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Although pure motor hemiplegia has not been reported after cerebral cortical infarction, occasional exceptions may occur. We provide three such examples. Necropsy study confirmed the site of lesion in one patient, and laboratory results (EEG and computerized axial tomography) suggested cortical involvement in the other two patients.

Attenuation of cerebral evoked responses after stimulation of the median nerve in the hemiplegic limbs suggested that an apparently pure motor hemiplegia in some patients may not have pure involvement of the corticospinal system. Frontoparietal metastasis, infarction in basis pontis and medullary pyramid, and occlusion of internal carotid artery in the neck resulted in pure motor hemiplegia in some individuals.

Motor nerve conduction velocities of the ulnar and common peroneal but not the median nerves were substantially reduced in the affected limbs in a series of hemiplegic patients. Slowing of conduction velocity of the common peroneal nerve was related to the reduction of skin temperature in the hemiplegic limbs. Brachial plexus latencies to biceps and deltoid muscles were longer in the affected than in the unaffected sides in five of 12 hemiplegic patients. Electromyograms (EMGs) of limb muscles showed absence of spontaneous activity in 83% of patients. Spontaneous EMG activities in 12 of the 13 patients were related to an associated subclinical neuropathy or plexopathy in the involved limbs. Entrapment andtraction causing subclinical or clinical neuropathy or radiculopathy may be present in some hemiplegic patients.

Thirty hemiplegic patients had simple muscle atrophy with reduced mean muscle cross sectional areas (predominantly type II fiber atrophy) and complex, multiple, or enlarged subneural apparatuses, many of which resembled subhuman endplates. Ultrastructural observations in a few patients revealed nonspecific responses of damage to sarcolemma and myofibrils. There was no correlation between structural changes and alteration of tone, sensory impairment, or site of lesion. We propose that hemiplegic amyotrophy results from a combination of disuse, loss of central "trophic" influence, and transsynaptic degeneration.

A 77-year-old man suddenly developed left hemiplegia without sensory impairment, visual or speech difficulties, loss of consciousness, or ataxia. He died one month later of pulmonary embolism, and a cystic infarction in the right medullary pyramid was the only lesion in the corticospinal system.