MYDRIASIS is one of the characteristic clinical signs of acute congestive (narrow-angle) glaucoma. It has long been known that in certain instances treatment with miotics of any type fails to bring about miosis or reduction in ocular tension. In such fulminating attacks, therefore, surgery must be performed under the adverse circumstances associated with high ocular tension, hyperemia, and congestion. This paper reports the results of investigations undertaken to determine the mechanism responsible for the miotic-resistant, dilated pupil of acute congestive (narrow-angle) glaucoma and to present certain possibilities regarding its origin. The most likely explanations are (1) increased tone of the dilator muscle as a result of reflex stimulation of the sympathetic nerves; (2) pressure paresis of the parasympathetic motor nerves to the iris sphincter as they pass through the suprachoroidal space; (3) disturbance of the local neurohumoral mechanism, resulting in interruption of stimuli to the muscle cells of the iris