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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Diagnosis requires bradykinesia PLUS at least one of: rest tremor or rigidity
- Rest tremor (4–6 Hz, pill-rolling) is the most recognisable feature but bradykinesia is the cardinal sign
- Levodopa (co-careldopa or co-beneldopa) is the most effective symptomatic treatment
- Dopamine agonists (pramipexole, ropinirole, rotigotine) are first-line alternatives, especially in younger patients — warn about impulse control disorders
- Diagnosis is clinical by a specialist — DaTSCAN can support diagnosis if uncertain
Overview
Parkinson's disease (PD) is a progressive neurodegenerative disorder resulting from loss of dopaminergic neurones in the substantia nigra pars compacta and the presence of Lewy bodies (intraneuronal inclusions of alpha-synuclein). Cardinal motor features are bradykinesia, rigidity, and rest tremor. PD also has important non-motor features including depression, cognitive impairment, REM sleep behaviour disorder, anosmia, constipation, and autonomic dysfunction. It is the second most common neurodegenerative disease after Alzheimer's disease.
Epidemiology
PD affects approximately 145,000 people in the UK with an incidence of ~15 per 100,000 per year. Mean age at diagnosis is ~65 years; it is uncommon under 50 (young-onset PD). Males are 1.5 times more commonly affected. Most cases are idiopathic. Risk factors include advancing age, male sex, family history (LRRK2, GBA gene mutations), pesticide exposure, and well water. Protective factors include smoking and caffeine (epidemiological association). 5–10% of cases have a monogenetic cause.
Clinical Features
Symptoms
Tremor: rest tremor, 4–6 Hz, pill-rolling, unilateral at onset, reduced by voluntary movement
Bradykinesia: slowness of movement, progressive fatiguing and decrement of repetitive movements (e.g. finger tapping)
Rigidity: lead-pipe rigidity, or cogwheel rigidity (superimposed tremor)
Postural instability: late feature — falls risk (not typically early)
Micrographia (small handwriting)
Non-motor: depression, anxiety, REM sleep behaviour disorder, anosmia, constipation, urinary frequency
Cognitive impairment and dementia (develops in ~80% over 20 years)
Signs
Bradykinesia: reduced facial expression (hypomimia/masked facies), reduced blink rate, slow monotonous speech
Asymmetric rest tremor (typically starts unilateral — if bilateral and symmetric from onset, consider alternative diagnosis)
Cogwheel rigidity at wrist/elbow (enhanced by contralateral limb activation)
Shuffling gait with reduced arm swing, festination (involuntary acceleration), freezing
Stooped posture
Postural instability (pull test positive) — late feature
Investigations
First-line
Clinical diagnosis by specialistDiagnosis is clinical — refer to neurologist or geriatrician with expertise in PD per NICE NG71. Bradykinesia + rest tremor or rigidity in an untreated patient
Second-line
DaTSCAN (dopamine transporter SPECT)Shows reduced dopamine transporter uptake in basal ganglia. Useful to distinguish PD from essential tremor or drug-induced parkinsonism
MRI brainNormal in PD — used to exclude structural causes (vascular parkinsonism, NPH, tumour)
Specialist
Genetic testingConsider in young-onset PD (<50 years) — LRRK2, PARK2 (parkin), GBA mutations
Levodopa challengeGood response to levodopa supports diagnosis of PD — poor response suggests atypical parkinsonism (MSA, PSP, CBD)
1
Pharmacological — motor symptoms
- Levodopa (co-careldopa e.g. Sinemet, or co-beneldopa e.g. Madopar) — most effective for motor symptoms. Warn about motor fluctuations with long-term use (wearing off, on-off, dyskinesias)
- Dopamine agonists (pramipexole, ropinirole, rotigotine patch) — less motor complications than levodopa, but less effective. WARN: impulse control disorders (gambling, hypersexuality, binge eating) — occurs in ~17%
- MAO-B inhibitors (rasagiline, selegiline, safinamide) — mild symptomatic benefit, can be used as monotherapy or adjunct
- Choice of initial therapy should be discussed with patient considering symptom control, motor complications, and side effects (NICE NG71)
2
Managing motor complications
- Wearing off: add COMT inhibitor (entacapone), or MAO-B inhibitor, or dopamine agonist; use modified-release levodopa
- Dyskinesias: reduce levodopa dose, add amantadine
- Consider advanced therapies if refractory: deep brain stimulation (STN or GPi), apomorphine infusion, levodopa-carbidopa intestinal gel (LCIG)
3
Non-motor symptom management
- Depression: SSRI or SNRI — avoid SSRIs with MAO-B inhibitors without specialist advice
- Dementia: rivastigmine (cholinesterase inhibitor — only one licensed for PD dementia)
- Psychosis/hallucinations: reduce dopaminergic medication; if persistent, quetiapine (low-dose) or clozapine (specialist only). Do NOT use typical antipsychotics (haloperidol) — worsen PD
- Constipation: macrogol laxatives
- Drooling: glycopyrronium, hyoscine patch, or botulinum toxin
4
Key principles
- Never abruptly withdraw dopaminergic medication (risk of neuroleptic malignant-like syndrome)
- Medications must be given on time when in hospital — delays worsen symptoms and can be dangerous
- DVLA: must inform DVLA at diagnosis. Can usually continue driving if safe to do so
- MDT: PD nurse specialist, physiotherapy, OT, SALT, psychology
Complications
- Motor fluctuations: Wearing off, on-off phenomenon, peak-dose dyskinesias — develop after ~5 years of levodopa in many patients
- Falls: From postural instability, freezing of gait, orthostatic hypotension
- PD dementia: Develops in ~80% over 20 years — treat with rivastigmine
- Impulse control disorders: Gambling, hypersexuality, binge eating — especially with dopamine agonists. Screen at EVERY review
- Psychosis/hallucinations: Visual hallucinations are common — may be drug-related or intrinsic to disease. Do NOT use typical antipsychotics
- Aspiration pneumonia: Leading cause of death in advanced PD — dysphagia from bulbar involvement
- Dopaminergic withdrawal: Abrupt cessation causes parkinsonism-hyperpyrexia syndrome (similar to NMS)
UKMLA Exam Tips
- 1Bradykinesia is the CARDINAL feature — must be present for diagnosis. Tremor alone is not enough
- 2Rest tremor (4–6 Hz, pill-rolling) — improves with action. Intention tremor = cerebellar disease, NOT PD
- 3PD tremor is typically asymmetric and unilateral at onset. Symmetric = consider alternative diagnosis
- 4Dopamine agonists: WARN about impulse control disorders at EVERY consultation — gambling, hypersexuality, binge eating
- 5Do NOT use metoclopramide or haloperidol in PD — they block dopamine receptors and worsen symptoms. Use domperidone for nausea
- 6Never abruptly stop levodopa or dopamine agonists — risk of parkinsonism-hyperpyrexia syndrome
- 7Red flags for atypical parkinsonism (MSA, PSP): early falls, rapid progression, poor levodopa response, early autonomic failure, vertical gaze palsy
practicetest your knowledge on parkinson's diseaseApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — neurology and beyond.
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