How to Recognize Tardive Dyskinesia

Differentiating tardive dyskinesia from other movement disorders can be challenging.

“One major criterion is the history of exposure to neuroleptic medications,” said Jeff Bronstein, MD, PhD, of the UCLA Health Movement Disorders Clinic. “The key is having had exposure to dopamine-blocking medications.”

Tsao-Wei Liang, MD, of Thomas Jefferson University in Philadelphia, agreed, saying the only way to diagnose tardive dyskinesia is if the patient has had a known drug exposure.

“You have to have a culprit agent,” Liang told MedPage Today. “There’s a clear correlation with medication exposure and the movement that develops in the patient’s history.”

Differentiation of Movements

Once that medication has been pinpointed, clinicians should note the patient’s distinct movement patterns and how they progress.

“Stereotypies, chorea, athetosis, and dystonia are the top four movements associated with tardive dyskinesia,” said Liang.

A stereotypy is a specific form of movement that can help differentiate tardive dyskinesia from other movement disorders, he said. A repetitive-type movement, a stereotypy usually starts as an oro-buccal-lingual motion in tardive dyskinesia and can look like lip-smacking, facial grimacing, or tongue movements.

The classic form of tardive dyskinesia begins generally in the lower face — mouth, tongue, and jaw — and neck, said Liang. “When I teach our residents and fellows to recognize tardive dyskinesia, I ask them to focus on the facial movements first.”

Bronstein added that oro-buccal-lingual stereotypies “can be very mild but become more severe with time with continued [drug] exposure.”

In one study, researchers analyzed videotapes of tardive dyskinesia patients and found that 96.1% had stereotypy. The presence of stereotypy in an adult “is highly suggestive” of prior exposure to dopamine receptor-blocking drugs, the research group concluded.

Tardive dyskinesia also can involve other parts of the body, including the neck, the eyes, the limbs, and the trunk, Liang pointed out.

It can include chorea, which involves brief abnormal involuntary muscle contractions. It also can include dystonia, which are uncontrolled, sustained muscle contractions that result in twisting and repetitive movements or abnormal fixed postures.

Athetosis — slower, irregular movement of the distal limbs, often looking like wiggling or writhing finger movements — also can emerge.

Although a patient could present with a variety of movements associated with tardive dyskinesia, it is more common to see one stereotype pattern movement, Liang observed. “It’s rare to see all different movements related,” he said. “It’s an interesting phenomenon … why do certain tardive dyskinesias look different from others?”

In contrast, movements such as bradykinesia, muscle rigidity, rhythmic tremor, and shuffling gait are more indicative of drug-induced parkinsonism rather than tardive dyskinesia, noted Kristen Ward, PharmD, of the University of Michigan College of Pharmacy in Ann Arbor, and Leslie Citrome, MD, of New York Medical College in Valhalla, in a recent review.

Ward and Citrome added that it is possible for patients treated with antipsychotics to have both drug-induced parkinsonism and tardive dyskinesia, but the former would precede the latter.

While movements associated with tardive dyskinesia typically set in after a few months use of a neuroleptic medication, drug-induced parkinsonism usually starts within a few weeks of starting a medication or raising its dose, according to DSM-5 criteria.

In rarer cases, tardive dyskinesia can appear months or years after treatment initiation. Drug-induced parkinsonism also can manifest several months or longer after starting a new drug.

Patients treated with dopamine-blocking agents can experience what’s known as withdrawal-emergent dyskinesia, a subtype of tardive dyskinesia. This manifests as involuntary movements after discontinuing a drug. “The dopamine receptors are kind of like recalibrating, and you’ll see these movements for [a few] months and then they go away,” John Lauriello, MD, also of Thomas Jefferson University, told MedPage Today.

The movements of withdrawal dyskinesia often look like classic tardive dyskinesia, marked by oro-buccal-lingual stereotypies. However, these symptoms are not permanent and sometimes rapidly improve. If the dyskinesia persists beyond 8 weeks, it is considered to be tardive dyskinesia, according to the DSM-5.

Imaging Aids

After a patient presents with involuntary muscle movements, dopamine transporter SPECT imaging (DaTscan) may help whittle down the final diagnosis, said Liang.

“The DaTscan evaluates how healthy the dopamine centers are,” he said. It can help to differentiate a drug-induced movement disorder apart from true Parkinson’s disease, he noted.

“If you have someone who was on a neuroleptic 6 months to 1 year ago and has these movements — and let’s say their movements are slowing down in their body, developing what looks like Parkinson’s, but they’re also having improvement — you may want to ask, ‘Was it truly the medication or not that led to this point?'”

While brain CT and MRI typically are normal in patients with tardive dyskinesia, these scans can help eliminate other causes of the movements, noted Bronstein.

A brain MRI is “probably the one imaging modality we would use if we’re not certain about the exposure and we want to delve a little further,” Liang said.

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