Ocular tracking of step-ramp targets by patients with unilateral cerebral lesions.
The relationship of sinusoidal smooth pursuit defects to pursuit defects with step-ramp targets in patients with cerebral lesions is unclear. We examined pursuit and saccades to both step-ramp and sinusoidal targets in 17 patients with unilateral cerebral lesions. Two types of pursuit defects were found. One group of three patients had ipsi-directional sinusoidal pursuit defects from lesions to the posterior internal capsule. Their chief abnormality with step-ramp targets was increased contra-directional pursuit. Their ipsi-directional step-ramp pursuit was often normal and disproportionately better than their ipsi-directional sinusoidal pursuit. Another patient with a parietal lesion had a second type of pursuit defect. He had low-normal sinusoidal pursuit bilaterally, but decreased ipsi- and contra-directional step-ramp pursuit. Also, he had an abnormal contra-directional drift after saccades to stationary targets. Despite these pursuit defects, saccadic accuracy did not show poor compensation for target motion in either patient type. The patient with the parietal lesion also had increased latencies for contralateral saccades. Recovery of pursuit was studied in one patient with an infarct of the posterior internal capsule. Initially he had a contra-directional bias that caused decreased ipsi-directional pursuit, increased contra-directional pursuit, and a contra-directional drift after saccades to stationary targets. Four months later, ipsi-directional pursuit and the post-saccadic drift to stationary targets had recovered, but contra-directional pursuit remained abnormally high. We conclude that lesions of descending pursuit tracts in the internal capsule are characterized by a contra-directional bias which recovers partly through a direction-specific adaptation. Lesions that affect the human homologue of posterior parietal cortex cause asymmetric bi-directional defects in pursuit initiation and increased contralateral saccadic latencies.
Barton
J J
JJ
Division of Neurology, Toronto Hospital, University of Toronto, Canada. jbarton@bidmc.harvard.edu
Sharpe
J A
JA
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001927:Brain Diseases / Q000473:pathology / Q000503:physiopathology*; D004292:Dominance, Cerebral / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010775:Photic Stimulation / Q000379:methods; D011698:Pursuit, Smooth / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D012438:Saccades / Q000502:physiology; D014786:Vision Disorders / Q000503:physiopathology; D014794:Visual Fields / Q000502:physiology