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Adie syndrome, sometimes known as Holmes-Adie’s syndrome or Adie’s Tonic Pupil, is a neurological disorder which affects the pupil of the eye and the autonomic nervous system.[1] It is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection which causes inflammation, and characterized by a tonically dilated pupil.[1]
Adie syndrome presents with three hallmark symptoms, namely abnormal pupil size (mydriasis), loss of deep tendon reflexes and diaphoresis.[1] Other signs may include hyperopia due to accommodative paresis, photophobia and difficulty reading.[2]
Clinical exam may reveal sectoral paresis of the iris sphincter and/or vermiform iris movements. The tonic pupil may become smaller (miotic) over time which is referred to as “little old Adie’s”.[3] Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity.[1] A normal pupil will not constrict with the dilute dose of pilocarpine.[3] CT scans and MRI scans may be useful in the diagnostic testing of focal hypoactive reflexes.[4]
The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s).[1] Pilocarpine drops may be administered as a treatment as well as a diagnostic measure, and should be applied three times daily.[1] Thoracic sympathectomy is the definitive treatment of diaphoresis, if the condition is not treatable by drug therapy.[1]
Adie’s syndrome is not life threatening or disabling.[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.[1]
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