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NEUROLOGY 1977;27:963
© 1977 American Academy of Neurology

Neuromuscular blockade with anti-axoplasmic antibodies

B. W. FESTOFF, M.D., A. S. ISRAEL, W. K. ENGEL, M.D. and R. B. ROSENBAUM, M.D.

Department of Neurology, University of Kansas Medical Center, Kansas City, KS, and the Neurology Service, Veterans Administration Hospital, Kansas City, MO (Dr. Festoff); the National Institute of Neurological and Communicative Disorders and Stroke, Bethesda (Dr. Engel); and the Department of Neurology, University of California Medical School, San Francisco.

In the process bf developing an immunopharmacologic method for identifying a "trophic" protein released from motor nerve terminals, a soluble fraction of peripheral nerve axoplasm was prepared. An attempt was made to eliminate contaminating myelin and basic protein. Antibodies were produced to soluble nerve proteins in all sheep immunized. On boosting, after a 6-week interval, the animals became weak, and some could not stand on the fifth day after injection. A distinct component of neuromuscular blockade was demonstrated electrically and in response to edrophonium. Because this syndrome was (1) in the broadest sense, an experimental allergic neuropathy but produced by a distinctly different antigen than has been utilized previously (the soluble nerve proteins represented the axoplasmic compartment) and (2) a clinical condition associated with a defect in neuromuscular transmission, this may represent a new and potentially important model in the study of neuromuscular and other neurologic diseases.

Reprint requests should be addressed to Dr. Festoff, Chief, Neurology Service, V. A. Hospital, Kansas City, MO 64128.

Presented in part at the 27th meeting of the American Academy of Neurology, Bal Harbour, Florida, April 1975.

Accepted for publication November 1976.






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