Propranolol treatment for neuroleptic-induced akathisia.

Sir: Akathisia, or motor restlessness, is a common and distressing side effect of antipsychotic or neuroleptic drug therapy. In extreme cases, akathisia could be mistaken for agitated psychosis, leading to an increase in the dose of the antipsychotic drug, which could further worsen the restlessness.1 Propranolol is a nonselective β-adrenergic blocker with no other autonomic nervous system activity. It is primarily and widely used as an antihypertensive agent, either alone or in combination with other antihypertensive medications. Here, we present a case of improvement of neuroleptic-induced akathisia with propranolol. Case report. Ms. A, a 46-year-old white woman, had a 20-year history of bipolar disorder, mixed type, diagnosed using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria.2 She had a history of multiple psychiatric hospitalizations, and her last hospitalization was in January 2004. She had no history of comorbid substance use disorder. Her medical history was significant for hypothyroidism, which has been well controlled with levothyroxine, 88 μg once a day, and acne grade 1 for which she has been taking tetracycline, 250 mg twice a day. Ms. A's initial presentation to our practice was in January 2004, at which time she was taking risperidone, 2 mg p.o. q.h.s., and carbamazepine, 200 mg p.o. q.a.m. and 400 mg p.o. q.h.s. At the time of her discharge from the hospital in February 2004, she was taking risperidone, 2 mg p.o. q.a.m., and lamotrigine, 50 mg p.o. b.i.d., as well as lorazepam, 0.5 mg at bedtime, as needed for insomnia. During the course of her outpatient treatment, she started to develop extreme paranoid ideations. In July 2004, risperidone was tapered in tandem with initiation of treatment with olanza-pine, 2.5 mg at bedtime, with the dose gradually increased to 10 mg at bedtime by December 2004. Within a week of the titration of the dose of olanzapine to 10 mg/day, she began to complain of restlessness. A diagnosis of akathisia was made based on the patient's subjective report of restlessness as well as the physician's objective assessment. Since no other medication changes had been made and since the patient denied any other symptoms of anxiety, the akathisia was attributed to an increase in the dose of olanzapine. A low dose of propranolol (10 mg twice a day) was initiated for managing the akathisia. Symptomatic improvement in akathisia was noticed within 2 days of initiation of propranolol. She reported no adverse effects from the use of propranolol. Motor restlessness has been proposed as the possible result of an imbalance between the central dopaminergic and β2-adrenergic systems. The improvement in akathisia from propranolol could thus be due to the β2 blocking property of propranolol.3 A blinded study has shown propranolol to be more efficacious than lorazepam in neuroleptic-induced akathisia.3 Furthermore, the low doses of propranolol used to treat akathisia do not significantly affect blood pressure.3 Presently, there is no definitive treatment of akathisia. Some other alternatives to propranolol in the treatment of akathisia include anticholinergic medications,4 benzodiazepines, or a reduction in the dose of neuroleptics. Propranolol could be a safe and efficacious treatment for neuroleptic-induced akathisia. However, studies representing larger patient populations and other neuroleptic medications are needed to corroborate these findings.