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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.
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]
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 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 ...
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]
William Adie was born in Geelong, Victoria, Australia, on 31 October 1886. He was educated at Flinders Street Model School, but had to leave school to support his family at the age of 13 when his father died in 1899. [1] He worked as an office errand boy, and an employer noticed his ability to learn.
The symptoms and signs associated with convergence insufficiency are related to prolonged, visually demanding, near-centered tasks. They may include, but are not limited to, diplopia (double vision), asthenopia (eye strain), transient blurred vision, difficulty sustaining near-visual function, abnormal fatigue, headache, and abnormal postural adaptation, among others.