Parkinson Disease — SAQ

Stem

A candidate is asked to manage a classic presentation of Parkinson Disease in an exam setting. Use precise definitions, scores, doses, and decision thresholds.

Core knowledge (model answer backbone)

Parkinson disease (PD) is a progressive neurodegenerative disorder characterised by loss of dopaminergic neurons of the substantia nigra pars compacta, with intracellular alpha-synuclein Lewy bodies. The cardinal motor features are TRAP: resting Tremor, Rigidity, Akinesia/bradykinesia (obligatory), and Postural instability. Diagnosis is clinical (MDS 2015 criteria); investigations exclude mimics. Treatment is symptomatic — levodopa combined with a peripheral decarboxylase inhibitor (carbidopa or benserazide) is the gold-standard and most effective therapy. Dopamine agonists, MAO-B inhibitors, COMT inhibitors and amantadine have defined roles; advanced disease uses apomorphine, levodopa-carbidopa intestinal gel, or deep brain stimulation. Long-term levodopa causes motor fluctuations and dyskinesia. Non-motor symptoms (anosmia, constipation, REM sleep behaviour disorder, depression, dementia, psychosis, dysautonomia) dominate late disease and drive disability. Dopamine-blocking drugs (metoclopramide, prochlorperazine, haloperidol) are contraindicated.

Red flags

• Asymmetric rest tremor plus bradykinesia or rigidity in an older adult - think Parkinson disease; assess with MDS 2015 criteria
• Early falls, vertical gaze palsy, symmetrical onset, early dementia or poor levodopa response - atypical parkinsonism (PSP, MSA, DLB); refer
• Young-onset parkinsonism (under 50) - exclude Wilson disease (ceruloplasmin, urinary copper, Kayser-Fleischer rings); consider genetic causes
• Acute deterioration in a known PD patient - never omit dopaminergic drugs; look for infection, aspiration, dehydration or drug omission

High-yield structure examiners expect

Cover: Overview & Definition, Classification, Epidemiology & Risk Factors, Pathophysiology, Clinical Presentation, Differential Diagnosis.

Key doses / thresholds (from topic teaching)

• under 0.2 g/L), raised 24-hour urinary copper
• despite at least 400 mg/day)
• up to 10 mg/kg/day) for severe rigidity/hyperthermi
• up to 8 mg three times daily**; prolonged-release
• trihexyphenidyl 1 to 2 mg twice daily, up to 6 to 15 mg/day**
• try up to 1000 mg/day but usually disappointing); treat f

Questions

a) Define the condition and give the most important classification or severity framework used in exams. (3 marks)

• Clear one-line definition matching standard teaching.
• Named classification / stages / types with discriminating features.
• One sentence on why classification changes management.

b) Outline pathophysiology in a mechanism chain that explains the main clinical features. (3 marks)

• Initiating insult → intermediate pathway → end-organ effect.
• Link at least two symptoms/signs to mechanism.
• Mention one complication pathway (e.g. shock, perforation, herniation, arrhythmia).

c) List discriminating clinical features and bedside assessment. (3 marks)

• Classic presentation plus one atypical group (elderly, pregnancy, child, immunocompromised).
• Named signs/manoeuvres if relevant.
• What must never be missed on exam/bedside (pregnancy test, airway, glucose, etc.).

d) Investigations with thresholds and one named score if applicable. (3 marks)

• First-line tests and what positive findings mean.
• Gold-standard or definitive investigation when needed.
• Score components reproduced exactly if a named score is standard for this topic.

e) Immediate resuscitation and definitive management with doses where standard. (3 marks)

• ABC / time-critical steps first.
• First-line drug(s) with agent + dose + route (or procedure steps).
• Escalation triggers (theatre, ICU, thrombolysis window, antidote, etc.).
• Disposition and safety-netting.

Marking tips

Full marks require specificity (numbers, names, doses) not generic "give antibiotics/fluids." Regional practice (ICMR / NICE / AHA) may be cited as alternative where relevant.