ISSN: 2577-4360
Authors: Alam M*, Abbas K, Usmani N and Mustafa M
Tardive dyskinesia (TD) is a potentially irreversible and disabling iatrogenic movement disorder characterized by involuntary, repetitive movements, predominantly affecting the orofacial region, trunk, and limbs. This severe adverse effect is associated with prolonged exposure to dopamine receptor blocking agents, particularly antipsychotic medications used in the treatment of psychiatric conditions such as schizophrenia and bipolar disorder. The pathophysiology of TD involves complex interactions between dopaminergic dysregulation, oxidative stress, neuroinflammation, and neuronal degeneration. Genetic factors, including variations in dopamine receptor genes, antioxidant pathways, and neuronal plasticity-related genes, contribute to individual susceptibility and symptom severity. While preventive measures, such as judicious use of antipsychotics and regular monitoring, remain the most effective strategies, once TD develops, management becomes challenging. Current pharmacological interventions, including vesicular monoamine transporter 2 (VMAT2) inhibitors, antioxidants, and alternative antipsychotics, provide symptomatic relief but do not consistently reverse the underlying pathology. Non-pharmacological approaches, such as deep brain stimulation, botulinum toxin injections, and rehabilitative therapies, can complement pharmacological interventions and improve functional outcomes and quality of life. Ongoing research efforts aim to elucidate the complex molecular mechanisms underlying TD and develop more targeted and personalized therapeutic strategies.
Keywords: Antipsychotics; Tardive Dyskinesia, D2 Receptor; Dopamine
