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Clinical application of eye movement tasks as an aid to understanding Parkinson’s disease pathophysiology

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Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder of the basal ganglia. Most PD patients suffer from somatomotor and oculomotor disorders. The oculomotor system facilitates obtaining accurate information from the visual world. If a target moves slowly in the fronto-parallel plane, tracking eye movements occur that consist primarily of smooth-pursuit interspersed with corrective saccades. Efficient smooth-pursuit requires appropriate target selection and predictive compensation for inherent processing delays. Although pursuit impairment, e.g. as latency prolongation or low gain (eye velocity/target velocity), is well known in PD, normal aging alone results in such changes. In this article, we first briefly review some basic features of smooth-pursuit, then review recent results showing the specific nature of impaired pursuit in PD using a cue-dependent memory-based smooth-pursuit task. This task was initially used for monkeys to separate two major components of prediction (image-motion direction memory and movement preparation), and neural correlates were examined in major pursuit pathways. Most PD patients possessed normal cue-information memory but extra-retinal mechanisms for pursuit preparation and execution were dysfunctional. A minority of PD patients had abnormal cue-information memory or difficulty in understanding the task. Some PD patients with normal cue-information memory changed strategy to initiate smooth tracking. Strategy changes were also observed to compensate for impaired pursuit during whole body rotation while the target moved with the head. We discuss PD pathophysiology by comparing eye movement task results with neuropsychological and motor symptom evaluations of individual patients and further with monkey results, and suggest possible neural circuits for these functions/dysfunctions.

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(adapted from Cui et al. 2003). Pink and green arrows in e schematically illustrate the possible circuits that include SEF, oculomotor vermis, caudal fastigal nuclei and vestibular nuclei for no-go instruction specific discharge during delay 2 of memory-based pursuit/saccade task. Reproduced and modified from Kurkin et al. (2014)

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Correspondence to Kikuro Fukushima.

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Fukushima, K., Fukushima, J. & Barnes, G.R. Clinical application of eye movement tasks as an aid to understanding Parkinson’s disease pathophysiology. Exp Brain Res 235, 1309–1321 (2017). https://doi.org/10.1007/s00221-017-4916-5

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