Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 7  |  Issue : 1  |  Page : 70-72  

Olanzapine induced tardive dyskinesia


1 Consultant Psychiatrist, Berhampore Mental Hospital, Berhampore, West Bengal, India
2 Department of Physiology, Burdwan Medical College, Burdwan, West Bengal, India
3 Department of Psychiatry, Pravara Institute of Medical Sciences (Deemed University), Rural Medical College, Loni, India

Date of Web Publication10-Dec-2013

Correspondence Address:
Suprakash Chaudhury
Prof. and Head, Department of Psychiatry, Pravara Institute of Medical Sciences (Deemed University), Rural Medical College, Loni - 413 736
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.122790

Rights and Permissions
  Abstract 

Olanzapine is considered to have significantly less risk of tardive dyskinesia (TD) compared to first generation antipsychotics. We describe two patients who developed TD after prolonged use of olanzapine. Both the patients received no medications prior to the treatment with olanzapine. They neither received any other medication along with olanzapine nor any injectible antipsychotics. In one patient, TD improved completely after withdrawal of olanzapine and treatment with clozapine, but recurred after a retrial of olanzapine. In the other patient, reduction of dose of olanzapine was tried without any success. Despite a substantially lower risk than first generation antipsychotics, TD is not entirely absent with olanzapine.

Keywords: Atypical antipsychotics, olanzapine, tardive dyskinesia


How to cite this article:
Chakraborty R, Chatterjee A, Chaudhury S. Olanzapine induced tardive dyskinesia. Med J DY Patil Univ 2014;7:70-2

How to cite this URL:
Chakraborty R, Chatterjee A, Chaudhury S. Olanzapine induced tardive dyskinesia. Med J DY Patil Univ [serial online] 2014 [cited 2023 Sep 22];7:70-2. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2014/7/1/70/122790


  Introduction Top


Tardive dyskinesia (TD) is a potentially persistent and disabling involuntary movement disorder that can occur with long-term antipsychotic treatment. TD usually involves the orofacial region, but arms, legs and body can be involved. Abnormal movements can include myoclonic jerks, tics, chorea and dystonia. They become most evident when patients are aroused, but ease during relaxation and disappear during sleep. [1] According to the DSM-IV, [2] these abnormal involuntary movements must have been present for at least 4 weeks and the antipsychotic medication should have been used for at least 3 months (1 month if the patient is sixty years or older) for the TD to have been caused by the use of antipsychotic drugs.

One of the major advantages of olanzapine, a second generation antipsychotic agent (SGA), is claimed to have a very low risk of causing TD compared to first generation antipsychotics (FGA). [1] Few reports also suggested that olanzapine improves TD in some patients, [3],[4] while there are now some reports of TD occurring after use of olanzapine5, [5],[6],[7],[8],[9],[10] although the incidence is still low. Literature search (pubmed, indmed) revealed no Indian report, but on manual search one report of olanzapine induced TD from India, [9] was found. However, history of prior treatment with typical antipsychotics in the patients raised doubts about the causative role of olanzapine in producing TD in some of these reports. [6],[7],[9] Here we describe two drug naïve patients who developed TD after they were treated with olanzapine monotherapy.


  Case Reports Top


Case 1

A thirty five year old married, Hindu male from very poor socioeconomic background, with an unremarkable past medical history, initially presented about three years back with fearfulness, irrelevant talk, hearing voices, belief that his neighbours were planning to harm him, insomnia and episodes of aggressive behavior of 8 month duration. He was diagnosed as schizophrenia as per International Classification of Diseases (ICD) 10 criteria and prescribed olanzapine 20 mg/day. Prior to that he was neither treated nor received any other medication for this illness. Gradually his symptoms improved and he continued taking olanzapine at same dose. Patient gradually became asymptomatic and was on regular medications for next 1 year and thereafter he started experiencing a peculiar slow rhythmic involuntary pouting and puckering movement of the lips. Gradually the movements increased considerably and the patient who by now was free from schizophrenic symptoms became very distressed. He was prescribed trihexyphenidyl 4 mg/day, but no improvement occurred. Patient continued taking olanzapine 20 mg/day and experienced gradually worsening lip movements for next 2 years. Biochemical, neuropsychological and imaging work-up was negative. The lip movements were diagnosed as tardive dyskinesia with a score of 12 on Abnormal Involuntary Movement Scale (AIMS). Olanzapine was immediately stopped and clozapine (Built up to 400 mg/day) was started. On follow up after four weeks, patient's AIMS score came down to four and after eight weeks, it came down to zero. Patient maintained the remission from schizophrenic symptoms. However because of poor economic status, patient communicated his inability to continue clozapine. Instead, he wanted to revert back to olanzapine since it was available at no cost from institute dispensary. Although we informed about the risk of relapse of TD symptoms, patient insisted on olanzapine retrial. Within four weeks of restarting olanzapine at a dose of 20 mg/day patient's TD movements recurred. Olanzapine was stopped immediately and he was advised to start clozapine. Unfortunately, patient was unable to procure clozapine and decided to stop taking medicines, despite being repeatedly warned about the possibility of relapse of schizophrenic symptoms. Since then, patient has not come for follow-up. Naranjo Adverse Drug Reaction Probability Scale, [11] indicated a highly probable relationship (score=10) between the tardive dyskinesia and olanzapine therapy in this patient.

Case 2

This thirty year old married, Hindu, male patient was hospitalized with a history of abnormal behaviour, irrelevant talk, auditory hallucinations, persecutory and grandiose delusions, and insomnia for 2.5 years. He was never treated prior to his admission. We measured his psychopathology according to Positive and Negative Syndrome Scale (PANSS) scale and the total score was 72 during admission. With a diagnosis of schizophrenia as per ICD 10 criteria, he was started on olanzapine 10 mg/day and gradually increased the dosage up to 25 mg/day. With this his symptoms showed remarkable improvement after eight weeks (PANSS score 30) and he was discharged. On his first follow-up after 1 month, he started having repetitive slow puckering movement of the lips. He was not taking any other medicines or substances as confirmed by his family members. A diagnosis of TD was made with a score of 7 on Abnormal Involuntary Movement Scale (AIMS). Olanzapine dosage was reduced to 20 mg/day, but TD movements showed no improvement. However, patient maintained remission of his schizophrenic symptoms. Patient and his family members declined to the option of clozapine for financial reason. Naranjo Adverse Drug Reaction Probability Scale [11] indicated a probable relationship (score=7) between the tardive dyskinesia and olanzapine therapy in this patient.


  Discussion Top


No accepted criteria have been set for the diagnosis of TD, but the presence of the Schooler and Kane criteria is often deemed to be sufficient for the diagnosis of tardive dyskinesia. [12] These include: 1) the use of antipsychotic drugs for at least 3 months; 2) involuntary movements of moderate intensity observed at least in one region or of mild intensity in at least two regions, 3) exclusion of other conditions that cause movement disorders. In both our cases, these 3 criteria were met. Risk factors for developing tardive dyskinesia include long-term therapy with FGAs at higher dosages, older age, female sex and concurrent affective disorders. the use of anticholinergics with neuroleptics, previous physical therapies (Electroconvulsive Therapy), the presence of other physical illness such as diabetes or an organic disorder, younger age of exposure and the presence of extrapyramidal symptoms early in treatment. [10],[13] In the two cases reported here none of these risk factors were present.

There is still no definitive treatment for TD. Nonetheless, therapeutic strategies used for TD include prevention, reversal, and suppression or clinical management. Patients who require antipsychotic treatment for extended times today have the opportunity of treatment with one of the SGA drugs and thus are at considerably reduced risk of developing TD. Clinical data with FGA treatment suggests that dyskinesia reversal occurs in persons with TD during ongoing treatment, however, still conferring future risk. Data suggest that this reversal may happen faster with SGA treatment than with the continued use of FGA drugs. TD reversal occurs frequently, although not inevitably, with cessation of antipsychotic treatment. The reversal occurs gradually over the course of months to years. Based on the simplistic formulation that relieving the brain of the inducing agent will allow the drug-induced tissue changes to reverse, then drugs such as clozapine or other newer antipsychotics, which have clinical efficacy with reduced dopamine-receptor occupancy, may reverse existent TD. [14] Other drug treatment strategies include benzodiazepines (notably clonazepam), vitamin E, melatonin, propranolol, amantadine, calcium channel blockers (especially nifedipine), tetrabenazine, reserpine, clonidine, buspirone, lithium carbonate and neuropeptides like ceruletide. Whereas each of these approaches provides clinical interest, none has developed into a therapeutic approach. [14]

These two cases highlight the troublesome occurrence of TD even with olanzapine which is by now an established first line treatment option of schizophrenia. Literature now suggests about 0.52% incidence rate of TD with olanzapine. [15] Interestingly in the first case, clozapine successfully corrected olanzapine induced TD. Research has suggested that olanzapine has a higher affinity and occupancy rate for D 2 receptor, [15] which may imply a higher than expected chance of inducing TD. The cases also highlight the issue of cost of treatment and its implication in medication compliance. Being unable to procure clozapine the second patient chose to tolerate the troublesome TD symptoms while the first patient ceased taking treatment altogether. The cases presented highlight the fact that despite a substantially lower risk than FGAs, TD is not entirely absent with olanzapine. Therefore, Psychiatrists must remain vigilant about onset of TD with these medications.

 
  References Top

1.Muench J, Hamer AM. Adverse effects of antipsychotic medications. Am Fam Physician 2010;81:617-22.  Back to cited text no. 1
    
2.American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4 th ed. Text Revision. Washington, DC: APA; 2000.  Back to cited text no. 2
    
3.Kucerová H. Olanzapine and improvement of tardive dyskinesia. Eur Psychiatry 2002;17:421-4.  Back to cited text no. 3
    
4.Kinon BJ, Jeste DV, Kollack-Walker S, Stauffer V, Liu-Seifert H. Olanzapine treatment for tardive dyskinesia in schizophrenia patients: A prospective clinical trial with patients randomized to blinded dose reduction periods. Prog Neuropsychopharmacol Biol Psychiatry 2004;28:985-96.  Back to cited text no. 4
    
5.Bella VL, Piccoli F. Olanzapine-induced tardive dyskinesia. Br J Psychiatry 2003;182:81-2.  Back to cited text no. 5
    
6.Dunayyevich E, Strakawsk SM. Olanzapineinduced tardive dyskinesia. Am J Psychiatry 1999;156:1662.  Back to cited text no. 6
    
7.Herran A, Vazquez-Barquero JL. Tardive dyskinesia associated with olanzapine. Ann Intern Med 1999;131:72.  Back to cited text no. 7
    
8.Bhanji NH, Margolese HC. Tardive dyskinesia associated with olanzapine in a neurolepticnaive patient with schizophrenia. Can J Psychiatry 2004;49:343.  Back to cited text no. 8
    
9.Mendhekar D, Aggarwal A. Olanzapine and trihexyphenidyl-induced tardive dyskinesia. Indian J Phrmacol 2005;37:26  Back to cited text no. 9
    
10.Zincir S, Bilgen AE, Erdem M, Gunay H, Bozkurt A. A case of tardive dyskinesia due to olanzapine treatment. Bull Clin Psychopharmacol 2012;22:268-70.  Back to cited text no. 10
    
11.Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239-45.  Back to cited text no. 11
    
12.Owens DG. Tardive dyskinesia. In: A Guide to the Extrapyramidal Side-effects of Antipsychotic Drugs. Cambridge, UK: Cambridge Üniversity Press; 1999. p. 166-226.  Back to cited text no. 12
    
13.Haddad PM, Sharma SG. Adverse effects of atypical antipsychotics: Differential risk and clinical implications. CNS Drugs 2007;21:911-36.  Back to cited text no. 13
    
14.Tamminga CA, Woerner MG. Clinical course and cellular pathology of Tardive Dyskinesia. In Neuropsychopharmacology-5 th Generation of Progress. In: Davis KL, Charney D, Coyle JT, Nemeroff C, editors. Philadelphia, Pennsylvania, PA: Lippincott, Williams and Wilkins; 2002. p. 1831-41.  Back to cited text no. 14
    
15.Shirazdi AA, Ghaemi SN. Side effects of atypical antipsychotics: Extrapyramidal symptoms and the metabolic syndrome. Harv Rev Psychiatry 2006;14:152-64.  Back to cited text no. 15
    




 

Top
   
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Case Reports
Discussion
References

 Article Access Statistics
    Viewed5228    
    Printed116    
    Emailed1    
    PDF Downloaded288    
    Comments [Add]    

Recommend this journal