Metabolic Patterns Associated With Non-Specific Magnetic Resonance Imaging Abnormalities in Temporal Lobe Epilepsy

Ryvlin, Philippe; Cinotti, L.; Froment, J.-C.; Bars, Didier Le; Landais, P.; Chaze, M.; Galy, G.; Lavenne, F.; Serra, Jeanne P.; Mauguı̀ere, François

doi:10.1093/brain/114.6.2363

Cited by 53 publications

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“…However, abnormal electrical activity, both ictal and interictal, is linked to reorganization of language cortex in TLE (Janszky et al, 2003). Furthermore, metabolic PET scans in TLE patients have demonstrated widespread interictal temporal lobe hypometabolism (Ryvlin et al, 1991), and altered anterior and inferior temporal lobe neurotransmitter function (Merlet et al, 2004). Therefore, the absence of significant comprehension deficits after ATL is likely to reflect a preoperative reorganization of the language system in the presence of left-lateralized TLE rather than an absence of language function in this region in the normal brain.…”

Section: Discussionmentioning

confidence: 99%

Converging Language Streams in the Human Temporal Lobe

et al. 2006

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There is general agreement that, after initial processing in unimodal sensory cortex, the processing pathways for spoken and written language converge to access verbal meaning. However, the existing literature provides conflicting accounts of the cortical location of this convergence. Most aphasic stroke studies localize verbal comprehension to posterior temporal and inferior parietal cortex (Wernicke's area), whereas evidence from focal cortical neurodegenerative syndromes instead implicates anterior temporal cortex. Previous functional imaging studies in normal subjects have failed to reconcile these opposing positions. Using a functional imaging paradigm in normal subjects that used spoken and written narratives and multiple baselines, we demonstrated common activation during implicit comprehension of spoken and written language in inferior and lateral regions of the left anterior temporal cortex and at the junction of temporal, occipital, and parietal cortex. These results indicate that verbal comprehension uses unimodal processing streams that converge in both anterior and posterior heteromodal cortical regions in the left temporal lobe.

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Section: Discussionmentioning

confidence: 99%

Converging Language Streams in the Human Temporal Lobe

et al. 2006

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“…More recently, some imaging studies have also suggested that there may be changes in the thalamus ipsilateral to the affected temporal lobe. Interictal positron emission tomography scans from several institutions have shown hypometabolism in the thalamus ipsilateral to the hypometabolic temporal lobe (40,41). There is also a recent report of thalamic atrophy ipsilateral to the atrophic hippocampus that was documented by volumetric measurements (42).…”

Section: Fig 2 A: Ca1mentioning

confidence: 99%

The Pathological Substrate of Limbic Epilepsy: Neuronal Loss in the Medial Dorsal Thalamic Nucleus as the Consistent Change

Bertram

Scott

2000

Epilepsia

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Summary:Purpose: The focus of research in limbic epilepsy has been the hippocampus because of its well-known pathology of hippocampal atrophy and sclerosis as well as the strong propensity for this structure to seize under a variety of circumstances. There is ample evidence, however, for pathological alterations in other regions of the limbic system in limbic/ mesial temporal lobe epilepsy, including the amygdala, the entorhinal cortex, and, in some cases, the thalamus. In this preliminary evaluation of the pathological substrate for limbic epilepsy, we wished to determine if there was consistent anatomic change at extrahippocampal sites.Methods: We compared paraffin sections of brains from rats with chronic spontaneous limbic epilepsy and age-matched controls to determine the consistency of the pathology at five sites: the hippocampus, amygdala, entorhinal cortex, piriform cortex, and medial dorsal thalamus.Results: In a qualitative evaluation of these sections taken from standardized positions, we found that the medial dorsal thalamic nucleus in the epileptic animals was the site that was consistently involved with neuronal loss. With all other sites, at least several animals had qualitatively normal tissue.Conclusions: This finding suggests that neuronal loss in the medial dorsal thalamus may be the consistent pathology in limbic epilepsy, at least in an animal model of the disorder. The presence of a structurally abnormal subcortical region with broad connections to the limbic sites involved with chronic epilepsy may have implications for our understanding of the pathophysiology of this disorder. Key Words: EpilepsyPathology-Thalamus-Hippocampus-Limbic.The mesial temporal lobe epilepsy syndrome has been associated with hippocampal pathology for many decades, and these changes of regional neuronal loss and gliosis, called hippocampal sclerosis, have become the pathognomonic finding for this condition. However, there have also been numerous observations of pathology in the adjacent regions of the amygdala, entorhinal cortex, and thalamus (1-4). A few reports have suggested that in some instances the extrahippocampal pathology is the primary change in selected patients with the mesial temporal lobe epilepsy syndrome (3). These observations indicate that the syndrome encompasses a more widespread pathology and that there may be more variability in the pathology from case to case. Understanding the nature and distribution of the pathology is a major component of developing a conceptual framework for this syndrome. There have been other observations made by a number of investigators that suggest that the pathological basis and pathophysiology are not confined to the hippocampus. One such observation is that the pattern of electrographic seizure onset is often regional, with the seizure beginning at multiple points within the temporal lobe at one time (5,6). A similar finding is that it is necessary to resect multiple structures in the mesial temporal region to effect a significant reduction in seizure frequency (7...

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“…It has been shown that there is interictal hypometabolism in TLE patients as well as in epileptic animals, which does not directly correlate with neuronal loss (Ryvlin et al, 1991;O'Brien et al, 1997;Foldvary et al, 1999;Dube et al, 2001). Thus, the regulation of metabolic pathways is most likely disturbed in the epileptic brain.…”

Section: Introductionmentioning

confidence: 99%

Metabolism is Normal in Astrocytes in Chronically Epileptic Rats: A ¹³C NMR Study of Neuronal—Glial Interactions in a Model of Temporal Lobe Epilepsy

Melø

Nehlig

Sonnewald

2005

J Cereb Blood Flow Metab

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The aim of the present work was to study potential disturbances in metabolism and interactions between neurons and glia in the lithium-pilocarpine model of temporal lobe epilepsy. Rats chronically epileptic for 1 month received [1-13 C]glucose, a substrate for neurons and astrocytes, and [1,2-13 C]acetate, a substrate for astrocytes only. Analyses of extracts from cerebral cortex, cerebellum, and hippocampal formation (hippocampus, amygdala, entorhinal, and piriform cortices) were performed using 13 C and 1 H nuclear magnetic resonance spectroscopy and HPLC. In the hippocampal formation of epileptic rats, levels of glutamate, aspartate, N-acetyl aspartate, adenosine triphosphate plus adenosine diphosphate and glutathione were decreased. In all regions studied, labeling from [1,2-13 C]acetate was similar in control and epileptic rats, indicating normal astrocytic metabolism. However, labeling of glutamate, GABA, aspartate, and alanine from [1-13 C]glucose was decreased in all areas possibly reflecting neuronal loss. The labeling of glutamine from [1-13 C]glucose was decreased in cerebral cortex and cerebellum and unchanged in hippocampal formation. In conclusion, no changes were detected in glial-neuronal interactions in the hippocampal formation while in cortex and cerebellum the flow of glutamate to astrocytes was decreased, indicating a disturbed glutamate-glutamine cycle. This is, to our knowledge, the first study showing that metabolic disturbances are confined to neurons inside the epileptic circuit.

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Metabolic Patterns Associated With Non-Specific Magnetic Resonance Imaging Abnormalities in Temporal Lobe Epilepsy

Cited by 53 publications

References 0 publications

Converging Language Streams in the Human Temporal Lobe

Converging Language Streams in the Human Temporal Lobe

The Pathological Substrate of Limbic Epilepsy: Neuronal Loss in the Medial Dorsal Thalamic Nucleus as the Consistent Change

Metabolism is Normal in Astrocytes in Chronically Epileptic Rats: A ¹³C NMR Study of Neuronal—Glial Interactions in a Model of Temporal Lobe Epilepsy

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Metabolic Patterns Associated With Non-Specific Magnetic Resonance Imaging Abnormalities in Temporal Lobe Epilepsy

Cited by 53 publications

References 0 publications

Converging Language Streams in the Human Temporal Lobe

Converging Language Streams in the Human Temporal Lobe

The Pathological Substrate of Limbic Epilepsy: Neuronal Loss in the Medial Dorsal Thalamic Nucleus as the Consistent Change

Metabolism is Normal in Astrocytes in Chronically Epileptic Rats: A 13C NMR Study of Neuronal—Glial Interactions in a Model of Temporal Lobe Epilepsy

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Metabolism is Normal in Astrocytes in Chronically Epileptic Rats: A ¹³C NMR Study of Neuronal—Glial Interactions in a Model of Temporal Lobe Epilepsy