Abstract
<h3>To the Editor.—</h3> In a recent article by Mogelnicki and associates (241:826, 1979) regarding the use of physostigmine in two patients to reverse a stupor that was apparently induced by the histamine H<sub>2</sub>antagonist cimetidine, the authors note two possible explanations for the observed events: First, physostigmine was acting specifically to reverse an anticholinergic stupor caused by cimetidine. Cimetidine would be classified with a wide variety of other drugs known to produce the central anticholinergic syndrome, which is manifested by stupor in severe cases. If physostigmine was reversing a central anticholinergic stupor produced by cimetidine, presumably at H<sub>2</sub>receptors in the CNS, the clinical manifestations of the anticholinergic syndrome in these two patients were unusual because the patients did not first manifest the usual initial mental changes associated with the central anticholinergic syndrome, such as delirium and agitation, before their conditions progressed to stupor. The second explanation of
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