Journal of Neuroscience, Vol 12, 2198-2210, Copyright © 1992 by Society for Neuroscience
Visual processing of motion-defined form: selective failure in patients with parietotemporal lesions
D Regan, D Giaschi, JA Sharpe and XH Hong
Department of Ophthalmology, Toronto Hospital, University of Toronto, Canada.
The following psychophysical data were obtained from 13 patients with
unilateral cerebral hemispheric lesions and 20 control subjects: speed
thresholds for detecting and for recognizing motion-defined letters, speed
thresholds for detecting coherent motion and for discriminating its
direction, and visual acuity for recognizing letters of 96% and 11%
contrast. Acuity was between 6/6 and 6/3 for all patients. Four patients
showed a selective loss of ability to recognize motion-defined letters,
while the ability to detect those same letters was spared, as was the
ability to detect coherent motion and discriminate its direction (type I
loss). Three patients showed a loss of ability both to recognize and to
detect motion-defined letters, while the ability to detect coherent motion
and discriminate its direction was spared (type II loss). All seven
patients who failed to recognize motion-defined letters had extensive
lesions in parietotemporal white matter underlying Brodmann cortical areas
18, 19, 37, 39, 21, and 22. The lesion was in the left hemisphere for three
patients and in the right hemisphere for the remaining four. The region of
overlap in these seven patients was not invaded by the lesion in any of the
other six patients, and none of these six patients showed a loss of ability
to recognize motion-defined letters. Three patients showed selective loss
of acuity for low-contrast letters with normal Snellen acuity. The lesions
in these three patients extended more posteriorly than in any other
patient, and their region of overlap was in white matter underlying areas
18 and 19. We conclude that (1) the loss of ability to recognize letters in
seven patients was specific to motion-defined letters rather than being a
general loss of letter-recognition ability, (2) this visual loss was
specific to motion-defined form rather than being a general failure of
motion processing, and (3) the visual loss was not produced by lesions that
did not involve the localized cerebral region specified above. To explain
the existence of type I and of type II loss with sparing of the detection
and discrimination of coherent motion, we propose that motion information
is processed hierarchically. We further suggest that homologs of the
socalled motion and color/form pathways (i.e., areas V1/MT/MST/7a and areas
V1/V4/IT) are interconnected to form a distributed system that is important
for the recognition of motion-defined form.(ABSTRACT TRUNCATED AT 400
WORDS)
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