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)

The histopathologic effects of methanol on the optic nerve were studied in four patients. Circumscribed myelin damage occurred behind the lamina cribrosa in each nerve. Axons were preserved. Demyelination also occurred in cerebral hemispheric white matter in one patient. This selective myelinoclastic effect of methanol metabolism is probably caused by histotoxic anoxia in watershed areas of the cerebral and distal optic nerve circulations. Juxtabulbar demyelination may cause optic disk edema in methanol poisoning by compressive obstruction of orthograde axoplasmic flow. Visual loss may be due to disruption of saltatory conduction. Retrolaminar demyelinating optic neuropathy is an early morphologic correlate of visual loss in methanol intoxication.

We have developed a simple procedure for assessing the ability of the visual pathway to extract a two-dimensional shape from motion. The test requires a patient to read motion-defined (MD) letters. These letters differ physically from the familiar contrast-defined (CD) letters that are dimmer or brighter than their surroundings in that the boundaries of MD letters are rendered visible exclusively by a step in velocity while the boundaries of CD letters are rendered visible by a step in luminance. Subjects viewed a random pattern of bright dots containing a perfectly camouflaged letter. Then the letter was revealed by moving dots within and outside the letter at equal speeds in opposite directions. Letter reading scores for 50 eyes of 25 patients with multiple sclerosis (MS) or optic neuritis were compared with norms based on 50 control subjects. When tested with large (50 arc min, i.e., 6/60) MD letters, 34/50 eyes of patients required abnormally high dot speeds to read letters, visual loss being sufficiently selective in 10 eyes that contrast sensitivity, Snellen acuity, 11%-contrast and 4%-contrast acuity were all spared. Four eyes were effectively motion blind in the sense that they could not read large letters even at our highest relative speed of 0.9 deg/s and the failure could not be attributed to reduced Snellen acuity. Our normal limit was 2.5 SD from the control mean and there were 1/50 false positives. Of the 34/50 eyes with elevated speed thresholds, 23 had normal Snellen acuities. The number of eyes abnormal for intermediate (11%) contrast CD letters, was 19/50 of which 8 had normal Snellen acuity, confirming our previous finding that MS can degrade the ability to see low-contrast objects while sparing Snellen acuity. We conclude that MD test letters can detect lesions that are not picked up by testing with CD test letters of high or low contrast. We suggest that the MD letter test can detect dysfunction in the human equivalent of a pathway in monkey brain that originates in large retinal ganglion cells, passes through the magnocellular layers of the lateral geniculate body, includes cortical area MT, and is involved in processing motion.

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