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Eye movements and the search for the essence of schizophrenia
1Department of Psychology, Harvard University, McLean Hospital, Consolidated Department of Psychiatry, Harvard Medical School, 33 Kirkland Street, MA 02138, Cambridge, USA. psh@wjh.harvard.edu
Abstract:
Clinical Schizophrenia has eluded precise description because of its protean phenotypic manifestations and variable clinical course, a variability that also makes it difficult to discover genetic linkages. Co-familial traits have higher recurrence risk rates than schizophrenia itself and might serve as pointers to the underlying physiology of schizophrenic illness. A dysfunction of smooth pursuit eye movements is one such co-familial trait that occurs in about 40 to 80% of schizophrenic patients and about 25 to 40% of their first degree relatives. The eye movement abnormality appears only when the subject tracks a moving target. We have traced this abnormality to a deficit in velocity sensitivity, a function that is regulated by a specific central nervous system network that includes the middle temporal and medial superior temporal areas of the extra-striate cortex. The higher familial recurrence risk of abnormal eye tracking, compared with that of clinical schizophrenia (about 5 to 8%), suggests that schizophrenic psychosis may be the rare form of a more prevalent disorder whose symptoms are much milder and more benign than the cognitive and behavioral disturbances of the clinical psychosis. From this vantage point, abnormal eye tracking can be viewed as one pleiotropic manifestation of schizophrenia, considered broadly, just as the café-au-lait spots of neurofibromatosis are a more benign and more frequent manifestation of that disease than are the neurofibromata.
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