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Clinical Pharmacist Colorado Mental Health Institute at Pueblo 1600 West 24th Street Pueblo, Colorado 81003-1411 fax 719/546-4259 terrie.sajbel{at}state.co.us
Assistant Chief of Medical Staff Institute for Forensic Psychiatry Colorado Mental Health Institute at Pueblo
Division Chief Institute for Forensic Psychiatry Colorado Mental Health Institute at Pueblo
Published Online, December 14, 2004. www.theannals.com, DOI 10.1345/aph.1E288
Case Report.
A 35-year-old man had a 22-year history of schizoaffective disorder that had been largely untreated. He had minimal intermittent antipsychotic exposure prior to admission to our hospital. Medication history included less than one-month trials of desipramine, fluoxetine, sertraline, olanzapine, and trifluoperazine at various times, with no reported movement disorder symptoms. His medical history was noncontributory; he had never undergone neuroimaging. He had not taken any antipsychotics for 5 months prior to or 4 months after hospital admission for acute psychotic exacerbation (July 2003).
On November 25, 2003 (day 1), abnormal movements were absent, and oral olanzapine 5 mg was initiated. The dose was increased to 10 mg daily on day 15 due to persistent symptoms. The patient's total Abnormal Involuntary Movement Scale (AIMS) score on day 10 was zero. After one month, he requested a medication change due to concern over weight gain; therefore, on day 34, aripiprazole was started at 10 mg/day. The aripiprazole dose was increased to 20 mg/day on day 55 due to continued psychosis, and olanzapine was discontinued.
On day 105, after 7 weeks of monotherapy with aripiprazole, the patient reported that his tongue felt large, slow, thick, and uncoordinated. These symptoms had emerged over a few days; he was noted to be talking with a lisp. The dyskinesia of his tongue manifested as rolling/writhing movements, exacerbated by purposeful movements (eg, finger tapping), and interfered with his sleep. He experienced episodic quivering of the upper lip; examination did not detect any other dyskinetic movements. The AIMS total score on day 105 was 8. Aripiprazole was discontinued and, within a day, the patient noted mild improvement. Within 10 days (day 115), the dyskinesia had resolved and the AIMS score on day 127 was zero. At the time of writing, the patient remained hospitalized. He was subsequently titrated onto quetiapine 500 mg/day and, after 2 months of therapy, had no recurrence of lingual dyskinesia.
Discussion.
This report describes the emergence of lingual dyskinesia with aripiprazole monotherapy. The absence of abnormal movements before starting this agent, the lack of concurrent therapy, and prompt resolution upon drug discontinuation suggest that aripiprazole may have produced the abnormal movements. The Naranjo probability scale indicated a probable relationship.4 It is doubtful that this reaction represented withdrawal dyskinesia given the short, low-dose olanzapine trial prior to aripiprazole, and the dyskinesia did not emerge until many weeks after olanzapine was discontinued. The patient's history of intermittent antipsychotic exposure, albeit limited, may have rendered him vulnerable to dyskinesias. It is notable that he did not experience similar symptoms in the setting of treatment with D2 receptor antagonists. This suggests that aripiprazole's partial agonist action may precipitate dyskinetic movements similar to those seen with full dopamine agonists in vulnerable individuals.5
References
This article has been cited by other articles:
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  M. J Grant and R. J Baldessarini Possible improvement of neuroleptic-associated tardive dyskinesia during treatment with aripiprazole Ann. Pharmacother., November 1, 2005; 39(11): 1953 - 1953. [Full Text] [PDF]
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