Delayed Gastric Emptying in Advanced Parkinson Disease: Correlation With Therapeutic Doses

Gastrointestinal dysfunction is often described in patients with Parkinson disease (PD), and gastrointestinal symptoms are usually attributed to gastroparesis. The consequent delayed gastric emptying (GE) may be an important pharmacokinetic mechanism underlying some of the response fluctuations that develop after long-term levodopa (L-dopa) therapy.The aim of this prospective study was to assess GE time by a liquid meal scintigraphy, in PD patients, and to correlate them with demographic, clinical, and therapeutic data.

Scintigraphy with radiolabeled albumin nanocolloids added to acidified orange juice was performed in 51 consecutive PD patients 1 hour after their usual dopaminergic therapy first dose and after a 12-hour fast. Demographic, neurologic, gastrointestinal, and pharmacologic data were collected.

Fifty-one patients were divided into 2 groups using the cutoff point obtained in normal subjects (40 minutes): group 1 included 29 patients with GE T½ of 27.60 ± 7.30 minutes (normal), group 2 showed a GE T½ of 84.90 ± 53.80 minutes (delayed). The most striking significant difference between the 2 groups was the dopa-decarboxylase inhibitor mean dose that was significantly higher in the group of patients with delayed GE (201.32 ± 97.26 vs 127.65 ± 79.74; P = 0.005).

The impairment of gastric motility, frequently represented in PD patients, occurs in approximately 42% of patients with motor complications. A mechanism that may explain the GE delay is the effect of L-dopa on dopaminergic receptors in the stomach. Therefore, the dosage of dopa-decarboxylase inhibitor, increasing the L-dopa concentration, may contribute to GE delay and its consequent effect on drug delivery and efficacy.