Parkinson`s Disease
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Transcript Parkinson`s Disease
Parkinson’s 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 GP’s 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
Alzheimer’s 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
Parkinson’s Disease Society (Scottish
Office)
Forsyth House, Lomond Court, Castle Business
Park
Stirling FK9 4TU
Tel: 01786 433811 • Helpline: 0808 800 0303
Email: [email protected]
Website: www.parkinsons.org.uk/scotland
Younger Parkinson’s Network
Tel: 01656 663 284
E-mail: [email protected]
Website: www.yap-web.net