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 Table of Contents  
Year : 2020  |  Volume : 25  |  Issue : 2  |  Page : 149-151

Olanzapine-induced choreoathetoid movements in a young patient of schizophrenia

1 Department of Psychiatry, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, Maharashtra, India
2 Undergraduate Intern at Seth G.S. Medical College and K.E.M. Hospital, Mumbai, Maharashtra, India

Date of Submission23-Aug-2020
Date of Decision19-Sep-2020
Date of Acceptance31-Oct-2020
Date of Web Publication23-Feb-2021

Correspondence Address:
Amey Y Angane
Department of Psychiatry, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmhhb.jmhhb_120_20

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Atypical antipsychotics like olanzapine are used in the management of schizophrenia due to their lower propensity to cause extrapyramidal symptoms. Yet, few case reports have suggested that olanzapine may cause tardive dystonia, dyskinesia, and oculogyric crisis. However, olanzapine has been never reported to induce nonrhythmic choreoathetoid movements in an adolescent patient within short periods of consumption. Here, we report a novel case of choreoathetoid movements with history of olanzapine consumption for 2 years. The patient presented with involuntary bilateral movements affecting her entire body for the past 4 months, and a diagnosis of olanzapine-induced choreoathetoid movements was made after excluding other neurological and inherited causes by performing necessary investigations. After olanzapine was tapered and stopped, the patient improved and has been subsequently maintained on clozapine. Thus, constant monitoring for movement disorders is needed, particularly in patients with risk factors, even with atypical antipsychotics like olanzapine, and this must play a vital role in management.

Keywords: Atypical antipsychotic, choreoathetoid movements, olanzapine, schizophrenia

How to cite this article:
Angane AY, Anvekar AR, Ghorpade GS, Unnithan VB. Olanzapine-induced choreoathetoid movements in a young patient of schizophrenia. J Mental Health Hum Behav 2020;25:149-51

How to cite this URL:
Angane AY, Anvekar AR, Ghorpade GS, Unnithan VB. Olanzapine-induced choreoathetoid movements in a young patient of schizophrenia. J Mental Health Hum Behav [serial online] 2020 [cited 2023 Mar 26];25:149-51. Available from: https://www.jmhhb.org/text.asp?2020/25/2/149/309962

  Introduction Top

Chorea is a dance-like complex movement characterized by involuntary, rapid, irregular, jerky, nonrepetitive movements distributed all over the body. Athetoid movements are characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, feet, and in some cases, arms, legs, neck, and tongue. The “dance-like” movements of chorea often occur with athetosis, which adds twisting and writhing movements. Walking may become difficult and include odd postures and leg movements.

Olanzapine is a second-generation (atypical) antipsychotic agent associated with a very low incidence of involuntary movements than observed with other typical antipsychotic drugs.[1] While involuntary movements are seen in 15%–30% of patients who have used antipsychotic drugs, most cases generally occur after the usage of typical antipsychotic drugs.[2] Although there are few reported cases in the literature of olanzapine inducing tardive dystonia, dyskinesia, and oculogyric crisis, olanzapine has been used to improve tardive symptoms of movement disorders due to the use of typical antipsychotics in patients with psychiatric illness like psychotic disorders.[3],[4],[5] There are no reported cases of olanzapine inducing generalized choreoathetoid movements distributed over the body.[2],[3],[4],[5] Here, we report a novel case of choreoathetoid movements in a young patient of schizophrenia, which developed after 2 years of treatment with olanzapine.

  Case Report Top

A 17-year-old right-handed female patient had been suffering from schizophrenia diagnosed as per the Diagnostic and Statistical Manual-5 Criteria for the past 2 years. She had been well maintained on olanzapine 20 mg for 2 years. For the past 4 months, the patient had complaints of involuntary movements of bilateral hands and feet when she presented to the psychiatry department of a tertiary care center.

The patient initially noticed involuntary twitching movements in her hands, feet, and face which progressed to a point where she had difficulty in walking without support, was frequently thrown off balance, and experienced difficulty in eating and performing her daily activities. These movements progressively increased over the past 4 months. There was a positive family history of schizophrenia in the patient's mother.

On neurological examination, the involuntary movements involved the distal part more than the proximal part of the limbs in the form of twisting movements of hands and legs. It was associated with oromandibular movements including pursing of lips and smirking. The patient was found to have a score of 12 on the Abnormal Involuntary Movement Scale (AIMS) at the time of presentation, with severe movements in the extremities and perioral region.[6] The AIMS is a clinician-rated scale that has 12 items which assess the severity as well as resulting distress and incapacitation caused by orofacial movements and extremity and truncal movements in patients who are being administered neuroleptic medications. Items are scored on a zero (none) to four (severe) basis.[6] Systemic examination of other systems was found to be uneventful.

On mental status examination, the patient was found to be conscious, co-operative, well oriented in time, place, and person, denied any delusions or hallucinations at present, and had a good insight regarding her psychiatric illness.

The patient had been prescribed olanzapine 20 mg for her symptoms of psychosis. She had been well maintained on olanzapine 20 mg for the past 2 years and was compliant with her medications.

On admission, all of patients' blood investigations were done which included a complete hemogram, serum electrolytes, fasting blood sugar, chest roentgenogram, electrocardiogram, and thyroid function tests, all of which were normal.

Due to the nature of movements and young age of the patient, Huntington's disease, Wilson's disease, and similar inherited neurological disorders were suspected and neurology consultation was sought. The patient was started on tetrabenazine 100 mg but found no relief from her symptoms. Huntington's disease was ruled out as genetic testing for CAG mutation analysis, and huntingtin protein came to be negative. The magnetic resonance imaging of the brain at the level of basal ganglia revealed no putaminal volume loss, no caudate head atrophy, and normal frontal horns. The patient was advised peripheral smear for acanthocytes and screening for Wilson's disease including urine ceruloplasmin and serum copper, all of which were negative. Slit-lamp examination of the corneas did not reveal any evidence of Kayser–Fleischer rings. There was no family history of any involuntary movements.

A diagnosis of olanzapine-induced choreoathetoid movements was made after excluding other possible causes. In 14 days, olanzapine was tapered and stopped while clozapine was added to prevent the recurrence of psychotic symptoms. The dose of clozapine was gradually increased to 100 mg. At the end of these 14 days, the patient had a score of 7 on the AIMS.

Over the next 14 days, tetrabenazine was also tapered and stopped and the patient was maintained on clozapine 100 mg. At the end of 14 days, the patient had a score of 3 on the AIMS and was subsequently discharged. Gradually, after 6 months of initiation of clozapine and withdrawal of olanzapine, the patient improved to reach a score of 0 on the AIMS. The patient's symptoms of schizophrenia were also managed.

The patient has since been maintained on clozapine 100 mg, and after 12 months of subsequent follow-ups, the improvement in her AIMS score has been maintained and there has been no relapse of any involuntary movements.

  Discussion Top

Atypical antipsychotic agents are preferred to typical antipsychotic agents as they have a lower propensity to induce extrapyramidal symptoms and tardive movements.[1] Olanzapine, a thienobenzodiazepine derivative, is a second-generation (atypical) antipsychotic agent. Compared with typical antipsychotic drugs, olanzapine has a greater affinity for serotonin 5-HT2A than dopamine D2 receptors and preferential action at mesolimbic dopaminergic pathway over nigrostriatal pathways, and this potent antagonism at dopamine and serotonin receptors is responsible for its actions.[1],[7]

Olanzapine has been found to have beneficial effects in psychiatric disturbances like bipolar disorder, schizophrenia and other psychotic disorders, mania, depression, and even in behavioral complaints occurring in other neurological disorders such as mental retardation, Parkinson's disease, Huntington's disease, and dementia.[8] Olanzapine has been found to have utility in movement disorders as it is a safer choice which mitigates the risk of aggravation of involuntary movements.[9] Furthermore, olanzapine has also been found to improve preexisting symptoms of tardive movements which may be caused by typical antipsychotics administered to patients of psychiatric illness, especially psychotic diseases. It is frequently used in Huntington's disease since it reduces chorea, is a mood stabilizer, augments antidepressants, and also encourages weight gain.[1],[8] However, excessive sedation and metabolic side effects such as diabetes mellitus and weight gain are some of the side effects that may limit its use.

Tardive movements like the choreoathetoid movements seen in our case can be attributed to dopamine receptor hypersensitivity in nigrostriatal dopamine pathway due to long-term antipsychotic medication use causing denervation hypersensitivity.[7] Due to this striatal dopaminergic-cholinergic imbalance and paradoxically increased nigrostriatal dopaminergic activity as a compensatory response to dopamine receptor blockade, olanzapine may cause choreoathetoid movements as was noted in our case. The risk factors noted in the literature for the development of tardive movements include older age, female sex, intellectual disability, specific gene polymorphisms which alter antipsychotic metabolism and dopamine functioning, diabetes, smoking, alcohol, and substance abuse along with the development of early parkinsonian side effects in ongoing therapy.[9] These factors can also put the patient at increased risk for choreoathetoid movements.

The differential diagnosis in young patients with development of involuntary movements includes Huntington's disease, Huntington's disease-like syndromes, Wilson's disease, spinocerebellar ataxia, benign hereditary chorea, dentatorubropallidoluysian atrophy, and neuroacanthocytosis, which need to be ruled out by consultant liaison with neurologists as was done in our case.

Although vesicular monoamine transporters and drugs such as baclofen and gabapentin have shown efficacy in the treatment of movement disorders induced by antipsychotic consumption, withdrawal of causative agent is required. A shift to antipsychotics like clozapine which has the lowest propensity to cause extrapyramidal symptoms is also needed, but the prognosis in many cases is poor due to delayed diagnosis, and hence, early detection as was done in our case needs to be a priority.[10]

Thus, constant monitoring and early detection of movement disorders even with an atypical antipsychotic like olanzapine, particularly in patients with risk factors for involuntary movements, will play a vital role in management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that their name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Bhana N, Foster RH, Olney R, Plosker GL. Olanzapine: An updated review of its use in the management of schizophrenia. Drugs 2001;61:111-61.  Back to cited text no. 1
Singh GP. Risperidone and olanzapine induced tardive dyskinesia: A critical review of reported cases. Indian J Psychiatry 2004;46:319-23.  Back to cited text no. 2
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Bavle AD, Kumar GM. Olanzapine-induced tardive oculogyric crises. Indian J Psychol Med 2013;35:423-4.  Back to cited text no. 3
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Aggarwal A, Jiloha RC. Olanzapine induced tardive dystonia. Indian J Pharmacol 2008;40:237-8.  Back to cited text no. 4
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Karaş H, Güdük M, Saatcioğlu Ö. Withdrawal-emergent dyskinesia and supersensitivity psychosis due to olanzapine use. Noro Psikiyatr Ars 2016;53:178-80.  Back to cited text no. 5
Guy W. ECDEU Assessment Manual for Psychopharmacology. Rockville, Md.: U. S. Dept. of Health, Education, and Welfare, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute of Mental Health, Psychopharmacology Research Branch, Division of Extramural Research Programs; 1976. p. 534-7  Back to cited text no. 6
Maloney AE, Sikich L. Olanzapine approved for the acute treatment of schizophrenia or manic/mixed episodes associated with bipolar I disorder in adolescent patients. Neuropsychiatr Dis Treat 2010;6:749-66.  Back to cited text no. 7
Grove VE Jr, Quintanilla J, DeVaney GT. Improvement of Huntington's disease with olanzapine and valproate. N Engl J Med 2000;343:973-4.  Back to cited text no. 8
Phillips W, Shannon KM, Barker RA. The current clinical management of Huntington's disease. Mov Disord 2008;23:1491-504.  Back to cited text no. 9
Solmi M, Pigato G, Kane JM, Correll CU. Clinical risk factors for the development of tardive dyskinesia. J Neurol Sci 2018;389:21-7.  Back to cited text no. 10


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