Horner syndrome

Last revised by Rohit Sharma on 27 Feb 2024

Horner syndrome classically presents as an ipsilateral enophthalmosblepharoptosis, 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.


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


There is an extremely long list of causes. The main ones include 3:

Central causes
Pre-ganglionic causes
Post-ganglionic causes

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