Objective: Quantitatively study visually-guided saccades (VGS) in Parkinson’s disease (PD).

Background: Visuomotor deficits such as hypometric VGS are present in PD despite the retained ability to accurately perceive the visual stimulus. These deficits sharply contrast with ‘blindsight’ where there is lack of visual identification of the object but preserved visually guided saccades. Normally the substantia nigra pars reticulata maintains tonic GABAergic inhibition on the superior colliculus; transient cessation of these neurons leads to timely saccade initiation. Disinhibition of the substantia nigra pars reticulata, as expected in PD, could therefore prematurely interrupt an ongoing saccade in both directions. Alternatively, impaired activation of the excitatory burst neurons (EBNs) could lead to slow saccades, while early activation of omnipause neurons (OPNs) and inhibitory burst neurons (IBNs) could result in premature breaks in the ongoing VGS and hypometria. We investigated the mechanisms for hypometric VGS in PD.

Methods: We used high-resolution oculography to analyze trajectory, curvature, amplitude, velocity, acceleration, and deceleration of VGS in 20 PD patients in the dopamine off period.

Results: We discovered unique properties of VGS in PD: they were slow, interrupted (vertical greater than horizontal), and had curved trajectories. The curvature in VGS were due to the fact that they were invariably misdirected and the patients had to make multiple changes in the trajectory to reach the intended target.

Conclusions: We suggest that saccade curvature in PD is not merely due to the mismatch in the velocity of relatively slower vertical and faster horizontal components, but also due to aberrant activation of the superior colliculus. We suggest that complete interruptions in the horizontal saccades may be caused by increased phasic inhibition of the superior colliculus due to increased activity of substantia nigra pars reticulata in PD. We further predict that irregularities and slowing, prominently seen in the vertical saccades, could be due to impaired function of reciprocally innervating saccade burst neurons leading to maladaptive feedback causing the premature activation of the superior colliculus.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/saccades-in-parkinsons-disease-hypometric-slow-or-maladaptive/