Early movement impairments in a patient recovering from optic ataxia

Since Balint's first description, optic ataxia has been considered as a pure visuomotor impairment produced by a lesion of the posterior parietal cortex. Beyond general agreement on the parietal involvement in visually guided behaviour, the exact role of the dorsal posterior parietal cortex in the temporal aspects of visuomotor control remains unclear. Recent evidence has indicated a specific involvement of the parietal cortex in the on-line visual guidance of movement. Here, we report the motor performance of, GT, a patient recovering from an optic ataxia due to a right focal lesion of the dorsal posterior parietal cortex. When asked to reach and grasp, with his left contralesional hand, different sized objects, located at different positions from his body, GT showed an apparently complete recovery from optic ataxia. However, the early kinematic aspects of GTs prehension movement were not normally tuned either by intrinsic or extrinsic visual properties of objects. At variance with both an age-matched control group and a neurological patient with a right internal capsule lesion and no sign of optic ataxia, GTs latencies to peak wrist acceleration and peak velocity were not modulated by object location. A similar defective pattern was present in GTs grasping component where, despite the sparing of the classical scaling of grip aperture, object size did not modulate the peak velocity of grip aperture. These results constitute evidence that the posterior region of the dorsal parietal cortex, besides playing a role in the on-line control of movement execution may also be involved in the programming of early kinematics parameters.