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Summary Parkinson's disease

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summary of pathophysiology and treatments

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  • May 16, 2024
  • 6
  • 2023/2024
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Parkinson’s
Pathophysiology of Parkinson’s
 chronic progressive neurodegenerative disease
 loss of dopamine neurons in the nigrostriatal pathway
 50-80% neurons lost before symptoms present
 presence of Lewy bodies in those neurons
o clumps of proteins e.g. alpha synuclein
o this is found primarily in the brain
o these proteins can build up leading to dysfunction
 changes to GABA glutamate pathway may contribute to non-motor and axial
symptoms
o axial: freezing, postural instability etc
Risk factors
 genetic factors
 exposure to neurotoxins
 head injury/brain injury
Motor Symptoms
 bradykinesia: slowness in initiating voluntary movement, or repetitive actions
 hypokinesia: reduced facial expressions, difficulty with fine movements
 tremor
o coarse tremor
o pill rolling tremor
 rigidity
o moves through the nigrostriatal pathway to the nasal ganglia
o to control smooth movements
o damage and death of dopamine neurons in the nigrostriatal pathway will
cause rigidity
Non-Motor Symptoms
 micrographia
o abnormally small, cramped handwriting
 swallowing and speech problems
 drooling
 loss of smell
 excessive sweating
 depression
 memory problems
 sleep disturbance
 constipation
 dizziness and falls
 urinary problems
 dementia
Aims for drug treatments for Parkinson’s
 only started when motor symptoms affect a patient’s ability to function
 aim is to increase dopamine levels in the brain
 treat symptoms only
 not curative or disease modifying (progression not affected)

,  treatments for non-motor symptoms
o symptomatic
o e.g., constipation → laxatives
Drugs used for motor symptoms
BNF!!!!!
levodopa
MAO-B inhibitors
dopamine agonists
COMT inhibitors
amantadine
anticholinergics
Treatment pathway for first-line therapy failure
 disease is progressing
 add a dopamine agonist and levodopa
 then add a COMT inhibitor
 amantadine or antimuscarinic for dyskinesia
 or if really advanced add an advanced therapy
What is levodopa?
 combined with dopa-decarboxylase inhibitor
 always!: CO-CARBEDOPA
 will not do anything if given alone
 most effective treatment
 treats motor symptoms of tremor, bradykinesia and rigidity
MOA levodopa
 also known as L-DOPA
 crosses the blood brain barrier via LAT1 on endothelial cells
 is decarboxylated to form dopamine
 by DOPA decarboxylase
 This supplemental dopamine performs the role that endogenous dopamine cannot
 due to a decrease of natural concentrations and stimulates dopaminergic receptors
Advice for prescribing levodopa
 low dose titrated up to limit side effects of
o postural hypotension
o nausea
o vomiting
o psychiatric effect
 initiate when symptoms interfere with daily activities
 until then use other first line therapies
o due to long term problems of levodopa
o decreased efficacy over time
o causes dyskinesias earlier in the disease (involuntary movements)
o but this is being looked at and not confirmed
 protein can alter its absorption
o so maybe space away from food to increase absorption
o or ask patient to have a low protein diet
What are MAO-B inhibitors?
 selegiline and rasagiline

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