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Published online before print February 25, 2009, doi:10.1212/01.wnl.0000345969.57574.f5)
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Volume 72, Number 20, May 19, 2009
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NEUROLOGY 2009;72:1747-1754
© 2009 American Academy of Neurology

Longitudinal and cross-sectional analysis of atrophy in pharmacoresistant temporal lobe epilepsy

B. C. Bernhardt, BSc, K. J. Worsley, PhD, H. Kim, PhD, A. C. Evans, PhD, A. Bernasconi, MD and N. Bernasconi, MD, PhD

From the Departments of Neurology (B.C.B., H.K., A.C.E., A.B., N.B.) and Mathematics and Statistics (K.J.W.), Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.

Address correspondence and reprint requests to Dr. Neda Bernasconi, Montreal Neurological Institute, 3801 University Street, Montreal, Quebec, Canada H3A 2B4 neda{at}bic.mni.mcgill.ca

Background: Whether recurrent epileptic seizures induce brain damage is debated. Disease progression in epilepsy has been evaluated only in a few community-based studies involving patients with seizures well controlled by medication. These studies concluded that epilepsy does not inevitably lead to global cerebral damage.

Objective: To track the progression of neocortical atrophy in pharmacoresistant temporal lobe epilepsy (TLE) using longitudinal and cross-sectional designs.

Methods: Using a fully automated measure of cortical thickness on MRI, we studied a homogeneous sample of patients with pharmacoresistant TLE. In the longitudinal analysis (n = 18), fixed-effect models were used to quantify cortical atrophy over a mean interscan interval of 2.5 years (range = 7 to 90 months). In the cross-sectional analysis (n = 121), we correlated epilepsy duration and thickness. To dissociate normal aging from pathologic progression, we compared aging effects in TLE to healthy controls.

Results: The longitudinal analysis mapped progression in ipsilateral temporopolar and central and contralateral orbitofrontal, insular, and angular regions. In patients with more than 14 years of disease, atrophy progressed more rapidly in frontocentral and parietal regions that in those with shorter duration. The cross-sectional study showed progressive atrophy in the mesial and superolateral frontal, and parietal cortices.

Conclusions: Our combined cross-sectional and longitudinal analysis in patients with pharmacoresistant temporal lobe epilepsy demonstrated progressive neocortical atrophy over a mean interval of 2.5 years that is distinct from normal aging, likely representing seizure-induced damage. The cumulative character of atrophy underlies the importance of early surgical treatment in this group of patients.

Abbreviations: GM = gray matter; TLE = temporal lobe epilepsy; WM = white matter.


Supplemental data at www.neurology.org

Editorial, page 1718

e-Pub ahead of print on February 25, 2009, at www.neurology.org.

Supported by a grant from the Canadian Institutes of Health Research (CIHR). B.B. was supported by the German National Merit Foundation and the German Academic Exchange Service.

Disclosure: The authors report no disclosures.

Received August 20, 2008. Accepted in final form December 15, 2008.


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