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Effect of memantine on CBF and CMRO 2 in patients with early Parkinson’s disease
Author(s) -
Borghammer P.,
Vafaee M.,
Ostergaard K.,
Rodell A.,
Bailey C.,
Cumming P.
Publication year - 2008
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2007.00943.x
Subject(s) - basal ganglia , memantine , cerebral blood flow , parkinson's disease , positron emission tomography , anesthesia , medicine , neuroprotection , psychology , nmda receptor , cardiology , neuroscience , central nervous system , disease , receptor
Objectives – Parkinson’s disease (PD) may be associated with increased energy metabolism in overactive regions of the basal ganglia. Therefore, we hypothesized that treatment with the N ‐methyl‐ d ‐aspartate receptor (NMDAR) antagonist memantine would decrease regional cerebral blood flow (rCBF) and oxygen metabolism in the basal ganglia of patients with early‐stage PD. Methods – Quantitative positron emission tomography (PET) recordings were obtained with [ 15 O]water and [ 15 O]oxygen in 10 patients, scanned first in a baseline condition, and again 6 weeks after treatment with a daily dose of 20 mg memantine. Dynamic PET data were analyzed using volume of interest and voxel‐based approaches. Results – The treatment evoked rCBF decreases in basal ganglia, and in several frontal cortical areas. The regional cerebral metabolic rate of oxygen (rCMRO 2 ) did not decrease in any of the a priori defined regions, and consequently the oxygen extraction fraction was increased in these regions. Two peaks of significantly decreased rCMRO 2 were detected near the frontal poles in both hemispheres, using a posteriori voxel‐based analysis. Conclusions – Although we did not find the predicted decrease in basal ganglia oxygen consumption, our data suggest that treatment with memantine actively modulates neuronal activity and/or hemodynamic response in basal ganglia of PD patients. This finding may be relevant to the putative neuroprotective properties of NMDAR antagonists.