Acute poliomyelitis for many years had been considered a disease specifically affecting the anterior horn cells of the spinal cord. Careful investigations have so extended our knowledge that the disease is now believed to be of a systemic nature, although one which has special predilection for motor spinal nuclei. Newer concepts of pathogenesis have afforded the opportunity for a fresh approach to problems of clinical management.1
During the past two years we have concentrated on the symptom complex of pain and spasm in acute poliomyelitis.2 We have been impressed by the regular occurrence of lesions in the sympathetic ganglions of patients who died of this disease. The observations of ganglion cell changes and interstitial productive inflammatory phenomena in the sympathetic ganglions, as well as of similar lesions of the internuncial and intermediolateral cell groups of the spinal cord and brain stem, have given a rational anatomic explanation for
SMITH E, GRAUBARD DJ, FALCONE J, GIVAN TB, ROSENBLATT P, FELDMAN A. CLINICAL MANAGEMENT OF ACUTE POLIOMYELITIS. JAMA. 1950;144(3):213–218. doi:10.1001/jama.1950.02920030001001
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