Ocular Motor Abnormalities in Neurodegenerative Disorders

CA Antoniades; C Kennard

Disclosures

Eye. 2015;29(2):200-207. 

In This Article

Alzheimer's Disease (AD)

Clinical Ocular Motor Manifestations

Abnormalities of eye movements in AD, especially saccades, have been reported in a number of studies.[6] Hypometric saccades, prolonged saccade latencies,[7–11] reduced peak velocities,[8] and disorganized visual scanning[10,12] have been noted. However, an early observation suggesting that prosaccadic latencies might prove to be a reliable index of dementia severity[13] was not confirmed.[7] Furthermore, results from studies looking at the saccadic gain and velocity in AD are controversial; some studies found impairment,[8,14] whereas other studies did not.[9,15]

Research Findings

Scinto et al[16] noted deficits in the generation of visually-guided saccades in AD, which they attributed to an attentional, rather than to an ocular motor source. However, two consistent impairments of saccades have emerged from AD research: (1) a high frequency of saccadic intrusions during attempted fixation;[11] and (2) visual capture by the target in the antisaccadic paradigm,[14,17–19] in which the subject has to suppress a reflexive saccade to a peripheral target and execute an endogenously driven saccade to an equal and opposite location. Interestingly, inhibition errors in the antisaccadic paradigm could be predicted by measures of dementia severity.[14,17,18,20] Antisaccades may provide not only a functional index of the dorsolateral prefrontal cortex, which is damaged in the later stages of AD, but also a tool for monitoring the progression of AD.[6] A more recent study[21] used an antisaccadic paradigm as a way of testing inhibitory control in AD patients. The results showed that AD patients were impaired relative to the mild cognitive impairement in participants and healthy controls. The antisaccadic task, therefore, might be a useful and relatively easy way of measuring executive function in AD.

Smooth pursuit eye movements in AD are also usually abnormal. Increased frequency of saccades during pursuit[22] may result from a disturbance in the pursuit system, due to a reduced gain (eye velocity divided by target velocity).[23] However, large-amplitude saccadic intrusions in the direction of target motion are also observed, probably reflecting increased saccadic distractibility.

Recently, a study by Kapoula et al[24] has looked into measuring fixational eye movements and in particular microsaccades, in a group of AD, minimal cognitive impairment, and healthy individuals. Microsaccade direction differed significantly in patients vs controls, but no abnormalities were observed in microsaccade dynamics (such as duration, intersaccadic intervals, peak velocity, and the peak duration—magnitude relationship) that are more directly related to the function of the brainstem saccade generator.[25] Such studies lend support to the idea that microsaccadic metrics may be a useful tool for an accurate diagnosis, as well as for evaluating ongoing therapies in neurodegenerative disorders, such as AD.

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