[1] It is named after the British neurologists William John Adie and Gordon Morgan Holmes, who independently described the same disease in 1931.

[4] Pupillary symptoms of Holmes–Adie syndrome are thought to be the result of a viral or bacterial infection that causes inflammation and damage to neurons in the ciliary ganglion, located in the posterior orbit, that provides parasympathetic control of eye constriction.

[5] Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity.

[6] The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s).

[1] As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.