16 Questions
What is the primary reason L-dopa is effective in treating Parkinson's disease?
It crosses the blood-brain barrier and is converted to dopamine
Which of the following is a potential neuroprotective effect of dopamine agonists?
May be neuroprotective
What is the primary mechanism of action of COMT inhibitors?
Blocking the breakdown of L-dopa in peripheral tissues
Which of the following antiparkinson agents is an antiviral agent that was discovered to have antiparkinson effects by chance?
Amantadine
What is the primary purpose of combining L-dopa with carbidopa?
To increase the absorption of L-dopa
What is the primary mechanism of action of MAO-B inhibitors?
Inhibiting monoamine oxidase type B
Which of the following is a potential problem with anticholinergic agents?
All of the above
What is the primary goal of coordinating rehabilitation sessions with drug therapy?
To optimize treatment timing
What is the estimated percentage of the population above 60 years that is affected by Parkinson's disease?
1%
What is the primary problem that leads to Parkinsonism?
Degeneration of dopamine-secreting neurons
Why is direct administration of dopamine ineffective in treating Parkinson's disease?
Dopamine cannot cross the blood-brain barrier
What is the purpose of carbidopa in L-DOPA therapy?
To prevent the premature conversion of L-DOPA to dopamine
What is the term for the decreased response to L-DOPA towards the end of the dose cycle?
End of dose akinesia
What is the purpose of inhaled L-DOPA (Inbrija)?
To treat 'off' episodes in patients already on L-DOPA therapy
What is a possible reason for the diminished response to L-DOPA therapy in long-term use?
Disease progression
What is the term for the fluctuations in response to L-DOPA within the dose cycle?
On-off phenomenon
Study Notes
Parkinson Disease
- Neurodegenerative disorder affecting 1% of the population over 60 years
- Classical symptoms include rigidity, resting tremor, bradykinesia, and postural instability
Neurological Basis of Parkinsonism
- Degeneration of dopamine-secreting neurons
- Decreased dopamine results in increased acetylcholine
- Other affected neurotransmitters include GABA, glutamate, 5-HT, and norepinephrine
Dopamine Replacement: Rationale for Levodopa Therapy
- Attempt to increase dopamine content in basal ganglia
- Levodopa (L-DOPA) is used as a precursor to dopamine, as it can cross the blood-brain barrier
- L-DOPA is converted to dopamine in the brain
Use of Carbidopa
- Carbidopa inhibits dopa decarboxylase, preventing premature conversion of L-DOPA to dopamine
- L-DOPA and carbidopa are often contained in the same pill (e.g. Sinemet)
Problems with L-DOPA Therapy
- Side effects: GI irritation, hypotension, psychotropic and behavioral effects, dyskinesias, and "freezing" of gait
- Fluctuations in response: end-of-dose akinesia, on-off phenomenon
- Diminished response in long-term use: benefits may be lost, or dyskinesias become intolerable, after 4 to 5 years
Inhaled L-DOPA
- Inhaled form of L-DOPA available (Inbrija)
- Used to treat "off" episodes in patients already taking levodopa/carbidopa
Other Parkinson Drugs
Dopamine Agonists
- Act like dopamine, directly stimulating dopamine receptors
- Longer t1/2, more stable responses
- Can be used as initial treatment in early PD
- May be neuroprotective
- Common agents: apomorphine, bromocriptine, cabergoline, pramipexole, ropinerole, rotigotine
- Problems: nausea, vomiting, confusion, hallucinations, postural hypotension, increased dyskinesia
COMT Inhibitors
- Inhibit catechol-O-methyltransferase (COMT) enzyme, allowing more L-DOPA to reach the brain
- May decrease fluctuations, increase "on time"
- Two specific agents: tolcapone, entacapone
- Can be combined with L-DOPA and carbidopa (Stalevo)
- Problems: GI distress, orthostatic hypotension, increased dyskinesia
Anticholinergic Agents
- Decrease acetylcholine influence, may help decrease rigidity and tremor
- Common agents: benztropine mesylate, biperiden, diphenhydramine, trihexyphenidyl
- Use limited by side effects
MAO-B Inhibitors
- Inhibit monoamine oxidase type B, prolonging dopamine effects in the brain
- Agents: selegiline, rasagiline
- Combined with L-DOPA to increase and prolong effects
- Problems: no major concerns
- Possible neuroprotective effects
Amantadine
- Blocks NMDA receptor in brain, decreasing influence of excitatory amino acids (glutamate)
- Decreased chance of dyskinesias
- Problems: orthostatic hypotension, psychotropic effects, skin discoloration
Anti-Parkinson Drugs: Impact of Rehabilitation
- Coordinate rehab sessions with drug therapy
- Optimal treatment time: 30 to 60 minutes after meds
- Recognize synergistic effects of physical rehab and drug therapy
This quiz covers the basics of Parkinson's disease, its symptoms, and the neurological basis of parkinsonism, including the role of dopamine and other neurotransmitters.
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