Olanzapine is an atypical antipsychotic with diverse receptor activities. Its greater affinity for serotonin 5HT2A receptors over dopamine D2 receptors accounts for the lower risk of extrapyramidal symptoms. Tic can be observed in transient tic disorder, Tourette's disorder, or medication-induced tic disorder, which could be a variant expression of tardive dyskinesia. De-arrangement of the dopaminergic pathway, including dopamine excess or super-sensitivity of post-synaptic dopaminergic receptors, is the main neurotransmitter abnormality of tic.1 Herein is reported a case of late-onset vocal tic in schizophrenia that was successfully treated with olanzapine monotherapy. A 48-year-old woman had been diagnosed with schizophrenia since 32 years of age. She had neither history of involuntary movement disorders nor family history of tic disorders or psychiatric disorders, including obsessive-compulsive disorder. Her initial psychiatric symptoms included commentary auditory hallucinations and persecutory delusions. Her symptoms remained stable under haloperidol 5–10 mg/day as an outpatient during the first 12 years. Late-onset extrapyramidal side-effects, including tremor and bradykinesia, were first noticed 4 years ago. The symptoms were attenuated largely by shifting the antipsychotic to quetiapine 200–400 mg/day, but the patient was lost follow up and visited several doctors in other hospitals with poor adherence to medication. After 2 months of medication discontinuation the patient revisited Taipei City Psychiatric Center with a complaint of vocal tic lasting for nearly 2 months, with unremarkable psychotic symptoms. The vocal tic was easily noticeable every 3–4 s throughout the day except for sleep and caused significant suffering, and difficulty in concentration as well as in interpersonal relationship. The neurologist confirmed the tic although magnetic resonance imaging of the brain and laboratory examinations produced normal results. The patient started receiving olanzapine monotherapy from 5 mg/day, titrating up to 10 mg/day thereafter. The vocal tic gradually subsided in 5 months. The patient has maintained the medication without re-appearance of the vocal tic for 2 years. She had been given haloperidol (2 mg/day) additionally for 2 months due to transient psychosis exacerbation. The patient resisted dose elevation of olanzapine during the exacerbated period for severe obesity (body height, 162 cm; bodyweight, 92 kg). Tics are known to be induced by a variety of drugs. Antipsychotic-induced tics may appear after years of continuous neuroleptic use in schizophrenia or weeks after neuroleptic withdrawal.2 Given the fact that the patient had no history of tic disorder and had been on antipsychotic since 32 years of age, we speculate that the tics might be explained by withdrawal from chronic antipsychotic exposure. Long-term use of antipsychotics could induce dopamine receptor hypersensitivity, in which withdrawal of the antipsychotic allowed hypersensitized receptors to respond to normal levels of dopamine and the appearance of tardive dyskinesia or tics.2 Olanzapine has been reported to improve tardive dyskinesia in 6 months of treatment after 5 years of antipsychotic therapy,3 as well as tardive dystonia, including in pharyngo-laryngeal dystonia, 2–6 weeks after decades of disease history.4, 5 Interestingly, olanzapine also appeared beneficial in treating the late-onset tic in the present case, possibly an uncommon manifestation of tardive dyskinesia. Its pro-cholinergic property seems to possess a potential antidyskinetic effect for drugs with post-synaptic cholinergic activity.6 It is postulated that olanzapine exerts its tic-reducing effect via this unique property. The present report shows the advantage of olanzapine monotherapy in treating late-onset simple vocal tics in a chronic schizophrenia patient following withdrawal of long-term antipsychotic treatment. Further studies to examine this effect and its mechanism are warranted.
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Cheng et al. (2007) studied this question.
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