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Review
. Nov-Dec 2001;24(6):313-23.
doi: 10.1097/00002826-200111000-00002.

Dyskinesia: L-dopa-induced and Tardive Dyskinesia

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Review

Dyskinesia: L-dopa-induced and Tardive Dyskinesia

O Rascol et al. Clin Neuropharmacol. .

Abstract

Neuroleptic induced tardive dyskinesia and L-dopa-induced dyskinesia are the two most common types of drug-induced abnormal involuntary movements. These two drug-induced dyskinesias are clearly different with respect to the offending drugs and the underlying disease, but they both share a number of intriguing similarities in terms of clinical phenomenology, epidemiology, risk factors, pathophysiological mechanisms and therapeutic responses. In both instances, it is believed that some dysregulation occurring at the level of the striatal dopaminergic receptors, and related non-dopaminergic neurotransmitters systems are playing a crucial role in the development and persistence of the mechanisms causing dyskinesia. These long-lasting functional changes, known as the "priming" phenomenon, are responsible for an impaired balance within the relays of the cortico-subcortical motor loops that release an inadequate output from the basal ganglia leading to an abnormal motor behavior. From a therapeutic perspective, there are also many similarities in the strategies proposed to manage these two dyskinesias. In both cases, unprimed patients not previously exposed to the offending drugs, are offered alternative medications to reduce, at least partly, the risk of occurrence of future dyskinesia: "atypical" neuroleptics in the place of "typical" neuroleptics, and dopamine agonists in the place of L-dopa. In both cases, once dyskinesias are present, in already "primed" patients, both types of dyskinesia appear to be poorly and only partly reversible. Based on limited clinical evidence, it is a common proposal to switch the dyskinetic subject from "typical" to "atypical" neuroleptics for tardive dyskinesia, or to switch from (or more pragmatically to substitute as much as possible) L-dopa to a dopamine agonist for L-dopa-induced dyskinesia. In both cases, efficacious symptomatic antidyskinetic interventions, to reduce the severity of a ready present dyskinesia, are rare. There are some uncontrolled data suggesting that dopamine depleting agents, like tetrabenazine, are possibly useful for tardive dyskinesia; however, there is more clinical evidence to support the efficacy of amantadine and functional surgery in parkinsonian patients with L-dopa-induced dyskinesia.

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