Abstract
Two cases of multiple sclerosis are reported in which attacks of pulmonary edema with recovery were observed during treatment with prostigmine. The mechanism by which prostigmine leads to pulmonary edema is explained through its muscarinic components which stimulate the secretion of the respiratory glands and produce bronchoconstriction. The free inflow of air is impeded and the consequent anoxia renders the dilated vessels more permeable. The suction of the descending diaphragm draws fluid into the alveoli. In neurological conditions in which an effect on the voluntary muscle is intended, prostigmine should be used in combination with atropine.

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