Part 6: Parkinson Disease Flashcards
Parkinson Disease
Neurodegenerative Disorder
1% of the population >60
Classic Parkinson Symptoms
Rigidity
Resting Tremor
Bradykinesia
Postural Instability
Parkinsonism primary cause
Degeneration of dopaminergic neurons in substantia nigra
Parkinsonism Neurological basis
Decreased dopamine results in increased ACh
Other neurotransmitters also effected
Dopamine Synthesis
Dopamine cant cross the blood brain barrier, Dopa can
Give L-Dopa to treat
Tyrosine–>Dopa–> Dopamine
Dopamine replacement: Levodopa
Attempt to increase dopamine content in basal ganglia
Levodopa (L-dopa) has dramatic effects in early stages
Carbidopa
L-dopa will be converted to dopamine before brain
Carbidopa inhibits dopa decarboxylase; prevents premature conversion
L-dopa side effects
GI irritation Hypotension Psychotropic, behavioral effects Dyskinesias Freezing of gait
End-of-dose akinesia
Decreased response toward end of dose cycle
May need sustained release
On-off phenomenon
Response fluctuates within the dose cycle
Long term L-dopa use
Benefits lost after 4-5 years
Tolerance or disease progression
Other antiparkinson medications
Dopamine agonists COMT inhibitors Anticholinergic agents MAO-B inhibitors Amantadine
Dopamine agonist problems
Nausea/vomiting
Confusion, Hallucinations
Postural Hypotension
Increased dyskinesia
COMT inhibitors
Allow more L-dopa to reach the brain
May decrease fluctuations, increase “on” time
Can be combined with L-dopa and carbidopa
Catechol-O-Methyltransferase
Enzyme that breaks down L-dopa in peripheral tissues
