ABSTRACT
Since amantadine was first reported to be useful in the treatment of Parkinson’s disease (PD) by Schwab et al. (1) in 1969, several clinical trials have tested the efficacy of amantadine alone or in combination with levodopa. Amantadine is a useful, welltolerated but second-line drug without the dramatic symptomatic effect of levodopa on the cardinal features of PD. It has been observed that discontinuation of amantadine in patients with PD may result in a dramatic worsening of the clinical state (2). Amantadine is a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor and can have a putative antidyskinetic effect, which has led to renewed clinical and theoretical interest in amantadine.
