Tardive akathisia: An analysis of clinical features and response to open therapeutic trials

Abstract

In recent years, there has been increasing recognition that akathisia occurs not only as an acute, self-limited complication of dopamine (DA) antagonist treatment, but also as a persistent form, called tardive akathisia. We represent a retrospective analysis of clinical features and therapeutic trials in 52 cases of this disorder. Although most patients developed this disorder after years of DA antagonist treatment (mean = 4.5 years), a significant proportion (34%) developed it within 1 year. The characteristic motor features included frequent, complex stereotyped movements. The legs were most frequently involved, showing marching in place and crossing/uncrossing. Trunk rocking, respiratory grunting and moaning, and complex hand movements such as face rubbing or scratching also occurred. In the 26 patients who were able to discontinue DA antagonists, akathisia persisted for years (mean = 2.7 years, range of 0.3-7 years) until abatement of symptoms or last follow-up. Younger patients were more likely to have remission or therapeutic suppression of akathisia at follow-up. In our experience, the catecholamine-depleting drugs reserpine and tetrabenazine were the most effective agents for suppressing symptoms, producing improvement in 87 and 58% of patients treated, respectively. However, improvement was limited in many patients, and at last follow-up only 33% of patients had complete abatement of their symptoms. In conclusion, tardive akathisia is a particularly disabling form of tardive dyskinesia, frequently persistent for years and often resistant to therapy.

Evidence-based guideline: Treatment of tardive syndromes

“…TDS includes not only lingual-facial-buccal dyskinesia but also the variant forms, collectively termed tardive syndromes. [2][3][4][5][6][7][8] In this guideline, tardive dyskinesia encompasses all forms of persistent dyskinesia caused by dopamine receptor blocking agents (DRBAs).…”

Clinical Characteristics and Predisposing Factors in Acute Drug-Induced Akathisia

“…presence of a nonorganic psychotic illness, making the pa¬ tient eligible for treatment with neuroleptics; (2) freedom from dopamine antagonists for a minimum of 2 weeks (6 weeks if a depot preparation had been used) prior to the day of admission; (3) freedom from acetylcholine (ACh) or ß-ad¬ renergic (ßA) antagonists for 2 weeks prior to admission; (4) freedom from nonneuroleptics known to sometimes cause or modify akathisia, eg, lithium carbonate, heterocyclic an¬ tidepressants, calcium channel antagonists, and serotonin reuptake inhibitors2; (5) absence of akathisia on day 1 on clinical assessment and a baseline global akathisia rating of 0; (6) no current replacement iron therapy; (7) no history of sympathomimetic use (including nonprescription forms) in the previous 2 weeks by patient report and a urine screen negative for amphetamines, cocaine, and phencyclidine; (8) giving an overall incidence of 21% in the first 2 weeks.…”

Antipsychotic-Induced Tardive Syndromes: Clinical Features and Treatment Approaches

“…Bacak ve gövde hareketleri en yaygın olanlarıdır. 8,10 Geç akatizi gelişimi için saptanan kesin bir risk faktörü yoktur. İleri yaş, kadın cinsiyet, demir eksikliği, baskın negatif belirtiler, bilişsel işlev bozukluğu ve afektif bozukluk tanısının olması olası risk etkenleridir.…”

“…Kadın-erkek oranı 2: 1 olarak bildirilmiştir. 10,11 Akatizi gelişme mekanizması iyi anlaşılma-mıştır. Striatum dışındaki alanlarda beyin dopamin reseptör blokajı nedeniyle olduğu düşünülmekte-dir.…”

“…Benzodiyazepinlerin potansiyel terapötik etkisi anksiyolitik ve kas gevşetici özellikleri ile ilgili olabilir. 10 Alfa-2 agonisti klonidinin yararı spesifik terapötik etki ya da sedasyon ile ilişkilidir. 13 Bir başka etkili klinik strateji tedaviye beta-adrenerjik bloker eklemektir.…”