DOI: 10.1097/01.jcp.0000169621.45443.ac
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PMID: 16012289
Issn Print: 0271-0749
Publication Date: 2005/08/01
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Excerpt
Different agents have been used for akathisia in the past. These treatments include beta-blockers, benzodiazapines, and anticholinergic drugs for neuroleptic-induced akathisia (NIA).
An atypical approach is to use a serotonin (5-HT2) antagonist such as cyproheptadine, mianserin, and trazadone.1-3 A previous study4 used the 5-HT2A/C antagonist mirtazapine to treat NIA. The mechanism by which this agent does this may be due to disinhibition of dopamine release in nigrostriatal projections.5,6 To date, all reports involving 5-HT2A/2C antagonists for treatment of NIA dealt with patients with a primary diagnosis of schizophrenia.
To date, there have been no studies looking at the effectiveness of a 5-HT2 antagonist for drug-induced akathisia in patients with bipolar disorder. We present 3 cases of patients with both bipolar disorder who developed drug-induced akathisia and were successfully treated with low-dose mirtazapine.
Mr. A is a 31-year-old African American male who was treated successfully for bipolar type I disorder with olanzapine 20 mg and no other concomitant medications. The patient had developed marked akathisia with this antipsychotic. Previously, many attempts had been made to resolve the akathisia by reducing the dose, using anticholinergics, and using beta-blockers; these attempts were either unsuccessful or poorly tolerated due to their own side effects. The patient was started on 7.5 mg mirtazapine and followed up 7 days later. At this time the patient has dramatically improved from baseline. The following score changes occurred on the Barnes Akathisia Scale7 (BAS) over 7 days: Objective (O) by 2 to 0; Subjective(S) by 2 to 1; Distress (D) from 2 to 1 point; and Global (G) from 4 to 1. Over the next 2 months the patient's dose of mirtazapine was tapered down but was unable to completely get off the medication without return of symptoms. The final dose was 3.75 mg. No reactivation of mania was noted.
Ms. B is a 37-year-old Caucasian female with a history of bipolar disorder type II. She had previously been treated with different antipsychotics with repeated episodes of dystonia or akathisia with these agents. The patient, already on oxcarbazepine 300 mg BID, was tried on aripiprazole 7.5 mg in an outpatient residents' clinic and followed up 10 days later. At this time, the patient developed moderate restlessness, inability to sit still as before, but with no anxiety; instead of discontinuing the aripiprazole, mirtazapine 7.5 mg was started with no change to any other medications. The patient reported reduction in symptoms over the next 2 days. The patient experienced complete resolution of symptoms and was able to tolerate up to 15 mg of aripiprazole. Mirtazapine was continued at the same dose and was well tolerated by the patient. BAS change from the time mirtazapine was started until 14 days later was: O from 3 to 1; S from 2 to 0; D from 2 to 0; and G from 3 to 0.
Ms. C was a 32-year-old African American female with a history of bipolar type II who was doing well on olanzapine 20 mg. The patient desired to be switched to an alternative agent secondary to weight gain and recent diagnosis of diabetes. The patient was started on aripiprazole 15 mg and the olanzapine was reduced to 10 mg. When the patient returned 7 days later she complained of a severe restlessness, constant pacing, and leg shaking but no increased anxiety. Mirtazapine 7.5 mg was initiated immediately with no changes to either the olanzapine or aripiprazole.
