We tested motion perception and smooth pursuit in 26 patients with uni
lateral 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 t
hree different frequencies, and an unpredictable horizontal step-ramp
target in the ipsilateral hemi-field. Six patients had defects in moti
on perception when the targets were moving towards the side of the les
ion ('ipsi-directional' defects) and two had bidirectional defects. Mo
tion perception defects occurred with lesions of the junction of Brodm
ann areas 19 and 37, a putative human homologue of the monkey V5 compl
ex. Seven patients had ipsi-directional pursuit defects, Jive of whom
had damage to the posterior limb of the internal capsule. Only two pat
ients had ipsi-directional defects of both motion perception and sinus
oidal smooth pursuit. Four patients had ipsi-directional defects of mo
tion 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 norm
al 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-directiona
l velocities with step-ramp targets. No patient group had a motion-spe
cific directional defect in saccadic accuracy. We conclude that neithe
r predictable nor unpredictable pursuit is necessarily impaired by les
ions of the 19/37 junction that cause ipsi-directional defects of moti
on perception. These dissociations between smooth pursuit and motion p
erception provide evidence that the pursuit system operates as an inte
rconnected network with parallel pathways, rather than as a simple seq
uential hierarchy of cortical areas.