Horner's Syndrome

Overview

Horner’s syndrome develops from injury to anywhere along the C8-T2 sympathetic pathway: as proximal as the hypothalamus to as distal as the post-ganglionic sympathetic fibers. Localizations include the hypothalamus, medulla, ciliospinal center of Budge (C8 - T2), superior cervical ganglion, carotid artery.

Findings

The complete syndrome consists of: 1 miosis; 2 ptosis; 3 apparent enophthalmos; 4 anidrosis and warmth of the face.

Common Causes

A lesion of the common carotid artery alone will spare the sympathetic supply to the face (travels with the external carotid artery) and a lesion of the carotid bifurcation will cause a complete Horner’s as both the eye and facial sympathetic innervation are lesioned.
The most obvious peripheral Horner’s occurs from lesions of the superior cervical ganglia and carotid artery.
A particularly important cause is squamous cell carcinoma of the lung which destroys the sympathetic chain in the thorax. It is rarely noted following carotid catheterization, but is common with severe migraine (Raeder’s paratrigeminal neuralgia), cluster headache and the autonomic trigeminal

migraine syndromes. It is a cardinal sign of carotid dissection in association with contralateral hemiparesis and facial pain.

The central Horner’s syndromes are noted most commonly with Wallenberg’s syndrome, but may be seen with any lateral brainstem lesion.
A “baby Horner’s” may occur following lesions of the frontal eye fields. This is usually noted as ptosis (decreased cortical innervation to the central caudal nucleus of the third nerve complex) most often ipsilaterally, but at times contralaterally with minimal miosis (decreased cortical–diencephalic

innervation) which also occurs ipsi- and contralaterally.

The Cocaine Test

Cocaine will not dilate the pupil (mechanism of its action is blockade of reuptake of dopamine and noradrenaline) and adrenaline dilates it more than usual (Cannon’s law of denervation supersensitivity).

Horner's Syndrome

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