Abstract
We tested motion perception and smooth pursuit in 26 patients with unilateral cerebral hemispheric lesions. We used random dot cinematograms to test motion direction discrimination. We measured pursuit gain as they followed a predictable sinusoidal target moving horizontally at three different frequencies, and an unpredictable horizontal step-ramp target in the ipsilateral hemi-field. Six patients had defects in motion perception when the targets were moving towards the side of the lesions ('ipsi-directional' defects) and two had bi-directional defects. Motion perception defects occurred with lesions of the junction of Brodmann areas 19 and 37, a putative human homologue of the monkey V5 complex. Seven patients had ipsi-directional pursuit defects, five of whom had damage to the posterior limb of the internal capsule. Only two patients had ipsi-directional defects of both motion perception and sinusoidal smooth pursuit. Four patients had ipsi-directional defects of motion perception alone, and five patients had ipsi-directional pursuit defects alone. The two patients with bi-directional defects in motion perception had normal sinusoidal smooth pursuit. Patients with lesions at the 19/37 junction and defects of motion perception alone had normal pursuit of unpredictable step-ramp targets in the ipsilateral hemi-field. In contrast, patients with ipsi-directional sinusoidal pursuit defects had decreased ipsi-directional and increased contra-directional velocities with step-ramp targets. No patient group had a motion-specific directional defect in saccadic accuracy. We conclude that neither predictable nor unpredictable pursuit is necessarily impaired by lesions of the 19/37 junction that cause ipsi-directional defects of motion perception. These dissociations between smooth pursuit and motion perception provide evidence that the pursuit system operates as an interconnected network with parallel pathways, rather than as a simple sequential hierarchy of cortical areas.
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