Abstract

To contribute to a better understanding of a poorly appreciated pioneer of therapeutic neurology, Mary Broadfoot Walker, MD. At a time when the treatment of myasthenia gravis (MG) was "a source of discouragement to the patient and a cause of nightmare for the physician," Mary Walker demonstrated that temporary relief of myasthenic symptoms could be produced by subcutaneous injection of physostigmine or neostigmine (Prostigmin; Roche, Basel, Switzerland). She also pioneered the concept of a circulating factor as the etiology of myasthenia and was the first to report hypokalemia in familial periodic paralysis. Throughout her career she was dependent on her salaried jobs as a medical officer in several large London hospitals and was thus forced to turn down an offer of an honorary staff position with research beds. Previously unpublished material written by persons who lived at the same time as Mary Walker is incorporated with the published record into an account of Mary Walker's accomplishments as assessed by her contemporaries. 1) Although Mary Walker's 1934 report on physostigmine for MG was ignored by most of those in clinical medicine at the time, those responsible for the financing of British medical research vainly hoped that it could be used as an example of the practical outcome of basic research. 2) Her 1935 demonstration of the beneficial effect of neostigmine (Prostigmin) was greeted with general skepticism because of the rapidity with which the patient's symptoms of myasthenic weakness improved, but she was soon vindicated by published confirmatory reports from several contemporaries. 3) Her 1938 demonstrations of what came to be known as "the Mary Walker effect" may have helped her reputation because subsequent published opinions of her contributions were generally favorable, although some people continue to disparage her even today. Mary Walker, with her brief case reports and her frequent demonstrations, not only offered symptomatic treatment for MG that has stood the test of time, but also provided the most convincing evidence at the time that the neuromuscular junction was the focus of the disease.

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