TY - JOUR
T1 - Saccades in Huntington’s disease
T2 - Predictive tracking and interaction between release of fixation and initiation of saccades
AU - Tian, J. R.
AU - Zee, D. S.
AU - Lasker, A. G.
AU - Folstein, S. E.
PY - 1991/6
Y1 - 1991/6
N2 - 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°;, 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.
AB - 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°;, 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.
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U2 - 10.1212/wnl.41.6.875
DO - 10.1212/wnl.41.6.875
M3 - Article
C2 - 1828547
AN - SCOPUS:0025859682
SN - 0028-3878
VL - 41
SP - 875
EP - 881
JO - Neurology
JF - Neurology
IS - 6
ER -