Neurology: Movement Disorders

• Parkinsonism: Approach to Movement Disorders | Parkinson's Disease | Treating Parkinson's Disease | Advanced Parkinson's Disease | Non-motor Symptoms of Parkinson's | Parkinson's Disease in Hospital | Atypical Parkinsonism | Drug-induced and Vascular Parkinsonism
• Tremor and dystonia: Tremor and Essential Tremor | Dystonia
• Hyperkinetic disorders: Huntington's Disease | Other Chorea and Ballism | Tics and Tourette Syndrome | Drug-induced Movement Disorders | Myoclonus | Restless Legs Syndrome
• Other: Inherited and Acquired Ataxias | Functional Movement Disorders
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🚶 Movement disorders are conditions with too little movement (parkinsonism) or too much (tremor, chorea, dystonia, tics, myoclonus). Parkinson's disease is the fastest-growing neurological condition in the world. Most movement disorders are diagnosed by careful observation; scans mainly help to exclude other causes. Parkinson's emergencies (missed doses, hyperpyrexia) are covered in the Neurological Emergencies chapter.
Your four questions for every patient: Is the movement too little or too much, and what does it look like? Could a drug be causing it? Are there red flags for atypical parkinsonism? What matters most to the patient - and are non-motor symptoms being treated too?

Approach to Movement Disorders

• Hypokinetic (too little): Parkinsonism - bradykinesia with rigidity, rest tremor or postural instability.
• Hyperkinetic (too much):
  • Tremor - rhythmic oscillation.
  • Chorea - irregular, flowing, "dance-like" movements that move from one body part to another.
  • Ballism - large flinging movements of a limb (severe chorea).
  • Dystonia - sustained muscle contractions causing twisting, abnormal postures.
  • Myoclonus - sudden, brief shock-like jerks.
  • Tics - repetitive stereotyped movements or sounds, preceded by an urge and briefly suppressible.
• Always ask:
  • Drugs (antipsychotics, antiemetics, valproate, lithium, SSRIs).
  • Family history.
  • Age of onset.
  • Speed of progression.
  • What makes it better or worse (rest, action, alcohol, stress, sleep).
• A video of episodes is very helpful.

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Parkinson's Disease

What it is: A progressive degenerative disease with loss of dopamine-producing neurones in the substantia nigra and Lewy bodies (alpha-synuclein). It affects about 1 in 37 people over their lifetime; it is commoner in men and with age (average onset about 60). About 5–10% have a genetic cause (e.g. LRRK2, GBA, PRKN - especially in young onset).

Diagnosis - clinical (UK Parkinson's Disease Society Brain Bank criteria):

• Bradykinesia - slowness, with decreasing size and speed of repeated movements (finger tapping). This is essential.
• Plus at least one of:
  • Rigidity - "lead-pipe", or "cogwheel" with tremor.
  • Rest tremor - 4–6 Hz, "pill-rolling", usually starting in one hand; reduced by movement, worse with stress.
  • Postural instability (a later feature).

Supportive features:

• Asymmetric onset that stays asymmetric.
• A good, lasting response to levodopa.
• Levodopa-induced dyskinesia.
• Slowly progressive course.

Other motor signs:

• Small handwriting (micrographia).
• Quiet voice (hypophonia).
• Reduced facial expression (hypomimia); reduced blinking.
• Shuffling gait with reduced arm swing; freezing.
• Stooped posture.

Early "prodromal" symptoms - often years before diagnosis:

• Loss of smell.
• REM sleep behaviour disorder (acting out dreams).
• Constipation.
• Depression and anxiety.

Investigations:

• Mainly clinical. Refer untreated suspected PD to a specialist (NICE NG71) - don't start treatment before the diagnosis is confirmed.
• DaTscan if it is unclear whether the tremor is parkinsonian (abnormal in PD and atypical parkinsonism; normal in essential tremor and drug-induced parkinsonism).
• MRI to exclude other causes if atypical features are present.

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Treating Parkinson's Disease

No treatment slows progression; all treatments improve symptoms. Start when symptoms affect daily life.

First-line choice (NICE NG71):

• Levodopa (with a decarboxylase inhibitor - co-careldopa or co-beneldopa) - the most effective drug.
  • Offer when motor symptoms affect quality of life.
  • Side effects: nausea (give domperidone at first), postural hypotension, hallucinations, sleepiness.
  • Long-term: Motor fluctuations ("wearing off", "on–off") and dyskinesia (involuntary writhing at peak dose).
• Dopamine agonists (non-ergot: ropinirole, pramipexole, rotigotine patch) or MAO-B inhibitors (rasagiline, selegiline, safinamide) - when motor symptoms don't yet affect quality of life.
  • Less effective, but less dyskinesia early on.
  • Dopamine agonist side effects:
    • Impulse control disorders - gambling, hypersexuality, compulsive shopping and eating. Warn patients and their carers, and ask at every review.
    • Excessive daytime sleepiness and sudden sleep attacks - driving risk.
    • Hallucinations, ankle oedema, postural hypotension.
  • Ergot-derived agonists (bromocriptine, cabergoline) cause heart valve and lung fibrosis - avoid, or monitor (echo).

Adding drugs for motor fluctuations ("wearing off"):

• Dopamine agonist, MAO-B inhibitor or COMT inhibitor (entacapone with each levodopa dose, or once-daily opicapone) - extends each levodopa dose. Entacapone turns urine orange.
• More frequent, smaller levodopa doses; controlled-release levodopa at night.
• Dyskinesia: Reduce doses; add amantadine.

Everyone:

• Parkinson's nurse specialist.
• Physiotherapy (gait, balance, falls), occupational therapy, speech and language therapy (voice, swallowing).
• Exercise - helps symptoms.
• Information on driving (tell the DVLA).
• Advance care planning as the disease progresses.

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Advanced Parkinson's Disease

When oral drugs can no longer give smooth control (severe fluctuations or dyskinesia), specialist options include:

• Apomorphine (a strong dopamine agonist given by subcutaneous injection or pump):
  • Injections rescue sudden "off" periods.
  • Needs domperidone cover at first (nausea).
  • Skin nodules.
• Levodopa infusions:
  • Foslevodopa–foscarbidopa (continuous subcutaneous infusion - NICE TA934).
  • Levodopa–carbidopa intestinal gel (through a PEG-J tube into the jejunum).
• Deep brain stimulation (usually the subthalamic nucleus):
  • For younger, cognitively intact patients with good levodopa response but troublesome fluctuations or tremor.
  • Doesn't help symptoms that don't respond to levodopa (e.g. balance, speech, cognition).
• Focused ultrasound (MR-guided) for drug-resistant tremor in selected patients.
• Late-stage problems:
  • Falls and freezing.
  • Dysphagia (aspiration pneumonia is a common cause of death).
  • Dementia.
  • Psychosis.
  • Immobility; weight loss.
  • Palliative care input is valuable.

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Non-motor Symptoms of Parkinson's

Non-motor symptoms often matter more to patients than tremor. Ask about them at every review.

• Depression and anxiety - common. SSRIs (watch for serotonin syndrome with MAO-B inhibitors at high doses), mirtazapine, CBT.
• Parkinson's disease dementia (develops after at least a year of motor symptoms; up to 80% eventually):
  • Rivastigmine or another cholinesterase inhibitor.
  • Memantine if these are not tolerated.
• Hallucinations and psychosis:
  • Look for triggers (infection, dehydration, new drugs).
  • Reduce drugs in this order - anticholinergics, amantadine, dopamine agonists, MAO-B and COMT inhibitors - then levodopa if needed.
  • If treatment is needed: quetiapine (off-label, low dose) or clozapine (with blood monitoring).
  • Avoid typical antipsychotics (haloperidol) and risperidone - they worsen parkinsonism.
• Orthostatic hypotension:
  • Review drugs; fluids, salt, compression stockings, raising the head of the bed.
  • Midodrine or fludrocortisone.
• Drooling: Speech therapy; glycopyrronium; botulinum toxin to the salivary glands.
• Sleep problems:
  • REM sleep behaviour disorder - melatonin or clonazepam; bed safety.
  • Daytime sleepiness - review dopamine agonists.
  • Night-time "off" symptoms - controlled-release levodopa or a rotigotine patch.
• Constipation - common and can affect drug absorption; laxatives.
• Urinary urgency and nocturia; erectile dysfunction.
• Pain - often linked to "off" periods.
• Weight loss and nutrition; dysphagia.
• Fatigue; apathy.

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Parkinson's Disease in Hospital

• Parkinson's medicines are time-critical - give them within 30 minutes of the usual time. Delays cause rigidity, falls, swallowing problems, aspiration and longer stays.
• Never stop levodopa suddenly - risk of parkinsonism–hyperpyrexia syndrome (like neuroleptic malignant syndrome).
• Nil by mouth or can't swallow:
  • Dispersible co-beneldopa via an NG tube.
  • Or a rotigotine patch (use a dose calculator, e.g. the OPTIMAL tool).
  • Get specialist advice.
• Drugs to avoid:
  • Antiemetics: Metoclopramide, prochlorperazine - use domperidone (or ondansetron, but not with apomorphine).
  • Antipsychotics: Haloperidol, risperidone - use low-dose quetiapine if needed, or lorazepam for acute agitation.
• Delirium: Common. Look for infection, constipation, urinary retention and drug changes.
• Assess swallowing and falls risk; early therapy input.

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Atypical Parkinsonism

Red flags suggesting it is not Parkinson's disease:

• Early falls (within the first year or two).
• Poor or no response to levodopa.
• Rapid progression.
• Symmetrical onset.
• Early autonomic failure.
• Vertical gaze palsy.
• Cerebellar signs.
• Early dementia or hallucinations.
• Early severe speech or swallowing problems.

• Treatment:
  • Try levodopa (some response in MSA early).
  • Manage symptoms (autonomic, falls, swallowing).
  • Multidisciplinary team and early palliative care.
• Survival is usually 6–10 years from onset.

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Drug-induced and Vascular Parkinsonism

• Drug-induced parkinsonism:
  • The commonest cause after PD.
  • Causes: Antipsychotics (especially typical ones and risperidone), metoclopramide, prochlorperazine, cinnarizine, valproate, lithium, tetrabenazine, amiodarone.
  • Usually symmetrical; tremor less prominent.
  • DaTscan normal.
  • Stop the drug if possible - recovery can take months. If an antipsychotic is essential, switch to one with lower risk (quetiapine, clozapine, aripiprazole).
• Vascular parkinsonism:
  • Due to small vessel disease.
  • "Lower-body parkinsonism" - gait problems and freezing with relatively normal arms.
  • Pyramidal signs; cognitive impairment; urinary problems.
  • Poor levodopa response. Manage vascular risk factors; physiotherapy.
• Normal pressure hydrocephalus - gait apraxia, urinary incontinence, cognitive decline (see the Brain Tumours, Spine and Other Neurology chapter).
• Other causes: Wilson's disease (young people), repeated head injury (boxers), carbon monoxide, manganese, post-encephalitic.

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Tremor and Essential Tremor

Types of tremor:

• Rest tremor - present at rest, reduced with movement: Parkinson's disease.
• Postural tremor - arms held out:
  • Essential tremor.
  • Enhanced physiological tremor - anxiety, caffeine, thyrotoxicosis, alcohol withdrawal, low glucose.
  • Drugs - salbutamol, lithium, valproate, SSRIs, ciclosporin, tacrolimus, theophylline, levothyroxine excess.
• Intention tremor - worse approaching a target: cerebellar disease (MS, stroke, alcohol).
• Dystonic tremor - jerky, irregular, with dystonia.
• Functional tremor - variable, distractible, changes frequency to match another movement (entrainment).

Essential tremor:

• Features:
  • The commonest movement disorder.
  • Bilateral postural and action tremor of the hands (writing, holding a cup).
  • Often head ("no-no") and voice tremor.
  • Family history (autosomal dominant) in about half.
  • Often improves with alcohol.
  • No bradykinesia or rigidity.
• Tests: TFTs; review drugs; DaTscan if unclear.
• Treatment (only if it affects function):
  • Propranolol (e.g. 40–160 mg daily, or as needed before events).
  • Primidone (start very low - 25 mg at night; sedation).
  • Topiramate, gabapentin as alternatives.
  • Botulinum toxin (head and voice).
  • Deep brain stimulation (thalamus) or focused ultrasound thalamotomy for severe tremor.

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Dystonia

What it is: Involuntary sustained or intermittent muscle contractions causing twisting movements and abnormal postures. It often has a "sensory trick" (geste antagoniste) - touching the face or chin eases it.

Types by distribution:

• Focal (the commonest in adults):
  • Cervical dystonia (spasmodic torticollis) - head turning or tilting, neck pain.
  • Blepharospasm - forced eye closure.
  • Writer's cramp and other task-specific dystonias (musicians).
  • Spasmodic dysphonia (voice).
• Segmental, multifocal or generalised - generalised dystonia usually starts in childhood (e.g. DYT1 gene).
• Dopa-responsive dystonia:
  • Children and young people.
  • Leg dystonia that is worse later in the day.
  • Dramatic response to low-dose levodopa - always try levodopa in young-onset dystonia.
• Secondary causes:
  • Drugs (acute dystonic reactions, tardive dystonia).
  • Wilson's disease - check copper studies in anyone under 50.
  • Stroke; cerebral palsy.

Treatment:

• Botulinum toxin injections - first line for focal dystonia (repeated every 3 months).
• Oral drugs: trihexyphenidyl (anticholinergic - younger patients), baclofen, clonazepam.
• Deep brain stimulation (globus pallidus) for generalised or severe dystonia.
• Physiotherapy.

Acute dystonic reaction (oculogyric crisis, torticollis, tongue protrusion) after antipsychotics or antiemetics, especially in young people: procyclidine 5–10 mg IV or IM.

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Huntington's Disease

What it is: An inherited neurodegenerative disease.

• Autosomal dominant - CAG repeat expansion in the HTT gene.
• 40 or more repeats - full penetrance; 36–39 - reduced penetrance.
• Anticipation - earlier onset in later generations, especially when passed from the father.
• Onset usually 30–50; death 15–20 years later.

Features - a triad:

• Movement:
  • Chorea.
  • Motor impersistence (can't keep the tongue out - "milkmaid's grip").
  • Abnormal eye movements (slow saccades).
  • Later rigidity, dystonia, dysphagia and falls.
• Psychiatric:
  • Depression (high suicide risk).
  • Irritability; apathy; obsessive behaviour.
  • Psychosis.
• Cognitive: Executive dysfunction progressing to dementia.
• Juvenile HD (onset before 20) - rigidity and seizures rather than chorea.

Diagnosis:

• Genetic testing (CAG repeat).
• MRI shows caudate atrophy.
• Predictive testing for at-risk relatives follows a structured counselling protocol (it is a life-changing result).
• Pre-implantation and prenatal testing are available.

Treatment (no disease-modifying therapy yet):

• Chorea: Tetrabenazine (can cause depression and parkinsonism) or antipsychotics (olanzapine, risperidone).
• Psychiatric: Treat depression (SSRIs), irritability and psychosis; monitor suicide risk.
• MDT: Speech and swallowing, nutrition (high calorie needs), physiotherapy, social care, advance care planning.
• Support for the family (Huntington's Disease Association).

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Other Chorea and Ballism

• Drugs: Levodopa (dyskinesia), the combined pill, phenytoin, stimulants, lithium.
• Metabolic:
  • Non-ketotic hyperglycaemia - one-sided chorea in older people with poorly controlled diabetes (bright basal ganglia on CT).
  • High or low calcium; high or low sodium.
  • Thyrotoxicosis.
  • Liver failure.
• Autoimmune:
  • Sydenham's chorea - rheumatic fever in children (weeks to months after strep throat).
  • SLE and antiphospholipid syndrome.
  • Autoimmune encephalitis (NMDA receptor).
• Pregnancy - chorea gravidarum (often previous Sydenham's or APS).
• Vascular - stroke in the subthalamic nucleus causes hemiballismus (violent flinging of the opposite limbs); usually improves over weeks.
• Blood: Polycythaemia vera.
• Inherited: Huntington's, Wilson's, neuroacanthocytosis, benign hereditary chorea, HD-like syndromes.
• Older people: "Senile chorea" is a diagnosis of exclusion.
• Treatment: Treat the cause; tetrabenazine or antipsychotics if disabling.

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Tics and Tourette Syndrome

• Tics:
  • Sudden, repetitive, non-rhythmic movements (blinking, shrugging) or sounds (sniffing, grunting).
  • A premonitory urge before the tic and relief afterwards.
  • They can be briefly suppressed.
  • Worse with stress, tiredness or relaxation.
• Tourette syndrome:
  • Multiple motor tics and at least one vocal tic for over a year, starting before 18 (usually 5–7 years).
  • Often peaks in early adolescence and improves in adulthood.
  • Coprolalia (swearing) affects only a minority.
• Associated conditions (common, and often more disabling than the tics): ADHD, OCD, anxiety, autism.
• Treatment:
  • Education and reassurance (school).
  • Behavioural therapy - habit reversal / CBIT, exposure and response prevention.
  • Drugs for disabling tics: aripiprazole, clonidine or guanfacine (also helps ADHD), risperidone.
  • Treat ADHD and OCD.
  • Deep brain stimulation in rare severe adult cases.
• Functional tic-like behaviours - sudden onset in teenagers, often after social media exposure; complex movements and words; managed as functional neurological disorder.

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Drug-induced Movement Disorders

⚠️ Safety Pearl: Metoclopramide causes acute dystonia in the young and parkinsonism and tardive dyskinesia in older people. The MHRA advises a maximum of 5 days' use.

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Myoclonus

• What it is: Sudden, brief, shock-like jerks (positive myoclonus) or brief lapses of muscle tone (negative myoclonus - asterixis).
• Normal (physiological): Hypnic jerks when falling asleep; hiccups.
• Causes:
  • Metabolic - uraemia, liver failure (asterixis), hypercapnia, low glucose, low sodium.
  • Drugs - opioids (especially in renal impairment - morphine metabolites), gabapentin and pregabalin, lithium, SSRIs, cefepime and other antibiotics.
  • Post-hypoxic - after cardiac arrest: early myoclonic status (poor prognosis) or later Lance–Adams syndrome (action myoclonus, better prognosis).
  • Epilepsy - juvenile myoclonic epilepsy, progressive myoclonic epilepsies.
  • Neurodegenerative - CJD (rapid dementia with myoclonus), Alzheimer's, corticobasal syndrome, MSA.
  • Spinal or segmental myoclonus.
  • Functional.
• Treatment: Treat the cause; review drugs. Levetiracetam, clonazepam or valproate for cortical myoclonus.

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Restless Legs Syndrome

What it is: An uncomfortable urge to move the legs.

• Worse at rest and in the evening or night.
• Relieved by movement.
• It disturbs sleep. Many also have periodic limb movements of sleep.

Causes and associations:

• Iron deficiency - check ferritin even if Hb is normal.
• Pregnancy.
• CKD (especially dialysis).
• Peripheral neuropathy.
• Family history (primary RLS).
• Drugs - antihistamines, antidepressants (SSRIs, mirtazapine), antipsychotics, metoclopramide.

Treatment:

• Iron replacement if ferritin is under about 75 µg/L (oral or IV).
• Lifestyle: Regular sleep, exercise, less caffeine, alcohol and smoking; leg massage.
• Stop trigger drugs.
• Drugs for frequent symptoms:
  • Gabapentin or pregabalin - now often preferred first.
  • Dopamine agonists (ropinirole, pramipexole, rotigotine) at low doses.
  • Watch for augmentation with dopamine agonists - symptoms become worse, earlier in the day and spread to the arms. This needs a switch.
• Low-dose opioids for refractory cases (specialist).

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Inherited and Acquired Ataxias

• Acquired causes (always check):
  • Alcohol (gait ataxia from anterior vermis damage).
  • Drugs (phenytoin, carbamazepine, lithium).
  • MS; stroke; tumours.
  • Hypothyroidism.
  • Vitamin E and B12 deficiency.
  • Coeliac disease (gluten ataxia).
  • Paraneoplastic (rapid onset - anti-Yo, anti-Hu, anti-Tr).
  • CJD.
  • MSA-C.
• Friedreich's ataxia:
  • Autosomal recessive (GAA repeat in FXN), the commonest inherited ataxia. Onset usually before 25.
  • Features:
    • Progressive ataxia and dysarthria.
    • Absent reflexes with extensor plantars.
    • Loss of vibration and joint position sense.
    • Pes cavus; scoliosis.
    • Hypertrophic cardiomyopathy (the main cause of death).
    • Diabetes.
    • Optic atrophy; hearing loss.
  • Omaveloxolone is licensed as the first specific treatment.
  • Monitor heart (ECG, echo) and glucose.
• Spinocerebellar ataxias (SCAs) - autosomal dominant, adult onset; many types (some with anticipation).
• Ataxia telangiectasia - childhood ataxia, telangiectasia (eyes, ears), immunodeficiency, cancer risk, raised AFP.
• Episodic ataxias - attacks of ataxia (EA2 responds to acetazolamide).
• Fragile X tremor-ataxia syndrome - older male carriers of fragile X premutations.
• Management: Physiotherapy, speech therapy, walking aids, treat reversible causes, genetic counselling.

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Functional Movement Disorders

What they are: Genuine involuntary movements caused by a problem with how the brain controls movement, not by structural damage. They are common in movement disorder clinics. Diagnosis is based on positive signs, not just excluding other conditions.

Positive signs:

• Functional tremor - distractibility (stops when the patient does a complex task with the other hand) and entrainment (takes on the rhythm of a tapping movement in the other hand).
• Functional dystonia - fixed postures, often after minor injury, with pain.
• Functional gait - dragging leg, knee buckling without falling, very slow.
• Functional jerks - variable; long delays before startle-related jerks.
• Sudden onset, often after a physical trigger (injury, infection, illness), with variable severity.

Management:

• A clear, positive explanation - what it is and that it can improve.
• Specialist physiotherapy (retraining movement with distraction techniques).
• Psychological therapy if relevant.
• Treat pain, fatigue, sleep and mood.
• Avoid unnecessary tests and drugs.
• About 1 in 10 also has another neurological condition (e.g. Parkinson's).

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios