What Is Tardive Dyskinesia?
Sometimes medications used to treat serious conditions can bring on serious conditions of their own. That’s the case with tardive dyskinesia (TD), a disorder marked by random and involuntary muscle movements that usually occur in the face, tongue, lips, or jaw.
It’s typically caused by long-term use of antipsychotic medications that block dopamine receptors, but it can be caused by some other drugs as well. Antipsychotic medications are used to treat a number of mental illnesses and mood disorders, including schizophrenia, bipolar disorder, and depression.
Tardive dyskinesia mainly causes these involuntary movements of the face, tongue, lips, or jaw:
It can also cause rocking, jerking, flexing, or thrusting of the trunk or hips and repetitive writhing, twisting, or dancing movements of the fingers or toes, according to the National Alliance on Mental Illness (PDF).
Antipsychotic drugs can cause tremor, too. This type of involuntary movement disorder is a rhythmic shaking of one or more body parts, whereas movements caused by tardive dyskinesia are irregular and unrhythmic.
RELATED: What’s the Difference Between Tremors and Dyskinesia Associated With Parkinson’s Disease?
Tardive dyskinesia is mainly caused by an older class of drugs used to treat psychiatric disorders. These antipsychotic medications, also called neuroleptic drugs, work by blocking dopamine receptors in the brain. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centers. It also plays a major role in motor functioning.
It's not clear why or how tardive dyskinesia symptoms begin, but they're thought to be related to the chronic blocking of dopamine receptors.
The older antipsychotic drugs that cause tardive dyskinesia include:
So-called second-generation, or atypical, antipsychotics can also cause tardive dyskinesia, according the American Academy of Neurology, although they are less likely to. These drugs include:
The following antidepressants may also cause TD, according to MedlinePlus:
Other drugs that can cause TD include:
It usually takes many months or years to develop symptoms of tardive dyskinesia, but the side effect can sometimes arise in just six weeks.
It’s possible, although rare, for tardive dyskinesia symptoms to start after a person has stopped taking a medication that can cause it, per the Cleveland Clinic.
According to a report published in June 2018 in the Journal of Neurological Sciences, some of the risk factors for developing tardive dyskinesia include older age, being female, and being white or of African descent. The longer a person has been ill, the more likely they are to develop the symptoms. People with diabetes, who smoke cigarettes, or who abuse alcohol or other substances may be at higher risk, too.
Dyskinesia can also develop in people with schizophrenia who haven’t used antipsychotics, a type known as spontaneous dyskinesia. It is estimated to occur in 25 percent of patients between 30 and 50 years old and in up to 40 percent of people 60 or older, per research. However, since most people with schizophrenia are treated with antipsychotics these days, spontaneous dyskinesia is rarely seen.
A doctor may make a diagnosis of tardive dyskinesia if a person is taking a medication that can cause it, has signs and symptoms of the problem, or has undergone testing to rule out other neurological or movement disorders that can cause similar symptoms. Other conditions that can cause involuntary or uncoordinated movements include Huntington’s disease, cerebral palsy, Tourette syndrome, and dystonia per the National Organization for Rare Disorders.
Doctors may also use a tool called the Abnormal Involuntary Movement Scale (AIMS) to detect tardive dyskinesia in people who are taking neuroleptic drugs and to track the severity of their symptoms over time. During an AIMS test, your doctor will gauge the involuntary movement throughout your body on a five-point scale, assessing the severity of movements. The AIMS may be administered before a neuroleptic drug is prescribed so the doctor has a baseline against which to compare future results, according to an article published in April 2022 in StatPearls.
The long-term prognosis for people with tardive dyskinesia varies. When diagnosed early, stopping the medication that is triggering symptoms can resolve the problem, though in some cases, the symptoms may persist indefinitely or worsen over time, according to an article published in 2021 in the journal Neuropsychiatric Disease and Treatment.
There is no standard treatment for tardive dyskinesia. Most likely, your doctor will adjust the medication thought to be causing the symptoms. In many cases, neuroleptic medications will be lowered to the lowest possible dose or discontinued if possible. But there’s limited evidence that lowering the dose, administering the drug intermittently, or stopping the drug altogether will reduce tardive dyskinesia symptoms.
Abruptly stopping a neuroleptic medication is not recommended because doing so can worsen tardive dyskinesia or even cause it in a person who is not already affected by it.
Two drugs, deutetrabenazine (Austedo) and valbenazine (Ingrezza), are approved by the U.S. Food and Drug Administration for the treatment of tardive dyskinesia. Both belong to a class of drugs known as selective VMAT2 (vesicular monoamine transporter-2) inhibitors. They are also referred to as dopamine-depleting drugs because of the effect they have in the brain.
Studies of valbenazine show it to be well tolerated, with fatigue or sedation as the main side effect.
More common side effects of deutetrabenazine are akathisia (restlessness), depression, and diarrhea. Deutetrabenazine has a black box warning for depression and suicidality, but data from studies of its effectiveness in treating tardive dyskinesia did not show an increased risk of suicide.
While both drugs have been found to suppress symptoms of tardive dyskinesia, they do not cure TD, and symptoms can recur if the drugs are stopped.
Some other drugs may improve tardive dyskinesia symptoms, but the evidence for them is considered insufficient to recommend them broadly as treatment for tardive dyskinesia.
Various alternative therapies have been studied for the treatment of tardive dyskinesia, but their effectiveness is unclear.
For example, there’s some evidence that branched-chain amino acids (BCAAs) — leucine, valine, and isoleucine — which are typically marketed as supplements for building muscle, can decrease TD symptoms. So far, researchers have deemed BCAAs promising and worth studying further.
Ginkgo biloba extract may also be effective in improving TD symptoms and “should be considered as treatment,” according to an article published in Neurology.
But these findings are still preliminary, and larger and higher-quality studies are needed before these or any other alternative therapies can be recommended for routine use.
Note that any supplement can cause side effects of its own, and many have potential interactions with prescription and over-the-counter drugs. So while preparations of BCAAs and ginkgo biloba are readily available for purchase at retail drugstores and online, it’s a good idea to discuss their use with your doctor before self-treating with these or any other dietary supplements.
When it comes to TD, the best strategy is prevention. That means judicious prescribing of antipsychotic drugs by healthcare providers, regularly monitoring patients for symptoms, and acting quickly to intervene and change treatment when symptoms occur.
Changing medications may also help. While all antipsychotics carry the risk of TD, the second generation of antipsychotics carry less of a risk, according to a meta-analysis published in October 2018 in World Psychiatry.
Tardive dyskinesia can interfere with eating, speaking, breathing, walking, and other activities of daily living.
The involuntary movements caused by tardive dyskinesia can also cause a person to feel embarrassed or self-conscious and to avoid social interaction. This self-isolation may compound the social isolation already experienced because of the mental or physical disorder necessitating taking the drug in the first place, per an article published in 2019 in Neuropsychiatric Disease and Treatment.
The low quality of life associated with tardive dyskinesia may lead some people to stop their drug therapy on their own, potentially leading to a relapse in their disease symptoms and, for some, the need for hospitalization.
According to a meta-analysis published in October 2018 in World Psychiatry, TD tends to occur in about 20 percent of people being treated with first-generation antipsychotics.
Research suggests that women and older patients are at a higher risk of developing the condition. In postmenopausal women in particular, incidence rates are as high as 30 percent.
In people being treated with second-generation antipsychotics, the rate of TD tends to be one-third of the rate of occurrence with first-generation medications, according to the World Psychiatry meta-analysis.
Research summarized in the summer 2017 issue of the Ochsner Journal suggests that being of African descent appears to elevate one’s risk of developing TD. An evaluation of 1,149 patients with TD found that in inpatient settings, African American patients were more likely to develop TD than Americans of European descent.
However, these results may not have taken into consideration the potential confounding factors, such as socioeconomic status and the ways in which doctors might treat African American patients differently with antipsychotics.
Tardive dyskinesia is one of several extrapyramidal side effects, which are commonly called drug-induced movement disorders. Others include:
While extrapyramidal symptoms are more likely to occur with first-generation antipsychotics, they can occur with second-generation antipsychotics as well.
Extrapyramidal symptoms can go away on their own or with treatment. However, they can be painful while they last, and without treatment, they can lead to serious and even life-threatening complications.
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