What is akathisia?
Akathisia is a movement disorder that is experienced as an intense inner restlessness and an urge to move that cannot be switched off. The name comes from a Greek word meaning “inability to sit,” and that is exactly what patients report. They pace, rock, shift their weight, and cross and uncross their legs, because staying still feels impossible.
Yet, akathisia is not simply a restless body. While it looks like fidgeting from the outside, it comes with an internal agitation that patients describe as one of the worst experiences of their lives, and it is impossible for someone who has not felt it to understand the terror it can carry.
Akathisia is, in nearly every case, caused by a drug. Antipsychotics, antidepressants, and anti-nausea medications can all cause it, and it can also appear during withdrawal from benzodiazepines, and it has been reported during withdrawal from antidepressants. Unfortunately, it is routinely mistaken for anxiety or a worsening of the original condition, and the usual response to worsening anxiety is a higher dose of the very drug that caused the problem.
Akathisia has been associated with self-harm and suicidal thinking, especially when nobody has named it. A patient deserves to hear the name of what is happening to them, because the name changes what happens next. So, what causes it, and why is it missed so often?
If you are in that dark place right now, do not wait for it to pass on its own.
- Call 911 or go to the emergency department for possible seizure activity, loss of consciousness, chest pain, or any symptom severe enough to frighten you.
- Call or text 988, the Suicide & Crisis Lifeline, if you have thoughts of self-harm or suicide.
- Contact your prescriber promptly if the restlessness is intensifying or you are tempted to change a dose on your own.
What causes akathisia?
The most common cause of akathisia is a drug that blocks dopamine, and antipsychotics are the biggest group. The older ones, such as haloperidol, carry the highest risk. Yet, the newer antipsychotics, including Seroquel (quetiapine), Zyprexa (olanzapine), and Abilify (aripiprazole), cause it as well, and Seroquel is often prescribed for nothing more than sleep.
Anti-nausea medications block dopamine too. Reglan (metoclopramide) and Compazine (prochlorperazine) are handed out for nausea and migraine, often in an emergency department, and the person goes home without a word about what the drug can do. The nausea is gone. The patient cannot sit down.
Antidepressants are the second big group. Selective serotonin reuptake inhibitors, or SSRIs, such as Zoloft (sertraline) and Lexapro (escitalopram), and serotonin-norepinephrine reuptake inhibitors, or SNRIs, such as Effexor (venlafaxine), can cause akathisia, most often in the first weeks of treatment or after a dose change.
Benzodiazepine withdrawal is the cause that gets overlooked. When a benzo is stopped or reduced too quickly, the loss of the drug’s effect at the GABA-A receptor can produce severe akathisia as part of benzodiazepine-induced neurological dysfunction, or BIND.
Why do such different drugs produce the same syndrome? For the dopamine blockers, one theory is that blocked dopamine signaling in the basal ganglia, the movement centers of the brain, produces the compulsion to move. For withdrawal, the mechanism is the loss of a brake rather than the blocking of a signal, and nobody fully understands either one.
What do akathisia symptoms feel like?
The hallmark akathisia symptom is a subjective sense of inner restlessness that the patient cannot ignore. From across the room it can look like anxiety. From the inside it feels like a compulsion, and patients often describe it as energy trapped inside the body that has to get out.
The visible signs are the body obeying that compulsion. Pacing back and forth, rocking while seated or standing, crossing and uncrossing the legs, marching in place, and swinging the legs while sitting are the classic movements. These are not habits. They are the only relief the person can find, and the relief lasts only as long as the movement does.
The mental side can be as bad as the physical. Intense anxiety, irritability, a sense of impending doom, and a feeling of being trapped in an uncomfortable body are common, and the distress gets worse with every attempt to hold still. Sleep suffers, because the restlessness does not stop at night.
Akathisia runs on a spectrum, from a restlessness the patient can partly suppress in public to constant movement that makes daily life impossible. Yet, both are the same condition, and both deserve the name.
Does benzodiazepine withdrawal cause akathisia?
It does, and withdrawal akathisia is one of the most distressing forms of BIND. Benzodiazepines enhance the effect of GABA, the brain’s main inhibitory neurotransmitter, at the GABA-A receptor. Take that enhancement away too fast and a nervous system that has adapted to it tips into a hyperexcitable state, and restlessness is one of the ways that state shows itself.
The faster the drug is removed, the higher the risk. Unfortunately, the fastest removals happen in addiction treatment facilities, where a patient on a prescribed benzo is “detoxed” on a schedule set by the insurance authorization rather than by the nervous system.
Physical dependence is not addiction. A person who has taken a benzodiazepine as prescribed for years is dependent, not addicted, and treating dependence as if it were addiction is how withdrawal akathisia gets manufactured.
Fortunately, there is a better way, and it has been in print for decades. The Ashton Manual recommends a slow, gradual taper, usually after a crossover taper to Valium (diazepam), precisely so that the receptors have time to recover at each step before the next reduction. While the manual never pretended that one pace fits everyone, its direction is always the same: slowly.
Withdrawal akathisia can persist for months after the last dose, as part of protracted withdrawal, and some patients experience it despite a careful taper. If akathisia appears during your taper, tell your doctor right away. The pace may need to be slowed or paused, and the doctor must be willing, because the nervous system sets the schedule and nobody else does.
Can Klonopin cause akathisia?
Klonopin, or clonazepam, can cause akathisia in three different situations, and none of them means the patient is imagining things. The rarest is a direct effect. In clinical experience, a small number of people respond to a benzodiazepine with agitation instead of calm, a paradoxical reaction, and restlessness of this kind can appear soon after the drug is started or the dose is raised.
The second is withdrawal that arrives while the person is still taking the drug. Klonopin is long-acting, so the gap between doses matters less than it does with Xanax. Yet, after months or years the receptor system adapts, and the same dose no longer holds it steady. The Ashton Manual describes this plainly: tolerance develops, and withdrawal symptoms can surface even while every dose is taken on time.
A common pattern we see in Klonopin akathisia is a patient who has taken the same dose for ten years and starts pacing at night. Unfortunately, they are told that their anxiety is back, and they leave with a higher dose. That patient’s anxiety has not come back. That patient has a drug effect.
The third, and the worst, is a sudden stop. A person runs out, a new doctor refuses to refill, or a rehab takes the pills away, and the brake comes off a nervous system that spent years adjusting to it. The Klonopin prescribing information lists an elimination half-life of roughly 30 to 40 hours, so the drug leaves slowly and the reaction to a cold turkey stop often builds over days, not hours.
How long does it last? Nobody can promise a timeline, and anyone who gives you one in days is guessing. Akathisia after an abrupt stop of clonazepam can persist for months, it tends to come in waves rather than a straight line, and it does improve as the receptors recover. That recovery is the treatment, and everything else is about protecting it.
What should happen after a cold turkey stop of clonazepam?
The truth is that a cold turkey stop should never have happened. The 2020 FDA benzodiazepine label update put it on every benzodiazepine label: abrupt discontinuation or rapid dose reduction can cause withdrawal reactions, including seizures, that can be life-threatening. Whoever told a dependent patient to “just stop” did not teach a lesson. They caused an injury, and the suffering that followed was never deserved.
Of course, the drug is now gone. Yet, the way back is not simply to wait it out. The right move is often a prescriber-guided reinstatement of the benzodiazepine, followed by a proper, slow Klonopin taper, and reinstatement is not a failure. It is the taper that should have happened the first time. That decision belongs to you and your prescriber together, never to you alone with a leftover bottle.
Why must the taper then be so slow, and why do the cuts get smaller as the dose falls? Think of a dimmer switch. While this is not a perfect analogy, the first quarter turn down from full brightness barely changes the room, and the last quarter turn before dark changes everything.
Benzodiazepine receptor occupancy is thought to work the same way. At higher doses most of the receptors are already occupied, so a small cut changes little. At low doses each remaining milligram holds a large share of the receptors, and the same cut is a much larger step.
That is why the Maudsley Deprescribing Guidelines describe hyperbolic tapering, in which each reduction is a fraction of the current dose rather than a fixed number of milligrams, so the steps shrink as the dose shrinks. Of course, the size and timing of each step belong to you and your prescriber, and no article should hand you a percentage. The principle is enough: the lower the dose, the smaller the cut.
One warning stands above everything else: never stop a benzodiazepine suddenly, and never let a taper turn into an abrupt stop. Sudden discontinuation can trigger seizures and can be life-threatening. However a taper is shaped, it should be gradual and medically supervised.
Why is akathisia so often mistaken for anxiety?
Is it anxiety? Is it the original illness coming back? Or, is it the drug? Akathisia is missed constantly in psychiatric medicine, and the reason is simple. Its symptoms overlap with anxiety, agitation, and psychomotor activation, and a doctor who is not specifically looking for akathisia sees a patient whose “underlying condition” is getting worse.
The consequences follow directly. If the restlessness is read as anxiety, the dose of the drug causing it is raised, or a second drug is added, and the akathisia intensifies. Patients who insist that something else is wrong are told that they are anxious and need to try harder to relax. Patients call this medical gaslighting, and they are right.
The distinction can be made in an ordinary office visit by anyone willing to ask. While anxious restlessness comes with worried thoughts and eases, at least a little, with reassurance, akathisia is a compulsion to move that the patient experiences as involuntary. And, the timing tells the story: the anxiety was there before the prescription, and the akathisia arrived with it or with a dose change.
Doctors who prescribe drugs with akathisia risk must watch for it in the first weeks and after every dose change, when a small change still works. Many patients end up in an emergency department instead, frightened by what is happening to them. The emergency department is the right place for a seizure or chest pain, and it is rarely the place where akathisia gets its name, so bring the word with you.
What is the treatment for akathisia?
Akathisia treatment begins with the cause. For medication-induced akathisia, the primary treatment is to reduce or discontinue the drug responsible, and for an antipsychotic or an antidepressant that means a gradual, planned taper rather than another abrupt stop that trades one injury for another.
Conventional psychiatry also has a short list of drugs it adds. Propranolol, a beta-blocker, is used to blunt the physical restlessness for some patients. Mirtazapine, a sedating antidepressant, is used in some settings for akathisia caused by antipsychotics. And, in acute hospital settings, benzodiazepines are sometimes given, which creates its own dependence problem and is no answer at all for akathisia that came from benzodiazepine withdrawal.
Those are options for the prescriber who started the offending drug to weigh with the patient, and they are not the deprescribing approach. The deprescribing approach is slower and plainer: identify the drug responsible, reduce it gradually, and give the nervous system time.
For withdrawal-induced akathisia, time and nervous system recovery are the most reliable treatment there is. Slow the taper, or pause it, and let the receptors catch up. The condition typically improves as the receptor systems recover, and while that can take months, it does come.
How can akathisia be prevented during medication changes?
Prevention is mostly slowness. Slow, gradual dose changes when starting, adjusting, or stopping a psychiatric medication are the most effective protection there is, and the Maudsley Deprescribing Guidelines set out hyperbolic taper schedules for antidepressants and benzodiazepines that reduce withdrawal effects during discontinuation.
A history matters. In fact, a patient who has had akathisia from one drug is at higher risk of getting it again from a related drug, and that history belongs in the chart and in every conversation about a medication change. If a doctor does not ask, it is not a bad idea to tell them anyway.
For benzodiazepine tapering, the Ashton Manual’s crossover taper to diazepam reduces the risk by providing stable blood levels and permitting very gradual reductions. Compounded liquid formulations make it possible to taper off of the drug by fractions of a milligram, which is the size of step a sensitive nervous system often needs.
Yet, the most powerful prevention is knowing the word. While the condition has a name and a mechanism, many patients have never heard of it, and they suffer in silence believing that it is anxiety or a personal failing. It is neither.
Where can you find help for akathisia and medication tapering?
Akathisia from a psychiatric medication or from benzodiazepine withdrawal calls for a physician who knows the condition on sight, and not every doctor does. Many patients have already met several who do not.
Is akathisia permanent? In most cases it is not, though after months of relentless symptoms it can feel that way. It ends as the nervous system heals, and the only thing anyone can do to hurry that along is to stop injuring it. Give the brain time, and it heals.
That principle is how Dr. Leeds practices. As an osteopathic physician and deprescribing specialist, he provides benzodiazepine and z-drug tapering and psychiatric medication deprescribing by telemedicine for patients located in Florida, using the Ashton Manual crossover taper for benzodiazepines and hyperbolic tapering in line with the Maudsley Deprescribing Guidelines for antidepressants and other psychiatric medications. He serves on the medical advisory board of the Benzodiazepine Information Coalition, and every taper is individualized and patient directed, with weekly visits for close monitoring.
If you suspect akathisia, from a medication you are taking now or from a taper or a sudden stop, contact Dr. Leeds through the contact form at drleeds.com.
This article is educational. It is not medical advice, and reading it does not create a doctor-patient relationship. Decisions about starting, continuing, or tapering any medication should be made with your own physician.
