Elevated nailfold plexus visibility aggregates in families and is associated with a specific negative symptom pattern in schizophrenia.

Twenty-four individuals with schizophrenia and 28 of their first-degree biological relatives were studied using clinical scales, functional ratings, and neuropsychological tests. An assessment of Nailfold Plexus Visibility (NPV) was also performed on these individuals. In keeping with the literature, we found an increased prevalence of high NPV in our schizophrenia subjects relative to controls and community norms, and also found that high NPV patients had significantly more negative symptoms and poorer social functioning. Measures of negative symptoms indicative of the deficit syndrome did a better job of distinguishing high from low NPV subjects than did more broadly defined negative symptom indices. As predicted, the prevalence of high NPV in first-degree relatives of high NPV schizophrenia subjects was increased compared with relatives of low NPV schizophrenia subjects. These two relative groups did not differ on overall level of schizotypy symptoms or on negative symptom schizotypy indices. However, relatives of low NPV patients scored significantly higher on scales of positive symptom schizotypy. Overall, these results support the hypothesis that high NPV is a marker of risk for a distinct subtype of schizophrenia.

Abnormal mechanisms of antisaccade generation in schizophrenia patients and unaffected biological relatives of schizophrenia patients.

Although errant saccadic eye movements may mark genetic factors in schizophrenia, little is known about abnormal brain activity that precedes saccades in individuals with genetic liability for schizophrenia. We investigated electrophysiological activity preceding prosaccades and antisaccades in schizophrenia patients, first-degree biological relatives of schizophrenia patients, and control subjects. Prior to antisaccades, patients had reduced potentials over lateral prefrontal cortex. Smaller potentials were associated with worse antisaccade performance. Relatives also exhibited reduced pre-saccadic potentials over lateral frontal cortex but additionally had reduced potentials over parietal cortex. Both patients and relatives tended toward increased activity over orbital frontal cortex prior to saccades. Results are consistent with lateral prefrontal dysfunction marking genetic liability for schizophrenia and underlying deficient saccadic control.