Synopsis
Identify parkinsonism clinically, refer suspected Parkinson disease untreated for expert confirmation and detect the temporal, autonomic, ocular, cortical and drug-related clues to alternative diagnoses.
- Parkinsonism requires bradykinesia plus rigidity, rest tremor or postural instability not better explained by another disorder; slowness alone is insufficient.
- True bradykinesia is progressive reduction in speed or amplitude during repetitive movement, seen in finger tapping, hand opening, pronation-supination, toe tapping or gait.
- Idiopathic Parkinson disease usually begins asymmetrically and combines limb signs with reduced arm swing, hypomimia, quiet voice and a good sustained levodopa response.
Key red flags
Sudden onset, clear focal deficits or stepwise lower-body gait decline is not typical idiopathic Parkinson disease and should trigger stroke, vascular, toxic, metabolic or structural investigation.
Investigation priorities
Confirm bradykinesia, define accompanying signs and compare the longitudinal pattern with recognised Parkinson and atypical criteria.
Management branches
Tremor, stiffness, slowness, gait or balance features raise possible Parkinson disease.
- Confirm objective bradykinesia, examine tremor and rigidity, observe gait and eye movements, measure standing blood pressure and screen cognition, mood, swallowing, sleep and falls.
- Reconcile prescribed and non-prescribed medicines, plotting dopamine-blocker exposure and symptom onset, and investigate any abrupt, focal or systemic presentation urgently.
Key medicines
No pre-referral dopaminergic trialDo not initiate a diagnostic test dose before specialist assessment when Parkinson disease is newly suspected.
Dopamine-blocking medicine reviewReduce or substitute only through the relevant psychiatric, medical or pharmacy plan; never use abrupt generic withdrawal.