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. 2019 Jan;12(1):1-13.
doi: 10.14802/jmd.18034. Epub 2019 Jan 30.

Abnormal Eye Movements in Parkinsonism and Movement Disorders

Ileok Jung  1 , Ji-Soo Kim  2   3
Affiliations

Abnormal Eye Movements in Parkinsonism and Movement Disorders

Ileok Jung et al. J Mov Disord. 2019 Jan.

Abstract

Abnormal eye movements are commonly observed in movement disorders. Ocular motility examination should include bedside evaluation and laboratory recording of ocular misalignment, involuntary eye movements, including nystagmus and saccadic intrusions/oscillations, triggered nystagmus, saccades, smooth pursuit (SP), and the vestibulo-ocular reflex. Patients with Parkinson's disease (PD) mostly show hypometric saccades, especially for the selfpaced saccades, and impaired SP. Early vertical saccadic palsy is characteristic of progressive supranuclear palsy-Richardson's syndrome. Patients with cortico-basal syndrome typically show a delayed onset of saccades. Downbeat and gaze-evoked nystagmus and hypermetric saccades are characteristic ocular motor findings in ataxic disorders due to cerebellar dysfunction. In this review, we discuss various ocular motor findings in movement disorders, including PD and related disorders, ataxic syndromes, and hyperkinetic movement disorders. Systemic evaluation of the ocular motor functions may provide valuable information for early detection and monitoring of movement disorders, despite an overlap in the abnormal eye movements among different movement disorders.

Keywords: Eye movements; ataxia; parkinsonism; saccades.

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Conflict of interest statement

Conflicts of Interest

The authors have no financial conflicts of interest.

Figures

Figure 1.
Figure 1.
Frequent square wave jerks (A), slowed and hypometric saccades (B), and impaired SP are characteristic findings of progressive supranuclear palsy syndrome. Saccades and SP are more severely impaired in the vertical direction (B). LH: horizontal position of the left eye, LV: vertical position of the left eye, LT: torsional position of the left eye, SP: smooth pursuit.
Figure 2.
Figure 2.
Patient with spinocerebellar ataxia type 2 shows slowed saccades especially in the vertical plane (A) and impaired smooth pursuit in both horizontal and vertical planes (B). LH: horizontal position of the left eye, LV: vertical position of the left eye.
Figure 3.
Figure 3.
Results of the vestibular function tests in a representative patient with spinocerebellar ataxia type 6. A. Caloric tests. The sum of the peak SPV of the nystagmus in response to each caloric stimulus is increased at 174°/s (normal range=45–157°/s). B. Rotatory chair test. The gains of the VOR are normal during sinusoidal horizontal accelerations. Gray areas represent the normal ranges (mean ± 2SD). C. Head impulse tests. Head impulses in the plane of each SCC revealed decreased gain of the VOR for all six semicircular canals with overt catch-up saccades during stimulation of the horizontal and posterior SCCs. The blue lines indicate head velocity and the red lines represent eye velocity. D. The head impulse VOR gain for the HC is negatively correlated with the ataxia score as measured using the ICARS. SPV: slow-phase velocity, VOR: vestibulo-ocular reflex, SCC: semicircular canal, LAC: left anterior SCC, LHC: left horizontal SCC, LPC: left posterior SCC, RAC: right anterior SCC, RHC: right horizontal SCC, RPC: right posterior SCC, ICARS: International Cooperative Ataxia Rating Scale, HIT-HC: head impulse testing in the horizontal semicircular canal plane.
Figure 4.
Figure 4.
Findings in a patient with episodic ataxia type 2. A: The patient shows gaze-evoked (filled arrow) and downbeat nystagmus (open arrow) during leftward gaze that decrease gradually. On resuming the neutral position (arrow head), upbeat nystagmus develops without rebound nystagmus in the horizontal plane. Upward deflection indicates rightward and upward eye motion. H: horizontal eye position, V: vertical eye position. B: Pedigree of the patient. Squares males, circles females, open symbols unaffected, solid symbols affected. C. The chromatograms of a part of exon 31 and intron 31 of CACNA1A show a heterozygous point mutation at the splice donor site (c.4953+1G>A).
Figure 5.
Figure 5.
Findings in a patient with paraneoplastic cerebellar degeneration. A and B: Recording of eye movements using 3-dimensional video-oculography shows spontaneous downbeat nystagmus (DBN) with decreasing slow phases, which increases without fixation (A). DBN increases during lateral gazes with horizontal gaze-evoked (hollow arrows), centripetal (arrows), and rebound nystagmus (arrow heads) (B). C and D: Whole body 2-deoxy-2-[F18]fluoro-D-glucose-positron emission tomography (FDG-PET) (C) and chest CT (D) show a hypermetabolic mass in the right lower lobe of the lung (arrows). E: Brain FDG-PET reveals increased metabolism, especially in the nodulus. F: The hypermetabolism observed on the initial PET disappeared after right lung lobectomy and chemotherapy.
Figure 6.
Figure 6.
In a patient with Huntington’s disease, the horizontal saccades are markedly slowed (A). In the vertical plane, slowing is more prominent during downward saccades. In contrast, vertical SP is severely impaired while the horizontal SP is relatively preserved (B). LH: horizontal position of the left eye, LV: vertical position of the left eye, SP: smooth pursuit.
Figure 7.
Figure 7.
Findings in a patient with Wilson’s disease. A: Kayser-Fleischer ring. Color external photograph shows Kayser-Fleischer ring (arrows), a golden-brown discoloration of the cornea due to deposition of sulfur-copper complexes within the Descemet’s membrane. B: T2-weighted MRIs reveal symmetrical high signal intensity lesions in the putamina, thalami, midbrain and pontine tegmentum. C: Video-oculographic recording (SMI®, Teltow, Germany) of saccades shows selective slowing of downward saccades while the velocities of horizontal and upward saccades are normal. D: Smooth pursuit is impaired in the vertical direction. LH: horizontal position of the left eye, LV: vertical position of the left eye.
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