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Old 07-09-2017, 03:43 PM
johnt johnt is offline
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Join Date: Apr 2009
Location: Stafford, UK
Posts: 1,059
15 yr Member
johnt johnt is offline
Senior Member
 
Join Date: Apr 2009
Location: Stafford, UK
Posts: 1,059
15 yr Member
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If you take levodopa on its own, much of it will be metabolised by DCC into dopamine before it gets to the brain. Dopamine cannot cross the BBB, so unless it is created in the brain it is wasted. Any dopamine formed outside the brain has the side-effect of causing nausea.

If a DCC inhibitor is used, less of the levodopa is metabolised outside of the brain, thus decreasing the nausea felt. Furthermore, if a DCC inhibitor is used, more of the levodopa gets into the brain, where it an be metabolised into dopamine. I don't think that it is quite right to say that the inhibitor causes dyskinesia, rather the effect of the inhibitor is to increase levodopa levels, and hence dopamine levels, in the brain. If these become too high, it leads to levodopa induced dyskinesia.

The question about mucuna pruriens is why does it for a given level of levodopa appear to cause less nausea?

John
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Born 1955. Diagnosed PD 2005.
Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg
Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg
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