Horner syndrome classically presents as an ipsilateral enophthalmos, blepharoptosis, pupillary miosis and facial anhidrosis due to disruption at some point of the oculosympathetic pathway.
Ptosis is due to interruption of the sympathetic motor innervation of the superior tarsal muscle which is a small muscle composed of smooth muscle fibers intimately associated with the undersurface of levator palpebrae superioris muscle. This muscle inserts into the tarsal plate of the upper eyelid and controls eyelid elevation and retraction.
Pathology
Horner syndrome can be anatomically classified into three types, depending on where the pathology affects the sympathetic pathway 1. Interestingly, postganglionic lesions do not tend to present with anhidrosis, as opposed to central or preganglionic lesions.
central: involves the first order neuron that starts in the hypothalamus and descends down the brainstem to the ciliospinal center (of Budge and Waller), at between C8-T1 4
preganglionic: involves the second order neuron that passes from the brainstem to the superior cervical ganglion in the neck, via the pulmonary apex 4
postganglionic: involves the third order neuron that ascends along the internal carotid artery to enter the cavernous sinus, where it joins the ophthalmic division of the trigeminal nerve
Etiology
There is an extremely long list of causes. The main ones include 3:
Central causes
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hypothalamic, thalamic or brainstem
ischemia (e.g. lateral medullary syndrome)
hemorrhage
tumor
demyelination
Pre-ganglionic causes
apical lung mass/tumor (Pancoast tumor)
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cervicothoracic spine
trauma
thyroid mass/goiter/tumor
mediastinal mass tumor
common carotid artery pathology
injury to superior cervical ganglion
Post-ganglionic causes
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internal carotid artery pathology
aneurysm
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