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ARTICLES: F. Riederer, R. Lanzenberger, M. Kaya, D. Prayer, W. Serles, and C. Baumgartner Network atrophy in temporal lobe epilepsy: A voxel-based morphometry study Neurology 2008; 71: 419-425 [Abstract] [Full text] [PDF]

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Network atrophy in temporal lobe epilepsy: A voxel-based morphometry study

Leonardo Bonilha, Jonathan J. Halford   (21 November 2008)

Reply from the authors

Franz Riederer, Christoph Baumgartner   (21 November 2008)

Network atrophy in temporal lobe epilepsy: A voxel-based morphometry study 21 November 2008
Leonardo Bonilha, Division of Neurology, Medical University of South Carolina 96 Jonathan Lucas Street, Suite 428, Charleston, South Carolina 29425-2272, Jonathan J. Halford Send Correspondence to journal: Re: Network atrophy in temporal lobe epilepsy: A voxel-based morphometry study bonilha{at}musc.edu Leonardo Bonilha, et al.	We read with great interest the article by Riederer at al. [1] The authors confirmed previous findings on mesial temporal lobe epilepsy (mTLE) showing that hippocampal atrophy is associated with a well-defined network of extra-hippocampal gray matter loss. They also demonstrated that cryptogenic temporal lobe epilepsy (cTLE) is associated with a pattern of gray matter atrophy. [2-4] Their results indicate that there are subtle differences in the anatomical distribution of damage in patients with mTLE compared to those with cTLE. The cTLE and mTLE groups had varying levels of epilepsy severity yet both groups exhibited extra-hippocampal atrophy and the pattern in each group was unique. Since VBM traditionally relies on the comparison of means of gray matter volume across different groups, reproducible findings on mTLE may indicate that patients with mTLE comprise a homogenous group. In comparison, patients with cTLE are likely more heterogeneous with outliers having pronounced brain damage. This may explain why the distribution of atrophy in cTLE is scattered across different brain areas and why previous studies have be unable to consistently observe differences between cTLE and controls. What is the primary cause of extra-hippocampal atrophy in TLE? Two common hypotheses are that brain atrophy in patients with TLE may be due to excitotoxic effect from seizures as they spread. Alternatively, it may be due to remote deafferentation from loss of hippocampal connections. Riederer et al. suggest that hippocampal atrophy alone is not responsible for causing brain atrophy yet plays a partial role in shaping the location and extent of atrophy. Further studies are needed to replicate these findings while considering the severity of epilepsy. It is possible that both recurrent seizures and hippocampal atrophy are necessary to generate a diffuse and homogeneous pattern of extra-hippocampal atrophy. References 1. Riederer F, Lanzenberger R, Kaya M, Prayer D, Serles W, Baumgartner C. Network atrophy in temporal lobe epilepsy: a voxel-based morphometry study. Neurology 2008;71:419-425. 2. Bonilha L, Kobayashi E, Rorden C, Cendes F, Li LM. Medial temporal lobe atrophy in patients with refractory temporal lobe epilepsy. J Neurol Neurosurg Psychiatry 2003;74:1627-1630. 3. Bonilha L, Rorden C, Castellano G, et al. Voxel-based morphometry reveals gray matter network atrophy in refractory medial temporal lobe epilepsy. Arch Neurol 2004;61:1379-1384. 4. Keller SS, Mackay CE, Barrick TR, Wieshmann UC, Howard MA, Roberts N. Voxel-based morphometric comparison of hippocampal and extrahippocampal abnormalities in patients with left and right hippocampal atrophy. Neuroimage 2002;16:23-31. Disclosure: The authors report no disclosures.
Reply from the authors 21 November 2008
Franz Riederer, Medical University of Vienna Waehringer Guertel 18-20, A 1190 Vienna , Austria, Christoph Baumgartner Send Correspondence to journal: Re: Reply from the authors franz.riederer{at}meduniwien.ac.at Franz Riederer, et al.	Bonilha and Halford hypothesize that cTLE might comprise a more heterogeneous disease group compared to mTLE because brain atrophy is more scattered. Furthermore, they contend that this may reflect outliers with more pronounced brain atrophy. [1] This interesting hypothesis cannot be verified by a voxel-based morphometry (VBM) approach that is based on comparisons of gray matter between groups. It cannot be determined whether more prominent focal atrophy in single patients or more discrete and widespread gray matter in all individuals is responsible for the pattern of atrophy we observed in the cTLE group. There is evidence from a PET study that metabolic dysfunction is more widespread in MRI-negative TLE compared to mTLE. [5] Comparing the individual patient with a control group has been performed in a VBM study on focal cortical dysplasias, but experience remains limited. [6] We look forward to improved VBM techniques so that these questions can be resolved. References 5. Carne RP, O'Brien TJ, Kilpatrick CJ, et al. MRI-negative PET-positive temporal lobe epilepsy: a distinct surgically remediable syndrome. Brain 2004;127:2276-2285. 6. Bonilha L, Montenegro MA, Rorden C, et al. Voxel-based morphometry reveals excess gray matter concentration in patients with focal cortical dysplasia. Epilepsia 2006;47:908-915. Disclosure: The authors report no disclosures.