Decision support only — not a substitute for NICE NG71, eTG, or your neurology/movement-disorder team. Diagnosis is clinical (MDS criteria) and should be reviewed for red flags over time. The two things that most often go wrong in hospital: dopaminergic doses given late or stopped, and dopamine-blocking drugs prescribed. Verify all doses.
1 Motor treatment — initiate, then chase the complications
Initiationlevodopa is most effective
Motor symptoms affecting quality of life.
Levodopa (with carbidopa/benserazide) first-line PD MED. DA agonist or MAO-B if QoL not yet affected. Don't delay levodopa out of dyskinesia fear LEAP.
Wearing-offend-of-dose
Benefit fades before the next dose.
Fractionate levodopa; add a COMT inhibitor (entacapone, opicapone), MAO-B inhibitor, or non-ergot dopamine agonist.
Dyskinesiapeak-dose
Involuntary movements at peak levodopa effect.
Reduce the per-dose levodopa, smooth delivery, add amantadine for troublesome dyskinesia.
Sudden "off" episodeson-demand rescue
Intermittent, disabling off periods despite an optimised oral schedule.
Fast-acting rescue: inhaled levodopa, sublingual or SC apomorphine. Frequent reliance signals the need for a continuous/advanced therapy.
Advanced therapiesrefractory fluctuations
Disabling fluctuations despite optimised oral therapy (~10%/yr become eligible).
DBS (STN/GPi) EARLYSTIM, levodopa-carbidopa intestinal gel, apomorphine/foslevodopa infusion, or MR-guided focused ultrasound lesioning — via a movement-disorder service.
Levodopa gives the best quality of life in early PD PD MED — the old "levodopa-sparing to avoid dyskinesia" instinct is outdated; dyskinesia tracks disease duration and dose, not merely when you start. Use non-ergot dopamine agonists (ergot agents cause cardiac/pulmonary fibrosis). Counsel everyone on impulse-control disorders before starting any dopaminergic. No therapy is disease-modifying yet — regular exercise is the closest thing we have.
2 Diagnose — and exclude the mimics
The clinical diagnosis
- CoreBradykinesia + rest tremor and/or rigidity (MDS criteria); typically asymmetric.
- SupportClear, sustained levodopa response; levodopa-induced dyskinesia.
- ProdromeREM sleep behaviour disorder, hyposmia, constipation, depression — precede motor signs by years.
Red flags for atypical
- GeneralEarly falls, rapid progression, poor levodopa response → not PD.
- Point toEarly autonomic failure → MSA; early dementia + visual hallucinations → DLB; vertical gaze palsy → PSP; cortical signs → CBD.
Don't be fooled
- Drug-inducedReview the med list — dopamine blockers (antipsychotics, metoclopramide, prochlorperazine) are the commonest reversible mimic.
- DaT scanSeparates degenerative parkinsonism from essential tremor / drug-induced — it does NOT distinguish PD from atypical.
3 Non-motor symptoms — they drive quality of life
Neuropsychiatric
- DementiaCommon; rivastigmine (cholinesterase inhibitor).
- PsychosisReduce/simplify dopaminergics first; if needed quetiapine or clozapine (pimavanserin where available). Never typical antipsychotics or most atypicals.
- MoodDepression & anxiety are common and under-treated — SSRI/SNRI.
Autonomic & sleep
- Ortho BPNon-pharm first; then fludrocortisone or midodrine.
- RBDMelatonin or clonazepam; protect the bed environment.
- Sleep attacksSudden-onset sleep & daytime somnolence with dopaminergics (esp. agonists) — warn about driving.
- GI/GUConstipation, urinary urgency, sialorrhoea, dysphagia — treat actively.
4 The safety traps — this is what gets tested & missed
Never stop abruptly
- RiskAbrupt withdrawal → acute akinesia / NMS-like Parkinson-hyperpyrexia. No "drug holidays."
- In hospitalGive doses on the patient's home schedule — "get it on time," allow self-medication. Ward drug rounds are too slow.
- NBMIf swallowing is unsafe, use a rotigotine patch or NG — don't just omit.
- ProteinErratic response? Take levodopa 30–60 min before meals — dietary amino acids compete for absorption.
Avoid dopamine blockers
- NeverMetoclopramide, prochlorperazine, haloperidol and most antipsychotics — they worsen parkinsonism.
- NauseaUse domperidone (peripheral) or ondansetron.
Impulse control disorders
- AskGambling, hypersexuality, shopping, binge eating — in ~14–17%, mostly with dopamine agonists.
- HiddenPatients conceal them — ask the patient and family directly; warn before starting.
- ManageReduce/switch the agonist — but taper (withdrawal syndrome).
5 The whole patient
Multidisciplinary care
- ExerciseA genuine intervention — regular exercise & physiotherapy improve symptoms and function, not just adjuncts.
- TeamPD nurse specialist, OT, speech (LSVT for voice; swallow/aspiration), dietitian.
- FallsAddress postural instability, orthostasis, and home hazards proactively.
Plan ahead
- CarersSupport carers; the non-motor burden falls heavily on them.
- ACPAdvance care planning — PD is progressive; revisit goals over time.
- ReferMovement-disorder service for diagnostic doubt, refractory fluctuations, or advanced-therapy assessment.
Sources.
NICE NG71 — Parkinson's disease in adults (levodopa first-line where motor symptoms affect QoL; non-ergot agonists; never withdraw antiparkinsonian drugs abruptly / no drug holidays; on-time dosing in hospital; counsel re impulse-control disorders, sleepiness, psychosis). MDS clinical diagnostic criteria for PD (2015). eTG (neurology).
Key trials: PD MED (levodopa superior QoL vs levodopa-sparing in early PD); LEAP (early vs delayed levodopa — no disease-modifying effect, no harm in treating); EARLYSTIM (DBS in earlier motor fluctuations).
Caveats: the PD-vs-atypical distinction evolves over follow-up — review the diagnosis. Advanced therapies and several agents are specialist-/PBS-governed in Australia — confirm criteria. Antiemetic and antipsychotic choice is constrained by the dopamine-blocking rule above. Verify all doses. Companion to the neuro set (stroke, seizures, migraine).