Eye Movement Abnormalities in Glaucoma Patients: A Review

Abstract

Glaucoma is a common condition that relies on careful clinical assessment to diagnose and determine disease progression. There is growing evidence that glaucoma is associated not only with loss of retinal ganglion cells but also with degeneration of cortical and subcortical brain structures associated with vision and eye movements. The effect of glaucoma pathophysiology on eye movements is not well understood. In this review, we examine the evidence surrounding altered eye movements in glaucoma patients compared to healthy controls, with a focus on quantitative eye tracking studies measuring saccades, fixation, and optokinetic nystagmus in a range of visual tasks. The evidence suggests that glaucoma patients have alterations in several eye movement domains. Patients exhibit longer saccade latencies, which worsen with increasing glaucoma severity. Other saccadic abnormalities include lower saccade amplitude and velocity, and difficulty inhibiting reflexive saccades. Fixation is pathologically altered in glaucoma with reduced stability. Optokinetic nystagmus measures have also been shown to be abnormal. Complex visual tasks (eg reading, driving, and navigating obstacles), integrate these eye movements and result in behavioral adaptations. The review concludes with a summary of the evidence and recommendations for future research in this emerging field.

Keywords: driving; eye movements; eye tracking; glaucoma; optokinetic nystagmus; saccades.

Figure 1

Schematic representation of trans-synaptic degeneration. Retinal ganglion cell atrophy leads to anterograde trans-synaptic degeneration along the optic nerve, optic tract, LGN, and optic radiation. Emerging theories suggest degeneration beyond these pathways, but this remains controversial.

Figure 2

Schematic representation of trans-synaptic degeneration on a cellular scale.

Figure 3

Efferent control of eye movement. (A) anterior (B) axial and (C) sagittal views of the anatomical origins of cranial nerves III, IV, and VI.

Figure 4

Depiction of a prosacadde, anti-saccade, and fixation task.

Figure 5

Forest plot of saccade latency as measured in milliseconds.,

Figure 6

Forest plot of peak saccade velocity data as measured by degrees/ second. Ballae et al report their velocities as degrees/ millisecond which is interpreted by the authors as a misprint.,,

Figure 7

Forest plot of fixation task data as measured by log-BCEA 95%. *Longhin et al did not report their range of BCEA values which provides a misleading effect size in this figure.,,

Figure 8

Summary of key points.

Figure 9

Study selection for review according to PRISMA criteria described in Moher et al 2009.