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Article
July 1976

Letters and Clinical Notes-Reply

Author Affiliations

Neurology Service and Neurology Research Laboratory
Veterans Administration Hospital Hines, IL 60141

Arch Neurol. 1976;33(7):519. doi:10.1001/archneur.1976.00500070061014
Abstract

In Reply.—  In their article, Moskowitz and Porter1 correctly stated the importance of recognizing a superimposed peripheral nerve lesion in hemiplegic patients. We agree that in occasional hemiplegic patients neural compression may occur, causing focal muscle atrophy and appropriate electromyoneurographic changes. In fact, in a brief communication2 we previously stated that impairment of nerve conduction velocities in some hemiplegic patients was related either to reduction of cutaneous temperature or neural compression, to which hemiplegic limbs were more susceptible than normal extremities. Moskowitz and Porter did not postulate peripheral nerve compression theory for hemiplegic amyotrophy, but Critchley3 listed the peripheral nerve hypothesis of Dejerine to explain muscle atrophy in hemiplegia. The point of our article is that although occasional hemiplegic patients may have a superimposed plexus traction or peripheral nerve compression, diffuse muscle wasting as noted by us and others3-4 rather than focal atrophy in the distribution of nerves or roots, muscle

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