Abstract

The primate middle cerebral artery (MCA) preparation has been studied as an animal model of human spasticity resulting from stroke. MCA occlusion in 3 squirrel monkeys was accomplished through a transorbital approach and animals were evaluated by ‘clinical’ examinations and studies of EMG responses to torque motor imposed joint displacement. Animals were transiently hemiparetic but not spastic postoperatively, although all were found to have a large infarct in MCA territory on post-mortem examination. The electromyographic (EMG) response of biceps in normal animals to torque motor imposed elbow extension consisted of both early (M1) and late (M2) components (Tatton et al. 1975). These components were unchanged following MCA occlusion. The EMG response to metacarpophalangeal joint extension in finger flexors of normal animals consisted solely of a long-latency (M2) component (Lenz et al. 1983a). Following MCA occlusion the M2 component in this muscle was decreased or absent, but a short-latency (M1) component appeared.

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