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NEUROLOGY 1996;46:1051-1054
© 1996 American Academy of Neurology

Gastric emptying in Parkinson's disease

Patients with and without response fluctuations

Ruth Djaldetti, MD, Jack Baron, MD, Ilan Ziv, MD and Eldad Melamed, MD

From the Department of Neurology (Dr. Djaldetti), Beilinson Medical Center, Petah Tiqva, Israel; Department of Nuclear Medicine (Dr. Baron), Elias Sourasky Medical Center, Tel Aviv, Israel; and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Supported in part by the National Parkinson Foundation, Miami, Florida.
Received February 27, 1995. Accepted in final form August 10, 1995.
Address correspondence and reprint requests to Dr. R. Djaldetti, Department of Neurology, Beilinson Medical Center, Petah Tiqva 49 100, Israel.

Delayed gastric emptying may be an important pharmacokinetic mechanism underlying some of the response fluctuations that develop after long-term levodopa therapy. We performed a radionuclide gastric emptying study using a standard Tc-99m colloid-labeled solid meal in 30 patients with Parkinson's disease (PD), 15 fluctuators with ``delayed-on'' and ``no-on'' phenomena, and 15 nonfluctuators. Fasting patients were given the standard meal, and gastric emptying was monitored with a gamma camera positioned over the stomach, recording data for 1 hour. PD patients had prolonged gastric emptying measured after 60 minutes compared with the normal control subjects (70.7 plus minus 16% versus less than 60%). Gastric retention measured after 1 hour was increased in patients with fluctuations compared with patients without fluctuations (77.4 plus minus 15.5% versus 64.0 plus minus 14.3%; p less than 0.05). Half-time emptying was significantly delayed in patients with, as compared with those without, response fluctuations (221 plus minus 202 minutes versus 85 plus minus 31 minutes; p less than 0.05). This demonstrates that delayed gastric emptying is common in PD patients and is more marked in those with response fluctuations. The stomach is an important target organ in PD, affected either by the basic PD pathology, chronic drug administration, or both.

NEUROLOGY 1996;46: 1051-1054




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