Clinical Nuclear Medicine

Skip Navigation LinksHome > December 2012 - Volume 37 - Issue 12 > Increased Adenosine A1 Receptor Levels in Hemianopia Patient...
Clinical Nuclear Medicine:
doi: 10.1097/RLU.0b013e31826392a7
Original Articles

Increased Adenosine A1 Receptor Levels in Hemianopia Patients After Cerebral Injury: An Application of PET Using 11C-8-Dicyclopropylmethyl-1-Methyl-3-Propylxanthine

Suzuki, Yukihisa MD, PhD*‡; Nariai, Tadashi MD, PhD†‡; Kiyosawa, Motohiro MD, PhD*‡; Mochizuki, Manabu MD, PhD*; Kimura, Yuichi PhD‡§; Oda, Keiichi PhD; Ishii, Kenji MD; Ishiwata, Kiich PhD

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Purpose: The aim of this study was to apply positron emission tomography (PET) with 11C-8-dicyclopropylmethyl-1-methyl-3-propylxanthine (MPDX), a radioligand for adenosine A1 receptor (A1R), to patients with hemianopia caused by brain injury to study neurorepair mechanisms in the brain.

Patients and Methods: Four patients with homonymous hemianopia and 15 healthy subjects were examined using PET to measure cerebral glucose metabolism, 11C-flumazenil (FMZ) binding to the central benzodiazepine receptor, and MPDX binding to A1R. Left and right regions of interest (ROIs) were selected, and semiquantitative data on the 3 kinds of PET examinations were obtained. The ROIs were referenced using the data for homologous regions in the contralateral hemisphere [ipsilateral/contralateral (I/C) ratio].

Results: The I/C ratios for cerebral glucose metabolism and FMZ binding were low in the primary visual cortex (PVC) and visual association cortex in all the patients, whereas MPDX binding increased in the PVC in patients 1 and 2. Patients 1 and 2 experienced improvement in their visual field after 1 year. However, the other 2 patients showed no changes. We observed an increase in MPDX binding to A1R in the injured portion of the PVC in the patients who recovered.

Conclusions: Evaluation of A1R by MPDX-PET may be useful for predicting prognosis and understanding the compensatory and reorganization processes in hemianopia caused by organic brain damage.

© 2012 Lippincott Williams & Wilkins, Inc.


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