A patient with a cavernous sinus thrombosis develops complete ophthalmoplegia, Horner syndrome, and loss of all facial sensation. The combination of a fixed dilated pupil alongside Horner syndrome in cavernous sinus pathology is explained by:

• A Simultaneous damage to CN III and CN IV, causing isolated upgaze paralysis
• B Horner syndrome causing mydriasis and CN III causing ptosis
• C CN VI damage causing abduction failure and CN VII causing loss of orbicularis oculi
• D Simultaneous damage to CN III (parasympathetic dilator inhibition) and sympathetic fibres (mydriatic function), with CN III palsy dominating causing mydriasis ✓

Explanation

In cavernous sinus disease, both CN III (which carries parasympathetic fibres causing pupilloconstriction via the ciliary ganglion) and postganglionic sympathetic fibres (which travel on the internal carotid artery through the sinus and cause pupillodilation) may be damaged. Horner syndrome alone causes miosis, but when CN III is also damaged, its unopposed dilator function is actually lost too — however, the parasympathetic constriction is the dominant control. With complete CN III palsy, the sphincter is paralysed and the dilator (adrenergic, direct sympathetic input to iris) causes mydriasis, overriding the Horner miosis. The net result is a mid-dilated or fully dilated fixed pupil depending on the relative degree of each lesion.

Reference: BD Chaurasia's Human Anatomy, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.