Abstract
Levodopa remains the mainstay of treatment for Parkinson disease (PD), but its use is associated with dyskinesias (LID) in many patients. LID likely reflect dysregulated release of dopamine combined with altered postsynaptic mechanisms due to pulsatile dopamine receptor stimulation. Dopamine D3 receptors are increased in animal models of LID, and experimental LID is attenuated by suppression of D3 signaling, but the relevance to LID in humans is uncertain.1 Payer et al.2 used PET with the D3-preferring dopamine receptor agonist [11C]PHNO. Compared to patients with PD without LID, those with LID had increased binding in the globus pallidus and decreased binding in the ventral striatum. In the dorsal striatum, PHNO binding was increased in both PD groups, but the difference between PD-stable and PD-LID was not significant. However, [11C]raclopride binding to D2 and D3 receptors was increased in patients with LID when controlling for levodopa dose.
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