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.
- Non-motor features can precede movement symptoms: anosmia, REM sleep behaviour disorder, constipation, depression and autonomic symptoms increase suspicion but are not independently diagnostic.
- NICE advises rapid referral, before starting treatment, to a specialist with expertise in differential diagnosis when Parkinson disease is suspected.
- Early recurrent falls or vertical gaze palsy suggest PSP; severe early autonomic failure or stridor suggests MSA; marked apraxia, cortical sensory loss or alien-limb phenomena suggest corticobasal syndrome.
- Dopamine-blocking antipsychotics and antiemetics commonly cause or worsen parkinsonism. The syndrome is often symmetrical, but asymmetry does not completely exclude a drug contribution.
- Vascular parkinsonism more often affects gait and lower limbs with cerebrovascular disease, while normal-pressure hydrocephalus adds cognitive and urinary features and ventriculomegaly.
- Structural MRI is used for atypical features or alternative pathology, not to prove routine Parkinson disease; dopamine-transporter SPECT helps when essential tremor and degenerative parkinsonism remain clinically indistinguishable.
- Review the diagnosis regularly, generally every six to twelve months, and reopen it when treatment response, progression or new signs no longer fit Parkinson disease.
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.
- Refer rapidly and untreated to a neurologist or geriatrician with diagnostic expertise, providing the chronology, examination, medicines, falls and functional impact rather than beginning a trial in primary care.
Key medicines
No pre-referral dopaminergic trialDo not initiate a diagnostic test dose before specialist assessment when Parkinson disease is newly suspected.This does not mean withholding established time-critical Parkinson medicines from a diagnosed patient; deterioration or swallowing failure needs urgent medicines reconciliation.
Dopamine-blocking medicine reviewReduce or substitute only through the relevant psychiatric, medical or pharmacy plan; never use abrupt generic withdrawal.Antipsychotic relapse, nausea control and withdrawal risks matter. If antipsychotic therapy remains essential, specialist selection of a lower motor-risk option is required.