What is neuroleptic induced akathisia

This paper highlights the need for its early recognition, provides a diagnostic guide and an approach to its management. Box 1. Key clinical points about akathisia Presents as a very distressing subjective feeling of restlessness and dysphoria Can be observed as fidgety movements of the legs, rocking from foot-to-foot, pacing, and inability to sit or stand still May be caused by medications across a number of categories, including antipsychotics, antidepressants and antiemetics Is associated with an increased rate of suicidal ideation Early recognition and treatment is crucial Case Ms D, aged 27 years, was admitted to a medical ward with a history of persistent abdominal pain, nausea and vomiting for about three months.

Subjectively, there could be one or more of the following: 14 feeling of restlessness or inner tension or discomfort, with special reference to the lower limbs an urge to constantly move the legs, and sometimes other parts of the body eg arms, trunk difficulty or inability in maintaining a posture for several minutes.

It usually lasts for less than six months and is characterised by intense dysphoria and restlessness. Chronic akathisia — lasts longer than six months after the last change in medication, and often includes mild dysphoria and restlessness, as well as some limb and orofacial dyskinesia.

Pseudoakathisia — believed to be a late stage of the chronic type. There are some motor manifestations, but there is no subjective awareness of restlessness. Tardive akathisia — a delayed onset, usually more than three months since a medication or dose change, and it is often associated with tardive dyskinesia. Withdrawal or rebound akathisia — due to discontinuing or decreasing an anticholinergic medication, usually occurring within six weeks.

Box 2. Summary of treatment recommendations for acute akathisia 21 Patient education eg akathisia, causes, treatment options Change in medication regimen eg reduce dose or stop and switch to an alternative medication Adjunctive treatment: beta-blockers eg propranolol 40—80 mg po daily 5HT 2A receptor antagonists eg mirtazapine 15 mg po daily, cyproheptadine 8—16 mg po daily benzodiazepines eg clonazepam 0. Competing interest: None.

Provenance and peer review: Not commissioned, externally peer reviewed. Ethical clearance In addition to obtaining informed written consent from the patient directly, the authors sought and obtained approval — Ethics Reference Number: HS H — from the Health Research Ethics Board at the University of Manitoba, Canada. Philadelphia: Wolters Kluwer, Diagnostic and statistical manual of mental disorders.

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The trials were of similar study design, they used same scale BARS for the evaluation of NIA and all trials assessed psychotic symptoms. Three trials were conducted by the same author, which presumably reduces the between-studies variance. We thank Hara Alexandri for her help in preparing the report.

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Clin Neuropharmacol 33 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Statement of Interests. Supplementary material. Laoutidis , Zacharias G. Address for correspondence: Zacharias G.

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This review assesses the role of benzodiazepines in the pharmacological treatment of this problem. To determine the effects of benzodiazepines versus placebo for people with neuroleptic-induced acute akathisia.

Further references were sought from published trials and their authors. All randomised clinical trials comparing benzodiazepines with placebo for people with antipsychotic-induced acute akathisia. Two reviewers, working independently, selected, quality assessed and extracted data. These data were then analysed on an intention-to-treat basis.