Tardive Dyskinesia (TD) is a neurological disorder characterized by involuntary, repetitive movements of the body. This condition is a potentially persistent side effect that can affect an estimated 20% to 30% of individuals who receive long-term treatment with the associated medications. TD typically develops after a period of exposure to these drugs. If you suspect you have TD, consult a medical professional for evaluation.
Recognizing the Involuntary Movements
These movements are often rhythmic and tend to be stereotypical in nature. They are frequently observed in the face and mouth, which is why they are sometimes referred to as orofacial dyskinesias. Common facial manifestations include involuntary grimacing, repetitive chewing motions, and excessive, rapid eye blinking.
Many individuals experience issues with the mouth and tongue, such as puckering or pouting of the lips, lip smacking, and the tongue thrusting or darting in and out of the mouth. These movements can interfere with speaking, eating, and general facial expression.
Movements are not limited to the head and neck; they can also affect the limbs and trunk of the body. In the extremities, the movements may appear as rapid wiggling of the fingers or toes, sometimes described as “piano playing” movements. More generalized movements can manifest as rocking of the torso, or involuntary pelvic thrusting motions, which are often more prominent when the individual is seated or standing still.
Medications Linked to the Condition
Tardive Dyskinesia primarily arises from the long-term use of medications that block dopamine receptors in the brain, particularly in areas controlling motor function. The most common cause is the use of antipsychotic medications, which are prescribed for conditions like schizophrenia and bipolar disorder. First-generation antipsychotics, such as haloperidol and chlorpromazine, carry a higher risk of inducing TD compared to the newer, second-generation (atypical) antipsychotics like risperidone or olanzapine.
While the risk is lower with second-generation agents, it is not eliminated, and exposure over time remains a concern. The duration of treatment plays a significant role, as the risk typically increases with longer periods of use and higher cumulative doses of the drug.
Beyond antipsychotics, other classes of drugs that block dopamine receptors can also precipitate the condition. Certain anti-nausea and gastrointestinal motility medications, most notably metoclopramide, have a strong association with TD, especially with extended use.
Seeking Professional Confirmation and Treatment
If involuntary movements are suspected, the first and most important step is to consult with the prescribing physician or a movement disorder specialist, such as a neurologist. Self-diagnosis is unreliable, and a professional evaluation is necessary to rule out other possible causes of abnormal movements. The formal diagnosis often involves a clinical assessment using standardized tools, most notably the Abnormal Involuntary Movement Scale (AIMS).
The AIMS scale is a clinician-administered assessment designed to rate the severity and location of the involuntary movements in the facial, oral, truncal, and limb regions. A definitive diagnosis requires that the abnormal movements persist for at least one month after a change in the offending medication or a reduction in its dosage. Early detection is important because it can influence the long-term course of the condition.
Management of the condition centers on a careful re-evaluation of the medication regimen that led to the movements. If medically appropriate, the first strategy may involve reducing the dose of the causative drug or switching to an alternative agent with a lower potential for inducing TD. However, such adjustments must be made cautiously to avoid worsening the underlying psychiatric condition or triggering a temporary increase in the dyskinesia, known as withdrawal dyskinesia.
Fortunately, there are now specific medications approved for the treatment of TD, which are typically used when symptoms are moderate to severe. These agents are known as Vesicular Monoamine Transporter 2 (VMAT2) inhibitors, including valbenazine and deutetrabenazine. VMAT2 inhibitors work by regulating the uptake of monoamines, like dopamine, into presynaptic vesicles, which helps to stabilize dopamine signaling in the brain’s motor pathways. These targeted treatments offer an effective way to reduce the severity of the involuntary movements, improving the patient’s quality of life even while they continue essential treatment for their underlying disorder.