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