Amantadine is contraindicated in persons with end stage kidney disease, given that the drug is cleared by the kidneys. It should also be taken with caution in those with enlarged prostates or glaucoma, due to its anticholinergic effects. Live attenuated vaccines are contraindicated while taking amantadine, as it may limit the efficacy of the administered vaccine. Chemical structure
Amantadine (brand names Gocovri, Symadine, and Symmetrel) is the organic compound 1-adamantylamine or 1-aminoadamantane, which consists of an adamantane backbone with an amino group substituted at one of the four methyne positions. Rimantadine is a closely related adamantane derivative with similar biological properties; both target the M2 proton channel of influenza A virus. Mechanism of action
Parkinsons disease
The mechanism of its antiparkinsonian effect is poorly understood. Amantadine is a weak antagonist of the NMDA-type glutamate receptor, increases dopamine release, and blocks dopamine reuptake. Amantadine probably does not inhibit monoamine oxidase (MAO) enzyme. Moreover, the drug has many effects in the brain, including release of dopamine and norepinephrine from nerve endings. It appears to be an anticholinergic (specifically at alpha-7 nicotinic receptors) like the similar pharmaceutical memantine.In 2004, it was discovered that amantadine and memantine bind to and act as agonists of the σ1 receptor (Ki = 7.44 μM and 2.60 μM, respectively), and that activation of the σ1 receptor is involved in the dopaminergic effects of amantadine at therapeutically relevant concentrations. These findings may also extend to the other adamantanes such as adapromine, rimantadine, and bromantane, and could explain the psychostimulant-like effects of this family of compounds.
Ocular origin
Ocular causes include:

Iritis
Keratitis
Blepharitis
Optic disc drusen
Posterior vitreous detachment
Closed-angle glaucoma
Transient elevation of intraocular pressure
Intraocular hemorrhage
Coloboma
Myopia
Orbital hemangioma
Orbital osteoma
Keratoconjunctivitis sicca testing

Neurologic origin
Neurological causes include:

Optic neuritis
Compressive optic neuropathies
Papilledema: "The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes." Generally, this transient visual loss is also associated with a headache and optic disk swelling. Multiple sclerosis can cause amaurosis fugax due to a unilateral conduction block, which is a result of demyelination and inflammation of the optic nerve, and "...possibly by defects in synaptic transmission and putative circulating blocking factors." Migraine
Idiopathic Intracranial Hypertension
Intracranial tumor
Psychogenic

Diagnosis
Despite the temporary nature of the vision loss, those experiencing amaurosis fugax are usually advised to consult a physician immediately as it is a symptom that may herald serious vascular events, including stroke. Restated, "because of the brief interval between the transient event and a stroke or blindness from temporal arteritis, the workup for transient monocular blindness should be undertaken without delay."