An Evaluation of Curare in Spasticity Due to Spinal-Cord Injuries

Abstract

IN 1850 Claude Bernard¹ demonstrated the site of action of curare to be the neuromuscular junction. His experiments have been verified by numerous investigators, and in 1935 West² and King³ clarified the mode of action and enumerated the pharmacologic properties of the drug. It was not until 1943 that Wintersteiner and Dutcher⁴ crystallized the quaternary ammonium salt, d-tubocurarine chloride. Recent availability of this pure preparation has stimulated clinical and pharmacologic investigations.The gross effects of curare on the normal human subject have been thoroughly investigated. The intrinsic musculature of the toes and eyes demonstrates early paresis, which successively involves the . . .