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13 Cards in this Set

  • Front
  • Back
Pathophysiology
Loss of SUBSANTIA NIGRA NEURONS
Loss of dopaegernic projections to the striatum
Environmental Factors
Pesticides
Toxins: MPTP
Well Water
Head Trauma
Smoking/coffee=protection
Genetic factors
Genetic component more obvious with early onset cases
Most likely a complex interaction with many other genes
Basal Ganglia
collection of nuclei in forebrain that make connections with motor cortex and the midbrain
Pathology of Parkinson's
Loss of neurons in the NIGRO STRIATAL PATHWAY
----Substantia niagra has dopamine containing neurons
----Project to the Basal Ganglia

Antipsychotics
Pathophysiology
Loss of neurons in the substantia nigra
Loss of striatal dopamine
Pathology of remaining neurons
--Lewy Bodies
--Mitochondrial Dysfunction
Neuropharmalogical Treatment
1. Increase activity in dopamine synapses
2. suppress activity in structures with heightened activity (symptom oriented!)
*Direct DA agonists
*ACh antagonists
*glutamate antagonists
*MAO inhibitors
L-DOPA
DA precursor
Mechanism of action:
-converted into DA in the brain
-Released by remaining neurons
DOPAMINE DOES NOT CROSS THE BBB
Problems with L-DOPA treatment
Converted into DA rapidly in the brain, so high doses are required, and high doses cause nausea
Long terms effects: dyskenesia (involuntary movement) and "on/off periods"
Carbidopa
Delays the conversion of LDOPA
DOES NOT CROSS BBB
Lower doses of LDOPA required, because more reaches the brain
Other Treatments
1. MAO-B Inhibitors: boost effects of ldopa, controls metabolism in the brain,
2. COMT inhibitors: prolong symptom relief by postponing metabolism of L-Dopa
GDNF
has been shown to reduce loss of DA neurons in rats
Protect neurons/Regenerate them?