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Background: Cognition is increasingly being recognized as an important aspect of psychotic disorders and a key contributor to functional outcome. In the past, comparative studies have been performed in schizophrenia and schizo-affective disorder with regard to cognitive performance, but the results have been mixed and the cognitive measures used have not always assessed the cognitive deficits found to be specific to psychosis. A set of optimized cognitive paradigms designed by the Cognitive Neuroscience Test Reliability and Clinical Applications for Schizophrenia (CNTRACS) Consortium to assess deficits specific to schizophrenia was used to measure cognition in a large group of individuals with schizophrenia and schizo-affective disorder., Method: A total of 519 participants (188 with schizophrenia, 63 with schizo-affective disorder and 268 controls) were administered three cognitive paradigms assessing the domains of goal maintenance in working memory, relational encoding and retrieval in episodic memory and visual integration., Results: Across the three domains, the results showed no major quantitative differences between patient groups, with both groups uniformly performing worse than healthy subjects., Conclusions: The findings of this study suggests that, with regard to deficits in cognition, considered a major aspect of psychotic disorder, schizophrenia and schizo-affective disorder do not demonstrate major significant distinctions. These results have important implications for our understanding of the nosological structure of major psychopathology, providing evidence consistent with the hypothesis that there is no natural distinction between cognitive functioning in schizophrenia and schizo-affective disorder.

Studies of neuropathology-cognition associations are not common and have been limited by small sample sizes, long intervals between autopsy and cognitive testing, and lack of breadth of neuropathology and cognition variables. This study examined domain-specific effects of common neuropathologies on cognition using data (N = 652) from two large cohort studies of older adults. We first identified dimensions of a battery of 17 neuropsychological tests, and regional measures of Alzheimer's disease (AD) neuropathology. We then evaluated how cognitive factors were related to dimensions of AD and additional measures of cerebrovascular and Lewy Body disease, and also examined independent effects of brain weight. All cognitive domains had multiple neuropathology determinants that differed by domain. Neocortical neurofibrillary tangles were the strongest predictors of most domains, while medial temporal tangles showed a weaker relationship with episodic memory. Neuritic plaques had relatively strong effects on multiple domains. Lewy bodies and macroscopic infarcts were associated with all domains, while microscopic infarcts had more limited associations. Brain weight was related to all domains independent of specific neuropathologies. Results show that cognition is complexly determined by multiple disease substrates. Neuropathological variables and brain weight contributed approximately a third to half of the explained variance in different cognitive domains.

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) neuropsychological battery was developed to evaluate cognitive impairments associated with Alzheimer's disease (AD). Previous studies have suggested that the battery is multi-dimensional, represented by either 3 or 5 dimensions. In this study a principal factor analysis was conducted using contemporary quantitative methods for determining the number of factors. Exploratory factor analysis of the CERAD battery and MMSE was conducted using one-half of the CERAD database (total N = 969). Glorfeld's modification of Horn's parallel analysis method suggested that there was 1 common factor in the variable matrix. Characterization of patterns of deficits in AD requires supplementation of measures derived from the CERAD and MMSE with other tests.

Background: In this study, we tested the hypothesis that low smooth pursuit gain in schizophrenia is related to an abnormality in motion perception., Methods: The subjects were 19 schizophrenics treated with clozapine and 19 controls. In addition to smooth pursuit and motion perception paradigms, sustained attention was also assessed using a continuous performance task (CPT)., Results: In the patient group, there was a statistically significant negative correlation between smooth pursuit gain and motion perception threshold (r = -0.60, P < 0.01). This relationship was not secondary to attention deficits as assessed by the CPT., Conclusions: Our results are consistent with the notion that the smooth pursuit gain deficit is related to a deficit in motion perception rather than in attention. Brain area V5 (also referred to as "MT' in macaque), located in the parieto-occipital region, is known to be critically important both for motion perception and gain. Thus, our results point to an abnormality in this area in schizophrenia.