With Walker's1 discovery that prostigmine alleviates the muscular weakness of myasthenia gravis and Wolf's2 finding that quinine abolishes the myotonus of congenital and atrophic myotonia, new impetus was given to the study of the pathophysiology of these disorders. The clinical observation3 that prostigmine exaggerates myotonia and that quinine exaggerates myasthenia established a relationship of opposition in response to drugs that accentuated the obvious contrast between these muscular states. It is this contrast that makes appropriate a comparative evaluation of their symptomatic response to pharmacologic antagonists.
It is two years since Walker's1 contribution and one year since Wolf2 suggested the use of quinine, so that an appraisal of the clinical usefulness of prostigmine and quinine is due. In this period we have studied, seen or been in indirect contact with nine patients with myasthenia gravis, nine patients with myotonia congenita and eighteen patients with myotonia atrophica.
KENNEDY F, WOLF A. QUININE IN MYOTONIA AND PROSTIGMINE IN MYASTHENIA: A CLINICAL EVALUATION. JAMA. 1938;110(3):198–202. doi:10.1001/jama.1938.02790030032008
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