scholarly journals Relevance of Removal of Limbic Structures in Surgery for Temporal Lobe Epilepsy

1991 ◽  
Vol 18 (S4) ◽  
pp. 628-635 ◽  
Author(s):  
André Olivier
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Clinical Evidence ◽  
Hippocampal Formation ◽  
Clinical Work ◽  
Limbic Structures

ABSTRACT:We have briefly reviewed the experimental and clinical evidence for the importance of the amygdala and hippocampal formation in temporal lobe epilepsy. More specifically, we have analyzed our own experience in patients with temporal lobe epilepsy investigated with intracerebral stereotaxic electrodes and operated by various modalities of resection. Our results, in agreement with previous experimental and clinical work, provide further evidence for an overwhelming predominance of limbic participation in temporal lobe epilepsy. As a result, more and more selective procedures are being carried out involving the mesial structures. However, this shift has been slow and progressive because of the proven value of cortico-amygdalo-hippocampectomy which provides excellent results on seizure tendency with low morbidity.

Temporal Lobe Epilepsy

2017 ◽  
Author(s):  
Edward H. Bertram
Keyword(s):  
Animal Models ◽  
Temporal Lobe Epilepsy ◽  
Entorhinal Cortex ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Focal Epilepsy ◽  
Neural Circuitry ◽  
Human Condition ◽  
Physiological Changes ◽  
Limbic Structures

Temporal lobe epilepsy, as discussed in this chapter, is a focal epilepsy that involves primarily the limbic structures of the medial temporal lobe (amygdala, hippocampus, and entorhinal cortex). In recent years animal models have been developed that mirror the pathology and pathophysiology of this disease. This chapter reviews the human condition, the structural and physiological changes that support the development of seizures. The neural circuitry of seizure initiation will be reviewed with a goal of creating a framework for developing more effective treatments for this disease.

scholarly journals Gene expression of glutamate metabolizing enzymes in the hippocampal formation in human temporal lobe epilepsy

Epilepsia ◽  
2012 ◽  
Vol 54 (2) ◽  
pp. 228-238 ◽  
Author(s):  
Tore Eid ◽  
Tih-Shih W. Lee ◽  
Yue Wang ◽  
Edgar Peréz ◽  
Jana Drummond ◽  
...  
Keyword(s):  
Gene Expression ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Metabolizing Enzymes ◽  
Human Temporal Lobe

scholarly journals Neurocysticercosis and microscopic hippocampal dysplasia in a patient with refractory mesial temporal lobe epilepsy

2006 ◽  
Vol 64 (2a) ◽  
pp. 309-313 ◽  
Author(s):  
Alexandre Valotta da Silva ◽  
Heloise Helena Martins ◽  
Carolina Mattos Marques ◽  
Elza Marcia Targas Yacubian ◽  
Américo Ceiki Sakamoto ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Refractory Epilepsy ◽  
Hippocampal Formation ◽  
Granular Cell ◽  
Mesial Temporal Lobe Epilepsy ◽  
Epidemiologic Studies ◽  
Neuronal Markers ◽  
Symptomatic Epilepsy ◽  
Mesial Temporal Lobe

Epidemiologic studies suggest that neurocysticercosis (NC) is the main cause of symptomatic epilepsy in developing countries. The association between NC and mesial temporal lobe epilepsy (MTLE) has been reported by several authors. Recent data have shown that the presence of NC does not influence the clinical and pathological profile in MTLE patients and suggest that not all cysticercotic lesions are inevitably epileptogenic. We describe a 50-years-old woman with partial seizures due to NC which evolve to MTLE. The patient was submitted to a corticoamygdalohippocampectomy to treat refractory epilepsy. An immunohistochemical study using neuronal markers was made on hippocampal formation. Besides the typical aspects of Ammon's horn sclerosis (AHS), the microscopic examination demonstrates cellular features of hippocampal malformation including dysmorphic neurons and focal bilamination of granular cell layer. We suggest that, in this case, a developmental disorder lowered the threshold for the NC-induced seizures and contributed to the establishment of refractory epilepsy.

Brain morphometric comparison of first-episode schizophrenia and temporal lobe epilepsy

1997 ◽  
Vol 170 (6) ◽  
pp. 515-519 ◽  
Author(s):  
W. B. Barr ◽  
M. Ashtari ◽  
R. M. Bilder ◽  
G. Degreef ◽  
J. A. Lieberman
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Hippocampal Volume ◽  
Brain Morphology ◽  
First Episode ◽  
Mr Images ◽  
Significant Group ◽  
Show Evidence ◽  
First Episode Schizophrenia

BackgroundConverging evidence has suggested that the abnormalities in brain morphology observed in schizophrenia are similar to those seen in temporal lobe epilepsy (TLE). The purpose ofthis study was to compare the features of these groups directly with measures of the brain using magnetic resonance (MR) morphometry.MethodMorphometric measures of ventricular and hippocampal volumes obtained from FLASH MR images were studied in 32 patients with first-episode schizophrenia (FES), 39 patients withTLE (21 left, 18 right), and 42 healthy controls.ResultsVentricular volumes in the FES and TLE groups were both significantly larger than those seen in controls and did not differ from each other. The FES group showed significantly larger temporal horns, while theTLE group had relatively larger frontal horns. Analyses of hippocampal volumes revealed a significant group by hemisphere effect. The FES group showed relative reductions in left hippocampal volume that were comparable only toTLE patients with seizures originating from the left hemisphere.ConclusionThe results indicate that FES and TLE groups both show evidence of ventricular enlargement. Lateralised morphological abnormalities of the hippocampal formation in FES and left TLE are comparable, and may be specific to temporolimbic regions.

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

2005 ◽  
Vol 25 (10) ◽  
pp. 1254-1264 ◽  
Author(s):  
Torun M Melø ◽  
Astrid Nehlig ◽  
Ursula Sonnewald
Keyword(s):  
Cerebral Cortex ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Neuronal Loss ◽  
Adenosine Diphosphate ◽  
Resonance Spectroscopy ◽  
Metabolic Disturbances ◽  
Nmr Study ◽  
Pilocarpine Model

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 [1-13C]glucose, a substrate for neurons and astrocytes, and [1,2-13C]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 13C and 1H 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 [1,2-13C]acetate was similar in control and epileptic rats, indicating normal astrocytic metabolism. However, labeling of glutamate, GABA, aspartate, and alanine from [1-13C]glucose was decreased in all areas possibly reflecting neuronal loss. The labeling of glutamine from [1-13C]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.

scholarly journals Cortical epileptogenesis of slowly kindled freely moving rats

2014 ◽  
Vol 60 (6) ◽  
pp. 249-253
Author(s):  
K. Orbán-Kis ◽  
Iringó Száva ◽  
T. Szilágyi
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Field Potential ◽  
Bipolar Electrode ◽  
Freely Moving Rats ◽  
Spontaneous Seizures ◽  
Freely Moving ◽  
Negative Field

Abstract Objective. Epilepsy is a neurological disorder that can be caused by many underlying pathologies. The epileptic and interictal manifestations that appear during the progression of chronic epilepsy are still not understood completely. One of the most frequent forms of this disease is temporal lobe epilepsy in which is clear involvement of the hippocampal formation. In order to study the electrografic progression of untreated seizures we used amygdala kindling in freely moving rats. Methods. Seven animals were implanted with bilateral hippocampal and prefrontal electrodes. A bipolar electrode, implanted in the lateral nuclei of the left amygdala was used for stimulation. The kindled group of animals was stimulated daily with the minimum current intensity needed to reach the afterdischarge threshold. Behavioral changes during kindling were scored according to the Racine scale. Results. The average seizure severity on the Racine scale was 2.6±0.4 by day 6 and 4.4±0.6 by day 20. The first spontaneous seizures appeared after 31 days of stimulation. During spontaneous seizures the preictal spike full width at half maximum increased gradually from 51±4msec to 110±5msec (p < 0.05) whereas the amplitude of the negative field potential deflection increased by 62% (p < 0.05). Conclusions. Our study showed that the progression of temporal lobe epilepsy, as seen in humans, can be reproduced in the kindling model with high fidelity. This study confirms in vivo the increase in preictal spike duration as well as the increase of the amplitude of negative field potential deflection during the preictal period.

scholarly journals Reduced Astrocytic Contribution to the Turnover of Glutamate, Glutamine, and GABA Characterizes the Latent Phase in the Kainate Model of Temporal Lobe Epilepsy

2011 ◽  
Vol 31 (8) ◽  
pp. 1675-1686 ◽  
Author(s):  
Silje Alvestad ◽  
Janniche Hammer ◽  
Hong Qu ◽  
Asta Håberg ◽  
Ole Petter Ottersen ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Time Window ◽  
Hippocampal Formation ◽  
Piriform Cortex ◽  
Mesial Temporal Lobe Epilepsy ◽  
Resonance Spectroscopy ◽  
Branched Chain ◽  
Latent Phase ◽  
Potential Biomarkers

The occurrence of spontaneous seizures in mesial temporal lobe epilepsy (MTLE) is preceded by a latent phase that provides a time window for identifying and treating patients at risk. However, a reliable biomarker of epileptogenesis has not been established and the underlying processes remain unclear. Growing evidence suggests that astrocytes contribute to an imbalance between excitation and inhibition in epilepsy. Here, astrocytic and neuronal neurotransmitter metabolism was analyzed in the latent phase of the kainate model of MTLE in an attempt to identify epileptogenic processes and potential biomarkers. Fourteen days after status epilepticus, [1-13C]glucose and [1,2-13C]acetate were injected and the hippocampal formation, entorhinal/piriform cortex, and neocortex were analyzed by 1H and 13C magnetic resonance spectroscopy. The 13C enrichment in glutamate, glutamine, and γ-aminobutyric acid (GABA) from [1-13C]glucose was decreased in all areas. Decreased GABA content was specific for the hippocampal formation, together with a pronounced decrease in astrocyte-derived [1,2-13C]GABA and a decreased transfer of glutamine for the synthesis of GABA. Accumulation of branched-chain amino acids combined with decreased [4,5-13C]glutamate in hippocampal formation could signify decreased transamination via branched-chain aminotransferase in astrocytes. The results point to astrocytes as major players in the epileptogenic process, and 13C enrichment of glutamate and GABA as potential biomarkers.

Sign in / Sign up

Export Citation Format

Share Document