<![CDATA[Background: Tardive dyskinesia (TD) is a complex, potentially irreversible movement disorder primarily associated with the long-term use of antipsychotic medications, particularly typical neuroleptic drugs. TD can develop during treatment and persist long after the discontinuation of the culprit medication. The etiology of this condition involves dysregulation of dopaminergic signalling, especially within the striatum, leading to activation of D2 dopamine receptors. This imbalance affects the homeostasis of neurotransmitters, including GABA and Glu. Chronic dopamine receptor antagonism incites neuroadaptive alterations that may linger post-therapy, resulting in abnormal involuntary movements affecting the orofacial regions, limbs, and trunk, which profoundly diminish patient quality of life. Case: A 29-year-old female with a known history of schizophrenia presented with sudden-onset neurological symptoms, notably persistent orofacial dyskinesias such as lip smacking and grimacing, which had developed over a 24-hour period. A thorough review of her medications indicated that lurasidone, classified as an atypical antipsychotic, was likely responsible for the onset of these dyskinetic movement features. Consequently, the physician opted to discontinue lurasidone and initiate valbenazine at 40 mg once daily with the intent of managing the dyskinetic symptoms while considering the overall psychiatric and medical treatment plan for the patient. Conclusion: The emergence of orofacial dyskinesias in this patient suggests a possible adverse reaction to lurasidone, necessitating re-evaluation of her psychopharmacological regimen. Valbenazine, a selective vesicular monoamine transporter 2 inhibitor, may provide a tailored approach to mitigate dyskinetic movements, while maintaining therapeutic efficacy in psychiatric care.]]>
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