Prior to 1990,<unk><unk>  could, "clinically, be divided into four identifiable symptom complexes, each with its underlying pathoetiology: embolic, hypoperfusion, angiospasm, and unknown."  In 1990, the causes of<unk><unk>  were better refined by<unk><unk>  Study Group, which has defined five distinct causes of transient monocular blindness: embolic, hemodynamic, ocular, neurologic, and idiopathic. Concerning the pathology underlying these causes (stay idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathy, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability."
Amaurosis fugax pathophysiology
Asperger syndrome pathophysiology
Sheehan's syndrome pathophysiology
Lesch-Nyhan syndrome pathophysiology
Sezary syndrome pathophysiology
Amnesia pathophysiology
Hyperhidrosis pathophysiology
Fragile X syndrome pathophysiology