Tardive dyskinesia often goes undiagnosed. Leading experts share advice on early detection and treatment.
Living with tardive dyskinesia can feel like facing an invisible challenge. This often-overlooked side effect of medications used to treat psychiatric conditions affects at least 600,000 people in the United States, according to Mental Health America. Yet despite its prevalence, many individuals remain undiagnosed — some estimates suggest as many as 65 percent may not realize they have it, per the National Organization for Tardive Dyskinesia.
Derived from Latin roots, tardive means delayed, and dyskinesia translates to abnormal movement. This disorder is characterized by involuntary, repetitive motions such as grimacing, excessive blinking, or rapid limb movements. For some, these symptoms emerge after years of medication use; for others, they can appear in as little as six weeks, according to MedlinePlus.
These movements can be disruptive and isolating, impacting self-esteem, relationships, and overall quality of life. Yet the path to recognizing and treating tardive dyskinesia is often fraught with barriers.
- Are healthcare professionals prepared to spot the signs early?
- What factors contribute to delays in diagnosis?
- And most importantly, can the progression of tardive dyskinesia be halted once it begins?
RELATED: Understanding the Different Types of Tardive Syndromes
To shed light on these questions, bpHope turned to three leading neuropsychiatrists, each with extensive experience in treating and researching tardive dyskinesia. Christoph U. Correll, MD, a professor of psychiatry and molecular medicine at the Donald and Barbara Zucker School of Medicine at Hofstra-Northwell in Hempstead, New York; Leslie Citrome, MD, MPH, clinical professor of psychiatry and behavioral sciences at New York Medical College in Valhalla, New York; and Stanley N. Caroff, MD, emeritus professor of psychiatry at Perelman School of Medicine at the University of Pennsylvania in Philadelphia.
Editor’s Note: This interview has been edited for length and clarity.
bpHope: Do you prefer using “tardive syndromes” to describe a broader range of symptoms, or do you stick with “tardive dyskinesia” since it’s more widely recognized?
Christoph Correll: A group of psychiatrists and neurologists have debated the best terminology for two years now. It’s tricky because tardive dyskinesia is a very well-recognized term, even though the condition is underassessed and undertreated.
It is a terminology recognized by psychiatrists and nurse practitioners, who comprise the bulk of the people who care for patients at risk for and diagnosed with tardive dyskinesia. People know what we’re talking about, which aligns with the American Psychiatric Association (APA) guidelines on what to do for screening and how to treat it.
BPH: What factors influence tardive dyskinesia’s progression, and are there early indicators of a higher risk for chronic or severe symptoms?
CC: Risk factors for the emergence of tardive dyskinesia include chronic use and higher doses of drugs that act as dopamine antagonists, co-use of anticholinergic medications, previous neuromotor side effects, such as dystonic reactions, akathisia (inner restlessness or need shift positions) or parkinsonism (slowed movements, rigidity, and tremors) as a side effect of the dopamine blocking medication, as well as higher age and female sex.
A history of substance abuse or diabetes are conditions that might reduce some of the buffer against the neurotoxic effects and may be the reason for the development of tardive dyskinesia secondary to antipsychotic use. When symptoms emerge, it’s difficult to know if they will stay the same, progress to moderate or severe tardive dyskinesia, or regress even if we discontinue the dopamine receptor antagonist drug. The risk factors that actually drove the initial emergence of tardive dyskinesias likely also affect progression.
BPH: Is tardive dyskinesia reversible, and if so, what factors most impact its reversibility?
CC: Tardive dyskinesia can be irreversible, but is not always so. Identifying tardive dyskinesia early when it is not severe gives you more chance to reverse it. Reducing the risk factors, such as curbing substance abuse, stabilizing blood sugar in someone who has diabetes, or lowering doses of dopamine-blocking medications when they lead to neuromotor side effects and using VMAT2 inhibitors [vesicular monoamine transporter inhibitors] could help mitigate the severity and reduce the symptomology to the degree that it might not be visible anymore.
VMAT2 inhibitors reduce the amount of dopamine in the nerves and are approved to treat tardive dyskinesia. Two are currently approved [by the U.S. Food and Drug Administration (FDA)] to treat tardive dyskinesia: deutetrabenazine (Austedo) and valbenazine (Ingrezza). We know that earlier identification and treatment of tardive dyskinesia is better than later.
BPH: How should clinicians adjust treatment to minimize the progression of tardive dyskinesia?
CC: The first step is to revisit whether the potentially causative medication is necessary. Can it be replaced with something else? We may be able to replace the dopamine receptor blocker with other medications if it’s given as augmentation for mood stabilization or depression. Other questions include: Can the dose be reduced without undercutting the medication’s efficacy? Can I reduce other risks, such as substance use or diabetes? There may also be a role for vitamin E in terms of minimizing progression.
BPH: Why do clinicians often overlook tardive dyskinesia?
CC: I think there are multiple reasons, and it is a real problem.
One issue is the false belief that tardive dyskinesia is mainly a concern from the era of first-generation antipsychotics. Clinicians assume second-generation antipsychotics, which cause less akathisia and Parkinsonism, have an almost negligible risk of tardive dyskinesia.
Additionally, clinicians prescribing antipsychotics are often not neurologists and may feel unequipped to assess tardive dyskinesia. Many don’t know how to use tools like the Abnormal Involuntary Movement Scale [AIMS], leading to a sense that this isn’t their responsibility.
For many decades, until 2017, there were no treatments for tardive dyskinesia, creating a mindset of, “Why look for it when there’s nothing to offer?” There may also be unconscious feelings of guilt, with clinicians thinking, “If I detect it, I might be seen as the culprit or even sued.” All of this contributes to a tendency to turn a blind eye and avoid assessing and addressing the issue.
BPH: What might improve diagnostic accuracy?
CC: I think there should be a standard. Patients on dopamine receptor–blocking antipsychotics should be assessed for tardive dyskinesia at every visit. Clinicians should at least routinely ask about and observe the patient for unusual movements, such as Parkinsonism (rigidity or slowness), akathisia (restlessness), or involuntary movements, especially in the face, that may be indicative of tardive dyskinesia.
A simple question like, “Since our last visit, have you noticed any unusual movements, or has anyone pointed out movements you didn’t intend to make?” should also be part of the routine. This can be done quickly and integrated into regular check-ins, alongside questions about weight or sleep, to catch potential issues like tardive dyskinesia early.
However, as suggested by the APA guidelines, a formal assessment with a tool such as the AIMS should be conducted at frequencies depending on the risk for tardive dyskinesia of the medication and the patient.
BPH: What specific steps could improve tardive dyskinesia diagnosis rates, particularly in settings where patients may not receive regular screenings?
CC: There’s a critical need for better tardive dyskinesia education among healthcare professionals, especially outside psychiatry. Regular assessments, such as with the AIMS, can greatly improve diagnosis rates. This 12-item tool takes just five minutes and is practical for routine care.
Tardive dyskinesia is often subtle, and because symptoms are involuntary, patients may not notice them. That’s why it’s essential to ask if they or others have observed unusual movements, combined with a quick physical assessment. Even if symptoms aren’t present, regular AIMS exams create a standard of care.
Clinicians should be trained to use the AIMS — it’s simple and efficient. The focus isn’t on scoring every visit but on identifying and addressing symptoms when they appear. APA guidelines recommend monitoring every three months for high-risk patients on first-generation antipsychotics, every six months for moderate-risk cases, and annually for low-risk individuals. Personally, I suggest checking more frequently when starting or adjusting medications, with at least a six-month AIMS assessment after baseline for all patients.
BPH: Why is it crucial for clinicians to distinguish tardive dyskinesia from other movement disorders, like acute extrapyramidal syndromes or drug-induced Parkinsonism?
Leslie Citrome: Tardive dyskinesia is often irreversible, while drug-induced Parkinsonism can be reduced or eliminated by lowering the antipsychotic dose, changing the antipsychotic, or stopping the antipsychotic.
In addition, the medication often used to address drug-induced Parkinsonism can make tardive dyskinesia worse, as well as interfere with cognition. On the other hand, treatment for tardive dyskinesia with VMAT2 inhibitors can make drug-induced Parkinsonism worse. Thus, a correct diagnosis is especially important.
BPH: What are the current treatment options for managing tardive dyskinesia, and how effective are they?
Stanley Caroff: Treatment for tardive dyskinesia depends on the severity of the abnormal movements and how much they impact a person’s life and functioning. Severe movements that can impair walking, talking, eating, resting, etc. ought to be treated, but treatment for even mild or subtle embarrassing movements should also be considered. Any treatment decision depends on a thorough discussion with your doctor and on your own health circumstances.
Talk with your doctor first about the indications and safety of any modifications to your current medications. If these measures are impractical or unsafe, then VMAT2 inhibitors are the only treatments that have been approved as safe and effective for suppressing tardive dyskinesia movements. Patients will experience a 30 percent decrease in severity, on average, with either of the currently approved VMAT2s, and one-third will have at least a 50 percent decrease in movements.
BPH: Are there side effects with VMAT2 inhibitors?
SC: These drugs have generally been well tolerated, with sedation as the most common side effect. Although they are effective and safe for most people, you should speak with your doctor about your own individual health status and whether you might be at risk for other side effects affecting your heart or liver and other reversible side effects like stiffness, restlessness, and tremors.
BPH: For patients with mild tardive dyskinesia symptoms who prefer to avoid additional medication, might supplements offer any benefit?
SC: There is only limited, inconclusive evidence of benefit for many other agents, including extracts of gingko biloba and vitamins B6 and E. Keep in mind that supplements may not be as closely regulated as approved pharmaceuticals. If you want to try any of them, discuss taking any supplements with your doctor.
CC: In very early or mild cases, I might consider starting vitamin E. While the data aren’t very strong, it has been shown to potentially help prevent TD progression. Typically, I’d start with 400 international units (IU) for four weeks, then increase to 800 IU for another eight weeks. If there’s no noticeable benefit after this period, it’s reasonable to discontinue it. Regular physical activity, enough sleep, and managing stress can all help lessen the symptom burden.
BPH: How can tardive dyskinesia affect a patient’s quality of life, and what can be done to mitigate these impacts? What about the effects on loved ones and relationships?
CC: Tardive dyskinesia can also cause collateral damage, affecting self-esteem and causing stigma. It causes physical problems but also psychological ones, such as hopelessness, depression, social withdrawal, and problems on the job.
The good news? All of these things could also be either shortened or even avoided if we can minimize the progression of tardive dyskinesia. Some patients may blame themselves. Don’t identify with the stigma. Try to get help, and if your doctor is not knowledgeable about it, or doesn’t want to pay much attention to it, demand that you are going to be seen by either a psychiatrist who specializes in the assessment and treatment of tardive dyskinesia or seek help from a movement specialist. Do not give up too early.
BPH: What are the top prevention strategies for tardive dyskinesia?
SC: The top prevention strategies for tardive dyskinesia include talking to your doctor about whether antipsychotics are indicated for your condition or whether alternative treatments may be effective. If antipsychotic treatment is necessary for your condition, discuss which antipsychotic is least likely to cause tardive dyskinesia.
Ask what dose will be prescribed and how long you must take the medication. Your doctor should screen you for abnormal movements before starting antipsychotics and then agree on a routine monitoring program to evaluate you regularly, at least every three months. In addition, get familiar with what tardive dyskinesia looks like so you can self-monitor for any abnormal movements and alert your doctor as soon as possible if you notice any.
BPH: What preventive steps should clinicians take when prescribing medications that might cause tardive dyskinesia?
SC: If antipsychotics are indicated, psychiatrists should select drugs that have a low risk for movement disorder side effects, use the lowest effective doses for the least amount of time, and screen frequently and regularly, at least every three months, for early signs of tardive dyskinesia. Frequent monitoring is especially important for people over the age of 40 who are at increased risk for tardive dyskinesia.
BPH: There’s a perception that second-generation antipsychotics rarely cause tardive dyskinesia. Is this accurate, or should clinicians be more cautious?
SC: Newer second-generation antipsychotics are about 2 to 3 times less likely to cause tardive dyskinesia than older drugs, but the risk is not zero. Additionally, some of these newer medications have been on the market for a shorter period, so long-term data on their risk of tardive dyskinesia may be limited. A conservative takeaway is that anyone receiving any dopamine receptor-blocking antipsychotic for any reason, over any sustained length of time, has some level of risk for tardive dyskinesia.
BPH: Could you describe withdrawal-emergent dyskinesia and whether it might occur with medication nonadherence or abrupt discontinuation?
SC: Withdrawal-emergent dyskinesias are movements resembling tardive dyskinesia that appear within one to two weeks of stopping oral antipsychotics or up to five weeks after discontinuing long-acting injectable antipsychotics. These dyskinesias typically resolve on their own within 4 to 12 weeks. They can occur due to treatment nonadherence or a decision to stop medication, but any changes in treatment should always be discussed with your doctor.
If the movements are mild and tolerable, they can simply be monitored until they resolve. However, if the movements are more severe and interfere with functioning, treatment may be necessary. In contrast, covert dyskinesias are true tardive dyskinesia symptoms that are masked during antipsychotic treatment and persist after the medication is discontinued.
BPH: There’s some confusion about tardive dyskinesia. Can you clarify a few common misconceptions?
SC: One misconception is that tardive dyskinesia only develops after a year or more of treatment. In reality, it can emerge within weeks to months in susceptible individuals.
Another misconception is that it only affects elderly people or those with chronic mental illnesses. The truth is that anyone, regardless of diagnosis or age, can develop tardive dyskinesia, although the risk does increase after the age of 40.
There’s also a belief that most people with tardive dyskinesia are unaware of it or aren’t bothered by it. But, over 50 percent of people with tardive dyskinesia report that it’s embarrassing or interferes with their functioning and quality of life. When severe, it can even be painful and compromise daily activities.
Finally, some think there are no proven treatments for tardive dyskinesia. However, two FDA-approved VMAT2 inhibitors have been shown to reduce tardive dyskinesia movements by at least 30 percent in half of the people treated, and they’re proven to be more effective than placebo.
These points are for general education and information. People should always consult their doctors about their circumstances and treatment options.
BPH: What are the latest advancements in research regarding tardive dyskinesia? Are there any promising directions that patients and clinicians should be aware of?
CC: There is hope. It’s important to fight against feelings of hopelessness and not view tardive dyskinesia as your fault. Don’t internalize the stigma or blame yourself. Instead, focus on getting the help you need. If your doctor isn’t knowledgeable about it or doesn’t take it seriously, insist on being seen by either a psychiatrist who specializes in tardive dyskinesia or by a movement disorder specialist. So don’t give up.
If someone hasn’t tried the newer VMAT2 inhibitors yet, there’s a chance their tardive dyskinesia symptoms could improve on deutetrabenazine or valbenazine, one of the two treatments that are approved by the FDA. For very severe cases, there’s even the possibility of brain stimulation targeting specific brain areas, which has been almost curative for some patients. Of course, this doesn’t work for everyone, but it’s important not to resign yourself to the idea that “this is just who I am now” or believe that nothing can be done.
A new non-dopamine-blocking antipsychotic was approved in September 2024. Cobenfy, an M1/M4 muscarinic agonist that reduces presynaptic dopamine release, is indicated for adults with schizophrenia. It doesn’t have a black box warning because of the risk of tardive dyskinesia so it may be helpful. We don’t know how much it will affect tardive dyskinesia risk, but having another class of medication that does not block postsynaptic dopamine receptors gives us hope.
Disclosures: Dr. Correll, Dr. Caroff, and Dr. Citrome have consulted for pharmaceutical companies, including Teva and Neurocrine Biosciences, both manufacturers of medications for tardive dyskinesia. The insights in this article are based on their professional expertise and clinical experience.
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