Abstract
Summary 1. Muscle spasm in poliomyelitis is of two types: A. Hypertonus B. Hyperirritable stretch reflex 2. The clinical characteristics of muscle spasm are described. 3. Muscle spasm is relaxed temporarily by spinal anesthesia or block of the myoneural junction in acute and subacute poliomyelitis. Intravenous pentothal decreases muscle spasm moderately in some patients and is ineffective in other patients. Muscle spasm in poliomyelitis has a neurogenic mechanism and is apparently the result of an increased discharge of nerve impulses through the motor neurons. 4. Evidence is presented to support the theory that the pathologic basis of muscle spasm in poliomyelitis is a lesion of internuncial neurons in the gray matter of the spinal cord. The muscle spasm is produced as a result of release of proprioceptive reflexes from inhibition. A. Muscle spasm has been produced in the experimental animal by temporary arrest of circulation in the spinal cord. Correlated with this muscle spasm, the spinal cord showed a lesion localized to the internuncial neurons, while the anterior horn cells appeared normal. B. In sixty-eight cases of poliomyelitis, review of the spinal cord pathology revealed an internuncial lesion in almost every patient. Twenty-six patients showed an internuncial lesion with relatively normal anterior horn cells. C. Measurements of chronaxie of muscles in fourteen patients with polimyelitis who exhibited marked muscle spasm demonstrated that there is no correlation of muscle spasm with anterior horn cell damage. Many muscles in spasm showed a normal chronaxie while other muscles in spams showed more or less marked increases in chornaxie. These results suggest that anterior horn cell destruction is not the basis of muscle spasm in poliomyelitis. D. Prostigmine, acting on the spinal cord to inhibit proprioceptive reflexes, relaxes muscle spasm and may be of therapeutic value in poliomyelitis.
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