In recent years radical changes in the therapy of poliomyelitis have been advocated which have stimulated reinvestigation of the pathologic physiology of the disease. The Kenny concept has placed emphasis on neuromuscular changes which obviously cannot be explained by the well recognized lower motor neuron paralysis in this disease.1 "Muscle spasm" and "incoordination" have been shown to be frequent and prominent symptoms of poliomyelitis.
"Muscle spasm" consists of at least two phenomena involving muscular hyperactivity in tonus and proprioceptive reflexes. The first phenomenon is a muscular rigidity or hypertonus which results in deformity (as in "foot retraction" or "foot drop") and limitation of passive motion (as in the rigidity of the back). The second type of change, which has been called "muscle spasm," is a limitation of passive motion which is at least in part the result of hyperirritable stretch reflexes in the muscles involved. As an example, in