Parkinson's Disease

Question 1

Aetiologies

Answer 1

• Parkinsonism “shaking palsy”- the clinical syndrome
  
  • mainly drugs, but also toxins / post encephalitis
  • V important to check Drug History
• Parkinson’s Disease
  
  • ​primary degeneration of dopaminergic neurons in the substantia nigra of basal ganglia, leading to reduced dopamine levels
  • idiopathic

Question 2

Epidemiology?

Answer 2

M > F

Question 3

Presentation

Answer 3

Triad of:

• resting tremor
• rigidity
• bradykinesia

Question 4

outline more specifically the presentation

Answer 4

• Resting tremor
  
  • 4-6Hz
  • “pill rolling tremor”
  • worse at rest, improves with voluntary movement
  • worse when pt is distracted
• Rigidity
  
  • cogwheel rigidity
• Bradykinesia
  
  • movements become smaller and slower

Question 5

outline some examples of bradykinesia seen in pts with parkinson’s

Answer 5

• shuffling gait
• handwriting gets smaller
• difficulty initiating movement ie from standing to walking
• reduced facial expression and movement
• difficulty turning around when standing

Question 6

what are some other features that may be seen?

Answer 6

• depression
• memory / cognitive impairment
• sleep disturbance
• postural instability
• anosmia

Question 7

What are Parkinson’s Plus syndromes?

Answer 7

group of neurodegenerative diseases which encompass parkinson’s symptoms, but have additional features that distinguish them from simple PD

Question 8

Outline some Parkinson’s Plus Syndromes

Answer 8

• Multi-sytem atrophy
  
  • degeneration of neurons in multiple systems in the brain
• Dementia with Lewy bodies
  
  • hallucinations
  • delusions
  • disorders of REM sleep
  • fluctuating consciousness
• corticobasal degeneration
• progressive supranuclear palsy

Question 9

how does progressive supranuclear palsy present?

Answer 9

• impaired vertical gaze
• falls

*assessment of cranial nerves in anyone who presents with a fall v important *

Question 10

Diagnosis?

Answer 10

clinical

Question 11

Mx?

Answer 11

• Levodopa
  
  • in combination with peripheral decarboxylase inhibitor
• COMT inhibitor
• Dopamine agonist
• Monoamine Oxidase-B Inhibitor

Question 12

expand on management options, ie action, side effects and example of each subtype

Answer 12

• Levodopa
  
  • in combination with peripheral decarboxylase inhibitor eg Carbidopa / Benserazide
  • most effective at controlling symptoms however becomes less effective over time, so other drugs given first and Levodopa started when these aren’t effective at managing symptoms anymore
• COMT inhibitor
  
  • example: Entacapone
  • given in combination with levodopa + decarboxylase inhibitor
  • action: increases effective duration of levodopa
• Dopamine agonist
  
  • S/E: pul fibrosis
  • example: Bromocryptine
  • not as effective as Levodopa in controlling symptoms
• Monoamine Oxidase-B Inhibitor
  
  • Action: helps to increase levels of dopamine

Question 13

s/e of levodopa

Answer 13

these occur when dose of dopamine is too high–> result in dyskinesias:

• dystonia: excessive muscle contraction
• chorea: involuntary movement that is jerking & random
• athetosis: involuntary twisting, writhing movement

Question 14

Use of Dopamine agonists and MAO-B Inhibitors?

Answer 14

they are given to delay use of levodopa and when symptoms no longer adequately controlled, given with levodopa to reduce dose needed of levodopa to control symptoms

Question 15

Outline the differences between parkinson’s and benign essential tremor in terms of:

• symmetrical / asymmetrical
• frequency
• pattern - with rest & movement
• change with alcohol

Answer 15