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Parkinson’s disease focussed examination covered here !
Parkinson’s disease is caused by degeneration of the dopaminergic neurons in the substantia nigra (part of the basal ganglia). This results in rigidity, tremor, bradykinesia and postural instability.
Clinical features tetrad
Rigidity Lead pipe rigidity, cogwheel rigidity, festinant gait Tremor Resting, pill-rolling Bradykinesia Slow shuffling gait, flexed trunk, slow monotonous speech, expressionless face, reduced blink rate, micrographia Postural instability Falls
Differential diagnosis of Parkinsonism
Parkinson’s disease
Vascular parkinsonism
Parkinson-plus syndromes
Multi-system atrophy (cerebellar signs, autonomic problems)
Progressive supranuclear palsy (vertical gaze palsy, axial rigidity)
Corticobulbar degeneration (apraxia, dementia, aphasia)
Lewy body dementia (dementia with some parkinsonian features)
Other causes
Iatrogenic, e.g. secondary medications
Wilson’s disease
Communicating hydrocephalus
Supratentorial tumours
Investigation
Parkinson’s disease is a clinical diagnosis – however, investigations may be required if the diagnosis is unclear:
Structural MRI: may be used to exclude some other causes of parkinsonism
Single-photon emission CT: may be used to differentiate Parkinson’s disease from other causes of tremor
Serum caeruloplasmin or 24-hour urinary copper excretion: to exclude Wilson’s disease
A patient presents to ED with chest pain and this trace. What would you do?
Interpretation management
Covered in OSCE Stations
Management
Pharmacological
Low potency:
Monoamine oxidase B inhibitors (e.g. rasagiline, selegiline)
For mild symptoms (no functional disability)
Moderate potency:
Dopamine agonists (e.g. ropinirole, pramipexole)
For moderate symptoms (most at diagnosis)
Take several weeks to work
Notable side effects: sleep attacks, impulse control disorders
High potency:
Levodopa (e.g. Madopar, Sinemet)
For severe symptoms/elderly
Given with peripheral decarboxylase inhibitor (e.g. carbidopa) to prevent peripheral conversion to dopamine
Notable side effects: ‘ on-off’/’wearing off’ phenomenon (increased immobility before the next dose is due after prolonged levodopa use); dyskinesias
Adjuncts to levodopa:
Dopamine agonists – reduce motor complications and levodopa dosage needs
Monoamine oxidase B inhibitors – reduce ‘off time’
COMT inhibitors (e.g. entacapone) – reduce ‘off time’
Apomorphine (subcutaneous) – for rescue therapy during ‘off time’
Amantadine (glutamate antagonist) – for levodopa-induced dyskinesias
Non-pharmacological
Multidisciplinary approach: input from neurologist, physiotherapist, occupational therapist, specialist nurse, GP, speech and language therapist
Supervised exercise
Home modifications
Consider associated conditions: dementia, depression, psychosis, sleep disturbance
Deep brain stimulation: considered in some refractory cases
Reference: NICE ‘NG71 Parkinson’s disease in adults’ 2017
Test yourself
What is the classic speed of the pill-rolling tremor in Parkinson’s disease?
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Which medications can cause parkinsonism?
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What are the clinical features of Wilson’s disease?
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