Quantitative assessment of muscular hypertonia resulting from cortical lesions in primates.
The effects of various cerebral cortical lesions on motor function and in particular on muscle tone have been studied quantitatively in the squirrel monkey (Saimiri sciureus) in an attempt to define the cause of muscular hypertonia and to develop a reliable model for human cerebral spasticity. Unilateral ablation of the primary motor area (MI), either alone or together with the supplementary motor area (MII), produced a contralateral hemiparesis especially marked for fine motor tasks, but did not cause hypertonia. Bilateral ablation of the supplementary motor area alone produced no impairment of motor function or change in muscle tone. Bilateral lesions of the primary motor area, either alone or together with the supplementary motor area, caused a disabling quandriparesis with striking hypertonia affecting chiefly the upper limb flexors and lower limb extensors. Quantitative electromyography revealed augmented stretch responses proportional to the rate of muscle lengthening. This velocity-dependent exaggerated stretch reflex, with a predominantly dynamic component reflecting hyperactivity of the Ia spindle afferents, is similar to that seen in human hemiplegic spasticity. Out results indicate that decorticate hypertonia depends upon the bilateral interruption of fiber tracts originating in motor cortex and distributed both ipsilaterally and contralaterally. Bilateral decortication in the primate seems to be a suitable laboratory model for the objective evaluation of measures proposed for the relief of spasticity in humans.