OPTIC ATAXIA: A SPECIFIC DISRUPTION IN VISUOMOTOR MECHANISMS

TLDR

Optic ataxia, a visuomotor disorder linked to unilateral parietal lesions, has been examined in 10 patients through film recordings of visually directed arm movements. In half of the patients, visuospatial perceptive tests were also administered to assess spatial processing. The study shows that optic ataxia is a distinct visuomotor impairment independent of visual space misperception, affecting both proximal and distal movement components equally, with error patterns varying by lesion side, indicating two parietally controlled visuomotor mechanisms with hemispheric asymmetry, and lesion mapping reveals consistent posterior parietal involvement while a weak overlap with hemispatial neglect suggests a double dissociation.

Abstract

Visually directed arm movements have been studied by film recordings in 10 patients with optic ataxia resulting from unilateral lesions of the parietal region, in 3 cases on the right and in 7 on the left. Half of the patients also underwent visuospatial perceptive tests. The results indicate the following. (1) Optic ataxia is a specific visuomotor disorder, independent of visual space misperception. (2) The proximal and the distal components of the movements are equally affected as shown in reaching and hand orientation tasks. (3) The percentages of spatial and orientation errors quantified, respectively, in these two situations show a different distribution across the different hand-field combinations according to the side of the lesion: whereas the right-damaged patients show a deficit essentially related to a field effect, the left-damaged patients show in addition to the latter an impairment related to a hand effect. These findings suggest that the 2 types of visuomotor mechanisms responsible for the proximal and distal components of visually-directed arm movements are controlled by the parietal cortex and that there should exist a hemisphere asymmetry in the functional organization of these mechanisms. (4) Reconstruction of the lesions drawn from CT scans in 8 of the patients shows a salient and constant involvement of the posterior parietal cortex, always including the intraparietal sulcus and either the superior part of the inferior parietal lobule or more often various parts of the superior parietal lobule. The weak co-occurrence of optic ataxia and hemispatial neglect, and their different lesion sites, indicate a double dissociation between these two symptoms.