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Mesial temporal lobe epilepsy: Clinical and neuropathologic findings of familial and sporadic forms

Summary Purpose: To evaluate the clinical and hippocampal histological features of patients with mesial temporal lobe epilepsy (MTLE) in both familial (FMTLE) and sporadic (SMTLE) forms. Methods: Patients with FMTLE (n = 20) and SMTLE (n = 39) who underwent surgical treatment for refractory seizures...

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Published in:Epilepsia (Copenhagen) 2008-06, Vol.49 (6), p.1046-1054
Main Authors: Andrade‐Valença, Luciana Patrízia A., Valença, Marcelo Moraes, Velasco, Tonicarlo Rodrigues, Carlotti, Carlos Gilberto, Assirati, João Alberto, Galvis‐Alonso, Orfa Yineth, Neder, Luciano, Cendes, Fernando, Leite, João Pereira
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creator Andrade‐Valença, Luciana Patrízia A.
Valença, Marcelo Moraes
Velasco, Tonicarlo Rodrigues
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Galvis‐Alonso, Orfa Yineth
Neder, Luciano
Cendes, Fernando
Leite, João Pereira
description Summary Purpose: To evaluate the clinical and hippocampal histological features of patients with mesial temporal lobe epilepsy (MTLE) in both familial (FMTLE) and sporadic (SMTLE) forms. Methods: Patients with FMTLE (n = 20) and SMTLE (n = 39) who underwent surgical treatment for refractory seizures were studied at the University of São Paulo School of Medicine at Ribeirão Preto. FMTLE was defined when at least two individuals in a family had clinical diagnosis of MTLE. Hippocampi from all patients were processed for Nissl/HE and Timm's stainings. Both groups were compared for clinical variables, hippocampal cell densities, and intensity of supragranular mossy fiber staining. Results: There were no significant differences between FMTLE and SMTLE groups in the following: age at the surgery, age of first usual epileptic seizure, history of initial precipitating injury (IPI), age of IPI, latent period, ictal and interictal video‐EEG patterns, presence of hippocampal atrophy and signal changes at MRI, and postoperative outcome. In addition, no differences were found in cell densities in hippocampal cornu ammonis subfields (CA1, CA2, CA3, CA4), fascia dentata, polymorphic region, subiculum, prosubiculum, and presubiculum. However, patients with SMTLE had greater intensity of mossy fiber Timm's staining in the fascia dentata‐inner molecular layer (p< 0.05). Discussion: Patients with intractable FMTLE present a clinical profile and most histological findings comparable to patients with SMTLE. Interestingly, mossy fiber sprouting was less pronounced in patients with FMTLE, suggesting that, when compared to SMTLE, patients with FMTLE respond differently to plastic changes plausibly induced by cell loss, neuronal deafferentation, or epileptic seizures.
doi_str_mv 10.1111/j.1528-1167.2008.01551.x
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Methods: Patients with FMTLE (n = 20) and SMTLE (n = 39) who underwent surgical treatment for refractory seizures were studied at the University of São Paulo School of Medicine at Ribeirão Preto. FMTLE was defined when at least two individuals in a family had clinical diagnosis of MTLE. Hippocampi from all patients were processed for Nissl/HE and Timm's stainings. Both groups were compared for clinical variables, hippocampal cell densities, and intensity of supragranular mossy fiber staining. Results: There were no significant differences between FMTLE and SMTLE groups in the following: age at the surgery, age of first usual epileptic seizure, history of initial precipitating injury (IPI), age of IPI, latent period, ictal and interictal video‐EEG patterns, presence of hippocampal atrophy and signal changes at MRI, and postoperative outcome. In addition, no differences were found in cell densities in hippocampal cornu ammonis subfields (CA1, CA2, CA3, CA4), fascia dentata, polymorphic region, subiculum, prosubiculum, and presubiculum. However, patients with SMTLE had greater intensity of mossy fiber Timm's staining in the fascia dentata‐inner molecular layer (p&lt; 0.05). Discussion: Patients with intractable FMTLE present a clinical profile and most histological findings comparable to patients with SMTLE. 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Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampal sclerosis ; Hippocampus - pathology ; Hippocampus - surgery ; Humans ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Middle Aged ; Mossy fiber ; Mossy Fibers, Hippocampal - pathology ; Nervous system (semeiology, syndromes) ; Neurology ; Neuronal Plasticity - genetics ; Neurons - pathology ; Neuropharmacology ; Pathology ; Pharmacology. 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Methods: Patients with FMTLE (n = 20) and SMTLE (n = 39) who underwent surgical treatment for refractory seizures were studied at the University of São Paulo School of Medicine at Ribeirão Preto. FMTLE was defined when at least two individuals in a family had clinical diagnosis of MTLE. Hippocampi from all patients were processed for Nissl/HE and Timm's stainings. Both groups were compared for clinical variables, hippocampal cell densities, and intensity of supragranular mossy fiber staining. Results: There were no significant differences between FMTLE and SMTLE groups in the following: age at the surgery, age of first usual epileptic seizure, history of initial precipitating injury (IPI), age of IPI, latent period, ictal and interictal video‐EEG patterns, presence of hippocampal atrophy and signal changes at MRI, and postoperative outcome. 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Antiepileptics. Antiparkinson agents</topic><topic>Atrophy</topic><topic>Biological and medical sciences</topic><topic>Electroencephalography</topic><topic>Epilepsy</topic><topic>Epilepsy, Temporal Lobe - diagnosis</topic><topic>Epilepsy, Temporal Lobe - genetics</topic><topic>Epilepsy, Temporal Lobe - pathology</topic><topic>Epilepsy, Temporal Lobe - surgery</topic><topic>Familial</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampal sclerosis</topic><topic>Hippocampus - pathology</topic><topic>Hippocampus - surgery</topic><topic>Humans</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mossy fiber</topic><topic>Mossy Fibers, Hippocampal - pathology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neuronal Plasticity - genetics</topic><topic>Neurons - pathology</topic><topic>Neuropharmacology</topic><topic>Pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Sclerosis</topic><topic>Sprouting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andrade‐Valença, Luciana Patrízia A.</creatorcontrib><creatorcontrib>Valença, Marcelo Moraes</creatorcontrib><creatorcontrib>Velasco, Tonicarlo Rodrigues</creatorcontrib><creatorcontrib>Carlotti, Carlos Gilberto</creatorcontrib><creatorcontrib>Assirati, João Alberto</creatorcontrib><creatorcontrib>Galvis‐Alonso, Orfa Yineth</creatorcontrib><creatorcontrib>Neder, Luciano</creatorcontrib><creatorcontrib>Cendes, Fernando</creatorcontrib><creatorcontrib>Leite, João Pereira</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Epilepsia (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andrade‐Valença, Luciana Patrízia A.</au><au>Valença, Marcelo Moraes</au><au>Velasco, Tonicarlo Rodrigues</au><au>Carlotti, Carlos Gilberto</au><au>Assirati, João Alberto</au><au>Galvis‐Alonso, Orfa Yineth</au><au>Neder, Luciano</au><au>Cendes, Fernando</au><au>Leite, João Pereira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mesial temporal lobe epilepsy: Clinical and neuropathologic findings of familial and sporadic forms</atitle><jtitle>Epilepsia (Copenhagen)</jtitle><addtitle>Epilepsia</addtitle><date>2008-06</date><risdate>2008</risdate><volume>49</volume><issue>6</issue><spage>1046</spage><epage>1054</epage><pages>1046-1054</pages><issn>0013-9580</issn><eissn>1528-1167</eissn><coden>EPILAK</coden><abstract>Summary Purpose: To evaluate the clinical and hippocampal histological features of patients with mesial temporal lobe epilepsy (MTLE) in both familial (FMTLE) and sporadic (SMTLE) forms. Methods: Patients with FMTLE (n = 20) and SMTLE (n = 39) who underwent surgical treatment for refractory seizures were studied at the University of São Paulo School of Medicine at Ribeirão Preto. FMTLE was defined when at least two individuals in a family had clinical diagnosis of MTLE. Hippocampi from all patients were processed for Nissl/HE and Timm's stainings. Both groups were compared for clinical variables, hippocampal cell densities, and intensity of supragranular mossy fiber staining. Results: There were no significant differences between FMTLE and SMTLE groups in the following: age at the surgery, age of first usual epileptic seizure, history of initial precipitating injury (IPI), age of IPI, latent period, ictal and interictal video‐EEG patterns, presence of hippocampal atrophy and signal changes at MRI, and postoperative outcome. In addition, no differences were found in cell densities in hippocampal cornu ammonis subfields (CA1, CA2, CA3, CA4), fascia dentata, polymorphic region, subiculum, prosubiculum, and presubiculum. However, patients with SMTLE had greater intensity of mossy fiber Timm's staining in the fascia dentata‐inner molecular layer (p&lt; 0.05). Discussion: Patients with intractable FMTLE present a clinical profile and most histological findings comparable to patients with SMTLE. Interestingly, mossy fiber sprouting was less pronounced in patients with FMTLE, suggesting that, when compared to SMTLE, patients with FMTLE respond differently to plastic changes plausibly induced by cell loss, neuronal deafferentation, or epileptic seizures.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>18294201</pmid><doi>10.1111/j.1528-1167.2008.01551.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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ispartof Epilepsia (Copenhagen), 2008-06, Vol.49 (6), p.1046-1054
issn 0013-9580
1528-1167
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source Wiley
subjects Adult
Anterior Temporal Lobectomy
Anticonvulsants. Antiepileptics. Antiparkinson agents
Atrophy
Biological and medical sciences
Electroencephalography
Epilepsy
Epilepsy, Temporal Lobe - diagnosis
Epilepsy, Temporal Lobe - genetics
Epilepsy, Temporal Lobe - pathology
Epilepsy, Temporal Lobe - surgery
Familial
Female
Follow-Up Studies
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Hippocampal sclerosis
Hippocampus - pathology
Hippocampus - surgery
Humans
Magnetic Resonance Imaging
Male
Medical sciences
Middle Aged
Mossy fiber
Mossy Fibers, Hippocampal - pathology
Nervous system (semeiology, syndromes)
Neurology
Neuronal Plasticity - genetics
Neurons - pathology
Neuropharmacology
Pathology
Pharmacology. Drug treatments
Sclerosis
Sprouting
title Mesial temporal lobe epilepsy: Clinical and neuropathologic findings of familial and sporadic forms
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