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Adie syndrome, also known as Holmes–Adie syndrome, is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). [1] It is frequently seen in females with absent knee or ankle jerks and impaired sweating.
Adie's pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear, but is believed to be the result of bilateral damage to the pretectal ...
Adie's pupil, which fails to constrict in response to light; aniridia, which is absence of the iris; and albinism, where the iris is defectively pigmented, may also cause this. Central cataracts, due to the lens clouding, disperses the light before it can reach the retina and is a common cause of hemeralopia and photoaversion in the elderly.
Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.
Tonic pupils are fairly common – they are seen in roughly 1 out of every 500 people. A person with anisocoria (one pupil bigger than the other) whose pupil does not react to light (does not constrict when exposed to bright light) most likely has Adie syndrome – idiopathic degeneration of the ciliary ganglion.
The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye. [3] In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at.
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Currently there is no treatment for this condition, but, it is usually self limiting. [1] Systemic administration of corticosteroids may be advised. [2] Even if the disease is resolved, the enlarged blind spot usually does not return to normal. [5]