Saccade Adaptation in Antipsychotic Naïve First-Episode Schizophrenia and Healthy Individuals

The primate oculomotor system and the underlying neural circuitry involved in the generation of saccades is well established. Because there are many brain systems involved in generating saccades, the oculomotor system makes for a good model to examine impaired brain functions in mental disorders believed to have widespread disruptions in neural circuitry like schizophrenia. Schizophrenia is a disabling disorder characterized by impaired cognitive and sensorimotor function. While it is believed several brain areas are affected in schizophrenia, recent studies have implicated the cerebellum to play a role. In addition to reported cerebellar abnormalities in schizophrenia in imaging studies, other studies have suggested that the cerebellum controls and mediates cognitive function similarly to the way it controls and mediates motor function. Thus, any dysfunction of the cerebellum can result in the variety of motor and cognitive deficits characteristic to schizophrenia. In the current study saccade adaptation, an oculomotor mechanism believed to heavily rely on the oculomotor vermis of the cerebellum, was assessed in healthy individuals and non-medicated first episode schizophrenia patients. Subjects performed visually guided saccades as well as a saccade adaptation paradigm in which the target is displaced during the saccade, inducing retinal error, i.e. error between the intended eye movement and target position. After repeated trials, healthy subjects gradually adapt to minimize retinal error by adjusting saccade amplitude to reach the new target position. Schizophrenia patients adapted as well as the healthy controls in that retinal error was reduced by similar amounts at similar rates across the trials of the adaptation task. Although adaptation was unimpaired in schizophrenia patients, findings in measures of saccade kinematics suggest dysfunction of the oculomotor vermis and possibly other areas of the cerebellum. Saccade dynamic characteristics provided more sensitive measures believed to better characterize the mechanisms of the cerebellum than latency and amplitude could provide alone. Patients facilitated similar adaptation by using different saccade kinematics from healthy controls. Another finding revealed schizophrenia patients had increased saccade amplitude variability, suggesting that any cerebellar deficits in maintaining saccade accuracy may have been compensated for while variability in saccade performance was not. The last finding revealed differences between the groups in timing parameters of certain saccade kinematics throughout all saccade types suggesting that other areas of the cerebellum not responsible for adaptation may also be affected in schizophrenia.