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Parkinsons Disease

Why I Chose This Subject


Common neurodegenerative disorder
120-230/100 000 in Scotland Expected increase of 25-30% in next 25 yrs

Complex condition which changes with time Huge social impact Uncertainty amongst GPs re prescribing New SIGN guideline this year

Clinical Background
PD-syndrome consisting of bradykinesia plus at least one of rigidity, resting tremor and postural disorder Parkinsonism-broader term but could be different aetiology from PD Average time from diagnosis to death is 13 years

Pathophysiology
Motor system-fine balance of inhibitory and excitatory inputs of basal ganglia and cerebellum Cerebellar output is excitatory, basal ganglia is inhibitory

Pathophysiology
Apoptosis of dopaminergic neurons in substantia nigra-leads to decrease in inhibition Disruption of signals to motor cortex via thalamus Smooth, coordinated movement is lost

Diagnosis Is Difficult
As is progressive disorder-can be hard in initial stages to diagnose accurately Poor specificity-advise pt & family this Recommendation that diagnosis should be made by a hospital clinician in SIGN Also useful way of getting MDT involved

Differential Diagnosis
Progressive supranuclear palsy Multi-system atrophy Alzheimers disease Lewy body dementia

Clues in Differentiating
Up to 20% of those with PD have one relative affected 30-50% have depressive symptoms 17% hallucinate 80% have ANOSMIA-may precede onset of PD

Investigations
Routine use of imaging not recommended Functional imaging most useful where there is uncertainty SPECT cheapest Can potentially detect very early disease as you can lose up to ~50% of dopamine receptors before showing signs of PD

Drug therapy
Does not slow or prevent disease progression Improves quality of life 5-10% respond poorly to all medications Trying to stimulate the dopaminergic system and control the resulting excitation in cholinergic pathways

Levodopa
Available for ~40 years Given with Dopa-decarboxylase inhibitor Co-beneldopa (Madopar) or Co-careldopa (Sinemet) Often get disabling dyskinesias at about 8 years of use Therefore often kept in reserve, especially in younger patients

Levodopa
Helps bradykinesia and rigidity (not really tremor) Small dose increments every few days 6-18 months to see improvement Nausea/flushing/sweating/neuropathy On-off effect End of dose deterioration

Dopamine Agonists
Ropinorole, Pramipexole, Pergolide Bromocriptine/Cabergoline now avoided due to cardiac valvulopathy and pleural, pericardial and retroperitoneal fibrosis Again-incremental increases Similar s/e profile, less motor complications but less improvement

Dopamine Agonists
If you initiate this you must tell patient about impulse control disorders and excessive daytime somnolence Hypotension particularly in first few days of treatment Good evidence in advanced PD to improve off time-transdermal Rotigotine Amantadine-weak dopamine agonist

However
Increasing Dopamine Agonists often worsens hallucinations
Patient preference

Other Treatments
COMT inhibitors
Entacapone provide some benefit in reducing off time

MAO-B inhibitors
Buccal selegiline or rasagiline can help motor complications (less commonly used)

Severe PD-can admit for subcutaneous Apomorphine infusion New treatments-dopamine pump if others fail

Antimuscarinics
Orphenadrine-helps drooling Often drooling is more unpleasant for family & they are delighted if you can improve this Procyclidine Best in drug-induced Parkinsonism s/e control

Other Features to Be Aware of


Depression-Citalopram (or Amitriptyline) Dementia in ~30% with late disease
Treat as per dementia guideline

Psychosis-low dose Clozapine or Quetiapine if monitoring impractical

Contacts
Parkinsons Disease Society (Scottish Office)
Forsyth House, Lomond Court, Castle Business Park Stirling FK9 4TU Tel: 01786 433811 Helpline: 0808 800 0303 Email: pds.scotland@parkinsons.org.uk Website: www.parkinsons.org.uk/scotland

Younger Parkinsons Network


Tel: 01656 663 284 E-mail: alunmorgan@btinternet.com Website: www.yap-web.net