Skip Navigation


Brain Advance Access originally published online on May 4, 2005
Brain 2005 128(8):1802-1810; doi:10.1093/brain/awh534
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
128/8/1802    most recent
awh534v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (11)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Joo, E. Y.
Right arrow Articles by Kim, B. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Joo, E. Y.
Right arrow Articles by Kim, B. T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Postoperative alteration of cerebral glucose metabolism in mesial temporal lobe epilepsy

Eun Yeon Joo1, Seung Bong Hong1, Hyun Jung Han5, Woo Suk Tae1, Jee Hyun Kim1, Sun Jung Han1, Dae Won Seo1, Kyung-Han Lee3, Seung-Chyul Hong2, Munhyang Lee4, Seunghwan Kim6 and Byung Tae Kim3

Departments of 1 Neurology, 2 Neurosurgery, 3 Nuclear Medicine and 4 Pediatrics, Samsung Medical Center and Center for Clinical Medicine, SBRI, Sungkyunkwan University School of Medicine, Seoul, 5 Department of Neurology, Myongji Hospital, Kwandong University, Goyang City and 6 APCTP/NCSL, Department of Physics, POSTECH, Pohang, Korea

Correspondence to: Seung Bong Hong, MD, PhD, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-Dong, Gangnam-Gu, Seoul, Korea 135-710 E-mail: sbhong{at}smc.samsung.co.kr

To investigate postoperative changes in the cerebral glucose metabolism of patients with mesial temporal lobe epilepsy (MTLE), statistical parametric mapping (SPM) analysis was performed on pre- and postoperative 18F-fluorodeoxyglucose PET (FDG-PET) images. We included 28 patients with MTLE who had undergone surgery and had been seizure-free postoperatively (16 had left MTLE and 12 right MTLE). All patients showed hippocampal sclerosis by pathology or brain MRI. FDG-PET images of the 12 right temporal lobe epilepsy patients were reversed to lateralize the epileptogenic zone to the left side in all patients. Application of the paired t-test in SPM to pre- and postoperative FDG-PETs showed that postoperative glucose metabolism decreased in the caudate nucleus, the pulvinar of the thalamus, fusiform gyrus, lingual gyrus and the posterior region of the insular cortex in the hemisphere ipsilateral to resection, whereas postoperative glucose metabolism increased in the anterior region of the insular cortex, temporal stem white matter, midbrain, inferior precentral gyrus, anterior cingulate gyrus and supramarginal gyrus in the hemisphere ipsilateral to resection. No significant postsurgical changes in cerebral glucose metabolism occurred in the contralateral hemisphere. Subtraction between pre- and postoperative FDG-PET images in individual patients produced similar findings to the SPM results, and additionally showed that postoperative glucose metabolism increased in the anterior thalamus in 12/28 patients (42.8%). SISCOM (subtraction ictal–interictal SPECT co-registered to MRI) performed in 17 patients showed ictal hyperperfusion in the ipsilateral temporal lobe, including the temporal stem white matter, midbrain, insular cortex and cingulate gyrus, bilateral basal ganglia and thalami, and multiple small regions in the frontoparietal lobes during seizures. This study suggests that brain regions showing a postoperative increase in glucose metabolism appear to represent the propagation pathways of ictal and interictal epileptic discharges in MTLE, whereas the postoperative decrease in glucose metabolism may be related to a permanent loss of afferents from resected anterior–mesial temporal structures.

Key Words: temporal lobe epilepsy; anterior temporal lobectomy; metabolism; 18F-FDG-PET; statistical parametric mapping

Abbreviations: AED = antiepileptic drug; FDG-PET = 18F-fluorodeoxy glucose positron emission tomography; MTLE = mesial temporal lobe epilepsy; ROI = region of interest; SPM = statistical parametric mapping; SISCOM = subtraction ictal-interictal SPECT co-registered to MRI; SPECT = single photon emission computed tomography; TLE = temporal lobe epilepsy

Received November 15, 2004. Revised February 17, 2005. Accepted April 8, 2005.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cereb CortexHome page
D. S. Rosenberg, F. Mauguiere, H. Catenoix, I. Faillenot, and M. Magnin
Reciprocal Thalamocortical Connectivity of the Medial Pulvinar: A Depth Stimulation and Evoked Potential Study in Human Brain
Cereb Cortex, June 1, 2009; 19(6): 1462 - 1473.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
S. Takaya, N. Mikuni, T. Mitsueda, T. Satow, J. Taki, M. Kinoshita, S. Miyamoto, N. Hashimoto, A. Ikeda, and H. Fukuyama
Improved cerebral function in mesial temporal lobe epilepsy after subtemporal amygdalohippocampectomy
Brain, January 1, 2009; 132(1): 185 - 194.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
S. Takaya, T. Hanakawa, K. Hashikawa, A. Ikeda, N. Sawamoto, T. Nagamine, K. Ishizu, and H. Fukuyama
Prefrontal hypofunction in patients with intractable mesial temporal lobe epilepsy.
Neurology, November 14, 2006; 67(9): 1674 - 1676.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.