Abnormal Pupillary Conditions

Although initially the affected pupil is larger than the contralateral pupil, with time it can become smaller. The pupil is very sensitive to acetylcholine (probably due to denervation supersensitivity), with strong, tonic constriction; this can be demonstrated by the vigorous miotic response to methacholine chloride and 0.1% pilocarpine. The intact sympathetic innervation is demonstrated by the normal response to cocaine.

ARGYLL ROBERTSON PUPIL

This was initially described in neurosyphilis or tabes dorsalis. The classic findings include a normal near or convergence reflex with normal pupillary responses to accommodation and an abnormal pupillary response to light. In addition, the pupils are small, irregular, and constrict with physostigmine and dilate variably with atropine and cocaine. The location of the lesion in the brain that causes the abnormal response is thought to be the rostral midbrain, near the periaqueductal gray. Although previously thought to be pathognomonic of neurosyphilis, it is now recognized in diabetes, viral encephalitis, multiple sclerosis, and other inflammatory and degenerative diseases of the brain.

HORNER SYNDROME

Horner syndrome results from loss of sympathetic innervation to the eye and is characterized by ptosis (droopy eyelid), miosis (constricted pupil), and facial anhidrosis (impaired facial sweating). Additional findings may include pigmentary changes in the iris. Pupillary reactions to light and accommodation are normal. The anisocoria (inequality in pupil size) is accentuated in dim light. The ptosis is due to paralysis of the Muller muscle; this is the sympathetically innervated smooth muscle of the upper eye lid. Acquired Horner syndrome may be central, preganglionic, or postganglionic. A central lesion may involve the first-order neuron at any point from the cell origin in the hypothalamus to its termination in the intermediolateral column of the spinal cord. Causes include brainstem infarction, tumor, and syringomyelia (cavitation in the spinal cord). Preganglionic Horner syndrome is due to involvement of the second-order neuron from its origin in the intermediolateral column to its termination in the superior cervical ganglion; causes include trauma or tumor of the cervical or upper thoracic spinal cord and lesion of the lower trunk of the brachial plexus, such as by tumors of the lung apex, jugular vein puncture, and thyroid surgery. Postganglionic Horner syndrome results from lesions of the third-order neuron in the sympathetic ganglion and the pathway leading to its termination in the face and eye, such as by extracranial carotid artery dissection, intracranial lesion in the carotid canal, or cavernous sinus pathology. Use of cocaine eye drops (which block the reuptake of norepinephrine) will help distinguish true Horner syndrome from physiologic anisocoria; 1 hour after instillation of 4% to 10% cocaine drops, a normal pupil will have dilated more than a pupil with sympathetic dysfunction (irrespective of site of lesion), increasing the baseline anisocoria. Apraclonidine, an alpha-adrenergic receptor agonist will cause the affected pupil to dilate (due to alpha-adrenergic supersensitivity), whereas the normal pupil will constrict. Pharmacologic testing will also differentiate between central, preganglionic, and postganglionic lesions. Hydroxyamphetamine (1%) drops instilled into the eye do not affect the pupil of Horner syndrome resulting from a lesion of the third-order postganglionic neuron, whereas a dilation occurs of normal pupils and in Horner syndrome with an intact third-order neuron due to release of norepinephrine. Similarly, 1% solution of phenylephrine hydrochloride will dilate the pupil in postganglionic lesions (third-order neurons) but not normal pupils.

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