Table of Contents Clinical features tetradDifferential diagnosis of Parkinsonism Investigation Management PharmacologicalNon-pharmacologicalTest yourself Learn the focussed examination too…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 RigidityLead pipe rigidity, cogwheel rigidity, festinant gaitTremorResting, pill-rollingBradykinesiaSlow shuffling gait, flexed trunk, slow monotonous speech, expressionless face, reduced blink rate, micrographiaPostural instabilityFalls 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 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? Oops! This section is restricted to members. Which medications can cause parkinsonism? Oops! This section is restricted to members. What are the clinical features of Wilson’s disease? Oops! This section is restricted to members.