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Interictal metabolic changes in episodic migraine: A voxel-based FDG-PET study

Authors
Kim, J. H.Kim, S.Suh, S-IKoh, S-BPark, K-WOh, K.
Issue Date
Jan-2010
Publisher
SAGE PUBLICATIONS LTD
Keywords
Episodic migraine; positron emission tomography; interictal glucose metabolism; insula; anterior cingulate cortex
Citation
CEPHALALGIA, v.30, no.1, pp.53 - 61
Indexed
SCIE
SCOPUS
Journal Title
CEPHALALGIA
Volume
30
Number
1
Start Page
53
End Page
61
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/117240
DOI
10.1111/j.1468-2982.2009.01890.x
ISSN
0333-1024
Abstract
Whereas there are many (H2O)-O-15-positron emission tomography (PET) studies demonstrating neuronal activation during acute migraine attacks, little information is available on the interictal (headache-free period) glucose metabolic changes in migraine. We therefore conducted voxel-based statistical parametric mapping analysis of F-18-fluorodeoxyglucose-PET to evaluate interictal metabolic differences between 20 episodic migraine patients (four with aura; three men; mean age 34.0 +/- 6.4 years) and 20 control subjects. Separate correlation analyses were performed to delineate a possible relationship between regional glucose metabolism and disease duration or lifetime headache frequency in migraine patients. Group comparison showed that migraine patients had significant hypometabolism in several regions known to be involved in central pain processing, such as bilateral insula, bilateral anterior and posterior cingulate cortex, left premotor and prefrontal cortex, and left primary somatosensory cortex (uncorrected P < 0.001, corrected P < 0.05 with small volume corrections). Correlation analyses showed that regional metabolism of the insula and anterior cingulate cortex had significant negative correlations with disease duration and lifetime headache frequency (uncorrected P< 0.001, corrected P< 0.05 with small volume corrections). Our findings of progressive glucose hypometabolism in relation to increasing disease duration and increasing headache frequency suggest that repeated migraine attacks over time lead to metabolic abnormalities of selective brain regions belonging to the central pain matrix.
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