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Quetiapine-Associated Tardive Dyskinesia

Quetiapine-Associated Tardive Dyskinesia

74 Taiwanese J Vol. 22 No. 1 2008

Quetiapine-associated Tardive

Hsing-Kang Chen, M.D.1, Chin-Bin Yeh, M.D.1,2, Wei-Wen Lin, M.D, Ph.D.1,2,3

Objective: To report a case of tardive dyskinesia in a patient treated with . Case report: A 51-year-old male had been treated with antipsychitics for 3 years, including clothiapine 40 mg/d, 2-4 mg/d, and 150 mg/d, individually. He was switched from zotepine to quetiapine 400 mg/d due to parkinsonism, which subsided 1 week after the change, however, the TD symptoms were subsequently noted 5 months later. These symptoms improved significantly after discontinuation of the quetiapine, but worsened after the quetiapine (400 mg/d) was again prescribed during admission to another hospital. In the beginning of his latest hospitalization, all were discontinued because the patient’s manic symptoms had been in full remission for at least 10 months. He was discharged 3 weeks after hospitalization with significant improvement of the TD symptoms. Conclusion: This single case report suggests that quetiapine might be associated with occurrence of TD symptoms although the frequency is presumably much rarer than that of conventional .

Key words: antipsychotics, tardive dyskinesia, quetiapine, bipolar disorder (Taiwanese J Psychiatry 2008;22:74-8)

observed. Herein, we report the case of a 51-year- Introduction old male with reemerging TD associated with quetiapine treatment. Second-generation antipsychotics (SGAs) are reportedly associated with much lower incidence of Case Report TD than conventional analogs. Of these, quetiapine has a low striatal D2 receptor-binding profile, with A 51-year-old married Taiwanese male the rapid release from D2 receptors [1] making it presented to our psychiatric ward with complaints less likely to cause of involuntary oral and facial movements that had (EPS) or tardive dyskenisia (TD). Although there persisted for about 3 weeks. He had experienced his are many case reports of associated SGA-induced first manic episode at the age of 38 years and was TD, to date, we only found three published articles subsequently admitted to our hospital. He involving eight cases where development or commenced treatment with lithium 900 mg/d, worsening of TD during quetiapine treatment was clothiapine 40 mg/d and clonazepam 4 mg/d in

1Department of Psychiatry, Tri-Service General Hospital 2Department of Psychiatry, National Defense Medical Center 3Peaceful Mind Clinic Received: January 31, 2007; revised: October 30, 2007; accepted: November 12, 2007 Address correspondence to: Dr Wei-Wen Lin, Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Cheng-Gung Road, Taipei 114, Taiwan Chen HK, Yeh CB, Lin WW 75

April 2001 (age 49 years). The clothiapine dosage mg/d, clonazepam 2 mg/d, midazolam 7.5 mg/d was raised to 120 mg/d and parkinsonism, and trihexiphenidyl 6 mg/d. including drooling and slurred speech, was noted His personal history was unremarkable except during this treatment, with the parkinsonism for the fact that he was a twin. He denied history of symptoms subsiding soon after discontinuation. He any before taking psychotropic was then switched to sodium 600 mg/d agents. He had also suffered herniation of and risperidone 2-6 mg/d in November 2001 due to intervertebral discs at C3/4, C5/6 and C6/7, which exacerbation of manic symptoms. Parkinsonism had been treated with radiculopathy and was developed again under risperidone 6 mg/d, conservative follow-up treatment for the preceding disappearing after its withdrawal and the addition 5 years. He also had a history of alcohol of an anticholinergic agent. In April 2003, he dependence starting at the age of 23 years but had suffered a manic relapse and sodium valproate abstained from April 2003. His twin brother also 1500 mg/d, clonazepam 4 mg/d and zotepine 150 had a similar history of alcohol dependence without mg/d were prescribed. Parkinsonism reemerged abstaining and bipolar I disorder. The patient’s and the zotepine was switched to quetiapine 400 early development and history were unremarkable. mg/day via cross titration. 4 mg/d was The patient was the youngest of the four children in also added and the parkinsonism improved 1 week his family. later. He was discharged without obvious EPS after Initial examination revealed a thin, adult male 3 weeks of hospitalization, and has been regularly of aged appearance relative to his chronological followed up at our outpatient clinic. age. He appeared anxious, with oro-facial Five months later, he experienced repetitive dyskinesia, repetitive and involuntary mouth and involuntary mouth opening and facial opening, and facial grimacing without trunk or limb grimacing. These movement problems persisted involvement. His vital signs were within normal despite decreasing the quetiapine dose to 200 mg/d range. No throat congestion or other signs of upper and the addition of trihexiphenidyl 4-6 mg/d. airway infection were noted. Mental status was Quetiapine was discontinued after 8 weeks, and the otherwise normal, with cranial nerve examination TD symptoms markedly improved 12 weeks later. also normal. Neurological examination revealed The trihexiphenidyl was stopped soon after the TD tingling sensations in the bilateral thumbs, and the improved. He visited another hospital for his neck index and ring fingers. pain and was referred to their psychiatric clinic for After admission, all medications were the residual TD symptoms where quetiapine 400 discontinued under the condition that full remission mg/d was prescribed again. The TD symptoms of his manic symptoms was achieved. His baseline promptly worsened and persisted for 3 weeks prior Abnormal Involuntary Movement Scale (AIMS) to his latest admission at our hospital. He then score was 21. One week after admission, we visited our outpatient clinic where we discontinued prescribed 4 mg/d for 10 days, the quetiapine for about 1 week and he was withdrawing it because of poor response. During admitted to our ward for further evaluation and this period, however, the TD symptoms did not management in April 2004 due to symptom worsen. Finally, he was maintained on clonazepam persistence. Immediately prior to this admission, 4 mg/d and lormetazepam 1 mg/d. The results of his medications had been sodium valproate 600 the laboratory tests and brain magnetic resonance 76 Quetiapine and Tardive Dyskinesia

imaging ordered by the neurologist were all free of movement disorders for at least 5 months unremarkable. The patient was discharged after 4 before developing TD, with the symptoms only weeks of hospitalization with an AIMS score of 7. emerging with the quetiapine treatment. His TD symptoms partially improved after tapering of the Discussion quetiapine, subsequently reemerging after further administration of the drug by another psychiatrist at Eight cases of quetiapine-associated TD have a different hospital. Thus, there is a temporal been reported, with five developing neuroleptic- relationship between the quetiapine administration induced EPS or TD prior to quetiapine and occurrence of the TD. It appears reasonable to administration (Table 1). Just three of the remaining assume, therefore, that the TD symptoms were cases had previously been free from EPS and TD. associated with the quetiapine administration. This demonstrates that, in most patients, these Trihexiphenidyl, an anticholinergic agent, dysfunctions are more likely to have been induced may exacerbate TD symptoms [2]; however, the by previous neuroleptic exposure than by link between the use of the anticholinergic and the quetiapine. Although our patient had experienced emergence of TD may be only an epiphenomena as parkinsonism after exposure to clothiapine, the subgroup of patients who develop EPS are zotepine and risperidone prior to the quetiapine thought to be more likely to receive anticho- administration, the symptoms disappeared soon linergics and also to develop TD [3]. In our case, after the withdrawal of clothiapine or addition of biperiden 2-6 mg/d was administered after the anticholinergic agents while discontinuing patient had developed TD for 2 months and risperidone or zotepine. In addition, he had been restarted at 4 mg/d for 10 days after a week’s

Table 1. Case reports of quetiapine-associated tardive dyskinesia

Duration of Diagnosis Quetiapine dose Previous Case no.; author Age/Sex quetiapine (DSM-IV) (mg/d) EPS/TD therapy (weeks) Ghelber et al., [8] 44/F 150 26 +/- 1 Ghaemi et al, [9] 25/M BPD, type I 125 6 -/- 2 Sharma et al., [10] 55/M MDD, recurrent 150 8 -/- 3 4 30/F BPD, type I 150 7 +/+ 5 48/F BPD, type II 225 12 +/- 6 54/F BPD, type I 300 10 +/+ 7 47/M BPD, type I 125 8 -/- 8 61/F MDD, recurrent 75 4 +/+ Chen et al, 2007, Jan 51 / M BPD, type I 400 24 +/- 9 Abbreviations: M = male; F = female; BPD = bipolar disorder; MDD = major depressive disorder. Chen HK, Yeh CB, Lin WW 77

hospitalization.; It was subsequently discontinued an explanation for low receptor occupancy and because of poor response, however. As the severity early clinical relapse upon withdrawal of of the TD symptoms did not change during this or quetiapine. Am J Psychiatry 1999; 156:876-84. period, it appears unlikely that the anticholinergic 2. Burnett GB, Prange AJ, Jr., Wilson IC, et al.: was responsible for the symptoms. We Adverse effects of anticholinergic antiparkinsonian drugs in tardive dyskinesia. an investigation of conclude, therefore, that the TD improvement was mechanism. Neuropsychobiology 1980; 6:109-20. not due to trihexyphenidyl administration but rather 3. American Psychiatric Association, Tardive that it was a consequence of the discontinuation of Dyskinesia: A Task Force Report of the American quetiapine. Psychiatric Association. Washington DC: Ameri- The risk factors for TD include long-term can Psychiatric Association, 1992. treatment with neuroleptics, increasing age, female 4. Jeste DV, Caligiuri MP, Paulsen JS, et al.: Risk of sex, alcoholism [4], and the presence of mood tardive dyskinesia in older patients. a prospective disorder[5] and cognitive disorder[6]. It has also longitudinal study of 266 outpatients. Arch Gen been suggested that acute EPS is a risk factor for Psychiatry 1995;52:756-65. TD [7]. Although he had abstained for about 1 year 5. Keck PE Jr., McElory SL, Strakowski SM, et al.: at the time of presentation, our patient had a long Antipsychotics in the treatment of mood disorders history of alcoholism as well as early-onset EPS and risk of tardive dyskinesia. J Clin Psychiatry and bipolar disorder, which may increase 2000;61 Suppl 4:33-8. vulnerability to the dyskinesic effects of quetiapine 6. Sandyk R, Kay SR, Awerbuch GI, et al.: Risk Factors for Neuroleptic-Induced Movement and cause a predisposition to TD. Disorders. Int J Neurosci 1991;61:149-88. In this presented case, it appears most likely 7. Casey DE: Clozapine: neuroleptic-induced extra- that the TD was resulted from the quetiapine pyramidal symptoms and tardive dyskinesia. administration. This suggests that there is a greater Psychopharmacology 1989;99 Suppl:S47-53. risk of TD with quetiapine therapy, especially in 8. Ghelber D, Belmaker RH: Tardive dyskinesia with high-risk patients. Large well-controlled trials of quetiapine. Am J Psychiatry 1999;156:796-7. quetiapine are needed, therefore, to assess the 9. Ghaemi SN, Ko JY: Quetiapine-related tardive incidence of, and risk factors for, this debilitating dyskinesia. Am J Psychiatry 2001;158:1737. dysfunction. 10. Sharma V: Treatment-emergent tardive dyskinesia with quetiapine in mood disorders. J Clin References Psychopharmacol 2003;23:415-7.

1. Seeman P, Tallerico T: Rapid release of drugs from D2 receptors:

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