Photo Credit: Artemis Diana
It is important for clinicians to understand the causes and symptoms of tardive dyskinesia to avoid common misdiagnoses and ensure effective management.
Tardive dyskinesia (TD) is a complex neurologic disorder characterized by involuntary, repetitive movements that can affect the face, lips, jaw, tongue, and limbs. These movements are often disfiguring and socially stigmatizing, leading to significant emotional and functional impairments. Understanding the causes, recognizing the symptoms, and distinguishing TD from other movement disorders are crucial for accurate diagnosis and effective management.
In an article published in the Primary Care Companion for CNS Disorders, researchers presented a case vignette and discussion to help clinicians diagnose and treat TD.
What is Tardive Dyskinesia?
TD is a hyperkinetic movement disorder resulting from long-term use of dopamine receptor–blocking agents commonly found in antipsychotic medications.
“TD typically presents after long-term use of dopamine-blocking medications but can also appear early in the treatment course, sometimes within the first month,” says psychiatrist Alex Dimitriu, MD, in an interview with Physician’s Weekly.
TD presents as involuntary, rhythmic, and stereotyped muscle movements, predominantly affecting the face and tongue but also extending to the limbs and trunk.
“It can be subtle, so it’s often missed. But traditionally, it’s oral movements like lip smacking. This can be confused with dry lips and not recognized,” says psychiatrist Howard R. Weeks, MD.
What Causes It?
The primary cause of TD is chronic exposure to dopamine receptor–blocking agents. These include first-generation antipsychotics, such as haloperidol and fluphenazine, which carry a higher risk for TD. Second-generation antipsychotics, including quetiapine and clozapine, generally have a lower risk but are not entirely without it. Other dopamine-blocking agents, such as certain antiemetics like metoclopramide and prochlorperazine, can also induce TD.
“The typical antipsychotics (ie, first generation) and atypical antipsychotics make patients more susceptible to TD, but at a reduced incidence,” explains Dr. Weeks.
The most widely accepted mechanism behind TD is dopamine supersensitivity. Long-term dopamine receptor blockade leads to upregulation of postsynaptic dopamine receptors, making them hypersensitive and resulting in involuntary movements.
“Higher doses and longer periods of exposure can increase TD risk for both first- and second-generation antipsychotics,” Dr. Dimitriu says.
Common Symptoms
TD manifests in various ways, including orofacial movements such as grimacing, tongue darting, lip smacking, or puckering. It can also involve limb movements characterized by rapid, jerking motions in the arms and legs. Trunk movements, including swaying or twisting motions of the torso, are also common.
Respiratory muscles may be affected in rare cases, leading to abnormal breathing patterns. These symptoms can lead to significant social stigma, impaired daily functioning, and emotional distress.
Commonly Mistaken Conditions
Accurate diagnosis of TD is critical, as other movement disorders can mimic its symptoms. These disorders include the following:
- Withdrawal dyskinesia occurs after the abrupt discontinuation of dopamine-blocking agents but usually resolves spontaneously.
- Edentulous dyskinesia is common in individuals with missing teeth, presenting with buccolingual movements but typically without tongue involvement.
- Benign essential blepharospasm causes involuntary eyelid movements.
- Meige syndrome involves progressive dystonic movements of the eyelids and oromandibular area, but it starts as focal dystonia before spreading.
- Huntington’s disease is a hereditary neurodegenerative disorder that causes choreiform movements but can be differentiated from TD through genetic testing and family history.
- Tic disorders and restless leg syndrome can mimic TD, although they have different underlying causes.
“Neurological tic disorders are the most common. Sometimes, tremors can be mistaken for TD. A careful history and neurological exam are crucial,” says Dr. Weeks.
The authors of the case vignette emphasized that early detection is vital, as “TD is often irreversible, disfiguring, and societally stigmatized, which likely explains its associations with poor daily functioning and adverse psychosocial outcomes. Therefore, clinicians should be vigilant for the emergence of TD and proactively mitigate symptom progression.”
