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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 syndrome [4] is tonic pupil plus absent deep tendon reflexes. Adie syndrome is a fairly common, benign, idiopathic neuropathy that selectively affects the ciliary ganglion and the spinal cord neurons involved in deep tendon reflex arcs. It usually develops in middle age, although it can occur in children. A variant of Adie syndrome, Ross ...
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.
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 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 the iris, especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.
However, if the eyes are asymmetrically affected, i.e. one eye's optic nerve is more damaged than the other, it will produce an important sign called an afferent pupillary defect. [citation needed] Defective light perception in one eye causes an asymmetrical pupillary constriction reflex called the afferent pupillary defect (APD). [citation needed]
Ross' syndrome consists of Adie's syndrome (myotonic pupils and absent deep tendon reflexes) plus segmental anhidrosis (typically associated with compensatory hyperhidrosis). [1] It was characterized in 1958 [2] [3] by A.T. Ross. [4] By 1992, eighteen cases had been documented. [5]
Nerves involved in the resizing of the pupil connect to the pretectal nucleus of the high midbrain, bypassing the lateral geniculate nucleus and the primary visual cortex. From the pretectal nucleus neurons send axons to neurons of the Edinger-Westphal nucleus whose visceromotor axons run along both the left and right oculomotor nerves .