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Tardive Dyskinesia (TD) Drug induced abnormal involuntary movements Tardive dyskinesia (TD) is a movement disorder that causes involuntary, repetitive body movements and is commonly seen in patients who are on long-term treatment with antipsychotic medications. However, several other classes of medications with different mechanisms are also associated with TD. Tardive dyskinesia is a side effect of antipsychotic medications. These drugs are used to treat schizophrenia and other mental health disorders. TD causes stiff, jerky movements of your face and body that you can't control. You might blink your eyes, stick out your tongue, or wave your arms without meaning to do so. Not everyone who takes an antipsychotic drug will get it. But if it happens, it’s sometimes permanent. Tardive dyskinesia causes stiff, jerky movements that you can't control. They include: Orofacial dyskinesia or oro-bucco-lingual dyskinesia: Uncontrolled movements in your face -- namely your lips, jaw, or tongue. Presentation might be as follows: Stick out your tongue without trying Blink your eyes fast Chew Smack or pucker your lips Puff out your cheeks Frown Grunt So if you have movements you can't control, let your doctor know right away. To ease your symptoms, your doctor may: Lower the dose Add another medication to what you’re taking to act as an antidote Switch you to a different drug Treatment and Prevention The goal is to prevent TD. When your doctor prescribes a new drug to treat a mental health disorder, ask about its side effects. The benefits of the drug should outweigh the risks. You might need to switch to a newer antipsychotic drug that may be less likely to cause TD. There are two FDA-approved medicines to treat tardive dyskinesia: Deutetrabenazine Valbenazine Both of these medicines work in similar ways to regulate the amount of dopamine flow in brain areas that control certain kinds of movements. Both can sometimes cause drowsiness. Medication-induced TD is a complex and unique neurologic disorder. While the reported incidence of TD seems to be less with atypical APDs compared to typical APDs, a risk of developing TD is associated with these medications, as well as others. A number of challenges with TD remain, including the ability to quantify the risk of TD caused by pharmacologic management, the difficulty of diagnosing TD even with DISCUS and other approaches, the exposure of older patients to both typical and atypical APDs, and the dyskinesia caused by other neurologic disorders. Additionally, the unclear pathophysiology of TD continues to be a problem for the successful treatment and management of the condition.