Treatment

Question 1

Why isn’t levodopa administered by itself?

Answer 1

It is easily metabolised to dopamine in the periphery which cannot cross the blood brain barrier

Question 2

What is the role of carbidopa?

Answer 2

AADC inhibitor - prevents the metabolism of levodopa

Question 3

Name inhibitors of COMT. Which is effective in both the CNS and PNS?

Answer 3

Talcapone - effective in both

Entacapone

Question 4

How does MOA-B inhibition work?

Answer 4

Reduces the metabolism of dopamine in the CNS = higher dopamine levels in synaptic cleft to bind to the post synaptic neuron

Question 5

How do dopamine receptor agonists work?

Answer 5

They mimic the action of dopamine by binding to the D1 and D2 receptors in the striatum. This means that when dopaminergic neurons deplete, the D1 and D2 receptors are still active.

Example = Pramipexole, rotigotine and ropinirole

Question 6

What is the main side effect that occurs from levodopa treatment? How does it occur?

Answer 6

Levodopa-induced Dyskinesia

As the disease progresses levodopa’a duration of response decreases and it’s therapeutic window (range between max and min effective dose) narrows. This means that dopamine is likely to rise above the therapeutic window which causes maximal antiparkinsonion effects (D1 and D2 pathways are over stimulated = higher activity through D1 and reduced activity through D2) leading to too much movement i.e dyskinesia