Named after British neurologist William Adie and Irish neurologist Sir Gordon Holmes after first describing the condition (calling it “pseudo-Argyll Robertson pupil” in 1931), Holmes–Adie syndrome (HAS) is characterized by pupillary dysfunction and areflexia. Though the exact cause is unclear, HAS appears to involve the degeneration of the ciliary ganglion resulting in postganglionic parasympathetic fiber impairment and ultimately dysfunction of the pupil. Most cases of HAS are idiopathic; however, cases have been linked to systemic infection (mainly viral), autoimmune diseases including paraneoplastic conditions and other systemic inflammatory diseases, orbital tumors and local trauma, and neuromuscular conditions, among many other published causes.