Intellectual decline in schizophrenia: evidence from a prospective birth cohort 28 year follow-up study. J Clin Exp Neuropsychol
ABSTRACT It is well established that IQ is lower among persons with schizophrenia than in the general population. However, it remains unclear if there is deterioration beyond a premorbid deficit. In order to assess the question of IQ deterioration, we assessed persons pre- and-post psychosis, comparing those who developed schizophrenia with those who did not. Twenty six patients with schizophrenia and 59 normal controls, evaluated at age 7 in the prospective, longitudinal, National Collaborative Perinatal Project (NCPP), were re-tested approximately 28 years later. We assessed change in an estimate of IQ based on the Vocabulary and Block Design tests from the Wechsler intelligence scales. Persons who later developed schizophrenia were significantly impaired on IQ compared to controls at age 7, especially on measures of attention. At age 35, persons with schizophrenia demonstrated significant impairment and deterioration on both IQ sub-tests compared to controls. Because impairment occurs by early childhood and subsequent deterioration occurs at an unknown period, designs with more frequent assessment of IQ through the premorbid, prodromal and early phases of illness are required to identify the key period of decline. Future research on this sample will evaluate the prospective roles of family history and perinatal complications on cognition, and assess the specificity of these findings.
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- "Attempts have also been made to correlate cortical gray matter loss in schizophrenia with changes in cognition given the presence of neuropsychological deficits and their known associations between various brain regions (Antonova et al., 2004). While the presence of premorbid cognitive deficits (Bilder et al., 2006), and occurrence of further decline after initial onset have been reported (Seidman et al., 2006), current evidence also strongly indicates that cognitive impairment appears to be stable after the first episode of illness (Heaton et al., 2001; Hill et al., 2004). Consequently, the presence of stable cognitive deficits in the face of progressive changes in brain structure during the chronic phase of schizophrenia is puzzling, and deserves confirmation and further investigation. "
ABSTRACT: Cortical abnormalities are considered a neurobiological characteristic of schizophrenia. However, the pattern of such deficits as they progress over the illness remains poorly understood. The goal of this project was to assess the progression of cortical thinning in frontal and temporal cortical regions in schizophrenia, and determine whether relationships exist between them and neuropsychological and clinical symptom profiles. As part of a larger longitudinal 2-year follow-up study, schizophrenia (n=20) and healthy participants (n=20) group-matched for age, gender, and recent-alcohol use, were selected. Using MRI, estimates of gray matter thickness were derived from primary anatomical gyri of the frontal and temporal lobes using surface-based algorithms. These values were entered into repeated-measures analysis of variance models to determine group status and time effects. Change values in cortical regions were correlated with changes in neuropsychological functioning and clinical symptomatology. Results revealed exaggerated cortical thinning of the middle frontal, superior temporal, and middle temporal gyri in schizophrenia participants. These thickness changes strongly influenced volumetric reductions, but were not related to shrinking surface area. Neuropsychological and clinical symptom profiles were stable in the schizophrenia participants despite these neuroanatomic changes. Overall it appears that ongoing abnormalities in the cerebral cortex continue after initial onset of schizophrenia, particularly the lateral aspects of frontal and temporal regions, and do not relate to neuropsychological or clinical measures over time. Maintenance of neuropsychological performance and clinical stability in the face of changing neuroanatomical structure suggests the involvement of alternative compensatory mechanisms.Schizophrenia Research 05/2012; 139(1-3):1-6. DOI:10.1016/j.schres.2012.05.002 · 4.43 Impact Factor
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- "In a preliminary report (Seidman et al. 2006), 46 % of individuals analyzed for this report (31 SCZ, 61 controls ) were studied, focusing only on IQ measures. "
ABSTRACT: BACKGROUND: Persons developing schizophrenia (SCZ) manifest various pre-morbid neuropsychological deficits, studied most often by measures of IQ. Far less is known about pre-morbid neuropsychological functioning in individuals who later develop bipolar psychoses (BP). We evaluated the specificity and impact of family history (FH) of psychosis on pre-morbid neuropsychological functioning.Method We conducted a nested case-control study investigating the associations of neuropsychological data collected systematically at age 7 years for 99 adults with psychotic diagnoses (including 45 SCZ and 35 BP) and 101 controls, drawn from the New England cohort of the Collaborative Perinatal Project (CPP). A mixed-model approach evaluated full-scale IQ, four neuropsychological factors derived from principal components analysis (PCA), and the profile of 10 intelligence and achievement tests, controlling for maternal education, race and intra-familial correlation. We used a deviant responder approach (<10th percentile) to calculate rates of impairment. RESULTS: There was a significant linear trend, with the SCZ group performing worst. The profile of childhood deficits for persons with SCZ did not differ significantly from BP. Neuropsychological impairment was identified in 42.2% of SCZ, 22.9% of BP and 7% of controls. The presence of psychosis in first-degree relatives (FH+) significantly increased the severity of childhood impairment for SCZ but not for BP. CONCLUSIONS: Pre-morbid neuropsychological deficits are found in a substantial proportion of children who later develop SCZ, especially in the SCZ FH+ subgroup, but less so in BP, suggesting especially impaired neurodevelopment underlying cognition in pre-SCZ children. Future work should assess genetic and environmental factors that explain this FH effect.Psychological Medicine 05/2012; 43(1):1-13. DOI:10.1017/S0033291712000773 · 5.43 Impact Factor
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- "It appears that different demographic characteristics across studies may also have contributed to the discrepant results. For example, studies that included more patients with a chronic course, older age, or other characteristics that may impair IQ (Seidman et al, 2006) may end up with a weaker association between rs1344706 and schizophrenia. "
ABSTRACT: ZNF804A gene polymorphism rs1344706 has been suggested as the most compelling case of a candidate gene for schizophrenia by a genome-wide association study and several replication studies. The current study of 570 schizophrenia patients and 448 controls again found significantly different genotype frequencies of rs1344706 between patients and controls. More important, we found that this association was modulated by IQ, with a stronger association among individuals with relatively high IQ, which replicated results of Walters et al, 2010. We further examined whether this IQ-modulated association also existed between the SNP and the intermediate phenotypes (working memory and executive functions) of schizophrenia. Data were available from an N-back task (366 patients and 414 controls) and the attention network task (361 patients and 416 controls). We found that the SNP and IQ had significant interaction effects on the intermediate phenotypes for patients, but not for controls. The disease risk allele was associated with poorer cognitive function in patients with high IQ, but better cognitive function in patients with low IQ. Together, these results indicated that IQ may modulate the role of rs1344706 in the etiology of both schizophrenia and its cognitive impairments, and pointed to the necessity of considering general cognitive function as indexed by IQ in the future studies of genetic bases of schizophrenia.Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 02/2012; 37(7):1572-8. DOI:10.1038/npp.2012.1 · 7.83 Impact Factor