Propranolol in the treatment of neuroleptic-induced akathisia

Abstract

Fourteen patients with neuroleptic-induced akathisia were treated with propranolol in an open trial. All patients demonstrated substantial improvement of their akathisia; nine of the 14 obtained complete remission. Response was quite rapid, occurring within 24 hours in most cases. Doses required for improvement were low (30-80 mg/day), and side effects were few. Lithium-induced tremor improved considerably, but symptoms of parkinsonism and tardive dyskinesia showed little change. Preliminary results with certain other beta blockers suggest that they are less effective than propranolol in the treatment of akathisia.

Heavy Alcohol Drinking Associated Akathisia and Management with Quetiapine XR in Alcohol Dependent Patients

“…Also, there was no change in the significance observed when drinking history markers were included. Other studies that have studied the efficacy of Propranolol [27] and Lorazepam [28] for treatment of akathisia have also reported time-course dependent alleviation of akathisia symptoms. There is substantial evidence that 5-HT2A antagonists are successful in treating akathisia symptoms, exclusively neuroleptic-induced akathisia [29].…”

“…Akathisia is generally associated with the sense of inner restlessness, mental uneasiness, unrest, or dysphonia, which can be intense [31]. The occurrence and reduction in akathisia have also been evaluated in several studies that have used atypical antipsychotics including Clozapine [22], Olanzapine [23], Quetiapine [24–26], Ziprasidone [27], and others.…”

Dopamine-receptor blocking agent-associated akathisia: a summary of current understanding and proposal for a rational approach to treatment

“…Doses of 60–120 mg/day have been demonstrated to be effective and well-tolerated for reducing DRBA-A symptoms. 94 – 97 The hypothetical mechanism of action, shared by the alpha-2 agonist clonidine, 98 is suppression of compensatory noradrenergic signaling that may trigger psychomotor activation associated with akathisia. D 2 stimulation in the locus ceruleus normally inhibits norepinephrine outflow, 99 so it follows that reduced dopamine signaling caused by DRBAs subsequently increases norepinephrine signaling in the midbrain as part of a feedback response.…”

“… 101 Comparative studies have shown cyproheptadine, zolmitriptan, and vitamin B6 produce similar levels of DRBA-A symptom reduction when compared with a range of doses (40–120 mg/day) of propranolol. 102 – 104 Serotonin 5-HT 2A receptor antagonists, such as mirtazapine, 105 – 110 trazodone, 111 fluvoxamine, 112 zolmitriptan, 103 mianserin, 113 and cyproheptadine, 102 represent another class of treatments for DRBA-A. 114 Blocking this receptor likely plays a role in reducing symptoms by increasing downstream dopamine signaling in areas of the brain affected by DRBAs.…”