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Comments on the paradoxic pupillary dilatation in optic neuropathy

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Abstract

REMOTE mild optic neuropathy may be suggested by the symptom. of monocular visual dimness lasting several days or weeks, and by diagnosis of demyelinating disease. Of more importance is the discovery of active but occult retrobulbar neuritis, which is common and seemingly relieved by treatment with adrenocorticotropin (ACTH) or corticosteroids. The diagnosis of such optic neuropathy, even when active, may be difficult. In mild cases the expected pain with eyeball movement is often absent, and even careful plotting of the visual fields does not reveal the usual central or paracentral scotoma. Even the visual acuity may not be demonstrably disturbed although the patient's symptom is cloudiness of vision. It is in such instances that abnormality of pupillary light reactivity can become diagnostic.

There are several simple ways to uncover the pupil hyporeactivity, but to Gunn1 goes the credit of popularizing the phenomenon that is often termed the Marcus Gunn pupil or the Marcus Gunn pupillary sign.2 Kestenbaum3 emphasized the importance of this finding and he described modifications. Both Kestenbaum and Duke-Elder4 have underscored the basic pathophysiology, whereas Daroff and Smith2 emphasize the clinical usefulness of the pupillary test.

Pupillary constriction to light, the pupillomotor force, is regularly impaired when optic nerve impulses are interrupted. In severe optic neuropathy the pupil is always dilated and there is little or no reaction to light. In moderately severe lesions there is no anisocoria, but diminished pupil reactivity to light is easily demonstrated. In the milder cases of unilateral optic neuropathy, covering one eye . . .


 

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