To the Editor: Paliperidone is associated with fewer extrapyramidal side effects (EPS) than typical antipsychotics. Here, we reported a case of schizophrenia with oral and tongue dyskinesia after aripiprazole treatment. The patient had improvement of dyskinesia after switching to paliperidone.

“Miss B” had her first episode of schizophrenia 1 year ago. The symptoms included delusion of persecution toward her colleagues, delusion of reference toward her boss, auditory hallucinations, and visual hallucinations. Her psychotic symptoms improved after the first 3 months of therapy with aripiprazole 15 mg/day. However, she had irregular, involuntary, persistent, and repetitive movements of mouth and tongue after aripiprazole treatment for 1 month. These movements were very irregular, either in intensity or direction. The intensity of movements varied over time and ranged from mild to moderate. The direction of tongue movements was random, in any possible direction, either within the oral cavity or outside the mouth. Her oral dyskinesia was not relieved after the aripiprazole was tapered to 10 mg/day in the 6th month and 5 mg/day in the 9th month. After 3 months of 5 mg/day aripiprazole therapy, her oral dyskinesia had still not responded to biperidin 2 mg/day. Because of the possibility of aripiprazole-related oral dyskinesia, the antipsychotic was switched to paliperidone. The irregular movements improved, with gradual decline in intensity, frequency, and duration within 1 month. No significant cholinergic rebound symptoms or side effects were noted after the abrupt switch. Her psychotic symptoms still remained stable. The remission of dyskinesia remained after therapy of paliperidone for the next 3 months.

This patient had improvement of dyskinesia after switching to paliperidone. The dose (3 mg/day) is relatively low for schizophrenia but equal to her previous aripiprazole dose of 5 mg/day. This patient had dramatic relief of dyskinesia side effects, which might be related to different binding patterns for neurotransmitter receptors of these two kinds of atypical antipsychotics. In a positron emission tomography study, 6–9 mg/day of paliperidone showed equal dopamine-binding at D2 receptors (around 70%–80%) over striatum and temporal cortex.¹ This patient just received 3 mg/day of paliperidone and had complete remission of dyskinesia. Lower binding of D2 receptors over striatum at the dose of 3 mg/day might be the reason. Aripiprazole has a well-known low risk of EPS, with incidence comparable to placebo, and it could modulate dopamine release over prefrontal cortex through the action on serotonin 5-HT_1A receptors.² The dopamine release is not observed over sriatum areas, and, with D2 occupancy over 90%, still did not produce EPS.³ Its tardive dyskinesia incidence is also comparable to placebo group without significant risk. However, this patient had dyskinesia side effects even using aripiprazole at a lower dose. The relatively higher antagonism over 5-HT_2A receptor of paliperidone than aripiprazole⁴ might provide another reason why this patient had remission of dyskinesia after the antipsychotic switch. 5-HT_2A antagonism also suppressed the abnormal involuntary movements and dyskinesia of dopamine-depleted rats after receiving dopamine agonists.⁵ These findings might help explain clinical phenomenon in this patient.