Abstract
Although cerebellar-like ataxia is a well known component of the ataxic hemiparesis (AH), the mechanism of hypermetria in AH has not been established. We describe a patient presenting a left AH following a right pontine infarction. We investigated the ballistic flexion movements of both wrists and the associated agonist and antagonist electromyographic (EMG) activities, before and after addition of inertial loads. At the time of motion analysis, neurological examination showed cerebellar-like dysmetria of the left side but the patient had recovered a normal strength. In the basal state (without addition of loads), movements of the left wrist were hypermetric. The duration of the agonist EMG activity was prolonged and the onset latency of the antagonist EMG activity was not delayed. Moreover, when a mass was added, the hypermetria was unchanged because the patient was unable to adapt appropriately neither the agonist, nor the antagonist EMG activity. We suggest that the hypermetria was due to an imbalance between the duration of the agonist EMG activity (the launching force) and the duration of the antagonist EMG activity (the braking force).
Published Version
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