Decomposing mechanisms of abnormal saccade generation in schizophrenia patients: Contributions of volitional initiation, motor preparation, and fixation release.

Clinical and theoretical models suggest deficient volitional initiation of action in schizophrenia patients. Recent research provided an experimental model of testing this assumption using saccade tasks. However, inconsistent findings necessitate a specification of conditions on which the deficit may occur. The present study sought to detect mechanisms that may contribute to poor performance. Sixteen schizophrenia patients and 16 healthy control participants performed visually guided and two types of volitional saccade tasks. All tasks varied as to whether the initial fixation stimulus disappeared (fixation stimulus offset) or continued during saccade initiation, and whether a direction cue allowed motor preparation of the specific saccade. Saccade latencies of the two groups were differentially affected by task type, fixation stimulus offset, and cueing, suggesting abnormal volitional saccade generation, fixation release, and motor preparation in schizophrenia. However, substantial performance deficits may only occur if all affected processes are required in a task.

Neural correlates of impaired volitional action control in schizophrenia patients.

Slowed initiation of volitional but not visually guided saccades indicates impaired volitional action control in schizophrenia patients (SZ). The present study aimed at identifying neural correlates of this specific deficit. Fourteen SZ and 13 healthy control participants (HC) underwent functional magnetic resonance imaging while performing volitional and visually guided saccades. SZ showed increased latencies in volitional but not in visually guided saccades. Brain activation during volitional saccades compared to visually guided saccades was increased in SZ compared to HC in several areas: the supplementary eye fields, suggesting inefficient production of volitional saccades; the prefrontal cortex, pointing to altered top down control on complex eye movements; and the left middle temporal area, suggesting changes in early sensory and attention processing during the volitional control of saccades in SZ.

Volitional saccades and attentional mechanisms in schizophrenia patients and healthy control subjects.

Schizophrenia (SZ) patients showed increased volitional saccade latencies, suggesting deficient volitional initiation of action. Yet increased volitional saccade latencies may also result from deficits in attention shifts. To dissociate attention shifting and saccade initiation, we asked 25 SZ patients and 25 healthy subjects to make saccades toward newly appearing (onset) targets and toward the loci of disappearing (offset) targets. Similar onsets and offsets were also used as attention cues in a Posner-type manual task. As expected, onsets and offsets had similar effects on attention. In contrast, saccade latencies were considerably longer with offset compared to onset targets, reflecting additional time for volitional saccade initiation. Unexpectedly, SZ patients had normal saccade latencies. Presumably, the expected deficit was compensated by decreased fixation-related neural activity, which was induced by the disappearance of fixation stimuli.