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ABSTRACT: Chronically institutionalized patients with schizophrenia have been reported to manifest cognitive and functional decline. Previous studies were limited by the fact that current environment could not be separated from lifetime illness course. The present study examined older outpatients who varied in their lifetime history of long-term psychiatric inpatient stay.
Community-dwelling patients with schizophrenia (n = 111) and healthy comparison subjects (n = 76) were followed up to 45 months and examined two or more times with a neuropsychological battery and performance-based measures of everyday living skills (University of California San Diego Performance-Based Skills Assessment Battery [UPSA]) and social competence. A mixed-effects model repeated-measures method was used to examine changes.
There was a significant effect of institutional stay on the course of the UPSA. When the schizophrenia patients who completed all three assessments were divided on the basis of length of institutional stay and compared with healthy comparison subjects, patients with longer stays worsened on the UPSA and social competence, while patients with shorter stays improved. For neuropsychological performance, both patient samples worsened slightly, while the healthy comparison group manifested a practice effect. Reliable change index analyses showed that worsening on the UPSA for longer stay patients was definitely nonrandom.
Lifetime history of institutional stay was associated with worsening on measures of social and everyday living skills. Neuropsychological performance in schizophrenia did not evidence the practice effect seen in the healthy comparison sample. These data suggest that schizophrenia patients with a history of long institutional stay may worsen even if they are no longer institutionalized.
Biological psychiatry 03/2010; 67(10):933-9. · 8.93 Impact Factor
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American Journal of Public Health 03/2010; 100(5):772-3; author reply 773. · 3.93 Impact Factor
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ABSTRACT: Anecdotal and biographical reports suggest that bipolar disorder may be associated with high IQ or creativity, but evidence for any such connection is weak.
To investigate possible associations between scholastic achievement and later bipolar disorder, using prospective data, in a whole-population cohort study.
Using individual school grades from all individuals finishing compulsory schooling in Sweden between 1988 and 1997, we tested associations between scholastic achievement at age 15-16 and hospital admission for psychosis between ages 17 and 31, adjusting for potential confounders.
Individuals with excellent school performance had a nearly fourfold increased risk of later bipolar disorder compared with those with average grades (hazard ratio HR = 3.79, 95% CI 2.11-6.82). This association appeared to be confined to males. Students with the poorest grades were also at moderately increased risk of bipolar disorder (HR = 1.86, 95% CI 1.06-3.28).
These findings provide support for the hypothesis that exceptional intellectual ability is associated with bipolar disorder.
The British journal of psychiatry: the journal of mental science 02/2010; 196(2):109-15. · 6.62 Impact Factor
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ABSTRACT: Cognitive processing inefficiency, often measured using digit symbol coding tasks, is a putative vulnerability marker for schizophrenia and a reliable indicator of illness severity and functional outcome. Indeed, performance on the digit symbol coding task may be the most severe neuropsychological deficit patients with schizophrenia display at the group level. Yet, little is known about the contributions of simpler cognitive processes to coding performance in schizophrenia (e.g. decision making, visual scanning, relational memory, motor ability). We developed an experimental behavioral task, based on a computerized digit symbol coding task, which allows the manipulation of demands placed on visual scanning efficiency and relational memory while holding decisional and motor requirements constant. Although patients (n=85) were impaired on all aspects of the task when compared to demographically matched healthy comparison subjects (n=30), they showed a particularly striking failure to benefit from the presence of predictable target information. These findings are consistent with predicted impairments in cognitive processing speed due to schizophrenia patients' well-known memory impairment, suggesting that this mnemonic deficit may have consequences for critical aspects of information processing that are traditionally considered quite separate from the memory domain. Future investigation into the mechanisms underlying the wide-ranging consequences of mnemonic deficits in schizophrenia should provide additional insight.
Biological Psychiatry 02/2010; 118(1-3):6-11. · 8.28 Impact Factor
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Sebastian Lundström,
Claire M A Haworth,
Eva Carlström,
Christopher Gillberg,
Jonathan Mill,
Maria Råstam,
Christina M Hultman,
Angelica Ronald,
Henrik Anckarsäter,
Robert Plomin,
Paul Lichtenstein, Abraham Reichenberg
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ABSTRACT: Despite extensive efforts, the causes of autism remain unknown. Advancing paternal age has been associated with various neurodevelopmental disorders. We aim to investigate three unresolved questions: (a) What is the association between paternal age and autism spectrum disorders (ASD)?; (b) Does paternal age moderate the genetic and environmental etiological factors for ASD? (c) Does paternal age affect normal variation in autistic-like traits?
Two nationally representative twin studies from Sweden (n = 11, 122, assessed at age 9 or 12) and the UK (n = 13, 524, assessed at age 9) were used. Categorical and continuous measures of ASD, autistic-like traits and autistic similarity were calculated and compared over paternal age categories.
Both cohorts showed a strong association between paternal age and the risk for ASD. A U-shaped risk association could be discerned since the offspring of both the youngest and oldest fathers showed an elevation in the risk for ASD. Autistic similarity increased with advancing paternal age in both monozygotic and dizygotic twins. Both cohorts showed significantly higher autistic-like traits in the offspring of the youngest and oldest fathers.
Phenomena associated with paternal age are clearly involved in the trajectories leading to autistic-like traits and ASD. Mechanisms influencing the trajectories might differ between older and younger fathers. Molecular genetic studies are now needed in order to further understand the association between paternal age and ASD, as well as normal variation in social, language, and repetitive behaviors in the general population.
Journal of Child Psychology and Psychiatry 02/2010; 51(7):850-6. · 4.28 Impact Factor
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Jolanta Zanelli, Abraham Reichenberg,
Kevin Morgan,
Paul Fearon,
Eugenia Kravariti,
Paola Dazzan,
Craig Morgan,
Caroline Zanelli,
Arsime Demjaha,
Peter B Jones,
Gillian A Doody,
Shitij Kapur,
Robin M Murray
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ABSTRACT: Overwhelming evidence suggests that compromised neuropsychological function is frequently observed in schizophrenia. Neurocognitive dysfunction has often been reported in other psychotic disorders, although there are inconsistencies in the literature. In the context of four distinct diagnostic groups, the authors compared neuropsychological performance among patients experiencing their first psychotic episode.
Data were derived from a population-based, case-control study of patients with first-episode psychosis. A neuropsychological test battery was administered to patients with a diagnosis of schizophrenia (N=65), bipolar disorder or mania (N=37), depressive psychosis (N=39), or other psychotic disorders (N=46) following index presentation, as well as to healthy comparison subjects (N=177). The presence of specific and generalized cognitive deficits was examined.
The schizophrenia group presented widespread neuropsychological impairments and performed significantly worse than healthy comparison subjects on most neuropsychological measures. Patients with other psychotic disorders and depressive psychosis also demonstrated widespread impairments. Deficits in patients with bipolar disorder or mania were less pervasive but evident in performance scores on verbal memory and fluency tests. Differences between the four patient groups and healthy comparison subjects and among the patient groups were attenuated after controlling for differences in general cognitive ability (IQ).
Early in their course, cognitive deficits are present in all psychotic disorders but are most severe and pervasive in schizophrenia and least pervasive in bipolar disorder and mania.
American Journal of Psychiatry 12/2009; 167(1):78-85. · 12.54 Impact Factor
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ABSTRACT: Cognitive decline has been described in elderly patients with schizophrenia, but the underlying pathology remains unknown. Some studies report increases in plaques and neurofibrillary tangles, but there is no evidence for an increased risk for Alzheimer's disease (AD) in elderly schizophrenics. Models of a decreased cerebral reserve suggest that increases in AD-related neuropathology below the threshold for a neuropathological diagnosis could be related to dementia severity in elderly schizophrenia patients. We tested this hypothesis in 110 autopsy specimens of schizophrenia patients, without a neuropathological diagnosis of AD or other neurodegenerative disorders. Furthermore, we assessed the effects of apolipoprotein E (ApoE) status, a known genetic risk factor for AD. Measures of density of neuritic plaques were obtained in five cortical regions, and the degree of hippocampal neurofibrillary tangles was rated. Dementia severity was measured prior to postmortem using the Clinical Dementia Rating (CDR) scale. multivariate analyses of variance were conducted with the factors dementia severity, by ApoE4 carrier status. Hippocampal neurofibrillary tangles correlated with increased dementia severity (p<.05). Neuritic plaque density increased with greater dementia severity (p<.005), and ApoE4 carrier status (p<.005), and these differences were magnified by the ApoE4 carrier status (p<.01). Even below the threshold for a neuropathological diagnosis of AD, neuritic plaques and hippocampal neurofibrillary tangles are associated with dementia severity in schizophrenia patients, even more so in the presence of genetic risk factors, suggesting that a decreased cerebral reserve in elderly schizophrenics may increase susceptibility for dementia.
Biological Psychiatry 11/2009; 116(1):90-6. · 8.28 Impact Factor
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Eugenia Kravariti,
Kevin Morgan,
Paul Fearon,
Jolanta W Zanelli,
Julia M Lappin,
Paola Dazzan,
Craig Morgan,
Gillian A Doody,
Glynn Harrison,
Peter B Jones,
Robin M Murray, Abraham Reichenberg
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ABSTRACT: Identifying neurocognitive subtypes in schizophrenia may help establish neurobiologically meaningful subtypes of the disorder, but is frequently confounded by differences in intellectual function between individuals with schizophrenia and controls.
To examine neuropsychological performance in individuals with epidemiologically based, first-onset schizophrenia and intellectually matched controls.
Using standard IQ and reading tests, we examined the proportions of 101 people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder and 317 community controls, falling into three a priori defined intellectual categories: 'stable good', 'deteriorated poor' and 'stable poor'. Neuropsychological function was compared between intellectually matched participants with schizophrenia and control subgroups.
Multiple deficits in executive function, processing speed and verbal memory, but not visual/spatial perception/memory, were detected in all participant groups with schizophrenia compared with controls. The average effect size across the affected domains ranged from small to medium to large in the stable good, deteriorated poor and stable poor subgroups of participants with schizophrenia, respectively.
Compared with intellectually matched controls, people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder show multiple deficits in executive function, processing speed and verbal memory.
The British journal of psychiatry: the journal of mental science 10/2009; 195(4):336-45. · 6.62 Impact Factor
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ABSTRACT: There is growing interest in the role of single genes in cognitive functions. Association studies are the most commonly applied method in this field. This method assumes that the genetic information affecting cognitive processes is "static" and unchanging. However, there is accumulating evidence that dynamic genomic and epigenetic alterations can modulate complex cognitive processes, and influence susceptibility to disorders associated with impaired cognitive functioning.
We present an overview of genomic and epigenetic mechanisms, and discuss the cognitive and psychiatric consequences of genomic and genetic abnormalities.
Genomic and epigenetic changes can affect complex cognitive functions, including learning and memory and are causative in several developmental and psychiatric disorders effecting language, social functioning and IQ.
Genomic and epigenetic disorders are "experiments of nature" that offer unique and valuable insight in to the physiology of general and specific cognitive functions.
Cognitive Neuropsychiatry 08/2009; 14(4-5):377-90.
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ABSTRACT: The male-to-female (M:F) ratio for autism spectrum disorders (ASD), typically about 4:1, appears to decrease with increasing paternal age, but this relationship has not been systematically tested. With 393 ASD cases from families with two or more ASD cases, we categorized paternal age into five age groups (<30, 30-34, 35-39, 40-44, 45+) and found that the M:F ratio was significantly decreased with increasing paternal age groups and remained so after also adjusting for maternal age. No significant relationship between maternal age group and the M:F ratio was observed. This study suggests that the M:F ratio is reduced with increasing paternal age consistent with de novo genetic or genomic anomalies arising more frequently as men age and then conceive children.
Journal of Autism and Childhood Schizophrenia 06/2009; 39(10):1487-92. · 3.06 Impact Factor
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Eugenia Kravariti, Abraham Reichenberg,
Kevin Morgan,
Paola Dazzan,
Craig Morgan,
Jolanta W Zanelli,
Julia M Lappin,
Gillian A Doody,
Glynn Harrison,
Peter B Jones,
Robin M Murray,
Paul Fearon
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ABSTRACT: Neurocognitive dysfunction is likely to represent a trait characteristic of bipolar disorder, but the extent to which it comprises 'core' deficits as opposed to those secondary to longstanding illness or intellectual decline is unclear. We investigated neuropsychological performance in an epidemiologically derived sample of patients with a first affective episode with psychotic symptoms and a positive history of mania, compared to community controls.
Using a nested case-control, population-based study, measures of episodic and working memory, executive function, processing speed, and visual-spatial perception were compared between 35 patients with a first affective episode with psychotic symptoms and a positive history of mania, and 274 community controls, as well as a subgroup of 105 controls matched on current IQ ('good' versus 'poor') and IQ trajectory ('stable', 'declined', or 'improved') with the patients (three controls per case).
Compared to the extended control sample, probands showed a suggestive deficit in short-term verbal recall, and a significant deficit in semantic fluency. Only the latter was detectable in the comparison with the IQ-matched controls. All other neurocognitive domains showed intact performance or nonsignificant deficits of small effect sizes compared to both control groups. Semantic fluency showed no association with symptoms or duration of untreated illness.
Patients with a first affective episode with psychotic symptoms and a positive history of mania show an isolated, selective deficit in semantic verbal fluency, against a background of generally preserved neurocognitive function. This pattern seems to contrast with the more widespread neuropsychological dysfunction seen in schizophrenia.
Bipolar Disorders 06/2009; 11(3):323-9. · 5.29 Impact Factor
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ABSTRACT: Factor analysis of symptom structure has proven to be a valuable tool to identify dimensions of symptoms in various psychiatric conditions. This study used exploratory and confirmatory factor analysis to examine symptom structures in depressed inpatients with unipolar (n = 718) or bipolar (n = 134) spectrum disorders who were rated at admission with a psychiatric rating scale. No differences in overall symptom severity on the scale were found in the 2 samples, although different factor structures were detected with exploratory analyses. These models were modified in a confirmatory modeling procedure to improve their fit to the data, resulting in models with good, but not perfect, fits. For people with bipolar disorders, a 5-factor model fit best, with depression loading with anxiety symptoms and in people with unipolar disorders, a 4-factor model with depression loading with vegetative symptoms was found. Our results suggest that similar levels of symptom severity may have different underpinnings in the 2 groups and suggest that more comparative studies of symptoms in these 2 conditions may be useful.
The Journal of nervous and mental disease 04/2009; 197(3):161-5. · 1.77 Impact Factor
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ABSTRACT: Clinical heterogeneity of autism likely hinders efforts to find genes associated with this complex psychiatric disorder. Some studies have produced promising results by restricting the sample according to the expression of specific familial factors or components of autism. Previous factor analyses of the restricted, repetitive behaviors and interest (RRBI) domain of autism have consistently identified a two-factor model that explains a moderate amount of variance. The identification of additional factors may explain more variance in the RRBI domain and provide an additional component of autism that may help in the identification of underlying genetic association.
We conducted factor analyses of RRBI symptoms with a sample that included verbal subjects meeting full criteria for autism aged 5 to 22 years (n = 245). Among affected sibling pairs (n = 126) we examined the familial aggregation of the identified factors. We also examined the associations of the factors with autism-related personality traits in fathers and mothers (n = 50).
The previously identified two-factor model - insistence on sameness (IS) and repetitive stereotypic motor behaviors (RSMB) - was replicated in our sample. Next, a second factor analysis that included the item for verbal rituals resulted in a four-factor model - IS, 'simple' RSMB, 'complex' RSMB, and a fourth factor including symptoms associated with intense preoccupations (IP). Of these four, both IS and IP were significantly familial among affected siblings, but only IP was significantly correlated with the broader autism phenotype traits of rigidity and aloofness in fathers.
The results support previous evidence for the IS factor, its familiality, and the identification of IP as an additional strong candidate trait for genetic studies of autism.
Journal of Child Psychology and Psychiatry 03/2009; 50(8):982-90. · 4.28 Impact Factor
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ABSTRACT: Accumulating evidence from epidemiological research has demonstrated an association between advanced paternal age and risk for several psychiatric disorders including autism, schizophrenia and early-onset bipolar disorder. In order to establish causality, this study used an animal model to investigate the effects of advanced paternal age on behavioural deficits in the offspring.
C57BL/6J offspring (n = 12 per group) were bred from fathers of two different ages, 2 months (young) and 10 months (old), and mothers aged 2 months (n = 6 breeding pairs per group). Social and exploratory behaviors were examined in the offspring.
The offspring of older fathers were found to engage in significantly less social (p = 0.02) and exploratory (p = 0.02) behaviors than the offspring of younger fathers. There were no significant differences in measures of motor activity.
Given the well-controlled nature of this study, this provides the strongest evidence for deleterious effects of advancing paternal age on social and exploratory behavior. De-novo chromosomal changes and/or inherited epigenetic changes are the most plausible explanatory factors.
PLoS ONE 01/2009; 4(12):e8456. · 4.09 Impact Factor
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ABSTRACT: Refractive errors (myopia, hyperopia and amblyopia), like schizophrenia, have a strong genetic cause, and dopamine has been proposed as a potential mediator in their pathophysiology. The present study explored the association between refractive errors in adolescence and schizophrenia, and the potential familiality of this association.
The Israeli Draft Board carries a mandatory standardized visual accuracy assessment. 678,674 males consecutively assessed by the Draft Board and found to be psychiatrically healthy at age 17 were followed for psychiatric hospitalization with schizophrenia using the Israeli National Psychiatric Hospitalization Case Registry. Sib-ships were also identified within the cohort.
There was a negative association between refractive errors and later hospitalization for schizophrenia. Future male schizophrenia patients were two times less likely to have refractive errors compared with never-hospitalized individuals, controlling for intelligence, years of education and socioeconomic status [adjusted Hazard Ratio=.55; 95% confidence interval .35-.85]. The non-schizophrenic male siblings of schizophrenia patients also had lower prevalence of refractive errors compared to never-hospitalized individuals.
Presence of refractive errors in adolescence is related to lower risk for schizophrenia. The familiality of this association suggests that refractive errors may be associated with the genetic liability to schizophrenia.
Schizophrenia Research 12/2008; 107(2-3):238-41. · 4.75 Impact Factor
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ABSTRACT: Evidence indicates an association between older parents at birth and increased risk for schizophrenia and autism. Patients with schizophrenia and autism and their first-degree relatives have impaired social functioning; hence, impaired social functioning is probably an intermediate phenotype of the illness. This study tested the hypothesis that advanced father's age at birth would be associated with poorer social functioning in the general population. To test this hypothesis, we examined the association between parental age at birth and the social functioning of their adolescent male offspring in a population-based study.
Subjects were 403486, 16- to 17-year-old Israeli-born male adolescents assessed by the Israeli Draft Board. The effect of parental age on social functioning was assessed in analyses controlling for cognitive functioning, the other parent's age, parental socioeconomic status, birth order, and year of draft board assessment.
Compared with offspring of parents aged 25-29 years, the prevalence of poor social functioning was increased both in offspring of fathers younger than 20 years (odds ratio [OR] = 1.27, 95% confidence interval [CI] = 1.08-1.49) and in offspring of fathers 45 years old (OR = 1.52, 95% CI = 1.43-1.61). Male adolescent children of mothers aged 40 years and above were 1.15 (95% CI = 1.07-1.24) times more likely to have poor social functioning.
These modest associations between parental age and poor social functioning in the general population parallel the associations between parental age and risk for schizophrenia and autism and suggest that the risk pathways between advanced parental age and schizophrenia and autism might, at least partially, include mildly deleterious effects on social functioning.
Schizophrenia Bulletin 10/2008; 34(6):1042-6. · 8.80 Impact Factor
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ABSTRACT: Advancing paternal age has been reported as a risk factor for neurodevelopmental disorders.
To determine whether advanced paternal age is associated with an increased risk of BPD in the offspring and to assess if there was any difference in risk when analyzing patients with early-onset BPD separately.
A nationwide nested case-control study based on Swedish registers was performed. Risk for BPD in the offspring of older fathers was estimated using conditional logistic regression analysis controlling for potential confounding of parity, maternal age, socioeconomic status, and parental family history of psychotic disorders.
Identification of 7,328,100 individuals and their biological parents by linking the nationwide Multigeneration Register and the Hospital Discharge Register.
A total of 13,428 patients with a BPD diagnosis on at least 2 separate hospital admissions was identified. Five healthy control subjects matched for sex and year of birth were randomized to each case. Main Outcome Measure Bipolar disorder based on ICD codes at discharge from hospital treatment.
An association between paternal age and risk for BPD in the offspring of older men was noted. The risk increased with advancing paternal age. After controlling for parity, maternal age, socioeconomic status, and family history of psychotic disorders, the offspring of men 55 years and older were 1.37 (95% confidence interval [CI], 1.02-1.84) times more likely to be diagnosed as having BPD than the offspring of men aged 20 to 24 years. The maternal age effect was less pronounced. For early-onset (<20 years) cases, the effect of paternal age was much stronger (odds ratio, 2.63; 95% CI, 1.19-5.81), whereas no statistically significant maternal age effect was found.
Advanced paternal age is a risk factor for BPD in the offspring. The results are consistent with the hypothesis that advancing paternal age increases the risk for de novo mutations in susceptibility genes for neurodevelopmental disorders.
Archives of general psychiatry 09/2008; 65(9):1034-40. · 12.26 Impact Factor
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ABSTRACT: Mounting evidence suggests that compromised neurocognitive function is a central feature of schizophrenia. There are, however, schizophrenia patients with a normal neuropsychological (NP) performance, but estimates of the proportion of NP normal patients vary considerably between studies. Neurocognitive dysfunction is also a characteristic of other psychotic disorders, yet there are inconsistencies in the literature regarding the similarity to impairments in schizophrenia. NP normality in psychotic affective disorders has not been systematically studied.
Data came from the Suffolk County Mental Health Project, an epidemiological study of first-admission patients with psychotic disorders. Respondents with a diagnosis of schizophrenia (N = 94) or schizoaffective disorder (N = 15), bipolar disorder (N = 78), and major depressive disorder (N = 48) were administered a battery of NP tests assessing 8 cognitive domains 2 years after index admission. Patients' performance profile was compared, and their NP status was classified based on 3 previously published criteria that vary in their stringency.
The 4 diagnostic groups had comparable NP performance profile patterns. All groups demonstrated impairments in memory, executive functions, and attention and processing speed. However, schizophrenia patients were more impaired than the other groups on all cognitive domains. Results were not attenuated when IQ was controlled. Prevalence of NP normality ranged between 16% and 45% in schizophrenia, 20% and 33% in schizoaffective disorder, 42% and 64% in bipolar disorder, and 42% and 77% in depression, depending on the criterion employed.
Evidence suggests that differences in NP performance between schizophrenia and psychotic affective disorders are largely quantitative. NP impairment is also common in psychotic affective disorders. A significant minority of schizophrenia patients are NP normal.
Schizophrenia Bulletin 06/2008; 35(5):1022-9. · 8.80 Impact Factor
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ABSTRACT: Evidence for a genetic association between autism and two single nucleotide polymorphisms (SNPs), rs2056202 and rs2292813, in the mitochondrial aspartate/glutamate carrier (SLC25A12) gene led us to ask whether any of the four previously identified familial traits in autism spectrum disorders (ASD) varied by these SNPs. In 355 ASD cases from 170 sibships we examined levels of the four traits in these SNPs using ANCOVA models. The primary models selected unrelated affected cases and used age and sex as covariates. An ancillary set of models used all affected siblings and included "sibship" as a random effects independent variable. We found significantly lower levels of routines and rituals associated with the presence of the less frequent A allele in rs2056206. No other significant differences were observed. The rs2056202 polymorphism may be associated with levels of routines and rituals in autism and related disorders.
American Journal of Medical Genetics Part B Neuropsychiatric Genetics 05/2008; 147(3):408-10. · 3.70 Impact Factor
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ABSTRACT: Previous studies have reported that as a group, individuals affected by psychotic and nonpsychotic disorders perform below norms on cognitive tests. Other studies have indicated that unaffected siblings of individuals affected by psychotic disorders also perform below norms on the same tests. We investigated cognitive performance on a large, population-based sample of individuals, affected at the time of testing by nonpsychotic disorders, and their unaffected siblings.
Subjects were taken from a population-based cohort of 523,375, 16- to 17-year-old male adolescents who had been assessed by the Israeli Draft Board. Cognitive test scores were examined in sib-pairs discordant for nonpsychotic (n = 19,489) and psychotic (n = 888) disorders and compared with 224,082 individuals from sibships with no evidence of mental illness.
There appears to be a gradient in cognitive performance (worst to best) from individuals currently affected by psychotic illnesses (Cohen's d = -.82), followed by individuals currently affected by nonpsychotic illness (Cohen's d = -.58), unaffected siblings of individuals affected by psychotic illness (Cohen's d = -.37), unaffected siblings of individuals affected by nonpsychotic illness (Cohen's d = -.27), and members of sibships with no evidence of mental illness. Unaffected siblings of both psychotic and nonpsychotic individuals from multiple affected sibships (more then one affected sibling) had worse cognitive test scores compared with unaffected siblings from simplex sibships (only one affected sibling).
The results support, but do not prove, the notion that cognitive impairment in psychiatric disorders is familial and cuts across diagnostic entities.
Biological psychiatry 04/2008; 63(6):602-8. · 8.93 Impact Factor
