Tardive dyskinesia (TD) is treatable, and for many people, symptoms can be significantly reduced or even reversed. Two FDA-approved medications, both in a class called VMAT2 inhibitors, are the primary treatment. Beyond medication, adjusting the drug that caused TD in the first place, certain supplements, and in rare cases surgical options can all play a role.
What Tardive Dyskinesia Looks Like
TD causes involuntary, repetitive movements that most often affect the face and mouth: lip smacking, tongue darting, jaw clenching, grimacing, or excessive blinking. It can also show up in the arms, legs, fingers, toes, and trunk as rocking, twisting, or writhing movements. These movements happen without your control and can range from barely noticeable to severe enough to interfere with eating, speaking, or social interactions.
TD develops as a side effect of medications that block dopamine receptors, most commonly antipsychotics used to treat schizophrenia, bipolar disorder, or severe depression. Some anti-nausea medications can also cause it. The condition typically appears after months or years of use, though it can sometimes emerge after the medication is stopped.
Doctors assess severity using the Abnormal Involuntary Movement Scale (AIMS), which rates movements in seven body areas on a 0-to-4 scale, from none to severe. This score helps track whether treatment is working over time.
FDA-Approved Medications: VMAT2 Inhibitors
The most effective treatment for TD is a class of drugs called VMAT2 inhibitors. These work by regulating how much dopamine gets packaged and released in the brain, which calms the overactive signaling behind the involuntary movements. Two are currently FDA-approved specifically for TD: valbenazine (Ingrezza) and deutetrabenazine (Austedo).
In phase 3 clinical trials, significantly more people taking these medications achieved at least a 50% reduction in their movement scores compared to placebo. The long-term results are even more encouraging. In one extended study of valbenazine lasting 48 weeks, movement scores dropped by an average of 10.2 points, and roughly 90% of participants saw their symptoms cut in half or more. A longer study of deutetrabenazine, running nearly three years, found a 6.6-point average reduction, with 67% of participants reaching that same 50% improvement threshold.
Deutetrabenazine is typically started at 12 mg per day, split into two doses, and gradually increased based on how you respond. The maximum is usually 48 mg per day. Valbenazine follows a simpler once-daily dosing schedule. Both medications require ongoing use; symptoms can return if you stop taking them. Common side effects include drowsiness and, less frequently, mood changes, so your prescriber will monitor you closely during the first few weeks of treatment.
Adjusting the Medication That Caused TD
A natural question is whether simply stopping or lowering the dose of the antipsychotic or other dopamine-blocking drug will fix the problem. The answer is more complicated than you might expect. Clinical evidence is actually insufficient to confirm that withdrawing the causative medication reliably improves TD. In some cases, stopping the drug abruptly can temporarily worsen the involuntary movements before any improvement occurs.
The American Psychiatric Association recommends considering withdrawal of the causative medication only in people who can safely tolerate it, meaning their underlying psychiatric condition won’t destabilize. For many people with schizophrenia or bipolar disorder, stopping antipsychotics simply isn’t an option. Switching from an older “typical” antipsychotic to a newer “atypical” one is sometimes tried, but the evidence supporting this approach is also limited.
That said, there is genuinely good news for people who are able to discontinue the causative drug. One study found that if a person stays off the medication for 18 months, the estimated probability of achieving a 50% reduction in involuntary movements is 87.2%. So while the process can be slow and isn’t always feasible, TD is far from always permanent.
Supplements: Vitamin E and Ginkgo Biloba
Vitamin E is one of the most studied supplements for TD, but the evidence is underwhelming for people who already have established symptoms. A Cochrane review of 13 trials involving 478 people found no clear improvement in TD symptoms with vitamin E compared to placebo. There was, however, a suggestion that vitamin E may help protect against worsening of symptoms over time. In other words, it might slow progression but won’t reverse movements that are already happening. It’s generally safe, which is why some clinicians still mention it, but it shouldn’t be relied on as a primary treatment.
Ginkgo biloba has more promising data. A randomized, double-blind trial tested a standardized extract called EGb-761 at 240 mg per day (split into three 80 mg doses) for 12 weeks in patients who continued taking their antipsychotics. The extract significantly reduced TD symptoms compared to placebo. The effect appears to be related to the supplement’s antioxidant properties, specifically its ability to boost a protective enzyme in the body. While this is encouraging, the evidence base is still small, and ginkgo biloba can interact with blood thinners and other medications, so it’s worth discussing with your prescriber before starting it.
Deep Brain Stimulation for Severe Cases
For people with severe TD that doesn’t respond to VMAT2 inhibitors or other approaches, deep brain stimulation (DBS) is a surgical option. This involves implanting thin electrodes in specific areas of the brain and connecting them to a small device, similar to a pacemaker, placed under the skin near the collarbone. The device sends electrical pulses that help regulate abnormal movement signals.
DBS is reserved for cases where medications have failed. Before surgery, you’ll undergo brain imaging studies like MRI to map exactly where the electrodes need to go. It’s not a first-line treatment and carries the risks of any brain surgery, but for people whose quality of life is severely affected and who haven’t found relief elsewhere, it can be a meaningful option.
What Recovery Looks Like
TD treatment is rarely an overnight fix. VMAT2 inhibitors typically show noticeable improvement within the first few weeks, but the full benefit often builds over several months of continued use. If you’re able to stop the medication that caused TD, the timeline is longer. Meaningful improvement may take a year or more, though the odds are strongly in your favor if you can stay off the drug for 18 months.
Some people achieve near-complete resolution of their symptoms. Others see a significant reduction that makes daily life much more manageable, even if some mild movements persist. The key factors that influence outcome include how long you had TD before starting treatment, your age (younger people tend to recover more fully), and whether the causative medication can be safely reduced or stopped. Early recognition and treatment consistently lead to better results, which is why regular movement screening during antipsychotic use matters so much.