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Classification & Assessment in Psychiatry · Paper A

Hemiballismus and chorea

The idea

Hemiballismus is the exam's most dramatic movement disorder: damage to a single nut-sized structure deep in the brain, the subthalamic nucleus, releases the brake on movement for one side of the body, and a calm limb turns into a large, violent, flinging swing — as if it were throwing something — almost overnight.

How it works

The subthalamic nucleus (STN) is a small basal ganglia structure whose normal job is to keep driving the globus pallidus internus (GPi), which in turn inhibits the thalamus and dampens movement.
A focal lesion — classically a small vascular stroke or haemorrhage, most often in an older patient with poorly controlled hypertension or diabetes — knocks out the STN on one side.
Losing STN drive to the GPi removes that inhibitory brake on the thalamus, so thalamic and cortical motor output goes unchecked on the side of the body opposite the lesion (basal ganglia lesions classically produce contralateral signs).
The clinical result is hemiballismussudden, large-amplitude, violent, flinging (ballistic) movements of the proximal arm and/or leg on one side, sometimes forceful enough to injure the patient or fling objects from their hand.
It typically appears acutely (hours to days) after the causative stroke, may partially settle over weeks as the acute injury resolves, and in an older or vascular-risk patient it is a stroke until proven otherwise.
Hemiballismus sits at one end of a spectrum of basal-ganglia hyperkinetic movement disorders that differ mainly in amplitude, speed and distribution: tremor and myoclonus are the smallest/fastest, tics are stereotyped and suppressible, chorea flows unpredictably, athetosis writhes slowly, dystonia holds a sustained posture, and hemiballismus is the largest-amplitude, most violent member of the family.

How to spot it

A stem describing sudden, violent, large-amplitude flinging movements of one arm and/or leg in an older patient with vascular risk factors (hypertension, diabetes, atrial fibrillation) is hemiballismus from a contralateral subthalamic lesion.
A stem describing smaller, flowing, dance-like movements moving unpredictably between the face and both hands, especially with a family history or a preceding sore throat, is chorea (Huntington's disease or Sydenham chorea respectively).
A stem with a sustained twisting posture or eyes deviating upward within hours-to-days of starting an antipsychotic is acute dystonia, not a primary movement disorder.
A stem with chewing, lip-smacking or tongue movements after years of continuous antipsychotic treatment is tardive dyskinesia.
A stem describing an inner urge to move and pacing, without a specific limb movement pattern, soon after starting an antipsychotic is akathisia.

Tell it apart

Hemiballismus vs chorea — hemiballismus is large-amplitude, violent, proximal and usually strictly unilateral from a focal lesion, whereas chorea is smaller-amplitude, flows unpredictably between distal body parts, and is often bilateral; the two sit on the same spectrum and can blend at the edges.
Hemiballismus vs athetosis — hemiballismus is fast and flinging, unlike athetosis's slow, continuous, writhing movements of the fingers and hands, which often merge with chorea (choreoathetosis) rather than looking ballistic.
Hemiballismus vs dystonia — hemiballismus produces a moving, flinging limb, whereas dystonia produces a sustained or intermittently sustained abnormal POSTURE (twisting, held), not a series of discrete flinging movements.
Hemiballismus vs tremor — tremor is a small, rhythmic, regular oscillation around a joint, unlike hemiballismus's irregular, large, non-rhythmic flinging.
Hemiballismus vs myoclonus — myoclonus is a brief, single shock-like jerk, whereas hemiballismus is a more sustained, flowing, violent swinging action of the whole limb.
Hemiballismus vs tics — tics are stereotyped, repeatable and at least partially suppressible with a preceding urge, unlike hemiballismus's involuntary, unsuppressible flinging.
Hemiballismus/chorea vs the drug-induced look-alikes a psychiatrist must not miss — acute dystonia appears within hours-to-days of starting or raising an antipsychotic as a sustained twisting posture (e.g. oculogyric crisis), tardive dyskinesia appears only after months-to-years of antipsychotic exposure as patterned orofacial chewing movements, akathisia is a subjective inner restlessness rather than an objective movement pattern, and drug-induced parkinsonism produces bradykinesia and rigidity rather than any hyperkinetic movement — none of these follow hemiballismus's acute, unilateral, vascular-lesion story.

Watch for

⚠️ Assuming any 'flinging' or 'jerky' movement in a vignette is hemiballismus — check amplitude (violent and large), distribution (usually unilateral, proximal) and cause (a focal contralateral subthalamic lesion, classically vascular) before naming it.
Assuming hemiballismus must affect the whole body — it is classically confined to one side (arm and/or leg); bilateral ballismus is rare and suggests a different, more diffuse process.
Mistaking a drug-induced movement disorder (acute dystonia, tardive dyskinesia, akathisia, drug-induced parkinsonism) for a primary basal ganglia lesion syndrome — always check the medication history and the time-course relative to starting the drug before reaching for a stroke-based diagnosis.
Assuming hemiballismus is always permanent — many cases partially or substantially improve over weeks as the acute injury settles, though some residual chorea can persist.

Use it again

First askis this movement pattern acute (hours-days, think focal lesion/stroke) or has it built up over months-years (think drug-induced or degenerative)?
Then describe the movement in your own words before matching to a name: a single brief jerk (myoclonus), a rhythmic oscillation (tremor), a sustained posture (dystonia), a flowing unpredictable dance (chorea), a slow writhe (athetosis), a suppressible stereotyped act (tic), or a violent proximal fling (hemiballismus)?
Check the medication history and the time since starting or changing a dopamine-blocking drug before assuming a primary neurological cause.
Note laterality — a strictly unilateral movement disorder in an adult with vascular risk factors points toward a focal contralateral lesion, classically the subthalamic nucleus for hemiballismus.

In detail

Hook — the exam's most dramatic movement disorder

Most movement disorders creep in slowly. Hemiballismus does the opposite: a person can be moving normally in the morning and, by the same afternoon, have one arm and leg flinging around violently, hard enough to knock things off a table or injure themselves. It happens because of damage to one small structure deep in the brain, and understanding that one structure is the key to understanding the whole family of movement disorders a psychiatrist is expected to name on sight.

Plain definition

Hemiballismus (from Greek roots meaning 'half' and 'throwing/jumping about') is sudden, violent, large, flinging movement of the arm and/or leg on ONE side of the body. 'Ballistic' here means the movement looks like a limb being thrown, the way you'd throw a ball with your whole arm, rather than a small twitch or tremor. It is caused by damage to the subthalamic nucleus (STN), a small, paired structure that sits deep in the brain as part of the basal ganglia (a group of structures that help smooth out and control movement), on the side OPPOSITE the affected limb.

The critical caveat — the drug history matters as much as the movement itself

Here is the trap almost everyone falls into: assuming that because a movement is unusual, jerky or embarrassing to the patient, it must be a primary neurological problem. In psychiatry, a huge proportion of the abnormal movements you will actually see on the wards are caused by antipsychotic medication, not by a stroke or a degenerative disease. Before you reach for hemiballismus, chorea or any other basal-ganglia diagnosis, always check: has this patient recently started, stopped or changed the dose of a dopamine-blocking drug? The answer to that single question, plus how long ago it happened, does more to narrow the diagnosis than the exact shape of the movement.

First principles — why damaging one small nucleus produces this exact movement

Picture the circuit as a braking system for movement. Normally, the subthalamic nucleus sends a steady stream of excitatory (go) signals to another structure, the globus pallidus internus (GPi). The GPi's job, in turn, is to inhibit the , which relays movement commands up to the motor cortex. So the STN, by driving the GPi, is indirectly keeping the brake pedal pressed down on movement — like a foot resting on the brake of a car via a chain of levers.

Now imagine a small stroke knocks out the STN on one side, usually in an older person with high blood pressure, diabetes, or another vascular risk factor. With the STN gone, its excitatory drive to the GPi disappears. The GPi's inhibition of the falls away. The thalamus and the motor cortex it feeds are now running with the brake released, and because circuits are 'crossed' (each side of the brain controls the opposite side of the body), the unchecked movement shows up on the side of the body OPPOSITE the lesion. That is the entire mechanism: one small structure lost, one brake released, one limb flinging.

Structured walk-through — from lesion to flinging limb, and where hemiballismus sits among its relatives

Picture 1,000 people who have a stroke. Only a small handful of them — well under 1%, so fewer than about 10 out of that 1,000 — will ever develop hemiballismus, because the stroke has to hit one small, specific structure (the subthalamic nucleus) rather than any of the far larger territories a stroke usually damages. That rarity is exactly why, when a vignette does describe it, the exam wants you to recognise it instantly rather than guess.

Hemiballismus does not exist in isolation — it is the most extreme member of a family of basal-ganglia hyperkinetic (excess-movement) disorders, and the exam repeatedly tests whether you can place a description at the right point on that spectrum. At the small, fast end sits tremor (a small, rhythmic back-and-forth oscillation) and (a single, sudden, shock-like jerk, too fast to stop voluntarily). A little further along sit tics (repetitive, stereotyped movements the patient can partially suppress, usually preceded by an urge).

Then comes chorea (irregular, flowing, unpredictable movements that seem to travel from one body part to another, usually on both sides), athetosis (slow, continuous, writhing movements, especially of the fingers and face, often blending with chorea), and (a sustained or repeatedly-held abnormal posture rather than a moving sequence). Hemiballismus sits at the far end: the largest amplitude, the most violent, and — unlike most of its relatives — usually confined strictly to one side of the body, because it comes from one discrete lesion rather than a more widespread process.

A second, separate but well-known cause worth knowing: in an older person, especially a woman, with poorly controlled diabetes, a hemiballismus-like or chorea-ballism picture can appear from very high blood sugar without ketones (non-ketotic hyperglycaemia) rather than from a classic stroke, sometimes with a characteristic appearance on brain imaging that resolves once the blood sugar is controlled. It is a good example of why the underlying cause always has to be actively looked for, not assumed.

Look-alikes and differentials

Looks similar	How to tell it apart
Chorea	Smaller amplitude, flows unpredictably between body parts, usually bilateral, from more diffuse pathology rather than one focal lesion
Athetosis	Slow, continuous, writhing movements (fingers, hands, face) rather than a violent, fast flinging swing
	A sustained abnormal POSTURE rather than a moving, flinging limb
Tremor	Small, rhythmic, regular oscillation, unlike hemiballismus's irregular, large-amplitude flinging
	A single, brief, shock-like jerk rather than a sustained, flowing violent swing
Acute dystonia (drug-induced)	Appears hours-to-days after starting/raising an antipsychotic, as a sustained twisted posture, not from a vascular lesion
Tardive dyskinesia	Appears only after months-to-years of antipsychotic exposure, as patterned orofacial chewing movements

Diagnosis — how it is actually established

The diagnosis starts clinically: recognising the specific movement pattern (violent, large-amplitude, unilateral flinging) in a patient with vascular risk factors, plus a sudden onset. This clinical impression is then confirmed with brain imaging (CT or, more sensitively, MRI), which classically shows an acute lesion in the subthalamic nucleus on the side opposite the affected limb, though occasionally the lesion involves the adjacent caudate, putamen or globus pallidus instead. Blood glucose should also be checked, since uncontrolled diabetes with very high blood sugar (without ketones) is a recognised alternative cause of a similar chorea-ballism picture, and correcting it, rather than treating a stroke, is the fix in that case.

Management — what is actually done, and whose guidance it rests on

Management runs on two separate tracks that should not be confused. The underlying cause is treated as its own problem: if it is a stroke, that means standard stroke care (secondary vascular prevention, blood pressure and diabetes control, and rehabilitation), following the same general stroke-management guidance used for any other stroke, such as NICE's guidance on stroke diagnosis and management; if it is non-ketotic hyperglycaemia, that means correcting the blood sugar.

Separately, the abnormal movement itself is treated only if it is severe, disabling, or dangerous to the patient — typically with a dopamine-receptor-blocking drug (a low-dose antipsychotic) or, in some cases, a GABAergic drug such as valproate, with drug choice and dosing following standard psychiatric prescribing references such as the Maudsley Prescribing Guidelines. Because many cases partially settle on their own over the following weeks as the acute swelling around the lesion resolves, a period of watchful waiting is often reasonable before starting a drug that carries its own side-effect burden.

Exam pearl

The exam's favourite trick with this whole family of disorders is to describe the MOVEMENT precisely and expect you to name the diagnosis without ever using its name — 'sudden, violent, flinging movements of one arm and leg' has to translate in your head to 'hemiballismus, think subthalamic nucleus, think stroke' just as automatically as 'chewing movements after years of antipsychotic treatment' has to translate to 'tardive dyskinesia'. Before you move on: could you explain to a friend, in one sentence, why a stroke in one small structure produces a violent flinging movement rather than weakness?

In one line

Hemiballismus is sudden, violent, large-amplitude flinging of one arm and/or leg from a stroke in the opposite subthalamic nucleus, releasing a brake on movement — and the exam wants you to place it correctly against chorea, athetosis, , tremor, tics, and the antipsychotic-induced look-alikes using the movement's shape, distribution and time-course, not the name of a drug or disease alone.