Extrapyramidal symptoms (EPS) are movement-related side effects caused by antipsychotic medications, and the first step in treating them is almost always adjusting the drug that’s causing them. EPS affect 50 to 75% of people taking older (first-generation) antipsychotics, though newer antipsychotics carry a lower risk. Treatment depends on which type of EPS you’re experiencing, how severe it is, and how quickly it started.
What EPS Looks and Feels Like
EPS isn’t a single symptom. It’s a group of movement problems that show up in different ways, and each type has its own treatment approach. The main forms are:
- Acute dystonia: sudden, involuntary muscle contractions that can twist your neck, jaw, or eyes into uncomfortable positions. This can start within hours or days of beginning a medication.
- Akathisia: an intense inner restlessness that makes it nearly impossible to sit still. People often describe it as feeling like they need to pace, shift weight, or move constantly.
- Drug-induced parkinsonism: symptoms that mimic Parkinson’s disease, including tremor, stiffness, slow movement, and a shuffling walk.
- Tardive dyskinesia: repetitive, involuntary movements, usually of the face, lips, tongue, or jaw. This develops after months or years of medication use and can be harder to reverse.
Because these types respond to different treatments, identifying which one you have is a critical first step.
Adjusting the Medication That’s Causing It
Regardless of the type, the frontline strategy is reviewing the medication behind the symptoms. Your prescriber will typically consider one of three options: lowering the dose, stopping the drug, or switching to a different antipsychotic with a lower EPS risk.
Newer (second-generation) antipsychotics generally cause fewer movement side effects than older ones. Among these, clozapine stands out for its very low incidence of EPS. Quetiapine also carries a notably low risk because of the way it interacts with dopamine receptors in the brain. Switching to one of these is a common move when EPS becomes a problem on another antipsychotic. That said, every medication swap involves trade-offs, so the decision depends on how well the current antipsychotic is controlling your primary condition.
Treating Acute Dystonia
Acute dystonia can be frightening. Muscles in the neck, face, or back suddenly lock into abnormal positions, and in rare cases the throat muscles tighten enough to affect breathing. Because of the urgency, treatment is usually given by injection, which starts working in about 20 minutes. If three doses don’t resolve the episode, emergency care is needed.
Once the acute episode is controlled, an oral anticholinergic medication is often continued for a period to prevent recurrence. These drugs work by blocking a chemical messenger called acetylcholine, which helps rebalance the signaling disruption caused by the antipsychotic. For dystonia that becomes chronic or primarily affects the face, Botox injections into the affected muscles can provide targeted relief.
Managing Akathisia
Akathisia is one of the most distressing forms of EPS. The constant urge to move can interfere with sleep, concentration, and quality of life, and it’s a major reason people stop taking their antipsychotic altogether.
The initial approach mirrors the general strategy: reduce the antipsychotic dose if possible, eliminate unnecessary antipsychotic combinations, or switch to a lower-risk drug. When medication changes alone aren’t enough, beta-blockers and benzodiazepines are the most effective add-on treatments. A large network meta-analysis comparing all available akathisia treatments found that benzodiazepines ranked highest for efficacy, followed closely by beta-blockers. A type of antidepressant that affects norepinephrine and serotonin also showed significant benefit compared to placebo. Anticholinergic drugs, which work well for other types of EPS, did not show a clear advantage for akathisia specifically.
Treating Drug-Induced Parkinsonism
When an antipsychotic makes you feel stiff, slowed down, or shaky in ways that resemble Parkinson’s disease, anticholinergic medications are the standard treatment. These are taken orally, typically starting at a low dose and increasing gradually based on response. Doses are usually split across two to four times per day.
Amantadine is another option. It works through a different mechanism, blocking a receptor involved in movement signaling in the brain. The standard starting dose is taken twice daily. Some people do better on amantadine because it tends to cause fewer side effects like dry mouth, blurred vision, and constipation that anticholinergic drugs are known for. It’s worth noting that anticholinergic side effects can be especially problematic for older adults, who are already at higher risk for confusion and memory issues from these medications.
Treating Tardive Dyskinesia
Tardive dyskinesia (TD) is the most stubborn form of EPS. Because it develops slowly over months or years of antipsychotic use, it doesn’t always resolve when the medication is changed. For decades, there was no FDA-approved treatment. That changed in 2017 with the approval of two medications that reduce involuntary movements by controlling how dopamine is packaged and released in the brain.
In clinical trials, the first of these drugs produced at least a 50% improvement in abnormal movements in about 40% of patients at the higher dose, compared to roughly 9% on placebo. The second drug showed similar results, with about 35% of patients achieving that same level of improvement versus 12% on placebo. These aren’t cures, but for many people with TD they represent a meaningful reduction in visible, involuntary movements of the face, tongue, and limbs.
Benzodiazepines are also used for TD, particularly when the newer medications aren’t an option. For severe tardive dystonia that doesn’t respond to medication, surgical options like deep brain stimulation exist, though these are reserved for the most treatment-resistant cases.
How EPS Is Monitored Over Time
If you’re taking an antipsychotic, your provider should be screening for involuntary movements on a regular basis. The standard tool is the Abnormal Involuntary Movement Scale (AIMS), a 12-item assessment where a clinician observes and rates movements in your face, lips, jaw, tongue, arms, legs, and trunk. Each area is scored from 0 (no movement) to 4 (severe), and the scores together give a picture of whether symptoms are developing, worsening, or improving with treatment.
The AIMS also captures how much the movements interfere with your daily life and whether you’re aware of them. Some people develop mild involuntary movements without noticing, which is one reason routine screening matters. Catching TD early, before it becomes moderate or severe, gives you the best chance of reversing it through medication changes. The assessment also tracks dental status, since ill-fitting dentures can sometimes mimic or worsen oral movements and need to be ruled out.
What Affects Your EPS Risk
Not everyone on an antipsychotic develops EPS. Your risk depends on several factors: the specific drug and its dose, whether you’re taking a first-generation or second-generation antipsychotic, your age, and your individual biology. First-generation antipsychotics cause EPS in an estimated 50 to 75% of users. Second-generation antipsychotics have a significantly milder side effect profile, though they aren’t risk-free.
Higher doses generally mean higher risk. Taking multiple antipsychotics at once also increases the likelihood. If you’ve had EPS before, you’re more likely to experience it again with future antipsychotic use. This history is important information to share with any new prescriber, since it can guide them toward lower-risk options from the start.