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T.M. Blekher, J. Tian, J. Wojcieszek, T. Foroud, R. Yee; Oculomotor Control in Parkinson’s Patients and Their Clinically Normal Siblings . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2920.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To characterize oculomotor control in a sample of individuals diagnosed with Parkinson’s disease (PD) and their clinically normal siblings. Methods: Subjects included 11 mildly– or moderately–affected PD patients (mean age 60 years), their 11 clinically normal siblings (mean age 58) and 11 normal controls (mean age 58). Eye movements of the subjects were recorded using a video based system (EyelinkII). The oculomotor testing paradigm included both traditional tests and a novel experimental procedure to assess visual scanning. Traditional tests elicited visually guided and volitional saccades, such as anti–saccade and memory–guided saccades. Visual scanning was recorded while the participants completed the Digit Symbol Subscale test. Basic saccade measures (latency, peak velocity, percentage of correct and reflexive saccade, etc.) and the number of searching saccades during visual scanning were quantified. A gaze shift fragmentation (multiple step patterns when target is reached by several hypometric saccades) was assessed over a sequence of three subsequent memory guided gaze shifts. Analysis of variance was used to test for significant difference between the PD patients, their siblings, and the control group. Post–hoc analysis was performed for those measures with significant group effect to identify pair–wise differences. Results: PD subjects and their clinically normal siblings demonstrated abnormally high incidence of gaze shift fragmentation while performing memory guided gaze shifts (percentage of multiple step pattern, mean: 50% PD group, 33% Sibling group, 10% control group; the PD versus control group, p=0.001; the siblings versus control group, p=0.02). Additionally, PD patients demonstrated a delay in the initiation of volitional saccades (p<0.05) and reduced number of searching saccades during visual scanning (p=0.004). No differences between groups were observed in a number of correct/reflexive volitional saccades, velocity of saccades, and a latency of visually guided saccades. Conclusions: Oculomotor dysfunction at early stage of PD is mainly characterized by a fragmentation of memory guided gaze shifts and delay in initiation of volitional saccades. The similar fragmentation abnormality exists in the clinically normal siblings of PD patients. Thus, the fragmentation abnormality may serve as a PD biological marker rather than a diagnostic criterion in early stage of PD.
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