Movement Disorders

Parkinson Disease

Pathophysiology and clinical phenotype

Parkinson disease (PD) is a progressive synucleinopathy defined clinically by parkinsonism: bradykinesia plus either rest tremor or rigidity. Motor signs usually emerge after approximately 50–70% substantia nigra pars compacta neuronal loss and ~80% striatal dopamine depletion. Degeneration disrupts basal ganglia circuitry: reduced nigrostriatal dopamine increases indirect pathway activity and reduces direct pathway facilitation, producing excessive inhibitory output from GPi/SNr to thalamocortical motor circuits. Lewy bodies contain misfolded α-synuclein; Braak staging proposes early olfactory bulb/dorsal motor vagal involvement, then pontomesencephalic, limbic and neocortical spread, correlating with hyposmia, REM sleep behaviour disorder, autonomic dysfunction, hallucinations and dementia.

Idiopathic PD is usually sporadic, but exam-relevant genetic associations include LRRK2 autosomal dominant PD, GBA as a major risk allele with greater cognitive/psychiatric burden, SNCA duplication/triplication, and early-onset recessive PRKN, PINK1 and DJ-1. The classic phenotype is asymmetric onset, 4–6 Hz “pill-rolling” rest tremor, cogwheel rigidity, decremental bradykinesia, reduced arm swing, hypomimia, micrographia, shuffling gait and later postural instability. Non-motor disease is not ancillary: constipation, urinary urgency, erectile dysfunction, orthostatic hypotension, anosmia, depression, apathy, pain, fatigue, sleep fragmentation, REM sleep behaviour disorder and cognitive decline are common and may dominate disability.

Diagnosis, staging and assessment

The MDS clinical diagnostic criteria require parkinsonism and classify PD as clinically established or probable according to supportive criteria, red flags and absolute exclusions. Supportive criteria include clear levodopa response, levodopa-induced dyskinesia, rest tremor, and either olfactory loss or cardiac sympathetic denervation on MIBG scintigraphy. Absolute exclusions include cerebellar signs, vertical supranuclear gaze palsy, frontotemporal dementia within 5 years, lower-limb-only parkinsonism for >3 years, normal presynaptic dopaminergic imaging, or absent response to high-dose levodopa despite at least moderate disease.

Assessment tool	Exam relevance
Hoehn and Yahr	Stage 1 unilateral; 2 bilateral without balance impairment; 3 postural instability but independent; 4 severe disability, able to stand/walk; 5 wheelchair/bed-bound.
MDS-UPDRS	Four domains: non-motor experiences, motor experiences, motor examination, motor complications; used in trials and longitudinal assessment.
DaTSCAN	Ioflupane SPECT demonstrates presynaptic dopaminergic deficit; sensitivity/specificity typically around 85–95% for degenerative parkinsonism versus essential tremor, but does not reliably distinguish PD from MSA/PSP/CBD.

Pharmacological management

NICE NG71 recommends offering levodopa when motor symptoms affect quality of life; if not, levodopa, a dopamine agonist or an MAO-B inhibitor may be considered after discussion of adverse-effect profiles. The PD MED trial showed better patient-rated mobility and quality-of-life outcomes with levodopa than levodopa-sparing initial therapy, despite more dyskinesia; CALM-PD showed pramipexole delayed dyskinesia compared with levodopa but caused more somnolence, oedema and hallucinations and less motor benefit.

Class	Typical dosing	Key adverse effects/exam points
Levodopa + dopa decarboxylase inhibitor	Co-careldopa or co-beneldopa often start 50/12.5 mg or 100/25 mg three times daily; titrate. Levodopa plasma half-life ~60–90 min.	Best symptomatic efficacy. Nausea, postural hypotension, hallucinations, dyskinesia, wearing-off. Avoid abrupt withdrawal: risk parkinsonism-hyperpyrexia syndrome.
Dopamine agonists	Pramipexole 0.088 mg TDS titrated; ropinirole 0.25 mg TDS titrated; rotigotine patch 2 mg/24 h upward.	Impulse-control disorders, sleep attacks, oedema, hallucinations; caution in elderly/cognitive impairment. Ergot agonists require valve monitoring and are rarely used.
MAO-B inhibitors	Rasagiline 1 mg OD; selegiline 5 mg BD; safinamide 50–100 mg OD.	Mild symptomatic benefit; adjunct for wearing-off. Serotonergic interaction risk is low but relevant with polypharmacy.
COMT inhibitors	Entacapone 200 mg with each levodopa dose, max 2 g/day; opicapone 50 mg nocte.	Prolong levodopa effect; dyskinesia, diarrhoea, orange urine. Tolcapone limited by hepatotoxicity.
Amantadine	100 mg OD–BD, renal adjustment.	Useful for dyskinesia; causes livedo reticularis, ankle oedema, confusion, hallucinations.

Motor complications and advanced therapies

With disease progression, short levodopa half-life and impaired striatal buffering produce wearing-off, delayed on, dose failures, freezing and peak-dose dyskinesia. Management includes fractionating levodopa, modified-release or intestinal gel in selected cases, adding MAO-B/COMT inhibitors, dopamine agonists, or amantadine for dyskinesia. Subcutaneous apomorphine is used as intermittent rescue or continuous infusion; antiemetic cover with domperidone may be required with ECG/QT caution.

Deep brain stimulation, usually subthalamic nucleus or GPi, is considered for medically refractory motor fluctuations or tremor in patients with good levodopa responsiveness and without uncontrolled psychiatric disease or significant dementia. STN DBS often permits levodopa reduction; GPi DBS may be preferred where dyskinesia or mood/cognitive concerns predominate. Non-pharmacological management is integral: PD specialist nurse input, physiotherapy for gait/balance, occupational therapy, speech and language therapy for hypophonia/dysphagia, exercise prescription, bone and falls risk reduction, and anticipatory management of autonomic, neuropsychiatric and palliative issues.

Essential Tremor

Essential tremor (ET) is the commonest pathological tremor syndrome, with prevalence rising from approximately 0.4–1% in the general population to 4–6% over age 65 years. It is classically an isolated bilateral upper-limb action tremor, present for at least 3 years, with or without head, voice or lower-limb tremor, and without other neurological signs. The 2018 International Parkinson and Movement Disorder Society classification separates ET from ET-plus, the latter denoting ET with additional “soft” signs such as impaired tandem gait, questionable dystonic posturing, mild memory impairment or rest tremor not sufficient to define another syndrome.

Pathophysiology and genetics

ET is increasingly viewed as a disorder of the cerebello-thalamo-cortical network, rather than a monosymptomatic benign tremor. Functional imaging and neurophysiology implicate abnormal oscillatory activity involving the cerebellar cortex, dentate nucleus, ventral intermediate nucleus of the thalamus and motor cortex. Pathological studies variably show Purkinje cell loss, torpedoes and altered GABAergic signalling; hence the responsiveness to agents enhancing inhibitory neurotransmission. Familial clustering is common: 30–70% report an affected first-degree relative, often with autosomal dominant inheritance and age-dependent penetrance. No single gene explains most cases; reported loci and genes include ETM1, LINGO1 association signals and rare variants, but routine genetic testing is not recommended.

Clinical phenotype and diagnostic approach

The defining tremor is a postural and kinetic tremor, usually 4–12 Hz, most evident during sustained posture, finger-nose testing, pouring water or spiral drawing. It is typically symmetrical or mildly asymmetric, worsens with anxiety, fatigue, caffeine and adrenergic stimulation, and may transiently improve with alcohol in 50–70% of patients. Head tremor is often “yes-yes” or “no-no”; isolated head tremor should prompt consideration of cervical dystonia. Voice tremor produces rhythmic quavering. Unlike Parkinson disease, ET lacks bradykinesia and rigidity; however, long-standing ET may develop rest tremor, creating diagnostic difficulty.

Feature	Essential tremor	Parkinsonian tremor	Dystonic tremor
Activation	Postural/kinetic; intention component possible	Rest tremor; re-emergent postural tremor	Postural/action, position-specific
Frequency	Usually 4–12 Hz	Typically 4–6 Hz	Variable, often irregular
Distribution	Bilateral hands; head/voice common	Asymmetric limb onset; jaw possible, head uncommon	Associated abnormal posture or sensory trick
Associated signs	None in pure ET	Bradykinesia, rigidity, reduced arm swing	Dystonic posturing, geste antagoniste

Assessment should actively exclude mimics: enhanced physiological tremor, thyrotoxicosis, anxiety, drug-induced tremor, alcohol withdrawal, neuropathic tremor, Wilson disease in younger patients and structural cerebellar disease. Relevant medications include β-agonists, lithium, valproate, ciclosporin/tacrolimus, amiodarone, SSRIs/SNRIs, tricyclics, methylxanthines and corticosteroids. In typical late-onset ET, investigations are limited; thyroid function tests, glucose, calcium and drug review are common exam-relevant exclusions. Serum caeruloplasmin, copper studies and slit-lamp examination are considered in young-onset tremor or hepatic/psychiatric features.

Severity scoring and prognosis

Severity is measured using validated tools such as the Fahn–Tolosa–Marín Tremor Rating Scale, the Essential Tremor Rating Assessment Scale and patient-centred disability measures. Spiral analysis and accelerometry quantify frequency and amplitude in trials but are not required routinely. ET is slowly progressive: tremor amplitude increases with age, while frequency may fall. Disability reflects writing, eating, drinking, occupation and social embarrassment. ET is not invariably benign; cohort studies suggest increased risk of gait ataxia, mild cognitive impairment and possibly incident Parkinson disease, though causality remains debated.

Management

Treatment is indicated when tremor causes functional impairment or distress. General measures include reducing caffeine and sympathomimetics, managing anxiety, weighted utensils, occupational therapy and avoidance of tremorogenic drugs. Intermittent therapy may suffice for performance-related tremor.

Therapy	Typical dosing	Key adverse effects / cautions	Exam points
Propranolol	10–40 mg orally before events; maintenance 40 mg twice daily, titrated to 120–320 mg/day. Half-life 3–6 h.	Bradycardia, hypotension, fatigue, depression, bronchospasm; avoid in asthma, heart block, decompensated heart failure.	First-line; best evidence for limb tremor; less effective for head/voice tremor.
Primidone	Start 12.5–25 mg nocte; increase slowly to 50–250 mg nocte or bd; usual 250–750 mg/day.	Acute nausea, ataxia, sedation, dizziness; induces hepatic enzymes; monitor FBC if long-term.	First-line alternative or add-on; metabolised to phenobarbital and phenylethylmalonamide.
Topiramate	Start 25 mg nocte; titrate to 100–400 mg/day.	Weight loss, paraesthesia, cognitive slowing, renal stones, teratogenic risk.	Probably effective; discontinuation due to adverse effects is common.
Gabapentin	300 mg tds, titrate to 1200–3600 mg/day.	Sedation, dizziness, oedema; renal dose adjustment.	Modest benefit; useful if comorbid neuropathic pain.
Benzodiazepines	Clonazepam 0.25–0.5 mg nocte/bd; alprazolam 0.25–0.5 mg prn or tds.	Dependence, falls, cognitive impairment, respiratory depression.	Reserved for anxiety-provoked tremor; avoid chronic use where possible.

The American Academy of Neurology evidence-based review classifies propranolol and primidone as established effective, each reducing tremor amplitude by roughly 50% in responders, though 30–50% have inadequate response or intolerance. Combination propranolol plus primidone may outperform either alone, particularly for head tremor, but adverse effects increase. Botulinum toxin may improve refractory hand, head or voice tremor, but hand weakness and dysphagia/dysphonia limit use; injections require EMG or kinematic targeting.

Advanced therapies

For severe medication-refractory ET, deep brain stimulation of the ventral intermediate thalamic nucleus provides substantial tremor suppression, often 60–90% contralateral limb benefit, adjustable and reversible but with risks of dysarthria, gait ataxia, infection and haemorrhage. Bilateral DBS improves bilateral tremor but increases speech and balance complications. MR-guided focused ultrasound thalamotomy creates a unilateral lesion; sham-controlled trial data showed approximately 47% improvement in hand tremor scores at 3 months versus minimal sham response, with persistent benefit in many patients but risks of paraesthesia, ataxia and gait disturbance. Lesional procedures are generally unilateral because bilateral thalamotomy carries unacceptable dysarthria and ataxia risk.

Chorea

Chorea is an involuntary hyperkinetic movement disorder characterised by brief, irregular, unpredictable, non-rhythmic movements that flow from one body part to another. It reflects dysfunction of basal ganglia motor circuits, particularly reduced inhibitory output from the internal globus pallidus/substantia nigra pars reticulata to the thalamus, causing excessive thalamocortical drive. In exam terms, chorea must be distinguished from myoclonus (shock-like, often stimulus-sensitive), tics (suppressible, preceded by urge), athetosis (slow writhing distal movements), ballism (proximal, flinging, usually subthalamic), and dyskinesia as a broader descriptive term.

Pathophysiology and classification

The canonical mechanism involves relative underactivity of the indirect pathway. Loss or functional impairment of striatal medium spiny neurons projecting to the external globus pallidus reduces subthalamic nucleus excitation of GPi, thereby reducing GPi inhibition of the thalamus. Huntington disease is the prototype, with early preferential degeneration of indirect pathway striatal neurons and later widespread cortical and striatal atrophy. Dopaminergic excess, NMDA/glutamatergic excitotoxicity, autoimmune basal ganglia injury, vascular lesions and metabolic derangements may produce a similar final phenotype.

Category	Key causes	Exam clues
Genetic/neurodegenerative	Huntington disease, dentatorubral-pallidoluysian atrophy, neuroacanthocytosis, benign hereditary chorea	Family history, psychiatric/cognitive features, caudate atrophy, acanthocytes or seizures in neuroacanthocytosis
Autoimmune/post-infectious	Sydenham chorea, SLE/antiphospholipid syndrome, autoimmune encephalitis	Child/adolescent post-streptococcal illness, carditis; thrombosis/miscarriage; encephalopathy/seizures
Metabolic/endocrine	Hyperthyroidism, hypoglycaemia, hyperglycaemic non-ketotic chorea, hepatic/renal failure, Wilson disease	Acute/subacute onset; abnormal glucose, thyroid, liver tests; Kayser-Fleischer rings, low caeruloplasmin
Drug/toxin-induced	Levodopa, dopamine agonists, antipsychotic withdrawal/tardive syndromes, anticonvulsants, oral contraceptives, cocaine	Temporal relationship; orofacial stereotypy in tardive dyskinesia; polypharmacy
Structural/vascular	Stroke, tumour, demyelination affecting basal ganglia/subthalamic region	Acute hemichorea/hemiballismus; contralateral lesion; vascular risk factors
Pregnancy-related	Chorea gravidarum	Often recurrence of Sydenham/SLE/APS-related chorea; usually improves postpartum

Huntington disease: high-yield prototype

Huntington disease is autosomal dominant due to a CAG trinucleotide expansion in HTT on chromosome 4. Normal alleles have <27 repeats; intermediate alleles 27–35; reduced penetrance 36–39; and full penetrance usually ≥40. Anticipation, particularly paternal transmission, reflects repeat expansion during spermatogenesis. Typical onset is age 30–50 years; juvenile disease, often with rigidity and seizures rather than chorea, is usually associated with very large expansions, commonly >60 repeats.

Clinical diagnosis rests on a triad of motor chorea/dystonia/parkinsonism, cognitive decline with executive dysfunction, and psychiatric disease, especially depression, irritability, apathy, obsessive-compulsive symptoms and psychosis. Suicide risk is increased, particularly around diagnosis and early functional decline. MRI may show caudate atrophy with enlarged frontal horns, but genetic testing is definitive after counselling. Predictive testing in asymptomatic adults requires formal pre-test counselling; testing minors is generally avoided unless clinically indicated.

Scoring and assessment

The principal scale is the Unified Huntington’s Disease Rating Scale (UHDRS). The motor section rates chorea, dystonia, eye movements, dysarthria, bradykinesia, gait and postural stability; each item is commonly scored 0–4, with higher scores indicating greater impairment. The Total Functional Capacity (TFC) score ranges from 13 normal to 0 severe dependency and stages Huntington disease: stage I 11–13, II 7–10, III 3–6, IV 1–2, V 0. This staging is useful in trials and prognosis, but MRCP questions often focus on recognising the syndrome and selecting appropriate investigations.

Investigation strategy

Investigation is guided by age, tempo, symmetry and systemic features. Acute unilateral chorea warrants urgent neuroimaging for stroke or structural disease. Subacute generalised chorea requires medication review and screening for glucose, renal/liver dysfunction, calcium, thyroid disease and autoimmune causes where indicated. In young patients, consider Wilson disease with serum caeruloplasmin, 24-hour urinary copper and slit-lamp examination; caeruloplasmin is typically <0.20 g/L but may be falsely normal as an acute-phase reactant. Sydenham chorea is supported by recent group A streptococcal infection: elevated antistreptolysin O or anti-DNase B titres, plus assessment for carditis.

Treatment principles and pharmacology

Treat reversible causes first: correct metabolic abnormalities, stop causative drugs, treat thyrotoxicosis, manage SLE/APS, and institute penicillin prophylaxis for Sydenham chorea when rheumatic fever criteria are met. Symptomatic treatment is justified when chorea causes falls, weight loss, social impairment or functional disability. In Huntington disease, the choice is influenced by psychiatric comorbidity: antipsychotics are preferred if psychosis, aggression or severe irritability coexist; VMAT2 inhibitors are useful when chorea predominates but may worsen depression or parkinsonism.

Drug/class	Typical adult dosing	Key cautions
Tetrabenazine, VMAT2 inhibitor	Start 12.5 mg once daily, increase weekly to 12.5 mg bd–tds; usual 25–75 mg/day. CYP2D6 genotyping/limits are relevant above 50 mg/day in some jurisdictions.	Depression, suicidality, akathisia, parkinsonism, QT prolongation; half-life of parent short, active metabolites approximately 4–8 h.
Deutetrabenazine, deuterated VMAT2 inhibitor	Start 6 mg once daily, titrate weekly by 6 mg/day; typical 12–48 mg/day in divided doses.	Similar but smoother pharmacokinetics; avoid in active suicidality or untreated depression.
Risperidone	0.5–1 mg nocte, titrate to 1–4 mg/day	Useful with behavioural symptoms; extrapyramidal effects, hyperprolactinaemia, metabolic effects.
Olanzapine	2.5–5 mg nocte, usual 5–10 mg/day	May help weight loss and insomnia; metabolic syndrome and sedation.
Haloperidol	0.5–1 mg bd, titrate cautiously	Effective but higher risk of parkinsonism, akathisia and tardive syndromes.

Evidence for tetrabenazine includes a pivotal randomised controlled trial in Huntington chorea showing a mean improvement in UHDRS chorea of approximately 5 units over 12 weeks versus placebo, but adverse neuropsychiatric effects limit use. Deutetrabenazine demonstrated significant chorea reduction in the First-HD trial with improved tolerability. Disease-modifying therapy for Huntington disease remains investigational; current care is multidisciplinary, including genetic counselling, physiotherapy, swallowing/nutrition assessment, advance care planning and treatment of depression with standard antidepressant approaches when indicated.

Dystonia

Dystonia is a hyperkinetic movement disorder characterised by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. Movements are typically patterned, twisting, may be tremulous, and are frequently precipitated by voluntary action with overflow activation. A key examination clue is the geste antagoniste or sensory trick, where light tactile input transiently improves dystonia, especially in cervical dystonia.

Pathophysiology and clinical phenomenology

Dystonia is increasingly conceptualised as a network disorder involving basal ganglia, cerebellum, thalamus, sensorimotor cortex and brainstem. Core mechanisms include impaired surround inhibition, maladaptive plasticity, abnormal sensory processing and defective motor learning. Neurophysiological studies demonstrate reduced intracortical inhibition and shortened cortical silent periods; clinically this explains overflow, task-specificity and co-contraction of agonist-antagonist muscles. Dopaminergic dysfunction is central in some genetic and acquired forms: GCH1-related dopa-responsive dystonia reflects impaired tetrahydrobiopterin synthesis and reduced dopamine production, whereas dopamine receptor blockade can cause acute dystonia or tardive dystonia.

Classification axis	High-yield categories	Exam relevance
Age at onset	Infantile <2 years; childhood 2–12; adolescence 13–20; adult >20	Childhood limb onset suggests genetic/generalised dystonia; adult focal onset is often idiopathic
Body distribution	Focal, segmental, multifocal, hemidystonia, generalised	Hemidystonia strongly suggests structural contralateral basal ganglia lesion
Temporal pattern	Persistent, action-specific, diurnal, paroxysmal	Diurnal fluctuation suggests dopa-responsive dystonia
Aetiology	Inherited, acquired, idiopathic	Acquired causes include drugs, Wilson disease, stroke, cerebral palsy, neurodegeneration

Important syndromes and differentials

Adult focal dystonias include cervical dystonia, blepharospasm, oromandibular dystonia, spasmodic dysphonia and task-specific dystonias such as writer’s cramp or musician’s dystonia. Cervical dystonia may present with torticollis, laterocollis, anterocollis or retrocollis and is commonly painful. Blepharospasm causes involuntary eyelid closure and must be distinguished from apraxia of eyelid opening, myasthenia gravis and hemifacial spasm. Oromandibular dystonia may mimic temporomandibular disease.

In any young patient, screen for treatable causes. Wilson disease should be considered particularly before age 40: serum caeruloplasmin may be low, but 24-hour urinary copper, slit-lamp examination for Kayser–Fleischer rings and hepatic assessment are often required. Dopa-responsive dystonia classically presents with childhood lower-limb dystonia, gait disturbance, diurnal worsening and sleep benefit; parkinsonism and brisk reflexes may occur. A levodopa trial is mandatory because response can be dramatic.

Assessment and scoring

There is no universal “stage” system analogous to Hoehn and Yahr. Severity is quantified using validated scales. The Burke–Fahn–Marsden Dystonia Rating Scale comprises a movement score assessing nine body regions and a disability score; it is widely used in generalised dystonia and DBS studies. Cervical dystonia is commonly scored with TWSTRS evaluating severity, disability and pain. Blepharospasm may be assessed using the Jankovic Rating Scale. In examinations, mention video documentation, functional impact, pain, swallowing/respiratory symptoms in cervical or laryngeal dystonia, and medication exposure.

Management

General principles

Management is phenotype-driven: remove offending drugs, treat underlying metabolic/structural disease, rehabilitate with physiotherapy and sensory retraining, and use botulinum toxin for focal dystonia. Genetic testing is considered for early-onset, generalised, familial or atypical cases; common genes include TOR1A, THAP1, GCH1 and KMT2B.

Treatment	Typical adult dosing	Key points
Levodopa trial	Co-careldopa 62.5 mg once or twice daily, titrate to 300–600 mg levodopa/day for at least 1–3 months if tolerated	Essential in childhood/young-onset dystonia; dopa-responsive dystonia may respond to low doses long term
Trihexyphenidyl	Start 1–2 mg daily; increase every 3–7 days; adult usual 6–30 mg/day, sometimes higher in specialist practice	Best evidence among oral drugs, especially young generalised dystonia; anticholinergic toxicity limits use
Baclofen	5 mg three times daily, titrate to 30–80 mg/day	Useful adjunct; sedation, weakness; intrathecal use reserved for severe refractory cases
Clonazepam	0.25–0.5 mg nocte or twice daily; titrate to 1–4 mg/day	Useful for dystonic tremor, myoclonus-dystonia or anxiety-associated exacerbation; dependence and sedation
Tetrabenazine	12.5 mg daily, titrate; usual 25–100 mg/day	May help tardive dystonia/choreo-dystonia; depression, parkinsonism, QT risk; VMAT2 inhibitor

Botulinum toxin is first-line for most focal dystonias, supported by randomised trial evidence and major movement disorder guidelines. Preparations include onabotulinumtoxinA, incobotulinumtoxinA, abobotulinumtoxinA and rimabotulinumtoxinB; units are not interchangeable. Effects begin after 3–7 days, peak at 2–6 weeks and last approximately 10–14 weeks, so reinjection is commonly every 12 weeks. For cervical dystonia, total onabotulinumtoxinA doses often range from 100–300 units, tailored by muscle selection, EMG or ultrasound guidance and prior response. Adverse effects include focal weakness, dysphagia, dry mouth and local pain; dysphagia is particularly associated with bilateral sternocleidomastoid injections or high anterior neck doses.

Acute drug-induced dystonia, usually after dopamine antagonists such as haloperidol, metoclopramide or prochlorperazine, is a medical emergency when laryngeal involvement occurs. Treat with intramuscular or intravenous procyclidine 5–10 mg or benztropine 1–2 mg; symptoms typically improve within minutes. Continue oral anticholinergic cover for 24–72 hours to prevent recurrence, and stop or reduce the causative drug.

Deep brain stimulation of the internal globus pallidus is indicated for medically refractory generalised or segmental dystonia, particularly primary genetic dystonia. Benefits evolve over weeks to months rather than immediately, and motor improvements of approximately 40–70% on BFMDRS have been reported in primary dystonia cohorts, with poorer responses in fixed skeletal deformity or secondary dystonia. Complications include infection, lead migration, dysarthria, stimulation-induced parkinsonism and hardware failure.