Dyskinesia refers to a category ofmovement disorders that are characterized by involuntary muscle movements,[1] including movements similar totics orchorea and diminished voluntary movements.[2] Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower extremities. Discoordination can also occur internally especially with the respiratory muscles and it often goes unrecognized.[3] Dyskinesia is asymptom of severalmedical disorders that are distinguished by their underlying causes.
Acutedystonia is a sustained muscle contraction that sometimes appears soon after administration ofantipsychotic medications.[4] Any muscle in the body may be affected, including the jaw, tongue, throat, arms, or legs. When the throat muscles are involved, this type of dystonia is called an acutelaryngospasm and is a medical emergency because it can impair breathing.[4] Older antipsychotics such ashaloperidol orfluphenazine are more likely to cause acute dystonia than newer agents. Giving high doses of antipsychotics by injection also increases the risk of developing acute dystonia.[4]
Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been onlevodopa (L‑DOPA) for prolonged periods of time. LID commonly first appears in the foot, on the most affected side of the body. There are three main types that can be classified on the basis of their course and clinical presentation following an oral dose ofL‑DOPA:[8][9]
Off-period dystonia – correlated to theakinesia that occurs before the full effect ofL‑DOPA sets in, when the plasma levels ofL‑DOPA are low. In general, it occurs as painful spasms in the foot. Patients respond toL‑DOPA therapy.[8][9]
Diphasic dyskinesia – occurs whenplasmaL‑DOPA levels are rising or falling. This form occurs primarily in the lower limbs (though they can happen elsewhere) and is usuallydystonic (characterized by apparent rigidity within muscles or groups thereof) orballistic (characterized by involuntary movement of muscles) and will not respond toL‑DOPA dosage reductions.[8][9]
Peak-dose dyskinesia – the most common form of levodopa-induced dyskinesia; it correlates with the plateauL‑DOPA plasma level. This type usually involves the upper limbs more (but could also affect the head, trunk and respiratory muscles), is choreic (of chorea), and less disabling. Patients will respond toL‑DOPA reduction but may be accompanied by deterioration ofparkinsonism.[8][9] Peak-doseL‑DOPA-induced dyskinesia has recently[update] been suggested to be associated with cortical dysregulation of dopamine signaling.[10]
Late-onset dyskinesia, also known astardive dyskinesia, occurs after long-term treatment with anantipsychotic drug such ashaloperidol (Haldol) oramoxapine (Asendin). The symptoms include tremors and writhing movements of the body and limbs, and abnormal movements in the face, mouth, and tongue – including involuntary lip smacking, repetitive pouting of the lips, and tongue protrusions.[11]
^abcBrian K. Alldredge; et al., eds. (2013).Applied therapeutics : the clinical use of drugs (10th ed.). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 1937.ISBN978-1609137137.
^abPranzatelli MR (September 1996). "Antidyskinetic drug therapy for pediatric movement disorders".J Child Neurol.11 (5):355–369.doi:10.1177/088307389601100503.PMID8877602.
^Chase TN, Oh JD, Konitsiotis S (April 2000). "Antiparkinsonian and antidyskinetic activity of drugs targeting central glutamatergic mechanisms".J Neurol. 247 Suppl 2:II36 –II42.doi:10.1007/pl00007759.PMID10991664.
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