کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
338440 547951 2010 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Deficits in visual sustained attention differentiate genetic liability and disease expression for Schizophrenia from Bipolar Disorder
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب رفتاری
پیش نمایش صفحه اول مقاله
Deficits in visual sustained attention differentiate genetic liability and disease expression for Schizophrenia from Bipolar Disorder
چکیده انگلیسی

BackgroundThere is mounting evidence for shared genetic liability to psychoses, particularly with respect to Schizophrenia (SZ) and Bipolar Disorder (BD), which may also involve aspects of cognitive dysfunction. Impaired sustained attention is considered a cardinal feature of psychoses but its association with genetic liability and disease expression in BD remains to be clarified.MethodsVisual sustained attention was assessed using the Degraded Symbol Continuous Performance Test (DS-CPT) in a sample of 397 individuals consisting of 50 remitted SZ patients, 119 of their first degree relatives, 47 euthymic BD patients, 88 of their first degree relatives and 93 healthy controls. Relatives with a personal history of schizophrenia or bipolar spectrum disorders were excluded. Performance on the DS-CPT was evaluated based on the response criterion (the amount of perceptual evidence required to designate a stimulus as a target) and sensitivity (a signal-detection theory measure of signal/noise discrimination).ResultsWe found no effect of genetic risk or diagnosis for either disorder on response criterion. In contrast, impaired sensitivity was seen in SZ patients and to a lesser degree in their relatives but not in BD patients and their relatives. These findings were not attributable to IQ, medication, age of onset or duration of illness.ConclusionsOur results argue for the specificity of visual sustained attention impairment in differentiating SZ from BD. They also suggest that compromised visual information processing is a significant contributor to these deficits in SZ.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Schizophrenia Research - Volume 124, Issues 1–3, December 2010, Pages 152–160
نویسندگان
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