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For the neurologist, examination of eye movements at the bedside is a traditional mainstay of anatomic localization and often provides diagnostic certainty in complicated clinical problems. For the basic neuroscientist, recording and analysis of eye movements, both in behaving monkeys and in normal humans, have become powerful tools to understand normal ocular motor control and to probe higher-level cerebral mechanisms that underlie attention, memory, and decision making. The antisaccade task is an example of such a useful eye movement paradigm.1–3⇓⇓ In this task, the subject has to cancel willfully a “reflexive” saccade to a suddenly appearing visual stimulus (i.e., …

We compared saccadic eye movements in 21 patients with Huntington's disease (HD) and 21 normal subjects. In a predictive tracking task, HD patients were unable to anticipate normally the timing and location of a visual target that alternated its position predictably (+/- 10 degrees, 0.5 Hz; mean latency of +170 msec in HD and -78 msec in normal subjects). HD patients and normal subjects, however, showed comparable decreases in saccade latency (110 msec in HD, 124 msec in normal subjects) when the fixation target was turned off 200 msec before (gap task) versus 200 msec after (overlap task) the appearance of an unexpected peripheral stimulus. Taken together, these findings support the idea that HD patients show greater defects in initiating internally generated than in initiating externally triggered saccades. This dichotomy is likely due to involvement of frontal lobe--basal ganglia structures in HD, with relative sparing of parietal--superior collicular pathways.

Article abstract-Eye movements were recorded from 20 mildly affected patients with Huntington’s disease (HD) who were divided into two groups, 10 patients with onset of symptoms before age 30 and 10 with onset of symptoms after age 30. In the younger onset group (HD 30) had peak saccade velocities lower than 300 deg/sec. Latencies for volitional saccades were greater than normal in the HD > 30 group, but were normal for the HD 30 group had an affected mother. These findings suggest that the pathophysiology of the slow saccades, initiation deficit, and excessive distractibility in HD are different. NEUROLOGY 1988;38427-431 In a recent study of eye movements in mildly affected patients with Huntington’s disease (HD), we found abnormalities of both the initiation of saccades as well as the ability to hold steady fixation.’ Most patients showed an increase in saccade latencies that was greater for saccades made on command (voluntary saccades) than for saccades made to the sudden appearance of a visual stimulus (reflexive saccades). All patients showed excessive distractibility; they had difficulty in suppressing a saccade to a suddenly appearing visual target even though they were instructed either to maintain straight-ahead fixation or to make a saccade in the direction opposite to the visual target. We attributed these abnormalities to involvement of the frontal eye fields or basal ganglia in HD. In the present study, we report further abnormalities of eye movements-saccade slowing andsaccade dysmetria-in the same group of patients, and compare these findings with their deficits in saccade initiation and in holding steady fixation. Slow saccades have been noted in patients with HD with a reported prevalence of 18% to 100%.2-10 While one study did seem to show a correlation between the age of the patient and the saccade ~elocity,~ few attempts have been made to correlate saccade slowing with other saccade abnormalities in HD or with patient age or severity or duration of illne~s.~J~J~ In contrast to the saccade initiation and the fixation deficits, which have been attributed to involvement of the basal ganglia or cerebral hemispheres, saccade slowing has usually been attributed to direct pathologic involvement of the intrinsic brainstem structures that generate the immediate premotor commands for saccadic eye movement~.~-~ Accordingly, to better understand the eye movement abnormalities in HD, we compared disor

We studied eye movements in 50 patients with Huntington's disease. Fixation was impaired in 73% of patients; such individuals had difficulty in suppressing saccades toward novel visual stimuli. Impaired initiation of saccades was manifest by increased reaction time (89%) and inability to make a saccade without head movement (89%) or blink (35%). Saccades and quick phases of nystagmus were slowed in 62%. Smooth pursuit was abnormal in 60%, and vergence in 33%. The vestibulo-ocular reflex and the ability to hold eccentric gaze were preserved even late in the disease.