Umut Günay, Candost Demiröz, Fatma Seher Kocaayan, İlay Dalkıran, Elif Tatlıdil
Tardive dyskinesia (TD) is a cluster of symptoms affecting orofacial, truncal, and extremity regions following prolonged exposure to antidopaminergic agents and may be life-threatening in severe cases. It is most commonly observed in patients receiving long-term antipsychotic treatment, such as individuals with schizophrenia. Lurasidone is a relatively novel antipsychotic that has been reported to induce tardive syndromes in patients with schizophrenia and bipolar disorder and has also been used as an augmentation strategy in treatment-resistant schizophrenia. In this report, we present an intriguing case in which TD improved following the addition of lurasidone to the patient's existing treatment, accompanied by a reduction in negative psychotic symptoms. The patient's Abnormal Involuntary Movement Scale (AIMS) score decreased from 20 to 8-9 after the initiation and subsequent dose increase of lurasidone. Additionally, the Positive and Negative Syndrome Scale (PANSS) total score decreased from 171 to 148, with particularly notable improvement in the negative symptom subscale. The beneficial effect of lurasidone on TD is hypothesized to be related to various receptor interactions of the current treatment, as well as 5-HT2A antagonism and preferential modulation of dopamine turnover in the prefrontal cortex rather than the striatum, as also observed with clozapine. Further studies are warranted to elucidate the underlying mechanisms of this phenomenon.