Pharmacologic Diagnosis of Pupillary Dysfunction

The diagnosis of anisocoria or of bilateral pupillomotor abnormality can be sharpened by the use of topical pharmacologic agents. Strong mydriatics or miotics override neural influences, so that any remaining anisocoria (or subnormal response) indicates iris disease, whereas elimination of anisoco-ria (or normal response) indicates a neural cause of the pupillary dysfunction.

For example, incomplete (or asymmetric) response to standard pharmacologic dilation (phenylephrine 2.5-10% with tropicamide 1%) suggests an iris structural abnormality, which may be more easily detected at slit-lamp after attempted dilatation. Conversely, incomplete miotic response to pilocarpine 1-2% may suggest previous pupillary sphincter trauma, or recent exposure to an anticholinergic agent (topically to the eye if unilateral, and perhaps systemically if bilateral).

In contrast, weak mydriatic or miotic agents can be used to highlight denervation supersensitivity when it exists. Within days of sympathetic denervation of the iris, the dilator muscle will exhibit supersensitivity to weak alpha-1 adrenergic agonists (epinephrine 0.1%, phenylephrine 1%, or most recently apra-clonidine 0.5-1%); such agents (or cocaine, below) are often used to distinguish Horner pupil from physiological anisocoria. Similarly, a weak cholinergic agonist (pilocarpine 0.06-0.12%) can demonstrate the cholinergic supersensitivity found in Adie tonic pupil.

Two additional agents are classically employed in the diagnosis of Horner pupil. Cocaine 10% solution has the unique property of preventing presynaptic norepinephrine reuptake; because of the steady baseline release of small amounts of norepinephrine into the neuromuscular cleft of the pupillary dilator muscle, the normal response to topical cocaine is pupillary dilatation. When baseline norepinephrine release is absent (because of either absence of the tertiary neuron or its neurochemical silence), cocaine will fail to dilate the Horner pupil.

Topical hydroxyamphetamine 1% causes release of stored presynaptic norepinephrine at the dilator’s neuromuscular junction. Therefore, lack of dilation in response to hydroxyamphetamine suggests absence of the tertiary neuron, helping to “localize” the lesion in the pupillary sympathetic chain.

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  • Category: Nervous diseases