Abstract
The pursuit system utilizes input from cerebral cortical pathways specialized for analyzing visual motion. Impaired smooth pursuit in humans with cerebral lesions usually signifies damage to posterior parietal hemispheric regions. The authors have recently studied horizontal smooth pursuit in 23 patients with discrete unilateral cerebral hemispheric lesions. Ten patients had pursuit asymmetry with lower gain when tracking toward the side of cerebral hemispheric damage. None had lower gain when tracking away. Two patients with lower ipsilateral gain had frontal lobe lesions. Areas of anatomical overlap of lesions associated with asymmetric pursuit in eight patients provide evidence for a pursuit pathway that originates in Brodmann's areas 19 and 39 (angular gyrus), and that these cortical areas are the human homologues of areas MT and MST in the simian cerebral cortex. A normal phase relationship between smooth eye motion and target motion in these patients indicated that prediction in the smooth pursuit system is resistant to cerebral hemispheric damage.The initiation of smooth pursuit in response to step-ramp targets was studied in 18 patients with focal cerebral hemispheric lesions. Seven patients had retinotopic pursuit defects, consisting of low smooth eye movement gain in both horizontal directions in the hemi field contralateral to the cerebral lesions. Only four of those seven patients had complete hemianopia and three had normal visual fields, indicating that ‘blindness’ for motion detection and/or motion generation can occur independently of damage to the geniculostriate pathway. Four patients with complete hemianopia occasionally made smooth eye accelerations to targets stepped into the blind hemifield, in the correct direction, but with low velocity. They did not adjust saccade amplitude to the direction or size of the target step.These measurements of steady state responses to sine wave targets and to step ramp targets enabled the authors to identify four classes of cerebral hemispheric smooth pursuit defects: (1) Ipsilateral low gain pursuit. Contralateral pursuit gain may be normal, low or high. (2) Bidirectional low gain smooth pursuit. (3) Retinotopic impairment of pursuit in both directions in the contralateral visual field. (4) Craniotopic paralysis of pursuit contralateral to the midline after acute non-dominant hemispheric lesions.
Published Version
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