Amantadine (Symmetrel®) was approved by the Food and Drug Administration in 1966 and was marketed as an antiviral agent. Its use as an antiparkinsonian agent was first described in 1969 when a woman with advanced PD serendipitously noted transient relief of tremor, rigidity, and bradykinesia, during a six-week course of flu prophylaxis with amantadine (1). Since that time, further studies confirmed a mild antiparkinsonian effect with amantadine (2). The use of amantadine has been limited, likely due to the development of dopamine agonists, better tolerance of levodopa with the advent of carbidopa, and the misconception of transient benefit, known as tachyphylaxis. Investigators have sought to examine the potential clinical uses for amantadine in the management of PD. Modulating effects of amantadine on motor complications in later stage PD have been documented in several studies (3-5).
Many different mechanisms of action have been proposed for the antiparkin-sonian effects of amantadine, but clear attribution has remained obscure. Traditional mechanisms for amantadine were usually ascribed to dopaminergic or anticholin-ergic mechanisms such as the proposed promotion of endogenous dopamine release
(6). However, further studies have demonstrated a variety of biologic effects beyond these systems. For instance, studies have suggested that amantadine possesses glutamate-blocking activity (7).
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