Eye tracking dysfunction (ETD) has been found in large numbers of schizophrenia patients and their first-degree relatives. Because of the many replications of the central findings, ETD has been proposed as a useful way of expanding the schizophrenia phenotype in genetic studies. We critically review the literature on ETD with respect to issues of measurement and the search for quantitative indices of ETD; syndrome and familial specificity of ETD for schizophrenia; statistical, interpretive, and methodological considerations in the use of mixture analysis; the association of ETD with clinically and psychometrically defined schizotypy; and the questions of trait stability and medication effects.

Increasing interest in the role of the frontal lobe in relation to psychiatric and neurologic disorders has popularized tests of frontal function. One of these is the antisaccade task, in which both frontal lobe patients and schizophrenics are impaired despite normal performance on (pro)saccadic tasks. We used positron emission tomography to examine the cerebral blood flow changes associated with the performance of antisaccades in normal individuals. We found that the areas of the brain that were more active during antisaccades than saccades were highly consistent with the oculomotor circuit, including frontal eye fields (FEFs), supplementary motor area, thalamus, and putamen.

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Background: Eye-tracking dysfunction has been found in many patients with schizophrenia and in about 40% of their first-degree biological relatives. We hypothesized that a deficit in motion processing is associated with eye-tracking dysfunction because both motion signals and the brain regions responsible for processing motion signals are implicated in the generation of smooth pursuit. We examined several aspects of visual perception, including motion perception, in patients with schizophrenia.

Schizophrenia patients and many of their relatives show impaired smooth pursuit eye tracking. The brain mechanisms underlying this impairment are not yet known, but because reduced open-loop acceleration and closed-loop gain accompany it, compromised perceptual processing of motion signals is implicated. A previous study showed that motion discrimination is impaired in schizophrenia patients. Motion discrimination can make use of position and contrast as well as velocity cues. Here, we report that the motion discrimination deficit, which occurs in both schizophrenic patients and in their first-degree relatives, involves a failure of velocity detection, which appears when judging intermediate target velocities. At slower and faster velocities, judgments of velocity discrimination seemed normal until we experimentally disentangled velocity cues from nonmotion cues. We further report that compromised velocity discrimination is associated with sluggish initiation of smooth pursuit. These findings point to specific central nervous system correlates of schizophrenic pathophysiology.Although schizophrenia is significantly influenced by genetic factors (1, 2), the clinical disorder occurs relatively infrequently; estimates vary from 3.5% to Ϸ8% in the nuclear families of schizophrenic probands (3). This low intrafamilial prevalence poses difficulties for studies of genetic linkage in schizophrenia. Certain physiological traits, however, although uncommon in the general population, occur more frequently than the clinical syndrome in first-degree relatives and suggest themselves as more penetrant alternative phenotypes for the study of the genetics and pathophysiology of schizophrenia (4). One of the more widely studied of these cofamilial traits is eye tracking dysfunction (5-7).Eye tracking dysfunction shows itself specifically in smooth pursuit eye movements, a tracking response to moving visual targets. Other kinds of eye movements, such as voluntary saccades (8, 9), vestibularly controlled eye movements (10), and the oculocephalic reflex (11), are normal in both patients and relatives. This set of findings indicates that the eye tracking dysfunction is specific to the smooth pursuit system and that its neuroanatomical substrate is above the brain stem.Several investigators have characterized the nature of the eye tracking dysfunction in schizophrenia as low closed-loop gain (the ratio of eye velocity to target velocity) with frequent compensatory catch-up saccades and low initial acceleration of the eye, both of which indicate that eye velocity lags behind target velocity (12-15). There may be two explanations for these findings: (i) Processing of velocity signals during target movement is deficient (16, 17); and (ii) general performance is inefficient when processing external signals (18).As evidence to support the hypothesis that deficient velocity processing is involved in eye tracking dysfunction, it is necessary to show that velocity discrimination is compromised in schizophrenic patients and that the sa...

Dopamine modulation via D(2) receptor blockade affects sensory processes in schizophrenia, shifting visual contrast detection from hypersensitivity in the unmedicated state to normal and even to hyposensitive levels. Thus, antipsychotic drug treatment may account for the inconsistent reports concerning visual contrast detection in schizophrenia.

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