Division of Neurology, University Health Network, University of Toronto, Toronto, Ontario, Canada
Address for correspondence: James A. Sharpe, M.D., Division of Neurology, University Health Network, 399 Bathurst St., ECW 5-042, Toronto, Ontario M5T 2S8, Canada. Voice: 416-603-5950; fax: 416-603-55596.
sharpej{at}uhnres.utoronto.ca
Ann. N.Y. Acad. Sci. 956: 143-154 (2002).
The mesodiencephalic junction is the site of the prenuclear
control of vertical eye motion. We measured vertical saccades,
smooth pursuit (SP), the vertical vestibulo-ocular reflex (VOR),
and its interactions with vision during active head motion in
21 patients with midbrain lesions causing palsy of vertical
saccades, upward, downward, or in both directions. Most patients
with limited slow or slowed saccades in one direction on clinical
examination had slowed saccades in the opposed direction. SP
gain was decreased in both directions in most patients, and
decreased upward or downward in few. VOR gain was subnormal
in both directions in many patients, and upward only in one;
phase lead of the VOR was recorded in 33% of them. Subnormal
SP and VOR gains were often dissociated. Visually enhanced VOR
gains were subnormal in both directions in many patients. Cancellation
of the VOR was impaired in many patients, both upward and downward
in most and upward in few patients. Gaze (eye plus head) tracking
gain was subnormal in 29% of patients. Defective SP and defective
cancellation of the VOR during head free tracking were often
dissociated. We conclude that VOR and SP gains are usually subnormal
in patients with paresis of vertical saccades. Impairment of
pursuit and the VOR are often dissociated. Phase lead of the
VOR implicates damage to velocity-to-position neural integrator
for vertical eye motion. These associations and dissociations
of impaired vertical eye motion signify discrete structural
and functional effects of supranuclear midbrain damage that
are undetected by examination of saccades.
