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Table of Contents
LETTER TO THE EDITOR
Year : 2021  |  Volume : 35  |  Issue : 4  |  Page : 208-209

Tetrabenazine for treating neuroleptic-induced tardive dyskinesia: A case report of a patient with chronic schizophrenia


Department of Psychiatry, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan

Date of Submission30-Mar-2021
Date of Decision29-Apr-2021
Date of Acceptance30-Apr-2021
Date of Web Publication21-Dec-2021

Correspondence Address:
M.D., Ph.D Cheng- Ho Chang
No. 386, Ta-Chung First Road, Tzuo-Yin District, Kaohsiung City 81362
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/TPSY.TPSY_40_21

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How to cite this article:
Ching PY, Pan CC, Chang CH. Tetrabenazine for treating neuroleptic-induced tardive dyskinesia: A case report of a patient with chronic schizophrenia. Taiwan J Psychiatry 2021;35:208-9

How to cite this URL:
Ching PY, Pan CC, Chang CH. Tetrabenazine for treating neuroleptic-induced tardive dyskinesia: A case report of a patient with chronic schizophrenia. Taiwan J Psychiatry [serial online] 2021 [cited 2022 Jan 27];35:208-9. Available from: http://www.e-tjp.org/text.asp?2021/35/4/208/332969



Neuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder. TD causes remarkable disturbances in patients with chronic schizophrenia who have received antipsychotic drugs for years. Tetrabenazine (TBZ) is used for treating TD in several countries [1]. We present the case of a male patient with chronic schizophrenia who received TBZ as a treatment for TD.


  Case Report Top


A 47-year-old male patient worked as a farmer in the suburb of Kaohsiung and is introverted and asocial. He started to have psychotic symptoms, including auditory hallucinations, bizarre behavior, and disorganized speech when he was 19 years old. He was first admitted to our hospital and diagnosed with schizophrenia in 1991.

For 10 years from 1991 to 2001, the patient had received a regimen including sulpiride (800 mg/day). He also received haloperidol (orally, 10 mg) as needed occasionally at that time. He had an episode of acute dystonia with symptoms of spasmodic torticollis and oculogyric crisis during his first admission. During the following courses, the main antipsychotic agent was risperidone from 2011 to 2016. On admission in May 2016, he showed obvious involuntary facial movements. The treating physician modified his regimen to olanzapine (15-20 mg/day), followed with another substitution with quetiapine.

From July 31 to September 28, 2018, the patient was admitted to our acute psychiatric ward. The chief complaint was persecutory delusion, auditory hallucinations, and social withdrawal for about two weeks before admission. In addition, his mother reported that he developed involuntary movement of his eyes, mouth, and trunk. The movements included grimacing, lip-smacking, chewing, protrusion of the tongue, and choreoathetosis of both upper limbs at a frequency of once per 10–15 seconds. Based on the clinical presentation and history, we diagnosed neuroleptic-induced TD. We changed the main antipsychotic drug to clozapine in consideration of the refractory psychotic symptoms. The psychotic symptoms were decreased in magnitude when the dosage of clozapine was titrated to 125 mg/day. But TD symptoms were still present after two weeks. The involuntary movements caused attention deficits and avoidance of social interaction. After reviewing the literature, we decided to give TBZ for TD treatment. The initial dosage was 12.5 mg/day, starting on August 27, 2018. He reached the maintenance dose of 25 mg/day on September 3, 2018. The symptoms were decreased in magnitude and frequency after a one-week course of treatment. We closely monitored him for possible TBZ side effects, such as sedation, somnolence, insomnia, depression, and increased suicidal thoughts. But he did not show any of those side effects.

The patient was regularly followed up at our outpatient clinic after discharge. He was admitted once in November 2018 for his worsened positive symptoms. His TD symptoms remained stable during the clinical follow-up. We used the abnormal involuntary movement scale (AIMS) [2], to measure the presence, severity, and changes in TD. [Table 1] presents the results.
Table 1: Changes of scores of abnormal involuntary movement before and after treatment of tetrabenazine

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  Comment Top


TD is a delayed-onset hyperkinetic involuntary movement disorder that results from exposure to dopamine receptor antagonists [3]. The prolonged use of typical and atypical antipsychotics, anti-emetics, and metoclopramide can cause side effects of TD. The prevalence of TD has been estimated to be 20%–40% of all patients receiving neuroleptics and the elderly and men have a higher risk of TD [4]. Treating TD remains challenging. Dose reduction or discontinuation of antipsychotic medication can worsen TD symptoms and pose a risk of triggering a psychotic relapse [5].

Vesicular monoamine transporters (VMATs) are presynaptic intracellular transmembrane proteins that play a critical rôle in the packaging, storage, and release of dopamine and other monoamines. Inhibition of VMAT2 decreases the dopamine release from the synapse and thereby reduces the hyperkinetic symptoms associated with TD [6]. TBZ, acting as an irreversible, high-affinity VMAT2 inhibitor, has shown promise in the treatment of hyperkinetic movement disorders [7]. The common side effects of TBZ are somnolence, acute akathisia, insomnia, fatigue, agitation, depression, anxiety, nausea, diarrhea, and  Parkinsonism More Details. TBZ can also increase the risk of suicidal ideation and neuroleptic malignant syndrome [8]. But these adverse events are dose-dependent and improve with dose reduction [9]. The initial recommended dose of TBZ is 12.5 mg/day in the morning. It should be titrated by 12.5 mg every week until reaching the most effective and still well-tolerated dose. The common effective dosage is around 37.5 mg/day and should be divided into a regimen of three times a day [6]. The exposure to TBZ metabolites is higher in patients with hepatic impairment than in healthy people. Therefore, TBZ is contraindicated in patients with liver diseases. TBZ is also contraindicated in patients who are suicidal and patients without treatment or with insufficiently treated depression.

Currently, TBZ is approved for the treatment of moderate to severe TD in some countries and is used and studied for off-label use in TD in the USA. A systematic review conducted by Caroff et al. in 2017 [9] included one double-blind cross-over study (n = 12) and seven open-label studies. The results showed that TBZ improves the symptoms in patients with TD. Nearly all studies with TBZ revealed changes in psychiatric status (depression) and secondary movement disorders (Parkinsonism and akathisia) as frequent side effects of treatment [9]. In our patient, TD symptoms were both subjectively and objectively lower after treatment with TBZ. At the latest follow-up, he still continuously took TBZ (25 mg/day). But we have only limited evidence to confirm that the improvement of TD can be attributed only to the therapeutic effect of TBZ or the combination of TBZ and clozapine. No self-reported side effects or symptoms of depression have been noticed. (The institutional review board at Kaohsiung Veterans General Hospital approved the publication of this case report (protocol number = KSVGH21-CT3-20 and date of approval = March 12, 2021), with the requirement of obtaining a written informed consent from the patient).


  Financial Support and Sponsorship Top


None.


  Conflicts of Interest Top


All authors declare no potential conflicts of interest in writing this letter-to-the editor.



 
  References Top

1.
Kaur N, Kumar P, Jamwal S, et al.: Tetrabenazine: Spotlight on drug review. Ann Neurosci 2016; 23: 176-85.  Back to cited text no. 1
    
2.
Guy W: Abnormal involuntary movement scale (117-AIMS). In: Guy W (ed): ECDEU Assessment Manual for Psychopharmacology. Rockville, Maryland, USA: National Institute of Mental Health, 1976: 534-37.  Back to cited text no. 2
    
3.
Waln O, Jankovic J: An update on tardive dyskinesia: from phenomenology to treatment. Tremor Other Hyperkinet Mov (N Y). 2013;3:tre-03-161-4138-1.  Back to cited text no. 3
    
4.
Liou CP, Fang CK, Hsu SC, et al.: Flupentixol decanoate-related tardive dyskinesia. Taiwanese J Psychiatry 2006; 20: 230-9.  Back to cited text no. 4
    
5.
Mejia NI, Jankovic J: Tardive dyskinesia and withdrawal emergent syndrome in children. Expert Rev Neurother 2010; 10: 893-901.  Back to cited text no. 5
    
6.
Eiden LE, Weihe E: VMAT2: A dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann N Y Acad Sci 2011; 1216: 86-98.  Back to cited text no. 6
    
7.
Solmi M, Pigato G, Kane JM, et al.: Treatment of tardive dyskinesia with VMAT-2 inhibitors: a systematic review and meta-analysis of randomized controlled trials. Drug Des Devel Ther 2018; 12: 1215-38.  Back to cited text no. 7
    
8.
Ondo WG, Hanna PA, Jankovic J: Tetrabenazine treatment for tardive dyskinesia: assessment by randomized videotape protocol. Am J Psychiatry 1999; 156: 1279-81.  Back to cited text no. 8
    
9.
Caroff SN, Aggarwal S, Yonan C: Treatment of tardive dyskinesia with tetrabenazine or valbenazine: a systematic review. J Comp Eff Res 2018; 7: 135-48.  Back to cited text no. 9
    



 
 
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