Parkinson disease and parkinsonism

• Parkinson disease is a chronic, progressive neurodegenerative disorder in which the dopamine-producing cells of the substantia nigra pars compacta die and Lewy bodies containing aggregated alpha-synuclein accumulate.
• It becomes clinically obvious only after roughly half the nigrostriatal neurons are lost. The cardinal motor problem is bradykinesia, with rigidity and rest tremor; postural instability comes later.
• Many symptoms are non-motor: anosmia, constipation, sleep disorder, depression, pain and later dementia. Several of these appear years before the first tremor.
• Idiopathic Parkinson disease is one cause of parkinsonism. Atypical parkinsonian syndromes, vascular disease, drug-induced cases and essential tremor must be distinguished because treatment and prognosis differ.
• Levodopa remains the most effective symptomatic drug. Dopamine agonists, MAO-B inhibitors, COMT inhibitors, amantadine, botulinum toxin and deep brain stimulation have defined roles. No drug has been proven to slow the disease (NICE NG71 recommendations 1.6).

By the end of this page you should be able to:

1. Define Parkinson disease, distinguish it from parkinsonism and classify idiopathic, genetic and secondary forms.
2. Explain the nigrostriatal dopamine pathway and how its failure produces the motor and non-motor features.
3. Recognise the early, motor and late clinical picture, including less obvious features such as masked facies, micrographia and freezing of gait.
4. Tell idiopathic Parkinson disease from essential tremor and from atypical and drug-induced parkinsonism, using clinical clues.
5. Plan investigations and know which tests NICE says to use or to avoid.
6. Outline management following NICE NG71 (dated 2017, last reviewed 19 December 2024), citing the role of the MDS evidence-based medicine reviews (Fox 2018, Seppi 2019) and the AAN practice parameter (Zesiewicz 2010).
7. Recognise and manage motor complications and indications for deep brain stimulation.
8. Identify drug-induced parkinsonism and its management.

Parkinsonism is a descriptive syndrome rather than a single disease: slowness of movement (bradykinesia), with rigidity and/or tremor and postural problems. Idiopathic Parkinson disease is one cause among many. Others include atypical neurodegenerative syndromes, vascular disease, structural lesions, normal pressure hydrocephalus, repeated head trauma, toxins and drugs.

• Idiopathic (sporadic) Parkinson disease, usually over 60 to 65 years. Most cases fall here.
• Genetic (monogenic or familial) Parkinson disease, accounting for about 10 to 15 per cent of cases, mostly early-onset or familial (Church 2026). ^[2]
• Secondary (acquired) parkinsonism: drug-induced, vascular, post-traumatic, post-encephalitic, toxic, metabolic or structural.
• Atypical parkinsonian syndromes: multiple system atrophy, progressive supranuclear palsy, corticobasal syndrome, dementia with Lewy bodies, some of which are now considered Parkinson disease-related synucleinopathies rather than "classical" Parkinson disease.

The Movement Disorder Society (MDS) Clinical Diagnostic Criteria for Parkinson's Disease (Postuma et al, 2015) grade confidence as clinically established or clinically probable Parkinson disease. NICE NG71 (2017) directs diagnosis clinically against the UK Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria, with review of the diagnosis every 6 to 12 months (see section 8). In one large cohort, over 90 per cent of cases diagnosed as early Parkinson disease fulfilled the MDS criteria (Malek et al, 2017). ^[1][4][8]

Parkinson disease affects about 1 per cent of adults over the age of 60 (Church 2026) and the burden is rising with population ageing. ^[2]

• Age: the dominant risk factor; incidence rises steeply after 60.
• Sex: men are affected somewhat more often than women in most series.
• Family history and genetic variants: mutations in several genes (SNCA, LRRK2, Parkin, PINK1, DJ-1, GBA1 and others) are linked to Parkinson disease. GBA1 variants increase risk up to five to six times. Overall, monogenic forms account for roughly 10 to 15 per cent of cases, and most of these are early-onset (Church 2026). ^[2]
• Environmental: pesticide and solvent exposure, and head trauma, are repeatedly associated; the evidence is associative.
• Prodromal non-motor features: constipation, REM sleep behaviour disorder, hyposmia and depression often precede the motor diagnosis by years but are risk markers rather than causes.

There are no proven modifiable risk factors that prevent Parkinson disease; prevention advice is therefore limited (see Prevention and screening).

Dopamine is synthesised in the substantia nigra pars compacta and released in the striatum. It facilitates movement through two routes: it excites the direct pathway (D1-like receptors) and inhibits the indirect pathway (D2-like receptors). Together these disinhibit the thalamus and allow a chosen movement to start and flow. (Church 2026)

• The pigmented dopamine neurons of the substantia nigra pars compacta degenerate, and aggregated alpha-synuclein accumulates in Lewy bodies and Lewy neurites.
• By the time tremor or slowness appears, more than half the dopaminergic neurons have already been lost (Church 2026).
• The synucleinopathy then spreads in a "prion-like" manner through connected central and peripheral neurons, explaining why constipation, sleep change and other non-motor features precede the motor illness (Church 2026).
• Beyond dopamine, cholinergic, serotonergic and noradrenergic systems also degenerate, contributing to dementia, depression, autonomic failure, pain and sleep disorder (Church 2026).

• Bradykinesia follows directly from loss of dopaminergic drive; of the cardinal features it tracks most closely with dopamine deficiency.
• Rigidity reflects the imbalance between dopamine and acetylcholine in the striatum.
• Rest tremor is not simple dopamine deficiency; it arises from rhythmic network activity and is the feature least responsive to levodopa.
• Postural instability appears later, reflecting pedunculopontine and brainstem involvement beyond the nigrostriatal system.

• Gross: pallor and depigmentation of the substantia nigra and locus coeruleus; the striatum looks relatively normal.
• Microscopic: loss of neuromelanin-containing dopaminergic neurons in the substantia nigra pars compacta; eosinophilic, round, intracytoplasmic Lewy bodies (alpha-synuclein, ubiquitin) in surviving neurons; Lewy neurites in processes; microglial activation; mitochondrial dysfunction (Church 2026).
• Braak staging describes the predictable spread of synuclein pathology from the lower brainstem and olfactory structures to the neocortex, mirroring the early prodromal and later cognitive features (Church 2026).
• Genetic Parkinson disease may be Lewy body negative in some forms (for example many Parkin cases), so absence of Lewy bodies does not exclude a genetic parkinsonism.

Hyposmia, constipation, REM sleep behaviour disorder, depression, anxiety, excessive daytime sleepiness, pain, and autonomic symptoms such as orthostatic dizziness. Recognising these helps the early suspicion but they are not diagnostic on their own.

• Slowness and stiffness interfering with routine tasks (shaving, buttons, writing getting smaller and smaller, "micrographia").
• Tremor of one hand, often starting in a finger, "pill-rolling", present at rest, improving with action, worse with stress, absent in sleep.
• Gait change: reduced arm swing, shuffling, shortening steps, festination, and later turning "en bloc".
• Dysphagia, hypophonia and drooling.
• Falls usually only in later disease; falls in the first year raise suspicion of an atypical syndrome (Church 2026).

• Inspection: expressionless or masked face, reduced blink, soft monotonous speech, drooling, flexed posture, loss of arm swing.
• Tremor: a slow rest tremor, often asymmetric; re-emerges after a latency when the hand is held out (re-emergent tremor).
• Rigidity: uniform "lead-pipe" resistance to passive movement, sometimes with superimposed "cogwheel" jerk; detectable in wrist, elbow and neck; synkinesis (mirror movement) can be elicited by repetitive movement of the opposite hand.
• Bradykinesia: slow, small, decrementing repetitive finger taps, hand opening/closing and foot taps; test both sides and compare.
• Postural stability: retropulsion test (pull test) is positive when corrective steps are taken or the patient falls; usually negative early.
• Gait: short steps, festination, freezing in doorways, turns with multiple small steps; assess turning and narrow-space freezing.
• Non-motor screen: blood pressure lying and standing (orthostatic hypotension), olfaction, sleep and mood screen, cognitive screen (MMSE or MoCA), bowel and bladder symptoms, pain.

The letters T-R-A-P summarise the motor picture: Tremor at rest, Rigidity, Akinesia or bradykinesia and Postural instability. Like all mnemonics it hides the fact that postural instability appears late and that non-motor symptoms precede the motor ones by years.

The table summarises the principal conditions to separate from idiopathic Parkinson disease. Judging which applies depends on the whole clinical picture rather than on any single sign.

Notes on the atypical syndromes: features described by Church (2026) include rapid progression compared with classical Parkinson disease; additional non-typical signs (early balance disorder, cognitive decline, autonomic failure, abnormal eye movements); MSA with early dysautonomia and rapid wheelchair dependence; PSP with early falls, swallowing problems and gaze palsy; corticobasal syndrome with asymmetric limb apraxia, alien limb and sensory loss; frontotemporal dementia with parkinsonism arising within 1 to 3 years; and the one-year rule separating dementia with Lewy bodies from Parkinson disease dementia. ^[2]

NICE NG71 is explicit about which tests help and which do not.

Tests NICE says not to use for diagnosing Parkinson disease: PET, structural MRI for the diagnosis itself (MRI is reserved for other parkinsonian syndromes), magnetic resonance volumetry and spectroscopy, acute levodopa or apomorphine challenge tests, and objective smell testing, except in trials (NICE NG71 1.2.8-1.2.14). NICE also recommends discussing donation of brain tissue to a brain bank for pathological confirmation (NICE NG71 1.2.4). ^[1]

A parkinsonian syndrome must first be established (bradykinesia plus at least one of rigidity, a rest tremor or postural instability not explained by vestibular, visual, cerebellar or proprioceptive causes). Exclusion criteria then remove secondary and atypical causes, and supportive criteria improve confidence. The criteria are clinical; final confirmation remains pathological.

MDS criteria again require bradykinesia plus rest tremor or rigidity, then weight supportive and absolute exclusion features to assign a diagnostic certainty of clinically established or clinically probable Parkinson disease. In a large recent-onset cohort more than 90 per cent of cases already diagnosed as Parkinson disease fulfilled these criteria (Malek et al, 2017). ^[4][8]

The Hoehn and Yahr scale stages motor disability from unilateral disease (stage 1) through bilateral disease (2), mild (3) and severe bilateral disease (4) to wheelchair or bed bound (stage 5). The MDS-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) is the gold standard for assessing motor and non-motor burden, daily activities and treatment complications (Church 2026). The diagnosis should be reviewed every 6 to 12 months because atypical features can emerge later (NICE NG71 1.2.5). ^[1][2]

Before starting treatment, discuss the person's clinical and lifestyle circumstances, preferences, goals and the potential benefits and harms of dopamine agonists, levodopa and MAO-B inhibitors (NICE NG71 1.3.1; Table 1 of that guideline copied below). Antiparkinsonian medicines must not be withdrawn abruptly nor allowed to fail suddenly (for example in gastroenteritis or after abdominal surgery) because of the risk of acute akinesia or neuroleptic malignant syndrome; "drug holidays" should not be undertaken. Medicines in hospital or care homes must be given at the right times, with adjustment only after discussion with a specialist (NICE NG71 1.3.2-1.3.4). ^[1]

• Offer levodopa to people in the early stages whose motor symptoms already affect their quality of life (NICE NG71 1.3.5). ^[1]
• Consider a choice of dopamine agonists, levodopa or an MAO-B inhibitor for people in the early stages whose motor symptoms do not yet affect quality of life (NICE NG71 1.3.6).
• Do not offer ergot-derived dopamine agonists as first-line treatment (NICE NG71 1.3.7); non-ergot agonists are preferred when an agonist is chosen (NICE NG71 1.3.11). ^[1]
• Levodopa is the most effective symptomatic treatment for Parkinson disease, but it does not slow or cure the disease (Church 2026); it also produces more motor complications, whereas agonists and MAO-B inhibitors are less powerful but cause fewer (NICE NG71 Table 1).
• Anticholinergics are generally avoided in older adults and must not be offered once dyskinesia or motor fluctuations have developed (NICE NG71 1.3.14; Church 2026).

• Levodopa with carbidopa or benserazide crosses the blood-brain barrier as a "Trojan horse" and is converted to dopamine inside the brain by DOPA decarboxylase; the peripheral inhibitor improves central delivery and reduces peripheral side effects. It is the usual mainstay as disease progresses (Church 2026). Formulations include immediate- and extended-release carbidopa/levodopa, Rytary, Crexont, Duopa gel infusion, inhaled levodopa (Inbrija) and foslevodopa-foscarbidopa (Church 2026; NICE NG71 1.8.4).
• Dopamine agonists (ropinirole, pramipexole, rotigotine; older ergot agents such as bromocriptine and pergolide) stimulate dopamine receptors directly. They may precede levodopa in younger patients to delay motor complications, but carry higher risks of impulse control disorders, somnolence and hallucinations (NICE NG71; Church 2026).
• MAO-B inhibitors (selegiline, rasagiline, safinamide) reduce central dopamine breakdown; selegiline and rasagiline give modest symptomatic benefit and safinamide additionally modulates glutamate release and sodium/calcium channel activity (Church 2026; NICE NG71 Table 1).
• COMT inhibitors (entacapone, tolcapone, opicapone) block peripheral metabolism of levodopa and are used as adjuncts when wearing-off occurs.
• Amantadine helps resistant tremor and levodopa-induced dyskinesia (NICE NG71 1.3.13; Church 2026).
• Apomorphine is a potent, short-acting dopamine agonist used in advanced disease as an intermittent rescue injection or continuous subcutaneous infusion (NICE NG71 1.8.1).
• Doses are individualised and should follow the specialist's prescription and the local formulary; NICE NG71 does not set fixed titration schedules and none are listed here.

• Seek advice from a specialist before modifying therapy once dyskinesia or fluctuations have appeared (NICE NG71 1.3.9).
• Offer a choice of dopamine agonist, MAO-B inhibitor or COMT inhibitor as adjunct to levodopa after discussing benefits and harms (NICE NG71 1.3.10).
• Choose a non-ergot dopamine agonist in most cases, with ergot agents reserved for women and men whose symptoms are not controlled by a non-ergot agonist (NICE NG71 1.3.11-1.3.12).
• Consider amantadine if dyskinesia is not adequately controlled (NICE NG71 1.3.13).
• Do not offer anticholinergics in the presence of dyskinesia or fluctuations (NICE NG71 1.3.14).

Approach drawn from NICE NG71 (1.5), the MDS evidence-based medicine review (Seppi 2019) and the AAN practice parameter (Zesiewicz 2010).

• Daytime sleepiness: advise against driving and review dopaminergic medicines; consider modafinil only after a detailed sleep history, review treatment at least every 12 months, and avoid modafinil in pregnancy (NICE NG71 1.5.1-1.5.3).
• REM sleep behaviour disorder: consider clonazepam or melatonin once medication causes have been reviewed (NICE NG71 1.5.5).
• Nocturnal akinesia: consider levodopa or oral dopamine agonists, then rotigotine (NICE NG71 1.5.6-1.5.7).
• Orthostatic hypotension: review antihypertensives, dopaminergics, anticholinergics and antidepressants, then consider midodrine (with monitoring for supine hypertension) and fludrocortisone if needed (NICE NG71 1.5.8-1.5.10).
• Psychosis (hallucinations, delusions): screen for these at every review and after medication changes; treat physical triggers; reduce Parkinson drugs where appropriate; consider quetiapine when there is no cognitive impairment; offer clozapine if standard treatment fails; avoid olanzapine and other antipsychotics, which can worsen motor features (NICE NG71 1.5.12-1.5.20). Lower doses than in other indications are required.
• Dementia: offer a cholinesterase inhibitor for mild to moderate Parkinson disease dementia; consider one for severe disease; consider memantine only if cholinesterase inhibitors are not tolerated or are contra-indicated (NICE NG71 1.5.22-1.5.24); manage dementia per NICE dementia guidance.
• Drooling: speech and language therapy approaches first; then consider glycopyrronium bromide or referral for botulinum toxin A (Xeomin, TA605 for chronic sialorrhoea). Other anticholinergics only if cognitive risk is thought minimal (NICE NG71 1.5.26-1.5.29).
• Depression: manage per NICE guidance for depression in adults with a chronic physical health problem (NICE NG71 1.5.11).
• Constipation, urinary urgency and pain: routine diet and fluid advice, pharmacological options (NICE NG71 1.7.10-1.7.12; Church 2026).

Offer Parkinson-specific physiotherapy and occupational therapy when balance, motor or activities-of-daily-living problems occur; consider earlier physiotherapy, occupational and speech therapy referral; involve Parkinson nurse specialists; encourage physical activity, protein redistribution without reducing total protein, and vitamin D supplementation; do not use creatine or over-the-counter supplements without professional advice (NICE NG71 1.7.1-1.7.15).

• Offer best medical therapy, including intermittent apomorphine injection or continuous subcutaneous apomorphine infusion.
• Do not offer deep brain stimulation if symptoms are controlled by best medical therapy; consider deep brain stimulation when they are not (NICE NG71 1.8.2-1.8.3). ^[1]
• Foslevodopa-foscarbidopa is an option under NICE TA934 (2023) for advanced levodopa-responsive disease with severe motor fluctuations or dyskinesia when other medicines are not enough and apomorphine or deep brain stimulation are unsuitable or no longer work (NICE NG71 1.8.4).
• Deep brain stimulation (usually targeting the thalamus, globus pallidus or subthalamic nucleus) reduces tremor, stiffness and slowness; patients may need much less levodopa afterwards, but like all treatments it is non-curative (Church 2026).

Offer opportunities to discuss prognosis, medicine side effects, advance care planning (ADRT, DNACPR, lasting power of attorney) and end of life; consider referral to palliative care at any stage (NICE NG71 1.9.1-1.9.4).

NICE advises not to use vitamin E, co-enzyme Q10, dopamine agonists or MAO-B inhibitors as neuroprotective therapy except in trials, and no agent is currently proven to slow progression. Only rehabilitation, exercise, fall prevention and treatment of non-motor problems can be offered as routine disease-modifying lifestyle care.

• Motor complications of levodopa (Church 2026): wearing-off (symptoms return before the next dose), unpredictable ON-OFF fluctuations, and peak-dose dyskinesia (choreic or dystonic involuntary movements at peak drug effect). These typically appear within 5 to 10 years of starting levodopa in about 80 per cent of patients. ^[2]
• Levodopa-induced dyskinesia is linked to higher doses and longer exposure; extended-release formulations, amantadine (including extended-release Gocovri) and infusion therapy can help (Church 2026; NICE NG71 1.3.13).
• Non-motor and disease complications: dysphagia and aspiration, falls and fractures, freezing of gait, autonomic failure, sleep disturbance, depression, psychosis, dementia, chronic pain, weight loss.

Parkinson disease is progressive and incurable at present. The rate of progression varies greatly between individuals. Early on the disease is driven by dopaminergic motor disability; later the problems are falls, dysphagia, cognitive and psychiatric decline and loss of independence. Death usually results from the consequences of immobility and aspiration, or from comorbidity, rather than from Parkinson disease itself. With specialist multidisciplinary care, dopaminergic control, exercise and early management of non-motor symptoms, quality of life can be maintained for many years. Mechanistic drug-induced cases usually recover (see Drug-induced parkinsonism).

No drug or test has been shown to prevent or screen for Parkinson disease. NICE NG71 recommends vitamin D supplementation, physiotherapy and exercise, fall precautions and review of bone health, and adherence to neuroprotective rules (no vitamin E, co-enzyme Q10, dopamine agonists or MAO-B inhibitors outside trials). Adequate protein and avoidance of dietary supplements are also advised. Routine population screening is not recommended; active case-finding through recognition of motor clues and prompt referral is the practical "prevention" of disability. Risk factors such as pesticide exposure justify occupational hygiene rather than drug prevention.

Drug-induced parkinsonism (DIP) is an often reversible syndrome of bradykinesia, rigidity and tremor produced by drugs. It is estimated to account for roughly 15 to 20 per cent of parkinsonian cases, can mimic Parkinson disease clinically and on examination, and remains underdiagnosed because it sits at the interface of different specialties (De Faria Sousa and Espinosa 2025). ^[3]

• D2 receptor blockade: typical and atypical antipsychotics, anti-emetics (metoclopramide, prochlorperazine). Risk rises with dose.
• VMAT2 inhibition/depletion: reserpine, tetrabenazine, deutetrabenazine, herbal Rauwolfia serpentina products.
• Mitochondrial/metabolic toxicity: valproate, cyclosporine, lithium (recovery may be incomplete).
• Calcium channel and metal-related: flunarizine, cinnarizine; manganese and iron overload.
• Polypharmacy can produce a cumulative DIP effect even when individual drugs are low risk.

• Symmetric bradykinesia and rigidity exceeding tremor; tremor when present is mild or postural rather than a resting pill-rolling tremor.
• Subacute onset weeks to months after starting or raising the drug.
• Women and adults over 65 are disproportionately affected, and psychiatric and gastrointestinal populations are most at risk.
• Absence of prodromal non-motor features (anosmia, constipation, REM sleep behaviour disorder, autonomic dysfunction) should raise suspicion.
• A French series reclassified 26 per cent of presumed Parkinson disease patients as DIP after careful medication review (De Faria Sousa and Espinosa 2025). ^[3]
• Imaging: DAT-SPECT shows preserved, symmetric striatal uptake, unlike the asymmetric reduction in Parkinson disease; cardiac MIBG scintigraphy and olfaction are typically normal in DIP (De Faria Sousa and Espinosa 2025).

• Withdraw or substitute the offending drug, and document avoidance to prevent re-exposure. An estimated 85 to 90 per cent of patients recover completely, usually within 6 to 12 months (median about 6 months); around 15 per cent have persistent symptoms beyond 12 months (De Faria Sousa and Espinosa 2025). ^[3]
• Taper psychiatric drugs gradually to avoid withdrawal. If antipsychotic treatment is still required, prefer low-D2-affinity agents such as quetiapine or clozapine; avoid olanzapine and typical antipsychotics. Replace metoclopramide with domperidone, which crosses the blood-brain barrier poorly, when an anti-emetic is needed (De Faria Sousa and Espinosa 2025; NICE NG71 1.5.19-1.5.20).
• Symptomatic support with amantadine, anticholinergics or physiotherapy can help. Levodopa gives little or no benefit in pure DIP, so a clear response should prompt reassessment for coexisting neurodegeneration (De Faria Sousa and Espinosa 2025).
• Patients and prescribers need education about re-exposure, and medicines reconciliation in high-risk populations.

• Pregnancy: modafinil is contraindicated in pregnancy or when pregnancy is planned (NICE NG71 safety advice). Otherwise care of pregnant patients with Parkinson disease is individual and multidisciplinary; in this material no pregnancy-specific dosing rule beyond that caution is provided (NICE NG71).
• Children: Parkinson disease is rare. Early-onset disease often has a genetic basis and should prompt genetic counselling and specialist review (Church 2026).
• Older adults: polypharmacy and comorbidity are higher, and anticholinergics carry greater cognitive risk; DIP is more common and non-motor problems dominate (NICE NG71; De Faria Sousa and Espinosa 2025). NICE also advises vitamin D supplementation, physiotherapy and falls prevention in older patients.
• Low-resource settings: where DaTSCAN or functional neuro-imaging are unavailable, diagnosis rests on the clinical skills of a trained specialist; stopping the offending drug, securing a reliable levodopa supply, physiotherapy, carer education and simple bedside checks such as lying and standing blood pressure become disproportionately important.

• Parkinson disease is a progressive synucleinopathy with loss of nigrostriatal dopamine neurons; clinical signs usually appear after more than half the relevant neurons are lost.
• Idiopathic Parkinson disease is one cause of parkinsonism; always consider drugs, vascular disease, atypical syndromes and essential tremor.
• The core motor picture is bradykinesia with rigidity or a resting tremor, usually asymmetric early; postural instability comes later.
• Non-motor features (hyposmia, constipation, REM sleep behaviour disorder, depression, pain, autonomic failure and later dementia) often precede motor diagnosis and dominate morbidity.
• Diagnosis is clinical against UK Brain Bank or MDS criteria; imaging is used to exclude or differentiate rather than to diagnose Parkinson disease (NICE NG71).
• DaTSCAN is considered only when essential tremor and parkinsonism cannot be distinguished clinically; PET, structural MRI, volumetry, spectroscopy, acute challenge tests and smell testing are not used to diagnose PD (NICE NG71).
• Levodopa is the most effective symptomatic drug; dopamine agonists and MAO-B inhibitors are alternatives in earlier or less disabling disease.
• Ergot dopamine agonists are not first-line; non-ergot agents are preferred; anticholinergics are avoided once dyskinesia or fluctuations appear.
• Motor complications (wearing-off, ON-OFF and peak-dose dyskinesia) typically appear within 5 to 10 years in about 80 per cent of patients on levodopa.
• Deep brain stimulation is considered only when symptoms are not adequately controlled by best medical therapy.
• No drug is proven to slow Parkinson disease: NICE advises against using vitamin E, co-enzyme Q10, dopamine agonists or MAO-B inhibitors as neuroprotection outside trials.
• Drug-induced parkinsonism is usually reversible once the drug is withdrawn; most recover in 6 to 12 months, and up to 85 to 90 per cent recover fully.
• Review the diagnosis every 6 to 12 months and involve physiotherapy, occupational therapy, speech and language therapy and Parkinson nurse specialists from the outset (NICE NG71).

• Essential tremor
• Multiple system atrophy
• Progressive supranuclear palsy
• Corticobasal syndrome
• Dementia with Lewy bodies
• Drug-induced movement disorders
• Neuroleptic malignant syndrome
• Dementia
• Autonomic neuropathy
• Depression in chronic physical illness