospital
   Frances R Frankenburg, MD is a member of the following medical
   societies: Alpha Omega Alpha and American Psychiatric Association
   Disclosure: Nothing to disclose.
   Chief Editor

   Eduardo Dunayevich, MD  Executive Director, Clinical Development, Amgen
   Eduardo Dunayevich, MD is a member of the following medical societies:
   American Psychiatric Association
   Disclosure: Lilly Research Laboratories Salary Other
   Additional Contributors

   Ronald C Albucher, MD Chief Medical Officer, Westside Community
   Services; Consulting Staff, California Pacific Medical Center

   Ronald C Albucher, MD is a member of the following medical societies:
   American Psychiatric Association

   Disclosure: Nothing to disclose.

   Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University
   of Nebraska Medical Center College of Pharmacy; Editor-in-Chief,
   Medscape Drug Reference

   Disclosure: Medscape Salary Employment
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   Cortical activation patterns during verbal working memory maintenance.
   Healthy controls (A), patients with schizophrenia (B), and
   significantly different activation between groups (subtraction of
   SZ-CO) (C) are shown. The time series plots in the middle column show
   activation associated with true memory maintenance (red lines) relative
   to the baseline activities (blue line). Bright parts in the middle of
   each plot represent 1-volume (1.5 s) after onset, and offset of the
   maintenance phase (4.5 secs). All p-values are corrected with false
   discovery rate of q< 0.005. Image courtesy of Kim J, Matthews NL, and
   Park S. An event-related fMRI study of phonological verbal working
   memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Cortical activation patterns during false memory trials. (A) False
   memory, baseline in controls (CO). (B) False memory, baseline in
   schizophrenia (SZ). (C) SZ – CO. All p-values are corrected with a
   false discovery rate of q< 0.005. The time course plots show false
   memory-related activities (yellow) and true memory-related activities
   (red) relative to the baseline (blue). Image courtesy of Kim J,
   Matthews NL, and Park S. An event-related fMRI study of phonological
   verbal working memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Magnetic resonance imaging showing differences in brain ventricle size
   in twins. The twin on the right has schizophrenia, whereas the twin on
   the left does not. Image courtesy of Dr. Daniel Weinberger, Clinical
   Brain Disorders Branch, National Institutes of Health.

   Previous
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Schizophrenia Treatment & Management

     * Author: Frances R Frankenburg, MD; Chief Editor: Eduardo
       Dunayevich, MD   more...


     * Overview
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     * Workup
     * Treatment
     * Medication
     *

   Updated: Dec 22, 2014
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     * Approach Considerations
     * Antipsychotic Pharmacotherapy
     * Other Pharmacotherapy
     * Psychosocial Interventions
     * Diet and Activity
     * Prevention
     * Other Treatments
     * Show All

   Multimedia Library
   References

Approach Considerations

   Treatment of schizophrenia requires integration of medical,
   psychological, and psychosocial inputs. The bulk of care occurs in an
   outpatient setting and probably is best carried out by a
   multidisciplinary team, including some combination of the following: a
   psychopharmacologist, a counselor or therapist, a social worker, a
   nurse, a vocational counselor, and a case manager. Clinical pharmacists
   and internists can be valuable members of the team.

   It is important not to neglect the medical care of the person with
   schizophrenia. Obesity, diabetes, cardiovascular disease, and lung
   diseases are prevalent in schizophrenia, and the person with
   schizophrenia often does not receive adequate medical care for such
   conditions.^[78]

   Antipsychotic medications (also known as neuroleptic medications or
   major tranquilizers) diminish the positive symptoms of schizophrenia
   and prevent relapses. Approximately 80% of patients relapse within 1
   year if antipsychotic medications are stopped, whereas only 20% relapse
   if treated. Children, pregnant or breastfeeding women, and elderly
   patients present special challenges. In all of these cases, medications
   must be used with particular caution.

   The choice of which drug to use for treatment of a patient with
   schizophrenia depends on many issues, including effectiveness, cost,
   side-effect burden, method of delivery, availability, and tolerability.
   Many studies have compared antipsychotic drugs with one another, but no
   broad consensus has been reached. In the absence of clinical or
   pharmacogenetic predictors of treatment response, the current treatment
   approach is largely one of trial and error across sequential medication
   choices.

   Although treatment is primarily provided on an outpatient basis,
   patients with schizophrenia may require hospitalization for
   exacerbation of symptoms caused by noncompliance with pharmacotherapy,
   substance abuse, adverse effects or toxicity of medications, medical
   illness, psychosocial stress, or the waxing and waning of the illness
   itself. Hospitalizations are usually brief and are typically oriented
   towards crisis management or symptom stabilization.

   Treatment of patients with schizophrenia, particularly during a
   psychotic episode, may raise the issue of informed consent. Consent is
   a legal term and should be used with respect to specific tasks. A
   person who is delusional in some but not all areas of life may still
   have the capacity to make medical and financial decisions.

Insurance concerns

   In the United States, patients with schizophrenia who are unable to
   work may be eligible for governmental programs, such as Medicare and
   Medicaid. These programs pay the cost of medical care. Unfortunately,
   if individuals begin to work and earn a sufficient salary, they may
   lose these benefits—an especially problematic occurrence when, as is
   often the case, their job provides minimal or no health benefits. This
   situation is complicated and must be monitored closely by professionals
   with a good understanding of health benefits.

   The impact of the American Affordable Care Act (ACA) on the care of
   schizophrenia has yet to be determined. Some parts of the ACA, such as
   the removal of exclusion of preexisting conditions as a barrier to
   getting insurance, and the removal of annual and lifetime benefit
   limits, will be helpful. The ACA mandates parity between care for
   medical and psychiatric illnesses.

   However, health plans in the new exchanges might not provide all of the
   services that are mentioned here, such as supported employment. As
   well, in the states that have chosen not to expand their Medicaid
   programs, patients with Medicaid as their insurer may continue to have
   difficulty in accessing care.[#Antipsychotic]
   Next

Antipsychotic Pharmacotherapy

   Before beginning antipsychotic medications, clinicians should warn
   patients and their families of adverse effects, and the slowness of
   response. The patient may be calmer and less agitated almost
   immediately, but alleviation of the psychosis itself often takes
   several weeks. Some clinicians routinely perform electrocardiography
   (ECG) before beginning treatment with antipsychotic medications and
   then as often as seems appropriate, for example if doses are increased
   or agents change. Because suicide is not uncommon in patients with
   psychotic illnesses, clinicians should write prescriptions for the
   lowest dosage that is consistent with good clinical care. Patients
   should be urged to avoid substance abuse. All medications should be
   given at lower dosages in children and elderly patients and used with
   great caution in women who are pregnant or breastfeeding.

   The first antipsychotic medications, chlorpromazine and haloperidol,
   were dopamine D2 antagonists. These and similar medications are known
   as first-generation, typical, or conventional antipsychotics. Other
   antipsychotics, beginning with clozapine, are known as
   second-generation, atypical, or novel antipsychotics.

   The conventional antipsychotic agents are available in generic forms
   and are less expensive than the newer agents. They are available in a
   variety of vehicles, including liquid and intramuscular (IM)
   preparations. Some of these agents (haloperidol and fluphenazine) are
   also available as depot preparations, meaning that a person can be
   given an injection of a medication every 2-4 weeks. Of the
   second-generation agents, risperidone is available as a long-acting
   injection that uses biodegradable polymers; olanzapine, paliperidone,
   and aripiprazole are also now available in long-acting injectable
   forms.^[79, 80, 81, 82]

   The first-generation antipsychotic drugs tend to cause extrapyramidal
   adverse effects and elevated prolactin levels. The second-generation
   drugs are more likely to cause weight gain and abnormalities in glucose
   and lipid control; in addition, they are often more expensive than the
   first-generation drugs.

Comparative efficacy of agents

   For some years, it was believed that the newer antipsychotic drugs were
   more effective, but there is now some uncertainty about that. An
   exception is clozapine, which consistently outperforms the other
   antipsychotic drugs.

   Phase 1 of the CATIE (Clinical Antipsychotic Trials of Intervention
   Effectiveness) study, a large nationwide trial that compared the
   first-generation antipsychotic perphenazine with the second-generation
   drugs olanzapine, risperidone, quetiapine, and ziprasidone, found that
   olanzapine was slightly better than the other drugs in terms of the
   patients choosing to stay on it, and number of hospitalizations, but
   also was associated with significant weight gain. Surprisingly,
   perphenazine performed about as well as the other 3 second-generation
   agents.^[83]

   In this and other studies the primary outcome, stopping the drug, may
   seem to be unusual. It is used because it reflects the “real-world”
   decision of the clinician and patient that the agent is either no
   longer tolerable or effective.

   In CUtLASS (Cost Utility of the Latest Antipsychotic drugs in
   Schizophrenia Study), a study from the United Kingdom, more than 200
   patients who were about to change antipsychotic medication were
   randomly assigned to either a first-generation or a second-generation
   agent. In this study, the first-generation drugs seemed to perform
   slightly better than the newer ones, as measured by the Quality-of-Life
   Scale.^[84]

   First-episode schizophrenia

   EUFEST (European First Episode Schizophrenia Trial) was a year-long
   open-label study conducted in nearly 500 patients in 13 European
   countries and Israel that, as did CATIE, used treatment discontinuance
   as the main outcome measure. The study found that patients were more
   likely to stop low-dose haloperidol than to stop olanzapine,
   quetiapine, ziprasidone, or amisulpride (not available in the United
   States); however, all medications were associated with similar
   decreases in symptoms.^[85]

   Similarly, the randomized, double-blind CAFE (Comparison of Atypicals
   for First Episode) study found few differences between olanzapine,
   quetiapine, and risperidone in 400 patients experiencing a first
   episode of psychosis, with all-cause treatment discontinuance rates in
   the vicinity of 70% by week 52. Drowsiness and weight gain were along
   the most common adverse events with all 3 drugs; in addition, insomnia
   was seen with olanzapine, a longer sleep time with quetiapine, and
   menstrual irregularities in women with risperidone.^[86]

   The Schizophrenia Patient Outcomes Research Team (PORT) of the
   University of Maryland recommended that any antipsychotic medication,
   with the exceptions of clozapine and olanzapine, can be used as
   first-line treatment for patients with schizophrenia who are
   experiencing their first episode of acute positive symptoms.^[87]

   According to a comprehensive review carried out by the Schizophrenia
   Patient Outcomes Research Team (PORT) of the University of Maryland,
   early treatment with any antipsychotic medication is associated with
   significant symptom reduction; first- and second-generation
   antipsychotics may have equivalent significant short-term efficacy.
   However, because of the adverse adverse-effect profile of clozapine and
   the significant metabolic risks associated with olanzapine, PORT
   advised that neither drug should be considered as a first-line
   treatment for first-episode schizophrenia.^[87]

   Noting that both responsiveness to treatment and sensitivity to adverse
   effects are greater in patients with first-episode schizophrenia than
   in those who have had multiple episodes, PORT recommended starting
   antipsychotic treatment for the former at doses lower than those
   recommended for the latter. An exception is quetiapine, which may not
   be effective in lower doses; in addition, low doses of aripiprazole or
   ziprasidone have not been evaluated in first-episode
   schizophrenia.^[87]

   Wunderink and colleagues followed just over 100 subjects participating
   in a study of first episode psychosis. Subjects were randomly assigned
   to antipsychotic medication dose reduction or dose maintenance. At 7
   years follow-up, they found that those treated with lower doses or no
   antipsychotics had more relapses and hospitalizations. This was not an
   unexpected finding. However, they also found that these lightly
   medicated patients overall were functioning better. They concluded that
   it seems that there are different responses of symptoms and functioning
   to medication.^[88]

   The National Institute of Mental Health (NIMH) has initiated a research
   project, Recovery After an Initial Schizophrenia Episode (RAISE), to
   determine whether coordinated and aggressive treatment in the earliest
   stages of illness can prevent long-term disability from schizophrenia.
   The RAISE Early Treatment Program (ETP), an integrated program
   delivered in community clinics, will be compared with the RAISE
   Connection program, a program offered in Baltimore and Manhattan in
   partnership with state mental health programs.

Choice of agent

   There is no clear antipsychotic drug of choice for schizophrenia.
   Clozapine is the most effective medication but is not recommended as
   first-line therapy because it has a high burden of adverse effects,
   requires regular blood work, and has not outperformed other medications
   in first-episode patients.^[89, 90]

   Numerous guidelines or algorithms for the treatment of schizophrenia
   are available. Treatment guidelines are recommendations that require
   clinical judgment in their application and must be regularly updated on
   the basis of new evidence.^[91]

   Few studies have examined the outcome of treatment using these
   algorithms. In a study from Canada, Agid et al described the outcome of
   treatment among 244 patients with first-episode schizophrenia who were
   treated according to a 2003 algorithm.^[92] If no response to the first
   antipsychotic was observed, a second antipsychotic was used. Most
   patients were treated with olanzapine or risperidone.

   Response rates fell from about 75% in the first trial to less than 20%
   in the second trial.^[92] The patients who did not respond to either
   trial were offered clozapine, and 75% responded. Unanswered questions
   from this study include the respective roles of first-generation and
   second-generation antipsychotic medications and when clozapine should
   be used.

   If the patient has not responded to a medication, physicians can switch
   medications or add another one. Using 2 or even 3 different
   antipsychotic agents together is common, though this practice lacks a
   compelling evidence base and does increase the complexity of the
   medication regimen.

   Nonetheless, in one large study, discontinuance of 1 of 2
   antipsychotics was followed by treatment discontinuance more often and
   more quickly than continuation of both antipsychotics were
   continued.^[93] A meta-analysis of 19 studies involving more than 1200
   subjects found a modest advantage for antipsychotic polypharmacy.^[94]

   Physicians sometimes choose what seems to be a simpler option than
   switching or adding medication, which is to increase the dose of the
   original medication. For example, quetiapine is sometimes prescribed at
   higher than approved doses for patients with schizophrenia or
   schizoaffective disorder. Honer et al found that dosages higher than
   800 mg/day did not show any advantage over dosages in the approved
   range.^[95]

   In a recent Cochrane review, authors studied quetiapine compared with
   other antipsychotics.^[96] Quetiapine seemed slightly less effective,
   but overall to have a slightly lower burden of adverse effects. Sixty
   percent of the patients started on quetiapine stopped taking it within
   a few weeks. The authors also noted that the clinical meaning of these
   many findings, many of them quite modest, remains unclear.

   PORT provided a detailed review addressing the choice of antipsychotic
   medications, including recommendations and discussions regarding acute,
   maintenance, first-episode, and targeted intermittent treatment, as
   well as treatment of individual symptoms.^[87]

Maximization of compliance

   Noncompliance with or nonadherence to pharmacologic therapy is
   difficult to estimate but is known to be common, and it is one of the
   reasons for the use of intramuscular (IM) preparations of antipsychotic
   medications. A regular routine of IM medication, such as every 2-4
   weeks, is preferred by some patients since it obviates the need to take
   medication every day. As well, it permits easier monitoring of
   medication adherence by the clinician. IM medication is less widely
   used in the United States than in Europe.

   Whether IM medication is superior to oral medication is not clear.

   A large trial that compared long-acting injectable risperidone with the
   psychiatrist’s choice of oral antipsychotic agent found, somewhat to
   the surprise of many, that injectable risperidone was not superior to
   the oral form and was associated with more side effects.^[97]

   In a meta-analysis of 21 randomized, controlled studies involving more
   than 5000 patients, the long-acting injectable agents were similar to
   the oral antipsychotics with regard to relapse prevention.^[98]
   However, in 10 studies using first-generation long-acting injectables,
   as well as studies published in or before 1991 (8 fluphenazine or
   long-acting injectable studies), the primary outcome with the
   long-acting injectable agents was superior to that with oral
   antipsychotics.

   Adherence is usually overestimated by both patient and physician.
   Nonadherence can be partial or complete, but even partial adherence is
   associated with relapse.^[99] In the past, nonadherence was thought to
   be due at least in part to the side effects of the conventional
   antipsychotic agents, such as akathisia. Nevertheless, nonadherence
   remains a major clinical problem, even with second-generation
   antipsychotic agents.

   Family members of people with schizophrenia, as well as clinicians
   providing care for them, should encourage them to take their
   medication, while at the same time respecting their autonomy. This is a
   difficult balance to achieve.

Adverse effects

   Patients tend not to be very adherent to antipsychotic medications, and
   this may, in part, be due to their adverse effects. Patients sometimes
   report they feel less like themselves, or less alert, when taking these
   medications. One troubling possibility is that while they are used to
   combat psychosis and in that sense to preserve brain functioning, these
   medications can actually interfere with the usual processes of the
   brain. Indeed, some practitioners have gone so far as to call
   haloperidol “neurotoxic” and suggest that it not be used. However,
   there may be adverse neurological effects with all of the antipsychotic
   medications, not just the conventional ones.

   For example, in an open-label 6-month pilot study in Canada, the
   reduction of risperidone or olanzapine dose by 50% improved cognitive
   function for stable patients with schizophrenia and did not lead to
   worsening of psychotic symptoms.^[100]

   The following are adverse effects typically associated with
   conventional antipsychotic agents and with the atypical antipsychotic
   risperidone at dosages higher than 6 mg/day:
     * Akathisia
     * Dystonia
     * Hyperprolactinemia
     * Neuroleptic malignant syndrome (NMS)
     * Parkinsonism
     * Tardive dyskinesia (TD)

   Akathisia is a subjective sense of inner restlessness, mental unease,
   irritability, and dysphoria. It can be difficult to distinguish from
   anxiety or an exacerbation of psychosis.

   Dystonia consists of painful and frightening muscle cramps, which
   affect the head and neck but may extend to the trunk and limbs.
   Dystonia usually occurs within 12-48 hours of the beginning of
   treatment or an increase in dose. Muscular young men are typically
   affected.

   Hyperprolactinemia is an elevation of the hormone prolactin in the
   blood, caused by the lowering of dopamine. (Dopamine inhibits the
   release of prolactin from the pituitary.) It is associated with
   galactorrhea, gynecomastia, and osteoporosis. In women it is associated
   with amenorrhea, and in men it is associated with impotence.

   NMS is marked by fever, muscular rigidity, altered mental state, and
   autonomic instability. Laboratory findings include increased creatine
   kinase levels and myoglobinuria. Acute kidney injury may result.
   Mortality is significant. NMS is thought to be less common in patients
   taking clozapine or other atypical antipsychotic agents.

   Parkinsonism consists of some combination of tremor, bradykinesia,
   akinesia, and rigidity.

   Tardive dyskinesia (TD) consists of involuntary and repetitive (but not
   rhythmic) movements of the mouth and face. Chewing, sucking, grimacing,
   or pouting movements of the facial muscles may occur. People may rock
   back and forth or tap their feet. Occasionally, diaphragmatic
   dyskinesia exists, which leads to loud and irregular gasping or “jerky”
   speech. The patient is often not aware of these movements. The
   incidence of TD is as high as 70% in elderly patients treated with
   antipsychotic agents. Risk factors for TD include older age, female
   sex, and negative symptoms.

   Physicians should warn patients, especially those being treated with
   conventional antipsychotic agents, about the risk of TD. Regular
   examinations, using the abnormal involuntary movement scale (AIMS),
   should be performed to document the presence or absence of TD.

   Anticholinergic effects

   Anticholinergic side effects occur with most antipsychotics (though
   risperidone, aripiprazole, and ziprasidone are relatively free of
   them). Such effects include the following:
     * Dry mouth
     * Acute exacerbation of narrow- or closed-angle glaucoma (if
       undiagnosed or untreated)
     * Confusion
     * Decreased memory
     * Agitation
     * Visual hallucinations
     * Constipation

   QT interval prolongation

   The QT interval is the interval between the beginning of the QRS
   complex and the end of the T wave on ECG. It reflects the time required
   for the ventricles to depolarize and repolarize. The QT interval
   corrected for heart rate is called the QTc. A prolonged QTc interval
   puts a person at risk for torsades de pointes, a malignant arrhythmia
   associated with syncope and sudden death.

   QTc intervals are lengthened by the conventional antipsychotic agents
   thioridazine, pimozide, and mesoridazine and, to a lesser extent, by
   the novel antipsychotic agent ziprasidone. (Mesoridazine is no longer
   available in the United States.) Risk is increased by individual
   susceptibility, heart failure, bradycardias, electrolyte imbalance
   (especially hypokalemia), hypomagnesemia, and female gender.^[101]

   No cases of torsades de pointes were reported in a large trial of more
   than 18,000 patients in 18 countries who were randomly assigned to
   receive either ziprasidone or olanzapine, though the event is so rare
   that this finding is not entirely surprising.^[102] No increase in
   nonsuicide mortality was reported. In particular, no increase in
   cardiac mortality was found, which is somewhat reassuring with respect
   to the cardiac safety of ziprasidone.

   Haloperidol has only a small influence on the ECG. Nevertheless, this
   agent has been implicated, albeit very rarely, in causing torsades de
   pointes.^[103]

   Clinicians should be alert to the ability of antipsychotic medications
   to cause ECG changes in patients with any of the above risk factors or
   in patients taking other medications that can lengthen the QTc
   interval. Particular caution is advised with regard to using these
   medications in patients who are elderly or medically ill.

   Altered glucose and lipid metabolism and weight gain

   Altered glucose and lipid metabolism, with or without weight gain, may
   occur with most antipsychotic agents, as can weight gain itself.^[104]
   Aripiprazole and ziprasidone are the antipsychotic drugs least likely
   to lead to these adverse effects, whereas olanzapine and clozapine are
   the drugs most likely to do so. The newer agents, asenapine,
   iloperidone, and lurasidone, may also share a lower liability for
   weight gain and metabolic disturbances.

   The mechanism of weight gain associated with psychotropic drugs is not
   understood. Sensitivity to insulin may be increased, or increased
   leptin levels may be present.

   A Danish study of the risk for diabetes with antipsychotics compared
   nearly 346,000 individuals who purchased antipsychotics and nearly 1.5
   million unexposed individuals and concluded that the rate ratio (RR)
   for risk with first-generation antipsychotics was 1.53, whereas the RR
   varied widely for second-generation antipsychotics (1.32; range,
   1.17-1.57).^[105]

   Stroup et al studied 215 patients whose psychotic symptoms were
   stabilized on olanzapine, quetiapine, or risperidone.^[106] After 24
   weeks, those who switched to aripiprazole had improved cholesterol
   levels and other metabolic factors, and they lost more weight than
   those who stayed on their original medication. Relapse or worsening of
   psychotic symptoms occurred no more frequently in patients who switched
   medications than in those who stayed on their original medication.
   However, patients who switched to aripiprazole were more likely to
   discontinue the assigned medication: 43.9% of those who switched
   discontinued their medication, whereas 24.5% of those who stayed on
   their original medication discontinued it. They concluded patients
   experiencing cardiovascular or metabolic adverse effects of an
   antipsychotic medication may fare better if they switch to a different
   agent, provided they are closely monitored.

   Weight gain is associated both with psychological problems (eg,
   decreased self-esteem) and with medical problems (eg, diabetes,
   coronary artery disease, and arthritis). Education about nutrition and
   exercise should be provided. Cognitive-behavioral therapy can be tried.

   It is unclear whether weight-reducing drugs should be added to
   antipsychotic therapy. In one randomized, placebo-controlled study
   conducted in 72 patients with first-episode schizophrenia who gained
   more than 7% of their predrug weight, metformin (1000 mg/day) was
   effective and safe in attenuating antipsychotic-induced weight gain and
   insulin resistance.^[107]

   Miscellaneous adverse effects

   All antipsychotic agents may be associated with esophageal dysmotility,
   thus increasing the risks of aspiration, choking, and the subsequent
   risk of pneumonia. Orthostatic hypotension can be problematic at the
   beginning of therapy, with dose increases, and in elderly patients.
   This problem is related to alpha[1] -blockade and seems to be
   particularly severe with risperidone and clozapine.

   Venous thromboembolism may be associated with the use of antipsychotic
   drugs. Patients treated with clozapine may be at particular risk for
   this complication; however, the reasons for this possible association
   are not understood.^[108, 109]

   Results from a prospective study indicated that in children and
   adolescents, long-term use of risperidone can negatively affect bone
   mass.^[110]

   Neurotoxic effects

   Some studies have explored the potential neurotoxic effects of
   antipsychotic medications; however, no clear conclusions have been
   reached. For example, Ho et al performed structural brain imaging in
   more than 200 patients with schizophrenia over 7 years and found that
   whereas patients treated with higher doses of antipsychotic medications
   seemed to lose gray matter throughout their brain (except the
   cerebellum), those treated with lower doses seemed to have a small
   increase in white matter.^[111]

   The clinical significance of these findings is unclear. It is not known
   whether these changes are directly associated with any clinical
   symptoms and whether they are reversible. It also is not known whether
   the higher medication doses were in response to the gray-matter loss or
   whether it was the other way around.

Monitoring of blood levels

   Regular measurement of blood medication levels in the blood would be
   helpful in schizophrenia, for the following reasons:
     * Patients may not always take their medications, and checking drug
       levels can detect this noncompliance
     * Patients may not always be the best reporters of side effects, and
       monitoring medication levels can occasionally help the clinician
       detect toxicity
     * Smoking tobacco products induces the liver enzyme CYP1A2 (though
       nicotine patches, nicotine inhalers, and chewing tobacco do not);
       this enzyme metabolizes a number of antipsychotic drugs, so that,
       for example, patients who stop smoking while being treated with
       clozapine or olanzapine often experience increased antipsychotic
       levels; a patient who has stopped smoking may have a variety of
       complaints, and checking drug levels can help determine their
       etiology

   For most antipsychotic medications, however, clear dose-response curves
   have not been established, and in clinical practice, drug levels are
   rarely monitored.

   There are 2 exceptions to this general statement. Plasma concentrations
   of haloperidol are correlated to some degree with clinical effects, and
   levels in the range of 15-25 ng/mL are thought to be optimal. Plasma
   concentrations of clozapine in the range of 300-400 ng/mL may be
   optimal.
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Other Pharmacotherapy

   Anticholinergic agents (eg, benztropine, trihexyphenidyl, and
   diphenhydramine) and amantadine are often used in conjunction with the
   conventional antipsychotic agents to prevent dystonic movements or to
   treat extrapyramidal symptoms. Akathisia is particularly difficult to
   treat, but it occasionally responds to an anticholinergic agent, a
   benzodiazepine, or a beta blocker.

   Many patients with schizophrenia are treated with other psychotropic
   medications in addition to antipsychotic agents. Polypharmacy in
   schizophrenia is supported by little rigorous evidence but is widely
   practiced nonetheless. Medications often used include antidepressants,
   mood stabilizers, and anxiolytic agents. Carbamazepine and clozapine
   should not be used together.

   Benzodiazepines are often used and are perceived as being quite safe.
   Nevertheless, they can be addictive and can lead to falls, especially
   in the elderly. There has long been a concern that they might increase
   mortality.^[70]
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Psychosocial Interventions

   Psychosocial treatment is essential for people with schizophrenia and
   includes a number of approaches, such as social skills training,
   cognitive-behavioral therapy, cognitive remediation, and social
   cognition training.^[112] PORT (see Antipsychotic Pharmacotherapy) also
   provides a detailed review of psychosocial interventions.^[113]

   Psychosocial treatments are currently oriented according to the
   recovery model. According to this model, the goals of treatment for a
   person with schizophrenia are as follows:
     * To have few or stable symptoms
     * To avoid hospitalization
     * To manage his or her own funds and medications
     * To be either working or in school at least half-time

   Hope, empowerment, choice, and community integration are emphasized in
   this treatment approach.

   A large study from China demonstrated the advantages of medication plus
   psychosocial intervention over medication alone.^[114] In the
   psychosocial intervention arm, each month patients and their families
   received 1 day of 4 types of evidence-based interventions:
   psychoeducation, family intervention, skills training, and
   cognitive-behavioral therapy. After 1 year, the patients in the group
   receiving the extra interventions were more compliant with their
   medications, had fewer rehospitalizations, and experienced better
   quality of life.

   Cognitive remediation, vocational rehabilitation, assertive community
   treatment, and family intervention are reviewed.

Cognitive remediation

   Cognitive impairment, a core feature of schizophrenia, is less dramatic
   than other symptoms of the disease (eg, hallucinations and delusions)
   but interferes with work, social relationships, and independent living.
   Cognitive impairment is not improved by medication.

   Cognitive remediation is a treatment modality derived from principles
   of neuropsychological rehabilitation and is based, in part, on the
   ideas that the brain has some plasticity and that brain exercises can
   encourage neurons to grow and can develop the neurocircuitry underlying
   many mental activities.

   Numerous different models of cognitive remediation are available. Some
   models use drill-based practicing of isolated cognitive skills with the
   aid of computers, whereas others help people develop strategies for
   overcoming areas of weakness. Other forms of this therapy are known as
   cognitive rehabilitation, cognitive enhancement, or metacognitive
   therapy.

   Cognitive remediation works best when patients are stable. Improvement
   occurs across numerous cognitive functions, and changes are found on
   brain imaging that reflect these changes in brain functioning.

   Cognitive remediation techniques are time-intensive and
   labor-intensive. Because cognitive deficits are multiple and vary from
   person to person, such techniques seem to work best when specifically
   tailored to each patient. When combined with other therapies, such as
   supported employment, cognitive remediation leads to clinically
   relevant improvements.^[115] These effects are durable, lasting even
   after the training has stopped.^[116]

   In a study by Grant et al, low-functioning patients with prominent
   negative symptoms were assigned to either recovery-oriented
   cognitive-behavioral therapy plus standard treatment or standard
   treatment; after 18 months, the authors found that both negative and
   positive symptoms had decreased in the group receiving the add-on
   cognitive therapy.^[117] The study was not blinded, and the treatment
   was delivered by enthusiastic doctoral level therapists; thus, the
   findings may not be widely generalizable.

   A study by Puig and colleagues also found cognitive remediation therapy
   to be effective. In the study, 50 patients between the ages of 12 and
   18 years with early onset schizophrenia were randomized to either
   cognitive remediation therapy plus usual treatment or usual treatment
   alone. Patients in the cognitive remediation group showed significantly
   greater improvements than patients in the usual treatment group in
   verbal memory, working memory, executive function, and cognitive
   composite scores, at the end of treatment and at 3-month follow-up. The
   cognitive remediation group also had greater improvements in daily
   living skills, global adaptive functioning, and self-perceived family
   burden.^[118]

   Cognitive therapy may be effective as a standalone treatment for
   schizophrenia.^[119, 120] For schizophrenic patients who cannot or will
   not take antipsychotic medication, cognitive therapy may be the most
   viable option. According to data from the first randomized trial of
   cognitive therapy as a standalone therapy for schizophrenia, structured
   treatment with a therapist significantly reduced the severity of
   psychiatric symptoms and improved personal and social functioning and
   some dimensions of delusional beliefs and voice hearing.^[119, 120]

   The study involved 74 individuals aged 16 to 65 years with
   schizophrenia spectrum disorders who had decided not to take or had
   stopped taking antipsychotics for at least 6 months.^[119, 120] Half
   were randomly assigned to cognitive therapy (26 sessions during a
   9-month period) plus treatment as usual and half to treatment as usual
   alone. After 18 months, 7 (41%) of 17 study participants receiving
   cognitive therapy had an improvement of more than 50% in the Positive
   and Negative Syndrome Scale (PANSS) total score compared with 3 (18%)
   of 17 receiving treatment as usual.^[119, 120]

   None of the antipsychotic medications currently available is
   particularly effective at addressing cognitive symptoms. A new
   initiative from NIMH, known as Measurement and Treatment Research to
   Improve Cognition in Schizophrenia (MATRICS), is a collaboration
   between various programs to develop tools for measuring cognition in
   clinical trials and aiding development of drugs that target these
   symptoms.

Vocational rehabilitation

   Most patients with schizophrenia would like to work; employment can
   improve income, self-esteem, and social status. However, few people
   with the disorder are able to maintain competitive employment.^[121]
   Supported employment programs currently thought to be most effective
   are those that offer individualized, supported, and rapid job
   assignments and that are integrated with other services. These programs
   are associated with higher rates of employment, but gains in other
   domains are surprisingly difficult to discern.^[122]

Assertive community treatment

   Assertive community treatment is a form of case management that is
   typically used for patients who have had multiple hospitalizations. The
   treatment involves active outreach to patients. Case managers usually
   have a fairly small outpatient load (about 10 patients) and are able to
   go into the community to work with their clients. The managers
   coordinate and integrate care by doing the following: they identify
   indications for treatment, make referrals to appropriate services, and
   promote engagement with interventions. This form of treatment is
   expensive but may be associated with better clinical and social
   outcomes and lower hospitalization rates.

Family intervention

   Schizophrenia affects the person’s whole family, and the family’s
   responses can affect the trajectory of the person’s illness. Familial
   “high expressed emotion” (hostile overinvolvement and intrusiveness)
   leads to more frequent relapses. Some studies have found that family
   therapy or family interventions may prevent relapse, reduce hospital
   admission, and improve medication compliance.^[123]

   The National Alliance for the Mentally Ill (NAMI) is a helpful advocacy
   group that is supportive for family members. NAMI also advocates
   funding and research.

Smoking cessation

   Most patients with schizophrenia smoke. This may be a result of
   previous conventional antipsychotic treatment, in that nicotine may
   ameliorate some of the adverse effects of these drugs. Smoking may also
   be related to the boredom associated with hospitalizations, the peer
   pressure from other patients to smoke, or the anomie associated with
   unemployment.

   Whatever the cause of the high incidence of smoking, the health risks
   from smoking are well known, and all schizophrenic patients should be
   encouraged to stop smoking.
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Diet and Activity

   Many psychotropic medications can cause weight gain and changes in
   glucose or lipid metabolism. Occasionally, a person with schizophrenia
   develops odd food preferences. Finally, many persons with schizophrenia
   have limited funds, do not cook for themselves, and live in areas where
   fast food outlets are abundant. Therefore, nutritional counseling is
   difficult but important.

   Because many psychotropic medications are associated with weight gain,
   and because of the many beneficial effects of exercise, persons with
   schizophrenia should be encouraged to be as physically active as
   possible.
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Prevention

   Many have wondered whether patients with schizophrenia would have a
   better prognosis if treatment could be started as early as possible. A
   study from Scandinavia found that early detection and intervention in
   first-episode psychosis led to higher recovery and employment rates at
   10-year follow-up.^[124]

   The North American Prodrome Longitudinal Study is exploring whether the
   incorporation of biologic measures into prediction algorithms can
   provide more accurate identification of young people who are at
   greatest risk for developing a psychotic disorder. The goal of this
   study is to establish objective criteria that can be used to develop
   preventive approaches.

   There are several studies of prodromal schizophrenia under way to
   inform early intervention strategies. In the absence of highly reliable
   methods of predicting schizophrenia, however, intervention during the
   prodromal stage could result in the unnecessary administration of
   antipsychotic medication to young people who are mistakenly identified
   as being at risk for schizophrenia.^[125]

   One approach to this problem is to use psychological therapies rather
   than pharmacotherapy. A German study of young people at risk for
   schizophrenia showed that the use of a psychological intervention
   involving cognitive-behavioral therapy, group skills training,
   cognitive remediation and multifamily psychoeducation delayed the onset
   of psychosis for at least 2 years.^[126]
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Other Treatments

   An entirely different kind of treatment for schizophrenia, still in its
   early stages, is transcranial magnetic stimulation (TMS). TMS involves
   the electromagnetic induction of an electric field in the brain.
   Standard TMS affects neurons within 1.5-2 cm from the scalp, and deep
   TMS can affect cells to a depth of 6 cm. The electric field changes the
   “excitability” of the neurons and seems to be safe with few adverse
   effects. TMS is mostly used for depression. However, early work
   suggests that TMS, in some cases, may decrease auditory
   hallucinations^[127] and negative symptoms^[128] in schizophrenia.
   Previous
   Proceed to Medication


   Contributor Information and Disclosures
   Author

   Frances R Frankenburg, MD  Professor, Department of Psychiatry, Boston
   University School of Medicine; Chief of Inpatient Psychiatry and
   Consulting Psychiatrist, Edith Nourse Rogers Memorial Veterans
   Administration Medical Center; Associate Psychiatrist, McLean Hospital
   Frances R Frankenburg, MD is a member of the following medical
   societies: Alpha Omega Alpha and American Psychiatric Association
   Disclosure: Nothing to disclose.
   Chief Editor

   Eduardo Dunayevich, MD  Executive Director, Clinical Development, Amgen
   Eduardo Dunayevich, MD is a member of the following medical societies:
   American Psychiatric Association
   Disclosure: Lilly Research Laboratories Salary Other
   Additional Contributors

   Ronald C Albucher, MD Chief Medical Officer, Westside Community
   Services; Consulting Staff, California Pacific Medical Center

   Ronald C Albucher, MD is a member of the following medical societies:
   American Psychiatric Association

   Disclosure: Nothing to disclose.

   Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University
   of Nebraska Medical Center College of Pharmacy; Editor-in-Chief,
   Medscape Drug Reference

   Disclosure: Medscape Salary Employment
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       trial. J Am Acad Child Adolesc Psychiatry. Aug 2014;53(8):848-58.
       [Medline]. [Full Text].
   140. Schoepf D, Uppal H, Potluri R, Heun R. Physical comorbidity and
       its relevance on mortality in schizophrenia: a naturalistic 12-year
       follow-up in general hospital admissions. Presented at: The 22nd
       European Congress of Psychiatry (EPA); March 3, 2014; Munich,
       Germany. Abstract FC07. Eur Arch Psychiatry Clin Neurosci. Feb
       2014;264(1):3-28. [Medline]. [Full Text].


   Previous
   Next

   Cortical activation patterns during verbal working memory maintenance.
   Healthy controls (A), patients with schizophrenia (B), and
   significantly different activation between groups (subtraction of
   SZ-CO) (C) are shown. The time series plots in the middle column show
   activation associated with true memory maintenance (red lines) relative
   to the baseline activities (blue line). Bright parts in the middle of
   each plot represent 1-volume (1.5 s) after onset, and offset of the
   maintenance phase (4.5 secs). All p-values are corrected with false
   discovery rate of q< 0.005. Image courtesy of Kim J, Matthews NL, and
   Park S. An event-related fMRI study of phonological verbal working
   memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Cortical activation patterns during false memory trials. (A) False
   memory, baseline in controls (CO). (B) False memory, baseline in
   schizophrenia (SZ). (C) SZ – CO. All p-values are corrected with a
   false discovery rate of q< 0.005. The time course plots show false
   memory-related activities (yellow) and true memory-related activities
   (red) relative to the baseline (blue). Image courtesy of Kim J,
   Matthews NL, and Park S. An event-related fMRI study of phonological
   verbal working memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Magnetic resonance imaging showing differences in brain ventricle size
   in twins. The twin on the right has schizophrenia, whereas the twin on
   the left does not. Image courtesy of Dr. Daniel Weinberger, Clinical
   Brain Disorders Branch, National Institutes of Health.

   Previous
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Schizophrenia Clinical Presentation

     * Author: Frances R Frankenburg, MD; Chief Editor: Eduardo
       Dunayevich, MD   more...


     * Overview
     * Presentation
     * DDx
     * Workup
     * Treatment
     * Medication
     *

   Updated: Dec 22, 2014
   What would you like to print?
     * Print this section
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     * History
     * Physical Examination
     * Complications
     * Show All

   Multimedia Library
   References

History

   Information about the medical and psychiatric history of the family,
   details about pregnancy and early childhood, history of travel, and
   history of medications and substance abuse are all important. This
   information is helpful in ruling out other causes of psychotic
   symptoms.

   The patient usually had an unexceptional childhood. In retrospect,
   family members may describe the person with schizophrenia as a
   physically clumsy and emotionally aloof child. The child may have been
   anxious and preferred to play by himself or herself. The child may have
   been late to learn to walk and may have been a bed wetter.^[59, 60]

   A noticeable change in personality and a decrease in academic, social,
   and interpersonal functioning often begin during middle-to-late
   adolescence. Usually, 1-2 years pass between the onset of these vague
   symptoms and the first visit to a psychiatrist.^[61] The first
   psychotic episode usually occurs between the late teenage years and the
   mid 30s.

   The symptoms of schizophrenia may be divided into the following 4
   domains:
     * Positive symptoms - Psychotic symptoms, such as hallucinations,
       which are usually auditory; delusions; and disorganized speech and
       behavior
     * Negative symptoms - A decrease in emotional range, poverty of
       speech, and loss of interests and drive; the person with
       schizophrenia has tremendous inertia
     * Cognitive symptoms - Neurocognitive deficits (eg, deficits in
       working memory and attention and in executive functions, such as
       the ability to organize and abstract); patients also find it
       difficult to understand nuances and subtleties of interpersonal
       cues and relationships
     * Mood symptoms - Patients often seem cheerful or sad in a way that
       is difficult to understand; they often are depressed

   Next

Physical Examination

   The findings from a general physical examination are usually
   noncontributory. This examination is necessary to rule out other
   illnesses.

   It is sometimes helpful to perform a neurologic examination as a
   baseline before initiating antipsychotic medications, because these
   drugs themselves can cause some neurological signs. Some patients with
   schizophrenia have motor disturbances before exposure to antipsychotic
   agents. Schizophrenia has been associated with left and mixed
   handedness, minor physical anomalies, and soft neurologic signs.

Mental status examination

   On a detailed mental status examination (MSE), the following
   observations may be made in a severely ill patient with schizophrenia:
     * The patient may be unduly suspicious of the examiner or be socially
       awkward
     * The patient may express a variety of odd beliefs or delusions
     * The patient often has a flat affect (ie, little range of expressed
       emotion)
     * The patient may admit to hallucinations or respond to auditory or
       visual stimuli that are not apparent to the examiner
     * The patient may show thought blocking, in which long pauses occur
       before he or she answers a question
     * The patient’s speech may be difficult to follow because of the
       looseness of his or her associations; the sequence of thoughts
       follows a logic that is clear to the patient but not to the
       interviewer
     * The patient has difficulty with abstract thinking, demonstrated by
       inability to understand common proverbs or idiosyncratic
       interpretation of them
     * The speech may be circumstantial (ie, the patient takes a long time
       and uses many words in answering a question) or tangential (ie, the
       patient speaks at length but never actually answers the question)
     * The patient’s thoughts may be disorganized, stereotyped, or
       perseverative
     * The patient may make odd movements (which may elated to neuroleptic
       medication)
     * The patient may have little insight into his or her problems (ie,
       anosognosia)
     * Orientation is usually intact (ie, patients know who and where they
       are and what time it is)

   Persons with schizophrenia may display strange and poorly understood
   behaviors. These include drinking water to the point of intoxication,
   staring at themselves in the mirror, performing stereotyped activities,
   hoarding useless objects, and mutilating themselves. Their wake-sleep
   cycle may be disturbed.
   Previous
   Next

Complications

Substance abuse

   Alcohol and drug abuse (especially nicotine) are common in
   schizophrenia, for reasons that are not entirely clear. For some
   people, these drugs provide relief from symptoms of the illness or the
   adverse effects of antipsychotic drugs, and the drive for this relief
   is strong enough to allow even patients who are impoverished and
   disorganized to find substances to abuse.^[62]

   Comorbid substance abuse occurs in 20-70% of patients with
   schizophrenia, particularly younger male patients, and is associated
   with increased hostility, crime, violence, suicidality, noncompliance
   with medication, homelessness, poor nutrition, and poverty. Drug use
   and abuse can also increase symptoms. For example, cannabis use has
   been shown to be associated with an earlier onset of psychosis and to
   correlate, in a bidirectional way, with an adverse course of psychotic
   symptoms in persons with schizophrenia. That is, people with more
   severe psychotic symptoms are more likely to use cannabis, and
   cannabis, in turn, seems to worsen psychotic symptoms.^[63] However,
   other research has shown that the use of cannabis is associated with
   better cognitive functioning.^[64]

   A register-based study of more than 3000 inpatients from Scotland who
   experienced substance-induced psychoses showed that episodes of
   psychosis induced from several types of illicit substances are
   significantly linked to a later clinical diagnosis of
   schizophrenia.^[65]

   Patients who abuse substances may fare better in dual-diagnosis
   treatment programs, in which principles from the mental health field
   can be integrated with principles from the chemical dependency field.

Depression

   Many patients with schizophrenia report symptoms of depression. It is
   unclear whether such depression is an independent problem, part of the
   schizophrenia, a reaction to the schizophrenia, or a complication of
   treatment. Addressing this issue is important because of the high rate
   of suicide in patients with schizophrenia.

   The research evidence for the use of antidepressant agents in
   schizophrenic patients is mixed. Further complicating the situation are
   the findings that antipsychotic agents may have antidepressant
   properties.^[66] One meta-analysis suggested that the addition of
   antidepressants to antipsychotics might help treat the negative
   symptoms of chronic schizophrenia, which can be difficult to
   distinguish from depression.^[67]

   Suicide attempts are lower in people treated with clozapine than with
   other antipsychotic agents.^[68]

Anxiety

   Many patients with schizophrenia report symptoms of anxiety. It is
   unclear whether such anxiety is an independent problem, part of the
   schizophrenia, a reaction to the schizophrenia, or a complication of
   treatment. Some adverse effects of medications, such as akathisia, may
   be experienced as anxiety. Anxiety may precede the onset of
   schizophrenia by several years.^[69]

   Treatment is keyed to the source of the anxiety. Antipsychotics usually
   relieve anxiety that is part of an acute psychotic episode; only
   limited data are available on treatment of comorbid anxiety disorders.
   Following treatment recommendations for primary anxiety disorder would
   be reasonable in many cases; however, fluvoxamine and other selective
   serotonin reuptake inhibitors (SSRIs) should be used cautiously in
   patients receiving clozapine; they can raise clozapine blood levels.
   Benzodiazepines may be helpful but carry their own risks.^[70, 71]

Obsessive-compulsive symptoms

   A number of patients with schizophrenia display obsessive-compulsive
   symptoms, such as the need to check, count, or repeat certain
   activities. As is similar to anxiety or depression, the connection
   between these symptoms and schizophrenia is not understood.
   Obsessive-compulsive symptoms are a known adverse effect of some
   antipsychotic medications, particularly clozapine. Patients with
   schizophrenia and obsessive-compulsive symptoms tend to do more poorly.
   There is no clear consensus on how to treat the obsessive-compulsive
   symptoms.

Violence

   Most people with schizophrenia are not violent. However, a few may act
   violently, sometimes as a result of command hallucinations or
   delusions.^[67] Because the violent acts carried out by these few
   patients may be unpredictable and bizarre, they are often highly
   publicized, and the intense publicity has the unfortunate consequence
   of exacerbating the stigma of the disease.

   Violence may be associated with substance abuse. However, the rate of
   violence in patients with schizophrenia who do not abuse substances is
   higher than that in people without schizophrenia.^[72, 73] Clozapine is
   sometimes recommended for treatment of patients with schizophrenia who
   are violent.
   Previous
   Proceed to Differential Diagnoses


   Contributor Information and Disclosures
   Author

   Frances R Frankenburg, MD  Professor, Department of Psychiatry, Boston
   University School of Medicine; Chief of Inpatient Psychiatry and
   Consulting Psychiatrist, Edith Nourse Rogers Memorial Veterans
   Administration Medical Center; Associate Psychiatrist, McLean Hospital
   Frances R Frankenburg, MD is a member of the following medical
   societies: Alpha Omega Alpha and American Psychiatric Association
   Disclosure: Nothing to disclose.
   Chief Editor

   Eduardo Dunayevich, MD  Executive Director, Clinical Development, Amgen
   Eduardo Dunayevich, MD is a member of the following medical societies:
   American Psychiatric Association
   Disclosure: Lilly Research Laboratories Salary Other
   Additional Contributors

   Ronald C Albucher, MD Chief Medical Officer, Westside Community
   Services; Consulting Staff, California Pacific Medical Center

   Ronald C Albucher, MD is a member of the following medical societies:
   American Psychiatric Association

   Disclosure: Nothing to disclose.

   Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University
   of Nebraska Medical Center College of Pharmacy; Editor-in-Chief,
   Medscape Drug Reference

   Disclosure: Medscape Salary Employment
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   Cortical activation patterns during verbal working memory maintenance.
   Healthy controls (A), patients with schizophrenia (B), and
   significantly different activation between groups (subtraction of
   SZ-CO) (C) are shown. The time series plots in the middle column show
   activation associated with true memory maintenance (red lines) relative
   to the baseline activities (blue line). Bright parts in the middle of
   each plot represent 1-volume (1.5 s) after onset, and offset of the
   maintenance phase (4.5 secs). All p-values are corrected with false
   discovery rate of q< 0.005. Image courtesy of Kim J, Matthews NL, and
   Park S. An event-related fMRI study of phonological verbal working
   memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Cortical activation patterns during false memory trials. (A) False
   memory, baseline in controls (CO). (B) False memory, baseline in
   schizophrenia (SZ). (C) SZ – CO. All p-values are corrected with a
   false discovery rate of q< 0.005. The time course plots show false
   memory-related activities (yellow) and true memory-related activities
   (red) relative to the baseline (blue). Image courtesy of Kim J,
   Matthews NL, and Park S. An event-related fMRI study of phonological
   verbal working memory in schizophrenia. PLoS One. 2010; 5(8): e12068.
   Magnetic resonance imaging showing differences in brain ventricle size
   in twins. The twin on the right has schizophrenia, whereas the twin on
   the left does not. Image courtesy of Dr. Daniel Weinberger, Clinical
   Brain Disorders Branch, National Institutes of Health.

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   Fact Sheet

Schizophrenia

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What is schizophrenia?

   Schizophrenia is a mental illness that affects about 1% of the adult
   population. Schizophrenia affects both men and women with equal
   frequency. It often appears in men in their late teens or early
   twenties, and with women in their twenties or early thirties (National
   Institute of Mental Health: The Numbers Count). Schizophrenia is often
   related to dissociative identity disorder (DID), also known as multiple
   personality disorder, in which someone alternates between different
   personalities. However, schizophrenia is not related to DID, but more
   so relates to the “split” between emotional expression and current
   experiences.

Symptoms of schizophrenia

   Schizophrenia often interferes with a person’s ability to think
   clearly, to distinguish reality from fantasy, to manage emotions, make
   decisions, and to relate to others. The symptoms of schizophrenia often
   include positive symptoms, behaviors that are present that should be
   absent, and negative symptoms, behaviors that are absent that should be
   present. Examples include

   Positive Symptoms
     * Delusions: Beliefs that may be possible but are not true (such as
       believing that people are plotting against you or tracking your
       behavior, or that you are the Messiah)
     * Hallucinations: When someone hears, sees, feels, or smells things
       that are not actually present (such as hearing voices that no one
       else can hear)
     * Disorganized speech (rambling or incoherent): Not being able to
       organize thoughts and communicating them in a way which other
       people can’t understand
     * Difficulty prioritizing tasks

   Negative Symptoms
     * Emotional flatness or lack of expression: When a person’s face,
       voice, and gestures seem flat
     * Lack of interest in life: Difficulty starting and following through
       on activities and having trouble doing simple things
     * Lack of pleasure: Not enjoying things they used to enjoy, including
       relationships and activities

   Other things besides schizophrenia may also cause similar symptoms,
   such as drug usage or a medical condition affecting the brain (head,
   injury, tumor, etc). Therefore, if you or someone you know is concerned
   about the symptoms described above, it is best to consult about the
   symptoms with a medical doctor for a complete checkup.

What causes schizophrenia?

   The exact cause of schizophrenia is not known. Like other medical
   illnesses such as cancer or diabetes, schizophrenia seems to be caused
   by a combination of genetics, environmental factors, and psycho-social
   factors. Examples include:
     * Genetics or family history: People who have first-degree relatives,
       such as parents, brothers, or sisters, have a higher risk of
       inheriting schizophrenia. However, genes only increase the chances
       of developing this illness; it does not depend on any single gene.
     * Biochemical factors: Research have indicated that the deficient
       activity of the neurotransmitters dopamine and glutamate, possibly
       play a role in developing schizophrenia.
     * Environment: Your prenatal environment, like if your mother had the
       flu when she was pregnant not receiving sufficient nutrition as a
       child, can put you at high risk of developing schizophrenia. Also,
       situations like being exposed to stress or trauma can increase
       risks.
     * Drug use: Some research suggest that drug misuse is related to the
       development of schizophrenia. It’s likely that substance misuse can
       bring on or worsen the symptoms and get in the way of the treatment
       of a person with schizophrenia.

Getting help

   Schizophrenia can be treated and people with schizophrenia can lead
   happy, fulfilling, productive lives. The most effective form of
   treatment is a combination of medications, professional counseling, and
   peer-to-peer and family support. If you have or think you have
   schizophrenia, seeking help is important. It should begin with a visit
   to a medical doctor, and sharing when you started experiencing
   symptoms. A general practitioner or psychiatrist may prescribe
   medication. Therapy or counseling with a psychiatrist, psychologist,
   social worker, or counselor can also help manage your symptoms and help
   you mange day to day tasks. Some who have schizophrenia may have
   periods of acute symptoms that require intensive treatment, such as
   hospitalization (if necessary).
   The National Alliance on Mental Illness has a weekly recovery support
   group for people living with mental illness in which people learn from
   each others’ experiences, share coping strategies, and offer each other
   encouragement and understanding. They also have resources for family
   and friends of a person who has schizophrenia. Check out the NAMI
   Connection to find a support group near you.

   Information for this fact sheet

   Substance Abuse and Mental Health Services Administration Schizophrenia

   National Alliance on Mental Illness (NAMI)

   Biological Psychology (11th Edition) by James W. Kalat

   Last edited by Kristie - March, 2014.

Where to Next?

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Op-Ed Contributor

The Violence in Our Heads

By T. M. LUHRMANN

Published: September 19, 2013

   STANFORD, Calif. — THE specter of violence caused by mental illness
   keeps raising its head. The Newtown, Conn., school killer may have
   suffered from the tormenting voices characteristic of schizophrenia;
   it’s possible that he killed his mother after she was spooked by his
   strange behavior and tried to institutionalize him. We now know that
   Aaron Alexis, who killed 12 people at the Washington Navy Yard on
   Monday, heard voices; many observers assume that he, too, struggled
   with schizophrenia.
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Keith Negley

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     * Signs of Distress Multiplied on Killer’s Path to Navy Yard
       (September 20, 2013)

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   T. M. Luhrmann

   To be clear: a vast majority of people with schizophrenia — a disease
   we popularly associate with violence — never commit violent acts. They
   are far more likely to be the victims of violence than perpetrators of
   it. But research shows us that the risk of violence from people with
   schizophrenia is real — significantly greater than it is in the broader
   population — and that the risk increases sharply when people have
   disturbing hallucinations and use street drugs. We also know that many
   people with schizophrenia hear voices only they can hear. Those voices
   feel real, spoken by an external, commanding authority. They are often
   mean and violent.

   An unsettling question is whether the violent commands from these
   voices reflect our culture as much as they result from the disease
   process of the illness. In the past few years I have been working with
   some colleagues at the Schizophrenia Research Foundation in Chennai,
   India, to compare the voice-hearing experience of people with
   schizophrenia in the United States and India.

   The two groups of patients have much in common. Neither particularly
   likes hearing voices. Both report hearing mean and sometimes violent
   commands. But in our sample of 20 comparable cases from each country,
   the voices heard by patients in Chennai are considerably less violent
   than those heard by patients in San Mateo, Calif.

   Describing his own voices, an American matter-of-factly explained,
   “Usually it’s like torturing people to take their eyes out with a fork,
   or cut off someone’s head and drink the blood, that kind of stuff.”
   Other Americans spoke of “war,” as in, “They want to take me to war
   with them,” or their “suicide voice” asking, “Why don’t you end your
   life?”

   In Chennai, the commanding voices often instructed people to do
   domestic chores — to cook, clean, eat, bathe, to “go to the kitchen,
   prepare food.” To be sure, some Chennai patients reported disgusting
   commands — in one case, a woman heard the god Hanuman insist that she
   drink out of a toilet bowl. But in Chennai, the horrible voices people
   reported seemed more focused on sex. Another woman said: “Male voice,
   very vulgar words, and raw. I would cry.”

   These observations suggest that local culture may shape the way people
   with schizophrenia pay attention to the complex auditory phenomena
   generated by the disorder and so shift what the voices say and how they
   say it. Indeed, that is the premise of a new patient-driven movement,
   more active in Europe than in the United States, which argues that if
   you treat unsettling voices with dignity and respect, you can change
   them.

   The Hearing Voices movement encourages people who hear distressing
   voices to identify them, to learn about them, and then to negotiate
   with them. It is an approach that flies in the face of much clinical
   practice in the United States, where psychiatrists tend to assume that
   treating such voices as meaningful encourages those who hear them to
   give them more authority and to follow their commands.

   Yet while there is no judgment from the scientific jury at this point,
   there is evidence that at least some people find that when they use the
   Hearing Voices approach, their voices diminish, become kinder and
   sometimes disappear altogether — independent of any use of drugs.

   This evidence is strengthened by a recent study in London that taught
   people with schizophrenia to create a computer-animated avatar for
   their voices and to converse with it. Patients chose a face for a
   digitally produced voice similar to the one they were hearing. They
   then practiced speaking to the avatar — they were encouraged to
   challenge it — and their therapist responded, using the avatar’s voice,
   in such a way that the avatar’s voice shifted from persecuting to
   supporting them.

   All of the 16 patients who received a six-week trial of that therapy
   found that their hallucinations became less frequent, less intense and
   less disturbing. Most remarkably, three patients stopped hearing
   hallucinated voices altogether, even three months after the trial. One
   of those three patients had heard voices incessantly for the prior 16
   years.

   The more we know about the auditory hallucinations of schizophrenia,
   the more complex voice-hearing seems and the more heterogeneous the
   voice-hearing population becomes. Not everyone will benefit from the
   new approaches. Still, they offer hope for those struggling with a grim
   disease.

   Meanwhile, it is a sobering thought that the greater violence in the
   voices of Americans with schizophrenia may have something to do with
   those of us without schizophrenia. I suspect that the root of the
   differences may be related to the greater sense of assault that people
   who hear voices feel in a social world where minds are so private and
   (for the most part) spirits do not speak.

   We Americans live in a society in which, when people feel threatened,
   they think about guns. The same cultural patterns that make it
   difficult to get gun violence under control may also be responsible for
   making these terrible auditory commands that much harsher.
   [meter.gif]

   T. M. Luhrmann is a professor of anthropology at Stanford University
   and a contributing opinion writer.

A version of this op-ed appears in print on September 20, 2013, on page A31
of the New York edition with the headline: The Violence in Our Heads.

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Overcoming Schizophrenia

   Each of us are in recovery, whether that be from: mental illness,
   substance abuse, abusive relationships, homelessness, etc. Whatever the
   situation, lets be an example to others that we can and do overcome
   tough situations by sharing our testimonies... Here is mine...

Pages

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     * Media
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The Author

   My Photo

   Ashley Smith
          Atlanta, Georgia, United States
          I am overcoming schizophrenia, and I believe others can too.
          Here is how I am managing my condition...

   View my complete profile

Tuesday, January 6, 2015

Starting the Conversation

   Many times limited information about mental illness leaves room for
   speculation and worry, which undoubtedly leads to fear, distancing
   oneself from discussions, and a poor outlook about the condition for
   oneself and the general public. However, a discussion about mental
   illness needs to be had to reduce confusion, isolation, and propaganda.
   Frequently, I share my story to reduce stigma and to promote the truth.
   Whenever I share my testimony of living with schizophrenia I usually
   get a warm and familiar response that goes something like: 'I know
   so-and-so with schizophrenia... I wish I would have talked to you
   sooner because your story helps me understand mental illness more.'
   Hearing that rekindles my desire to further articulate my crisis
   history and present-day recovery to share hope and to reduce the lies-
   the lie that recovery is not possible, the lie that life is over if you
   have a diagnosis, and the most ignorant lie; the lie that we should not
   talk about it.
   Sometimes people are reluctant to ask me questions in the beginning
   because they don't want to get too personal, but I welcome the
   conversation because the discussion provides insight and understanding.
   For me, sharing my story is so therapeutic, it enables me to release
   the dreadful experience of living with the condition, but in a
   constructive manner.
   The misinformation circulated about schizophrenia and other mental
   illnesses have an invisible muzzle on that must be eradicated and
   destroyed. My hope is for society to remove that mouthpiece and to have
   a lively dialogue about the truth- the truth that people can and do get
   better living with mental illness, and that an individual like you,
   your relative, or your partner can live a fulfilling life in recovery.
   There needs to be a frank conversation about mental illness in order to
   reduce stigma, help others, and to break the cycle of suffering.
   Talking about my mental illness helps me and others to talk openly
   about our dark moments and hopeful life after crisis.
   To help start a conversation I encourage you to read my book, What's On
   My Mind? A Collection Of Blog Entries From "Overcoming Schizophrenia."
   Available in Paperback or e-Book online at Amazon.com.
   Also, if you have a question about schizophrenia I encourage you to
   ask, you may also email me: ashley@emminc-recovery.org.
   Finally, I am inviting you to an event in Atlanta, Georgia where I will
   start a mental health conversation, Mental Health Day At The Capitol on
   Tuesday, January 20, 2015, 8AM - 12PM located at the Freight Depot, 65
   Martin Luther King Jr. Drive, Atlanta, GA 30303. The deadline to
   register is January 15th. For details visit the Georgia Mental Health
   Consumer Network, Inc.
   Posted by Ashley Smith at 4:52 AM 1 comment: Links to this post
   Labels: Georgia Mental Health Consumer Network, Mental Health Day At
   The Capitol, Schizophrenia, Speaking Engagement, Stigma

Sunday, December 7, 2014

My Enemy- Depression Or My Responsibilities?

   How often do you confuse your mental health deterioration and physical
   ailments for your mental illness, opposed to the burdens that you put
   on yourself with an active lifestyle?
   Over the past few months I've struggled with the physical ramifications
   of "depression," or what I thought was my depression. I've had partial
   work days as the result of my fatigue and lack of energy. I've felt:
   drained, off balanced, and uneasy. In fact, I visited my mental health
   doctor and primary care doctor for help. My mental health doctor
   realized my poor sleeping habits were the outcome of lack of direction
   or not taking my medication as prescribed which was in the morning and
   NOT at night. Finally, when my primary care doctor performed several
   blood tests without issues he explained to me what my problems were, an
   "active lifestyle."
   Now, I know what I should do to help myself with this concern of lack
   of energy- continue to take my medication, resume taking vitamins and
   create more time for self care. I've struggled with managing my self
   care because I want to help those around me, so I lessen my "me-time"
   and volunteer additional support to peers at work and friends outside
   of work... I cannot continue on this routine. I spoke to a peer who is
   also in recovery and we plan to check in with each other to hold
   ourselves accountable to our new self care regimens. We've practiced
   this before but let it go, now I'm ready to pick up our check in
   routine to get myself back focused and well. Peer support helps a lot,
   and I need it again. I'm glad I have a better understanding of my
   problems and situation.
   How do you balance your self care for good mental health?
   Posted by Ashley Smith at 8:49 PM No comments: Links to this post
   Labels: Balance, Depression, Medication, Peer Support, Self Care

Sunday, November 9, 2014

My Medication Schedule

   Recently, I've had to revise my medication schedule. For the last two
   months I've had problems staying asleep, and I've been talking to my
   mental health doctor under monthly basis to resolve my poor sleeping
   habits. On the last visit we discovered I was taking one of my
   prescriptions at night when it should've been taken in the morning. In
   fact, my pill bottle said to take the medicine in the mornings, but I
   wanted to change my medication regimen for my convenience. However, I'm
   going back to a morning routine. I will set my cell phone alarm as a
   reminder to take my medicine before I leave the house. I am hopeful
   that this change will help me sleep better. It's interesting how small
   changes can either create big problems or solutions. I think my
   sleeping patterns will improve along with my energy level and ability
   to manage high productivity at work.
   How do you manage your medication regimen to fit within your routine?
   Posted by Ashley Smith at 10:30 AM 2 comments: Links to this post
   Labels: Doctors, Medications, routine
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My Recovery at a Glance

     * Detrimentally in Denial
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     * From the Terrors of Psychosis to Hope and a Better Life
     * Good Doctor Bad Doctor
     * Lack of Trust: A Byproduct of my Mental Illness
     * When Coping Isn't Coping Anymore

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News & Views

   15 November 2013

Five myths – and the facts – about schizophrenia

Stand Up for Schizophrenia

   Rethink Mental Illness conducted a survey in 2011 that suggested 90 per
   cent of us can’t separate fact from fiction when it comes to
   perceptions about schizophrenia.

   The poll of more than 2,000 UK adults revealed five top myths
   associated with the illness, which we're republishing here in honour of
   Schizophrenia Awareness Week...

   Myth 1: People with schizophrenia have a split personality

   Fact: This is the most common myth, but it’s completely false. The word
   ‘schizophrenia’ literally translated means ‘split mind’ which has
   caused a lot of confusion. People with schizophrenia do sometimes
   experience delusions and hallucinations but they do not have two
   separate personalities.

   Myth 2: People with schizophrenia have the same physical health as
   everyone else

   Fact: Many people do not realise the impact schizophrenia has on
   people’s physical health. The physical effects of mental illness,
   combined with the side effects of anti-psychotic medication and
   lifestyle factors mean people with the illness have a life expectancy
   20 years lower than average.

   Myth 3: People with schizophrenia can’t recover

   Fact: Around 30% of people with schizophrenia will have a lasting
   recovery and around 20% will show significant improvement. Around 50%
   will have a long-term illness, which may involve further episodes of
   becoming unwell and times of being better.

   Myth 4: People with schizophrenia need to be monitored at all times

   Fact: When people with schizophrenia are getting access to the
   treatment and support they need, there is no reason why they cannot
   lead happy and productive lives. Some people with schizophrenia live
   with family or in supported housing, but many of those affected live
   independently and are active members of society.

   Myth 5: People with schizophrenia are dangerous

   Fact: Violence is not a symptom of schizophrenia and people with the
   illness are for more likely to be the victims of violence than the
   perpetrators.

   Find more facts in our information sheet.


Stand Up for Schizophrenia

   Find out more by visiting our liveblog


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   People with schizophrenia have "split personalities."

   "Split personalities" or "multiple personalities" are not a symptom of
   schizophrenia; in fact, these symptoms indicate a different mental
   illness called dissociative identity disorder. A child with
   schizophrenia may react inappropriately to situations, but that
   reflects distorted thinking, hallucinations or delusions.

   People with schizophrenia are dangerous.

   A few people with schizophrenia suffer from delusions that make them
   prone to violent outbursts, but the vast majority of people with this
   disorder tend to withdraw when they become symptomatic. People with
   schizophrenia are more likely to be victims of violence or suicide than
   harmful to other people. Substance abuse, along with schizophrenia,
   increases the risk of aggressive behavior.

   Schizophrenia comes on suddenly.

   In fact there are early signs of developing schizophrenia that tend to
   appear during adolescence, though they may not be recognized: declining
   school work, difficulties with friends and family, problems with
   organizing information. An individual may not hear voices, but might
   hear whispers, which he can't make out.

   All people with schizophrenia see things that aren't there.

   About a fifth of people with schizophrenia have visual hallucinations,
   but hearing voices is much more common, occurring in 70 percent of
   people with the disorder. A few also experience tactile hallucinations
   or odd smells.

   If one of your parents has schizophrenia, you probably will too.

   A family history of schizophrenia does increase your risk of developing
   it, but not as dramatically as most people think. With no family
   history, you have a 1 percent risk of developing schizophrenia. Your
   risk rises to 2 percent if someone in your extended family has it—an
   aunt, uncle or cousin. If one of your parents has it, 10 percent. An
   identical twin with the disorder gives you a 50 percent risk of
   developing it, too.

   Schizophrenia is purely genetic.

   Along with genetics, research has shown that stress and family
   environment can play a role in triggering psychosis. A household with a
   lot of expressed affect—conflict and emotional drama—can increase
   risks.

   Schizophrenia is untreatable.

   Schizophrenia is not curable, but with consistent medication and other
   therapy it is a manageable chronic illness, like diabetes or heart
   disease.

   People with schizophrenia can't lead normal lives.

   Wrong. With medication and behavioral treatment to learn to manage
   symptoms, people can, indeed, live productive, happy lives.

   Medications turn people with schizophrenia into zombies.

   If a person with schizophrenia who's on anti-psychotic medication is
   lethargic and listless, it's a result of either the schizophrenia
   itself or overmedication.

   For a complete guide to schizophrenia, see our Mental Health Guide.

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Myths about Schizophrenia

Misconceptions:  What Schizophrenia is NOT

   Here are some common myths about schizophrenia that need to be
   dispelled:

   MYTH: People with schizophrenia have a split personality, or multiple
   personalities.
   FACT: The word “schizophrenia” derives from “schizo,” meaning split or
   fractured, and “phrenia,” meaning mind. Thus, schizophrenia describes
   the breaking apart of one's mental functions, not the splitting apart
   of one's personality. “Split personality” is an entirely different
   disorder, now called dissociative identity disorder.

   MYTH: People with schizophrenia have sub-normal intelligence.
   FACT: While people with schizophrenia have cognitive impairments, this
   is not the same as a lack of intelligence. Those with schizophrenia
   demonstrate the same average intelligence as the rest of the
   population.

   MYTH: Schizophrenia is caused by child abuse, terrible parenting. or an
   otherwise horrible childhood.
   FACT: Neglect or abuse has not been shown to be an important factor in
   the development of schizophrenia. As has been stated, there are both
   genetic (inherited) and environmental factors associated with
   schizophrenia, and childhood experiences have not been cited as a
   strong environmental factor.

   MYTH: Schizophrenia makes a person bad, lazy, or uncaring.
   FACT: “Laziness” and “lack of concern” are misunderstandings or
   mislabels of certain “negative” symptoms of schizophrenia.

Schizophrenia is often misunderstood—and stigmatized

   The media all too often portrays people with schizophrenia as violent
   and dangerous. They sensationalize the disease by featuring chronic
   patients whose symptoms are not being treated.

   How often have you seen characters in film and/or television programs
   portrayed as seeing images and talking to themselves, or as living on
   the street and having poor personal hygiene—and been told that these
   characters have schizophrenia?

   These depictions are unfortunate—not only because they perpetuate
   society's lack of understanding of schizophrenia, but they create
   greater stigma for mental illnesses in general.

About Schizophrenia

     * what is schizophrenia?
     * Symptoms of Schizophrenia
     * Schizophrenia Treatment
     * myths about schizophrenia

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Schizophrenia Treatment

There have been many advances in schizophrenia research

   Brain imaging revolutionized medical research on schizophrenia. Until
   brain imaging technology was invented, the medical world knew very
   little about schizophrenia, because there was so little understanding
   of how the brain operates. Now that it's easier to study the brain,
   scientists have found many differences between brains of people with
   schizophrenia and those without. These discoveries have helped doctors
   know more about the nature and course of the illness and how treatable
   schizophrenia actually is.

Schizophrenia is not curable, but can be managed with effective treatment

   Treatment for schizophrenia must necessarily address both biological
   and psychological issues. Biological issues are addressed with
   medications, while psychological issues are addressed with
   psychotherapy.

   Dramatic advances have been made since the late 1980s in developing
   drugs to treat schizophrenia due to research innovations as described
   above. Some of these medications include antipsychotic drugs such as
   clozapine, risperidone, olanzapine, quetiapine, aripiprazole and
   azenapine. Such medications, when supplemented with effective
   psychotherapy, have helped tens of thousands of people with
   schizophrenia experience productive and rewarding lives.

   Even more recently, special forms of cognitive behavioral therapy (CBT)
   have been developed that can reduce the intensity of positive symptoms,
   such as hallucinations, that do not respond well to medication. These
   new therapies are growing in popularity, and are being tested for their
   effects in patients who are in very early stages of the illness.

About Schizophrenia

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Symptoms of Schizophrenia

What are the initial symptoms of schizophrenia?

   Schizophrenia often begins with psychosis, or a “break with reality.”
   (The word “psychosis” means a defective or lost contact with reality.)
   When a person is psychotic, they usually cannot tell whether their
   perceptions, thoughts and beliefs are real or not.

   Initial symptoms usually appear in late adolescence or early adulthood.
   It is possible to develop schizophrenia as a young child or as an older
   adult, but that is unusual.

“Positive” and “Negative” symptoms of schizophrenia

   Psychiatry uses the terms “positive” and “negative” to classify the
   symptoms of schizophrenia.

   “Positive” symptoms refer to the experiences a person with
   schizophrenia has that are not common to others. Examples include
   delusions (unreal beliefs) and hallucinations (unreal perceptions).

   “Negative” symptoms represent the absence of capacity common to persons
   without schizophrenia. Examples include:
       -avolition (lack of ability to plan behavior)
       -flat affect (an impaired ability to express emotions and other
   non-verbal information)
       -cognitive impairments (difficulty with logic and comprehension)

What pattern, if any, do symptoms follow?

   Over time, the “positive” symptoms of schizophrenia may come and
   go—sometimes spontaneously, sometimes as the result of treatment.

   “Negative” symptoms are more likely to persist—and are often more
   disabling. They are also more often misunderstood. For example,
   avolition can be interpreted as “laziness” or “lack of willpower” and
   flat affect can be interpreted as “having no concern about others.”

About Schizophrenia

     * what is schizophrenia?
     * Symptoms of Schizophrenia
     * Schizophrenia Treatment
     * myths about schizophrenia

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What is Schizophrenia?

Schizophrenia is a brain disorder

   Schizophrenia is an illness that primarily impacts the brain, like
   epilepsy, Parkinson's, or Alzheimer's. Schizophrenia affects thoughts,
   perceptions and the capacity to reason. For those affected, that
   translates into impairments in their ability to process information,
   learn and remember.

Schizophrenia occurs twice as often as Alzheimer's disease.

   Schizophrenia affects approximately 1 person in 100, or 1% of the
   population. To put that number in context, it is twice as many people
   as have Alzheimer's disease, and the same number of people as serve in
   the U.S. military today.

Schizophrenia is not gender or geography specific

   Schizophrenia is found in every culture around the world. Also, it
   affects both men and women almost equally—although men who develop
   schizophrenia generally do so earlier in life and with more severe
   symptoms.

What causes schizophrenia?

   Scientists haven't yet discovered what causes schizophrenia. Currently,
   the causes are thought to involve both genetic (inherited) and
   environmental (biological, acquired) factors.
   Genetic, or Inherited, Factors: The risk of developing schizophrenia
   goes up when one has a close relative who also has the disorder,
   indicating a genetic component.
   Environmental, or Biological, Factors: Environmental factors that have
   been associated with schizophrenia include viral infection or very poor
   nutrition during the fetal period.

Schizophrenia is not curable, but can be treated effectively

   Even though schizophrenia is not curable, it can be managed with
   effective treatment.  Today, a person with schizophrenia who receives
   appropriate treatment can lead a productive, rewarding life.

About Schizophrenia

     * what is schizophrenia?
     * Symptoms of Schizophrenia
     * Schizophrenia Treatment
     * myths about schizophrenia

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Schizophrenia Myths & Facts

   Myth:  Schizophrenia is a split personality

   Fact:  People with schizophrenia have only ONE personality.  The word
   'schizophrenia' comes from the Greek word meaning 'split mind' and this
   is perhaps where the confusion started.  The diagnosis of Schizophrenia
   was first introduced into the medical lexicon by the Swiss
   psychiatrist, Dr Eugen Bleuler in 1911.

   Myth:  People who have schizophrenia are always violent

   Fact:  People who have schizophrenia are unlikely to be violent and are
   frequently the victims of violence.  This is another very common and
   unfounded myth that is exacerbated by the media.  There is an increased
   risk of violence, especially early in the course of the illness before
   help has been received, however this risk is low.   There is an
   increased risk of self-harm among people with schizophrenia and this is
   linked to an increase in the rate of completed suicide.  Often, because
   of the nature of the illness, violence is self-directed either through
   fear, delusional thinking or the decision to 'no longer cope' with the
   illness.  It is fair to say that a person with schizophrenia has more
   to fear from the general community than the reverse, as they are often
   on the receiving end of quite severe stigmatisation, misunderstanding
   and outright discrimination.

   Myth:  People with schizophrenia are developmentally delayed

   Fact:  People with schizophrenia are NOT developmentally delayed.  This
   myth has its basis in the treatment programs in the nineteenth and
   early twentieth century..  During this period, people with a
   developmental delay and people with a mental illness were placed in
   asylums together and this is probably where the confusion arose.

   Myth:  People with schizophrenia have low intelligence

   Fact:  People with schizophrenia are not low in intelligence.  As with
   any population, there is a variation, but this is not a characteristic
   of the illness.  People with schizophrenia have won the Nobel Prize.

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About Schizophrenia

Learning about schizophrenia

   If you , or your friend, relative or partner has been diagnosed with
   schizophrenia, then this is the best section for you to start
   browsing.  Here you will find a wealth of information on
   schizophrenia.  Below you will find a short summary of what
   schizophrenia actually is and to the left of this page is a menu
   detailing the more specific elements of schizophrenia.  Have a look at
   this first if you are new to schizophrenia.

   If you are a carer:  in addition to reading the material on
   schizophrenia produced in this section of the web site, you might also
   like to read information written specifically for carers and friends.
   If you have a mental illness, browse through this section on
   schizophrenia or have a look at other mental illnesses.  You can also
   go directly to the consumer section that deals with treatment and
   recovery processes.

What is schizophrenia?

   "For me, schizophrenia severely ruptured the relationship I had enjoyed
   with myself prior to the illness.  My sense of being in the world, my
   thought processes and indeed the very way my senses perceived the world
   go through involuntary changes.  I was plunged at times into a
   confusing and frightening world ruled by my own paranoias and
   delusions...Prior to developing schizophrenia the workings of my mind
   had been unquestioned.  Suddenly I was being told by a psychiatrist
   that I could not always trust my own thoughts and senses.  I felt that
   my own mind had betrayed me.  How could I ever trust it?  Self had
   become a traitor and was working against my own good" (Simon, a person
   who has experienced schizophrenia).

   Schizophrenia is a condition characterised by disturbances in a
   person's thoughts, perceptions, emotions and behaviour.  It affects
   approximately one in every 100 people worldwide and commonly begins in
   adolescence or early adulthood.  Schizophrenia is probably not a single
   disease, rather a cluster of diseases, which have overlapping signs and
   symptoms.  It is therefore important to acknowledge the unique
   experience of each person living with schizophrenia.

   While schizophrenia can be a devastating illness for the people who
   experience it as well as for their families, it is important to
   recognise that there is hope.  Treatments, both medical and
   psychosocial, are becoming more effective.  Recently introduced early
   intervention programs are demonstrating encouraging outcomes for people
   with early psychosis and the concerns of consumers and their carers,
   such as those relating to empowerment and quality of life, are being
   increasingly recognised.

   Schizophrenia is a complex disorder with few generalisations holding
   true for all people diagnosed.  In practice, there appears to be as
   many forms of schizophrenia as there are individuals experiencing the
   illness.


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Schizophrenia Symptoms

   "The consumer who lives with schizophrenia is more than a complex
   presentation of signs and symptoms. Not only does this person
   experience the internal effects of the illness, they also feel the
   interaction between their internal physical and psychological
   experience, and the external social world" (Paul, a Mental Health
   Professional).

   There are a number of signs and symptoms that are characteristic of
   schizophrenia, however, the expression of these symptoms varies greatly
   from one individual to another. No one symptom is common to all people.
   As such, diagnosis and treatment must always be tailored to the
   individual's unique experience of schizophrenia.

   The symptoms of schizophrenia can be divided into a number of groups:
     * Positive symptoms, for example, hallucinations, delusions and
       disorganised thinking
     * Negative symptoms, for example, loss of motivation and ability to
       experience pleasure in life
     * Cognitive symptoms, for example difficulty in concentrating or
       planning
     * Mood and anxiety - depression and anxiety is common

Positive symptoms

   The positive symptoms of schizophrenia (also referred to as 'psychotic'
   or 'active' symptoms) reflect an excess or distortion of normal
   functioning and include the following:

Delusions

   Delusions are false personal beliefs held with extraordinary conviction
   in spite of what others believe and in spite of obvious proof or
   evidence to the contrary. They may revolve around many themes. For
   example, a person experiencing delusions may believe they are being
   spied on, tormented, followed or tricked (persecutory). Or they may
   believe gestures, comments, passages from books, television and other
   environmental cues are directed specifically at them (referential).
   Delusions may be bizarre (believing your thoughts have been removed by
   an outside force) or realistic (believing you are being followed by the
   police). Delusions will occur during some stage of the disorder in
   ninety percent of people who experience schizophrenia.

Hallucinations

   Hallucinations can occur in any of the five senses but the most common
   are auditory. These are usually experienced as voices which are
   perceived as distinct from the person's own thoughts. For example, the
   person may hear voices repeating or mimicking their thoughts, arguing,
   commenting on their actions (often in a critical manner) or telling
   them what to do (command hallucinations). Hallucinations of any form
   occur in over 70 per cent of people who experience psychotic illnesses.
   Auditory hallucinations occur in 60-90 per cent of people with
   schizophrenia, while visual hallucinations occur in 15-50 per cent.

Disorganised Thinking

   This is usually expressed through abnormal spoken language. For
   example, the person's conversation jumps erratically from one topic to
   another, new words may be created, the grammatical structure of
   language breaks down and speech may greatly speed up or slow down.

Disorganised Behaviour

   This can be manifested in a variety of ways. A person with
   schizophrenia may, for example, aimlessly wander, display child-like
   silliness or become unpredictable agitated. Or they may display
   behaviour that is considered inappropriate according to usual social
   norms, such as wearing many layers on a hot day, muttering aloud in
   public or inappropriately shouting or swearing. Disorganised behaviour
   can lead to problems in organising meals and maintaining hygiene. It
   may be difficult to link disorganised behaviour in adolescents
   to psychosis as teenagers are often intrinsically disorganised.

Catatonic Behaviour

   This refers to states of muscular rigidity and immobility, stupor and
   negativism, or to states of wild excitement. The person may hold fixed
   or bizarre bodily postures for extended periods of time and resist any
   effort to be moved. Catatonic behaviour is very rare in developed
   countries (Cutting, 1996).

Negative symptoms

   The negative symptoms of schizophrenia (also referred to as 'deficit'
   symptoms) reflect a loss of normal functioning and include the
   following:

Loss of Motivation (Avolition)

   This may involve lack of energy, apathy or seeming absence of interest
   in what were usually routine activities. People experiencing avolition
   may be inattentive to grooming, personal hygiene, have difficulty
   making decisions and have difficulty persisting at work, school or
   household chores.

Loss of Feeling or an Inability to Experience Pleasure (Anhedonia)

   This may manifest itself through having a lack of interest in social or
   recreational activities or through failure to develop close
   relationships. It may mean that the simple pleasures of life, like
   appreciating a beautiful sunset, being no longer enjoyed.

Poverty of Speech (Alogia)

   The person's amount of speech is greatly reduced and tends to be vague
   or repetitious. People showing signs of alogia may be slow in
   responding to questions or not respond at all.

Flat Presentation (Affective Flattening)

   This can be indicated by unchanging facial expressions, poor or no eye
   contact, reduced body language and decreased spontaneous movements. A
   person experiencing affective flattening may stare vacantly into space
   and speak in a flat, toneless voice. Flat affect refers to the outward
   expression of emotion and not the inner experience. this can be
   associated with a blunting of affect where people lose their
   sensitivity and ability to communicate emotion.

   However, the negative symptoms are difficult to assess because they
   commonly precede an acute episode of illness and commonly persist.

   It is also possible a person may have schizophrenia but be
   symptom-free. The symptoms may only emerge during an acute episode.

Cognitive symptoms

   Cognitive dysfunction is usually present in people with schizophrenia.
   A large body of research demonstrates schizophrenia is associated with
   cognitive impairments including problems with attention, concentration
   and memory. This is often associated with difficulties in understanding
   social relationships and understanding what the other people may be
   thinking. This is called social cognition.

Mood and Anxiety

   People with schizophrenia commonly become depressed and anxious at
   stages of their illness. depression can be a reaction to being
   psychotic or it can arise without any identifiable stressor. It can
   also contribute to people being amotivated, tired and angry.
   Unfortunately a small number of people with schizophrenia commit
   suicide and this is usually linked with feeling depressed.
   Anxiety can be a reaction to some of the positive symptoms of
   psychosis, part of the process of recovery or arise partly out of the
   socially isolated lives that many people with schizophrenia live. It
   can limit the ability of people to get out and engage with the
   community.

Are there any early warning signs?

   Yes. Usually before a person develops psychosis or schizophrenia, there
   is a period where 'something is not quite right'. During this time they
   may withdraw from their family and friends, have changes in their
   appetite and sleep patterns, find it difficult to concentrate and
   consequently have difficulties at school or work. The person may find
   this period very disturbing, even frightening, and may not want to talk
   about what is happening to them. This period is referred to in medical
   language as the ‘prodrome’.

   The prodrome is the period of disturbance or mild symptoms that occurs
   before the onset of an illness. The prodrome for schizophrenia can be
   anything from a month to several years. New research is suggesting that
   if early interventions are begun during this period, the prospects for
   recovery or a milder course of illness are increased.

   Some early warning signs and symptoms of psychosis are:
     * Changes in thinking: Difficulty in concentrating, poor memory,
       preoccupation with odd ideas, increased suspiciousness.
     * Changes in mood: Lack of emotional response, rapid mood changes,
       inappropriate moods.
     * Changes in behaviour: Odd or unusual behaviour.
     * Physical changes: Sleep disturbances or excessive sleep and loss of
       energy.
     * Social changes: Withdrawal and isolation from family and friends.
     * Changes in functioning: Decline in school or work performance.

   Remember: none of these symptoms by themselves indicate the presence of
   schizophrenia or another mental illness. But if they are severe,
   persistent or recurrent, professional help should be sought as soon as
   possible.

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Schizophrenia Causes

Possible causes of schizophrenia

   The causes of mental illness are linked to several factors which can be
   summarised into three main groups:

Biological factors

     * which arise from physiology, biochemistry, genetic make-up and
       physical constitution and the drugs that they might abuse

Psychological factors

     * including the person's upbringing, emotional experiences and
       interactions with people

Social factors

     * that are associated with the person's present life situation and
       sociocultural influences

Stress

     * Exposure to stressors, both environmental and social may overwhelm
       a person's coping ability and may as a result contribute to the
       onset of mental illness.

   No single cause of schizophrenia has been identified to date; there are
   most likely to be several contributing factors.  It is probable that
   there is an interaction between the consumer's biological
   vulnerability, stress or change in the environment and the consumer's
   ability to deal with these environmental factors in terms of their
   social skills and supports.  A less stressful environment may decrease
   the risk of onset in a person with a predisposition to schizophrenia or
   their relapse with another episode of the illness.

We know that schizophrenia is NOT caused by:

     * Domineering mothers or passive fathers
     * Poverty
     * Weakness of character or personality
     * Bad parenting
     * Sinful behaviour

Possible Contributing Factors:

   NB:  These are possible causal factors.  None, in their own right cause
   Schizophrenia.  They may, particularly in combination increase the risk
   of developing Schizophrenia.

Genetics

   Twin, family and adoptions studies suggest that genetic factors play an
   important role in the development of schizophrenia.  For example, the
   child of one parent with schizophrenia has about a 10 per cent chance
   of developing schizophrenia; if both parents have schizophrenia, the
   risk is increased to 40 per cent.  By comparison, the risk of
   schizophrenia in the general population is about one per cent.  The
   list below indicates the chances of developing schizophrenia during a
   life time:
     * General Population 1%
     * Brother or sister has schizophrenia 8-10%
     * One parent has schizophrenia 12-15%
     * paternal twin has schizophrenia 14%
     * Identical twin has schizophrenia 50%

   Schizophrenia has a large number of genes implicated in its cause (like
   other disease such as high blood pressure).   It is likely that no
   single gene “causes” schizophrenia.  Rather there is a large number of
   genes that increase the risk of getting schizophrenia.   These genes
   are important in different aspects of the way the brain develops and
   the way brain cells communicate to each other.  If an individual has a
   large number of these genes and is placed in a stressful environment
   this makes getting schizophrenia more likely.   Some of these genes
   also play a part in other severe psychiatric disease such as bipolar
   disorder.  This is one of the reasons that it can be difficult to
   diagnose these illnesses – they really do overlap.

Environment

   Possible environmental factors include obstetric complications, the
   mother’s exposure to influenza during pregnancy or starvation.  It has
   also been suggested that stress, trauma even migration can lead to the
   emergence of schizophrenia.  Family factors causing stress may affect
   the course of the illness but there is no convincing evidence that they
   have a causative role.

Neurodevelopmental Factors

   Schizophrenia appears to be a neurodevelopmental disorder.   That is
   the changes that cause the illness have been occurring from the
   earliest stages of development even in utero, and may continue to
   influence the development of the brain over the first 25 years of
   life.   This also means that we could influence or change the
   likelihood of getting the illness by identifying these factors and
   intervening early.   At present we are unable to do this
   satisfactorily.

Drug Misuse

   Substance misuse, including cannabis, is important in the development
   of schizophrenia in some people.  It is well established that substance
   misuse may precipitate or worsen the symptoms and interfere in the
   treatment of a person with schizophrenia.

Biochemical Factors

   The neurodevelopmental and genetic factors that we described above have
   an effect upon the development of the brain and the expression or
   amounts of many brain chemicals and neurotransmitters.
   Neurotransmitters (the substances that allow communication between
   nerve cells) have long been thought to be involved in the development
   of schizophrenia and many of the treatments for schizophrenia affect
   neurotransmitter function.  Although there are no definitive answers
   yet, this is a very active area of schizophrenia research.

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    3. 5 Ridiculous Myths You Probably Believe About Schizophrenia

5 Ridiculous Myths You Probably Believe About Schizophrenia

   By Amanda Mannen,  Amanda Davenport September 15, 2014 748,582 Views
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   [javascript]

   It's not that Hollywood doesn't portray mental illness -- movies love
   to include schizophrenic characters. It's just that they're usually
   serial killers. Unfortunately, since most people don't know anyone who
   has schizophrenia (at least, as far as they know), this means a lot of
   what you think about the disease is bullshit.

   Cracked has already told you a lot about mental illness myths, even
   telling you what movies get wrong about mental institutions. Well, we
   wanted to know what it was like to deal with schizophrenia on
   day-to-day basis, so we sat down with a woman who suffers from it. She
   says ...

#5. It's Not Multiple Personalities

         [javascript] Image Source/Digital Vision/Getty Images, Ryan
                        McVay/Photodisc/Getty Images

   The "voices" I hear are not too terribly different from the
   self-critical voices everyone has in their heads -- except I can hear
   them as clearly as if someone were standing right next to me. Oh, and
   they're assholes. There are two distinct male voices that I hear (that
   is, when I'm not on medication, or it decides to randomly stop working
   for a few days). One tells me to hurt myself or other people, and
   another calls me the sort of names you generally only hear in the
   comment section of any internet article about feminism.

          [javascript] Thomas Northcut/Digital Vision/Getty Images
   Except with him, I have clinical proof that his penis is non-existent.

   This gets into a lot of the confusion about what schizophrenia actually
   is -- a lot of old movies portrayed it as multiple personality disorder
   (or the clinical term, "disassociate identity disorder"). It's true
   that both often involve hallucinations and voices in your head, but
   Hollywood always writes these illnesses purely according to whatever
   will make the freakiest plot twist (sadly, I do not go to sleep and
   wake up as Brad Pitt, or even Edward Norton).

                        [javascript] 20th Century Fox
                    "I am Jack's inaccurate plot twist."

   The key difference is that for me, these voices never "take over" --
   I'm always conscious and in control of myself. They can make it hard to
   focus when real people are trying to talk to me, but otherwise, I'm
   more aware of my surroundings than what you'd expect based on what
   you've seen in movies. For example, there's a scene in Girl,
   Interrupted in which a schizophrenic character who'd been badly burned
   in the past suddenly realizes the extent of her disfigurement. That
   movie is based on a book based on a true story, so I don't know if that
   really happened, but I assure you, I know what I look like (fabulous,
   in case you were wondering).

   There are levels of severity, of course, just like with any illness --
   some sufferers are incapable of even basic communication, so it's
   literally impossible to know what they're experiencing. But neither
   version tends to show up in movies -- this kind of mental illness is
   usually an excuse to have the main character suddenly realize they were
   the killer all along, or to create an ambiguous Black Swan or American
   Psycho situation. But that brings me to a crucial point ...

#4. Voices Don't Make You Do Terrible Things

           [javascript] Darrin Klimek/Digital Vision/Getty Images

   Back when all of this first began, one of the voices started giving me
   graphic instructions to kill a particularly dickish teacher I had. This
   troubled me, to say the least. This was before I knew that everyone
   regarded me as a potential serial killer, so I went to the school
   counselor, who immediately flipped precisely all of her shit(s). That's
   an understandable reaction, but fear of that response is what keeps a
   lot of mentally ill folk from getting help -- it took a lot of pleading
   to convince her that I wasn't going to return to school with an Uzi. In
   fact, the only time I've come anywhere close to violence since was the
   result of a medication called Haldol that I was taking, which causes
   mood swings. Even then, it was pretty much limited to screaming at my
   husband to get off my back about the damn dishes.

                 [javascript] gemenacom/iStock/Getty Images
     Not that medication side effects are really necessary for "they're
                 soaking" to escalate into a shouting match.

   It doesn't help that, according to pop culture, lots of murderers get
   off with a "the voices made me do it!" insanity plea (in reality, that
   defense is rarely tried, and when it is, it usually doesn't work). And
   again, Hollywood doesn't help, creating characters like Donnie Darko,
   who are commonly mistaken for schizophrenic and who allow their voices
   to convince them to do things like damage school property and listen to
   anything Drew Barrymore has to say.

   I won't speak for all schizophrenics, but for the most part, we don't
   like our voices. Why would we ever do anything simply because those
   jerks told us to? Think back to your middle school bully -- how would
   you respond if he tried to talk you into committing horrible crimes,
   but couldn't threaten you bodily harm (because he himself had no body
   -- for the purposes of this example, your middle school bully is a
   ghost). You'd tell him to fuck off and leave you alone, or at least run
   away. Sadly, the latter is what many of us end up doing. I have a
   schizophrenic friend (our parties are great) who believes the voices
   are government agents who are out to get him, so he holes up in his
   house all day, trying to hide from them. I'm willing to bet they've
   told him to do a lot of things that, as detached from reality as he is,
   he has still never even considered.

          [javascript] Medioimages/Photodisc/Photodisc/Getty Images
           "Fuck you, G-Men. Pepsi on cereal? That's just stupid."

   And his case is typical -- the violent crime rate is no higher among
   schizophrenics than it is in the rest of the population. What they are
   more likely to do is simply withdraw from society -- many become
   depressed and/or have problems with substance abuse. A sad, pitiful
   little man hiding in his house all day is probably a far cry from the
   raving psychopath you're imagining, and that's a big reason why ...

#3. You Can't Necessarily Tell Who Has It

             [javascript] Comstock Images/Stockbyte/Getty Images

   That's right -- we could be among you right now and you might never
   even know it. The one time Hollywood did schizophrenia reasonably well
   was when they took a true story and proceeded to make up a lot of
   stuff, with a little movie you might have heard of called A Beautiful
   Mind. What's accurate is how, through much of the film, John Nash is
   pretty damn functional. He gets married, he graduates from Princeton
   ... shit, those are things that most "normal" people can't even manage.
   For a long time, nobody suspects there's anything wrong with him.

   That's because schizophrenics aren't necessarily drooling, twitching
   blobs of humanity -- it can actually be really hard to tell when
   they're having an episode. A lot of the symptoms of paranoia can be
   mistaken for simple social awkwardness. The only difference is that I
   also happen to think cameras are following me everywhere, which I'm
   probably not going to tell you about, and if I did, you would probably
   think I'm merely stoned, because people absolutely have.

              [javascript] Jupiterimages/Stockbyte/Getty Images
     Switch "probably" to "totally" if you're within 50 feet of any Taco
                                    Bell.

   For example, one of my problems is that if I make eye contact with a
   stranger in public, I'm suddenly convinced that they know what I'm
   thinking -- they can see it on my face somehow, and make no mistake,
   they are judging me. I have a real problem with eye contact in general
   -- when to make it, when to look away, oh god I've been looking away
   for too long, they think I'm weird, just look, dammit. Sound familiar?

   It's hard for non-experts to distinguish. The only person who ever
   caught on was a psychology professor who noticed my eyes darting around
   the room over the course of a semester. One day, he asked me to stay
   after class. Expecting to be chided for not paying attention and
   preparing for an uncomfortable chit chat, I was instead asked "Did you
   know you have schizophrenia?" (I did, so it was all good). Even my own
   family doctor was surprised to learn that I had schizophrenia, adding
   "You look so normal," apparently because I wasn't currently throwing
   feces at her.

             [javascript] Comstock Images/Stockbyte/Getty Images
    Of course, when you've got a blank check to fling poop, it's awfully
                  tempting to cash it in those situations.

   Another thing Russell Crowe and crew got right is that while
   schizophrenia isn't curable, it is treatable. But ...

                               [316922_v1.jpg]
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   Schizophrenia

Schizophrenia Myths and Facts

     * By Connie Brichford | Medically reviewed by Kevin O. Hwang, MD, MPH

Much of what is commonly believed about schizophrenia is wrong.

Related

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   Schizophrenia is an illness that affects more than 2 million Americans.
   And while the condition ranks high in the public's consciousness, our
   collective understanding of it is low. There are a number of myths
   about people with schizophrenia, generally based on the underlying
   false assumption that the experiences of schizophrenia are the same
   from person to person.

   Ken Duckworth, MD, medical director for the National Alliance on Mental
   Illness (NAMI), says it's hard to generalize about people with
   schizophrenia: "It's extremely complicated. No two people with
   schizophrenia are the same."

   Schizophrenia: Myths and Realities
   Myth: People with schizophrenia have "split personalities." This is the
   perhaps the most pervasive myth about the disease, and it is
   perpetuated in the news, movies, and television shows.

   Reality: This is a symptom of a different illness entirely. "Split
   personalities" or "multiple personalities" are not a symptom of
   schizophrenia; in fact, these symptoms indicate a different mental
   illness called Dissociative Identity Disorder.
     * This misperception may originate from the word "schizophrenic"
       which describes the "split mind" that people with schizophrenia
       seem to exhibit. "Split mind refers to the mismatch between thought
       and feeling. A person may be telling a very sad or distressing
       story while smiling, or may be afraid of things that are completely
       mundane," Duckworth says.
     * A person with schizophrenia may react inappropriately to
       situations, but that does not mean that he or she has multiple
       personalities.

   Myth: People with schizophrenia are dangerous. This is also perpetuated
   in the media and in movies and television shows.

   Reality: Some people with schizophrenia may be dangerous, but most are
   not. Some people with schizophrenia may be prone to violent outbursts,
   but the vast majority of people with this disorder tend to withdraw
   from society when they become symptomatic.

   Duckworth says, "Again, it's complicated. The truth is that most people
   are completely benign. But, another truth: There is a small subset of
   the population that can be dangerous, usually people who are also using
   drugs or alcohol. And, around 10 percent kill themselves, which is
   inherently violent."
     * There is evidence that suggests that psychoses can and do fuel
       violent behaviors, but the actual numbers don't justify a fear of
       all people with schizophrenia. People with psychotic symptoms
       account for only 5 percent of violent crime, and some estimate the
       number closer to 1 percent.
     * In fact, people living with schizophrenia are in greater danger of
       being victimized by both violent and non-violent crimes than the
       general population.

   Myth: People with schizophrenia will never get better. The public
   perception is that people with schizophrenia are doomed.

   Reality: Many people recover. "People do pretty well over time.
   Symptoms sometimes lose their intensity," Duckworth says. Most people
   can find relief from symptoms, and as many as half of people with
   schizophrenia can experience significant or even complete recovery with
   treatment.

   The Media's Role in Perpetuating Schizophrenia Stereotypes
   The media are partially responsible for how we perceive schizophrenia —
   as Duckworth says, "American media has contributed to mass confusion
   about it." In a 2003 survey of American newspapers, Duckworth and his
   colleagues found that in 28 percent of articles in which the words
   "schizophrenia" and "schizophrenic" appeared, the words did not refer
   to the illness, but rather were invoked as metaphor. "Schizophrenic"
   was used to describe the erratic behavior of the weather, the stock
   market, and even the New England Patriots' football team.

   However, newer, more sensitive and complex portrayals of schizophrenia
   in the media can help us change our understanding of this disease.
   There may be a trend toward moving away from using "schizophrenic" to
   mean "crazy" or "bad." A 2008 segment of MTV's True Life documentary
   series called "I Have Schizophrenia" allowed young people with the
   disorder to share their experiences in their own words. And the
   Oscar-winning film A Beautiful Mind portrayed the life of mathematician
   John Nash, who lived and worked with schizophrenia. More realistic and
   nuanced portrayals like these give mental illness advocates reason to
   be optimistic.

   Last Updated: 3/9/2012

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Myths about Schizophrenia

   Myths about Schizophrenia

   Although schizophrenia was first described over a hundred years ago and
   we have been studying it closely ever since, we still do not fully
   understand it. Consequently schizophrenia is surrounded by more than
   its fair share of myths about its causes and features. Here are a few
   of them:

   1. People with schizophrenia are always dangerous

   It is one of the commonest and most enduring myths around schizophrenia
   that all people suffering from this condition become dangerous. Whilst
   the myth is not founded, it is the case that people living with
   schizophrenia are more at risk of dangerous behaviour such as suicide
   or violence when they are poorly.

   Studies have found that between 10 and 23% of people who are
   experiencing acute psychosis may exhibit violent behaviour and this
   probably accounts for around 30 homicides out of a total of about 600
   per year in the UK.^1,2 Whether this is proportionately more than the
   general population, taking into account the young age group of
   schizophrenics, remains a matter of some debate.

   Schizophrenia is predominantly an illness of young people: 70% of all
   cases being diagnosed between the ages of 16 and 25. It also happens
   that most violent crime is carried out by young people. So although the
   proportion of homicides committed by people with schizophrenia is
   greater than the incidence of schizophrenia in the population as a
   whole, the statistics are skewed by the age of the attacker and it is
   by no means clear that people with schizophrenia are more likely to
   commit violent crimes than people who do not have the condition.
   Suicide by people with schizophrenia account for more deaths in the UK
   than traffic collisions

   Suicide by people with schizophrenia account for more deaths in the UK
   than traffic collisions

   Thankfully homicide remains a comparatively small part of the overall
   mortality rate for this condition. The much larger part is the problem
   of suicide in schizophrenia which accounts for over 2,000 deaths a year
   in the UK. (More deaths in fact than are caused by road accidents).
   This tragically high figure represents about one in 10 of those
   diagnosed.

   With these figures in mind it is safe to conclude that most people with
   schizophrenia will never exhibit dangerous behaviour of any kind and
   that when they do they are much more likely to harm themselves than to
   harm other people.

   More about this subject is available in our advice sheet on
   dangerousness.

   2. Schizophrenia is very rare

   Schizophrenia affects people from all walks of life and social
   backgrounds. It exists in all races and societies and strikes people in
   all age groups. The average incidence is about one percent. That is to
   say that about one person in every 100 will experience an episode of
   the illness at some time during their life.^13 Today, about 280,000
   people are being treated for the condition by the NHS in the UK. So the
   condition is much more common than many people think.

   3. Schizophrenia is caused by a bad upbringing

   In particular bad mothering was thought to cause schizophrenia in
   offspring for much of the 20th century. This belief found widespread
   support from the followers of Sigmund Freud’s psychoanalytic theories
   but it is worth noting that Freud himself believed that schizophrenia
   probably had physical origins and refused to treat it by
   psychoanalysis.

   The various psychoanalytic theories reflected the belief that traumatic
   experiences in early childhood, often forgotten and unacknowledged,
   affected the development of the child’s “ego”. Later, so the theory
   goes, under the stress of adolescence the ego disintegrates and the
   person regresses to an infantile condition.^3

   Freida Fromm-Reichman the German psychoanalyst who saw the family
   upbringing as being the cause of schizophrenia

   Freida Fromm-Reichman the German psychoanalyst who saw the family
   upbringing as being the cause of schizophrenia
   In 1948 Fromm and Reichman took this a stage further and came up with
   the concept of schizophrenogenic families. That is a family environment
   that gives rise to schizophrenia in the offspring. In the 1960s and
   1970s the growth of the anti-psychiatry movement gave the belief added
   impetus.

   In the past such family theories have been widespread amongst
   professionals who have seen the person’s family as being part of the
   problem rather than as an important factor in the overall therapeutic
   solution. Families were often denied information about their loved
   one’s condition and people suffering from psychotic episodes were
   sometimes removed from their supportive family home to live in seedy
   bedsits where they were often unable to cope with the pressures of
   everyday life and were targetted by predatory or anti social
   neighbours. The families were then stigmatised as being the cause of
   their loved ones problems. The theories which gave rise to these abuses
   were often not tested by evidence and thankfully we have left them
   behind. However it is still possible to occasionally encounter older
   professionals who stubbornly cling to these beliefs.

   3. Schizophrenia is caused by abuse during childhood

   With society’s growing awareness of the issue of child abuse during the
   1990’s and into the 21st century came the hypothesis that experiences
   of abuse during childhood and adolescence caused schizophrenia later in
   life. Whilst such experiences of abuse are undoubtedly psychologically
   damaging there is currently no research evidence of a link with
   schizophrenia.

   In fact the theory that trauma in earlier life can cause schizophrenia
   later is not new and has been around since the nineteenth century. It
   has been the subject of a good deal of research particularly during the
   latter half of the twentieth century. The weight of evidence suggests
   that the link does not exist.^4 This is perfectly logical, after all if
   childhood trauma did cause schizophrenia later in life we would expect
   to see epidemics of schizophrenia amongst groups like concentration
   camp survivors or the victims of the blitz and that simply did not
   happen.

   4. Schizophrenia is just a sane reaction to an insane world

   British psychoanalyst R.D. Laing who became the doyen of the
   anti-psychiatry movement of the 1960’s.

   British psychoanalyst R.D. Laing who became the doyen of the
   anti-psychiatry movement of the 1960’s.
   This bizarre theory was the brainchild of British psychoanalyst Ronald
   Laing who became the doyen of the anti-psychiatry movement of the
   1960’s. The theory grew out of the idea that often the person diagnosed
   with schizophrenia was the scapegoat for the social turbulence of a
   dysfunctional family environment and may in fact paradoxically be the
   sanest member of the family group. Although this idea gained a great
   deal of popularity, in later life Laing himself became increasingly
   disillusioned with it.^5

   5. Schizophrenia doesn’t exist

   Dr Thomas Ssasz, American psychoanalyst who believed that schizophrenia
   was a myth.

   Dr Thomas Ssasz, American psychoanalyst who believed that schizophrenia
   was a myth.
   In the middle of the 20th century there were those in the
   anti-psychiatry movement who proposed that schizophrenia didn’t exist
   at all and that it was simply an invention of the psychiatry
   profession. Dr Thomas Szasz a psychoanalyst in the USA became well
   known for this theory. He called schizophrenia a fake disease and the
   sacred symbol of psychiatry.^6 Perhaps if he had ever had to endure a
   day living with the voices he would not have resorted to this potty
   notion.

   6. Anti-psychotic medication is just a chemical cosh

   Although the early anti-psychotics (called typical) did have sedating
   effects and in high doses could cause people on them to become slow and
   lethargic, anti-psychotics are not used principally for that effect but
   for the benefit that they bring in helping to alleviate the positive
   symptoms of schizophrenia such as the delusions and hallucinations.^8

   Chlorpromazine (Largactil) the first of the antipsychotic drugs

   Chlorpromazine (Largactil) the first of the antipsychotic drugs
   Unfortunately these early antipsychotics were often misleadingly called
   “major tranquillisers”, a term which has stuck to this day and
   unfortunately leads to much confusion about their role. When the first
   psychiatrists to study their use, the Frenchmen Jean Delay and Paul
   Deniker, first used the antipsychotic chlorpromazine in psychiatry, it
   was precisely the fact that the drug had a more precise effect in
   calming their patients than the other tranquillisers in use at the
   time, that attracted them to it. It was later found that this effect
   was not due to sedation but because the chlorpromazine acted directly
   to reduce the hallucinations and delusions. ^14

   Before the advent of the antipsychotic drugs most people with a
   diagnosis of schizophrenia were confined in one of the large asylums,
   like this one on the edge of Dartmoor, sometimes for many years

   Before the advent of the antipsychotic drugs most people with a
   diagnosis of schizophrenia were confined in one of the large asylums,
   like this one on the edge of Dartmoor, sometimes for many years
   The beneficial humanitarian affect of the antipsychotic drugs should
   not be underestimated. Before the introduction of these drugs in the UK
   about 70% of people with a diagnosis of schizophrenia were continuously
   confined in mental hospitals: today it is only about 5%. ^14

   The more modern atypical forms of anti-psychotics have less sedating
   effect and are preferred nowadays over the older type of typical ones.
   The guidance given by NICE to NHS doctors working in the UK is that
   newer atypicals should be used in preference to the older typicals in
   new cases of schizophrenia, where the person is acutely ill or where
   side effects are being experienced from the use of an older typical
   drug. ^7

   7. Schizophrenia is a split personality

   One of the popular myths about schizophrenia is that it involves a
   split personality: a Jekyl and Hyde personality. This is not the case.
   Although the term schizophrenia literally means a split mind and was
   coined by Dr Eugen Bleuler, a Swiss psychiatrist, the condition does
   not really manifest itself in that way. It would be more accurate to
   regard the condition as one in which the mind becomes confused and
   disordered. ^8

   8. People with schizophrenia will be severely disabled for life

   Whilst in theory this shouldn’t be so, in practice there is, at least
   in the UK , some truth in this.

   Our experience of schizophrenia from over a century of study tells us
   reliably that about 25% of people who experience an episode of
   psychosis will go on to recover completely and have no further problems
   in their life. We also know now that given proper treatment a large
   proportion of the remainder will be substantially recovered and will go
   on to achieve a high level of functioning. ^9

   Yet in the UK today only about 13% of people with a diagnosis of
   schizophrenia are in any kind of work.^10 So clearly there is an
   enormous disparity between the clinical outcomes and the social
   outcomes. Why is this so? Clearly this is an area that needs much
   greater study, in particular in view of the fact that the number of
   people with schizophrenia in work at the moment in the UK is actually
   declining.

   There may be a number of factors at work here. Some would blame a
   benefits culture that gives people “on the sick” very few incentives to
   seek work. Others would blame the stigma that people with schizophrenia
   face from employers when looking for work.

   Another factor may be arguably that many of those professionals caring
   for people with schizophrenia see permanent unemployment as being the
   natural lifestyle for people with a diagnosis of schizophrenia and have
   little ambition for the people in their care. Others may be loathe to
   put their patients under the stress of looking for work in an
   increasingly competitive jobs market for fear of provoking a relapse in
   their condition.

   Whatever the reason we believe that this issue is an area that should
   become absolutely key in our study of this condition and development of
   our treatment models in future years. Many thousands of bright and
   intelligent people who could be making a creative contribution to the
   wellbeing and prosperity of our society are currently consigned to a
   life of low achievement because of these issues. After all other
   countries, notably Italy and Cuba, have much better outcomes in terms
   of employment for people living with schizophrenia.

   This is not however a problem unique to people with schizophrenia. Most
   people with physical disabilities also experience other people in
   society who wrongly assume that they are incapable of achieving.

   9. If it’s genetic, then we can do nothing about it

   Research has shown that there are a number of factors that can
   contribute to a successful recovery including reducing family stress,
   useful occupation, talking therapy and reducing stress from financial
   problems.^11

   We also know that early diagnosis and treatment with antipsychotic
   medication will improve prospects of a good recovery enormously. ^12
   Another factor that is crucial to a successful recovery is having a
   good recovery strategy. Living one day at a time may be an appropriate
   strategy for coping with a crisis but later it is necessary to start
   identifying goals in your life and plotting a path towards achieving
   those goals.^8

   Having a genetic predisposition to suffering with schizophrenia in no
   way guarantees that you will suffer from it and even if you do there is
   no need for an episode of schizophrenia to necessarily be a life
   sentence.

   10. If it’s genetic, then let’s get rid of the bad genes

   Hartheim Euthanasia Centre in Germany where over 18,000 people with
   disabilities including people with schizophrenia were killed during the
   Third Reich.

   Hartheim Euthanasia Centre in Germany where over 18,000 people with
   disabilities including people with schizophrenia were killed during the
   Third Reich.
   This was of course exactly what the Germans tried to achieve during the
   Third Reich. Then people with schizophrenia were simply killed by the
   use of gas chambers in the hope that the defective genes could be
   eliminated from the race.

   Apart from the humanitarian and ethical considerations, this approach
   has three serious flaws. First of all it is not clear whether the
   genetic factor consists of one gene acting alone or several acting in
   combination so the process is almost certainly more complicated than
   may appear at first sight.

   Secondly, as we have said before, simply having the right genes for
   schizophrenia in no way guarantees that you will suffer from it
   yourself. For instance, if you are an identical twin with a sibling who
   has schizophrenia you only have a 50% chance of suffering from it
   yourself even though you share all the same genes.

   And lastly, genes with adverse affects on the species tend to be bred
   out of the gene pool during the natural process of evolution and the
   fact that the schizophrenia gene has survived this long implies that it
   must impart beneficial traits to the species in addition to the adverse
   one. Eliminating the schizophrenia gene would therefore almost
   certainly cause as much harm to the gene pool as benefit. There is
   already some prima facie evidence for this. People with schizophrenia
   are thought to have a reduced incidence of certain physical illnesses
   such as rheumatoid arthritis and some cancers.

   It is also worth remembering that during most of the twentieth century,
   the practice both in the UK and USA was to confine people with
   schizophrenia in one of the large mental asylums where they had very
   little opportunity to reproduce. Yet during that time the incidence of
   schizophrenia in those countries actually increased slightly. So
   clearly the genetic issue is more complicated than we may at first
   infer.

   Conclusion

   Sadly schizophrenia attracts many ideas and beliefs that just don’t
   stand up to the evidence. Over the last hundred years we have
   accumulated an enormous amount of research evidence to guide the way
   that we treat and respond to schizophrenia. However it still receives
   less research funding than other physical conditions such as heart
   disease or cancer. If we are to finally blow away all of these myths
   and the others that will surely follow in their path we need
   governments to fund much more research into this life changing
   condition.

   References

   1. Fazel S, Reinharth J, Serper M, Singh J, 2011, Structured Assessment
   of Violence Risk in Schizophrenia and Other Psychiatric Disorders: A
   Systematic Review of the Validity, Reliability, and Item Content of 10
   Available Instruments, Published in Schizophrenia Bulletin September
   2011.

   2. Rollin H, 1980, Schizophrenia at Home, Published in Coping with
   Schizophrenia, Burnett Books. P23.

   3. Howe G, 1986, Schizophrenia A Fresh Approach, David & Charles, P26.

   4. Fuller Torrey E, 2001, Surviving Schizophrenia, Quill, P166.

   5. Fuller Torrey E, 2001, Surviving Schizophrenia, Quill, P171.

   6. Fuller Torrey E, 2001, Surviving Schizophrenia, Quill, P171.

   7. Reveley A, 2006, Your Guide to Schizophrenia, Hodder Arnold, P74.

   8. Author’s personal experiences.

   9. Fuller Torrey E, 2001, Surviving Schizophrenia, Quill, P130.

   10. Warner R, 2000, The Environment of Schizophrenia, Brunner
   Routledge, P73.

   11. Jones S and Hayward P, 2004, Coping with Schizophrenia, One World,
   P45.

   12. Howe G, 1991, The Reality of Schizophrenia, Faber and Faber, P61.

   13. Reveley A, 2006, Your Guide to Schizophrenia, Hodder Arnold, P13.

   14. Cutting J and Charlish A, 1995, Schizophrenia, Thorsons, P124.
   Download PDF Version of This Page

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