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Lancet: Volume 353, Number 9166 22 May 1999 Riluzole for levodopa-induced dyskinesias in advanced Parkinson's disease Doron Merims, Ilan Ziv, Ruth Djaldetti, Eldad Melamed Dyskinesias are a common and frequently disabling side-effect of chronic levodopa therapy in patients with Parkinson's disease.1 The causes of these levodopa-induced involuntary movements are not fully understood, but excess formation of dopamine in striatum from exogenous levodopa and overstimulation of supersensitive dopaminergic receptors may play an important part. Pharmacological treatment of these dyskinesias is unsatisfactory. Decrease or discontinuation of levodopa or the addition of dopamine-receptor blocking neuroleptics can suppress or even abolish the dyskinesias, but the parkinsonian signs and symptoms soon worsen and may become life threatening. Steroetaxic pallidotomy and chronic subthalamic stimulation by implanted electrodes are effective antidyskinetic strategies but carry certain risks and cannot be widely used.2 The success of these surgical approaches may be partly owing to inhibition of glutameric transmission within the basal ganglia circuitry. This mechanism suggests that glutamergic overactivity beyond the dopaminergic synapses may participate in the generation of dyskinesias and raises hope that its suppression may be beneficial without causing loss of levodopa efficiency and parkinsonism deterioration. Indeed, NMDA receptor antagonists such as amantadine3 and dextrometorphan4 can lessen such dyskinesias. ---------------------------------------------------------------------------- ---- Department of Neurology, Rabin Medical Center, Belinson Campus and Tel Aviv University Medical School, Petach Tiquva 49100, Israel (Eldad Melamed)