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06-18-2017, 02:23 AM | #1 | ||
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Boxtel et al. write [1]:
"Classically, the worsening of clinical signs in patients given very low dose antiparkinsonian drugs is explained by a preferential stimulation of presynaptic dopaminergic receptors ... limiting release of endogenous dopamine." This observation complicates the prescribing process: a baseline result, followed by a negative result is not, in itself, adequate to conclude that an antiparkinson medication is not efficacious. It may also explain why I perform fairly well in the morning before taking the first dose of the day, but get worse briefly while the drug's absorbed up to working levels. I often go 12 hours, 8 half-lives of levodopa, overnight between doses, so the drug has almost been washed out. It also suggests that too much exogenous levodopa may lead to a decrease in endogenous dopamine production. This would favour the "runway" hypothesis of dosing, rather than the, I think, currently favoured "use or lose" hypothesis. Reference: [1] "Drug Benefits and Risks: International Textbook of Clinical Pharmacology" edited by C.J. van Boxtel, B. Santoso, I.R. Edwards 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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"Thanks for this!" says: | jeffreyn (06-18-2017), moondaughter (06-18-2017) |
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