Pathology of Epilepsy

Kim, Jung Ho

doi:10.1006/exmp.2001.2372

Cited by 24 publications

(16 citation statements)

References 152 publications

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“…29,32 Hippocampal findings often were not provided 24 -26 or hippocampal sclerosis has been diagnosed in case of 25 or 30% average neuronal loss from Ammon's horn, 34,35 which does not match with the amount of neuronal loss in AHS. 1,4,36,37 Studies reporting correlations between microdysgenesis and postsurgical outcome 24,25,27 did not address outcome-relevant factors other than histopathology, for example, duration of epilepsy 38 or amount of mesial resection. 39 Diagnostic criteria of microdysgenesis often included structural features encountered in normal temporal brain areas, for example, columnar arrangement of cortical neurons, molecular layer neurons, or single white matter neurons.…”

Section: Discussionmentioning

confidence: 99%

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Kasper¹,

Stefan²,

Paulus

2003

Annals of Neurology

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The interrelationship of mesial temporal lobe epilepsy (MTLE), hippocampal sclerosis, and febrile convulsions still remains an enigma. Additional microscopical cortical dysplasia or microdysgenesis has been suggested as pre-existent susceptibility factor rendering the affected brain vulnerable to the development of MTLE after initial precipitating injuries such as febrile convulsions. Twenty-four MTLE cases with histopathologically definite hippocampal sclerosis were examined for clearly defined features of microdysgenesis and further signs of neocortical dysplasia. Although unequivocal signs of dysplasia were absent, 29.2% of cases showed cortical neuronal clustering, 25.0% showed perivascular clustering, and 20.8% showed increased white matter neurons. The features of microdysgenesis studied here were not linked with each other and were not related to initial precipitating injuries, positive family history, or any other clinical parameter. Their suggested fundamental role as dysplastic factor within development of hippocampal sclerosis and MTLE is not confirmed.

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Section: Discussionmentioning

confidence: 99%

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Kasper¹,

Stefan²,

Paulus

2003

Annals of Neurology

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“…Patients with CCMs often present with epilepsy or progressive focal neurological deficits as a result of repetitive lesional bleeding (4,22).…”

Section: Discussionmentioning

confidence: 99%

“…Arteriovenous malformations; Cavernous malformations; Gene arrays; Gene expression Cerebrovascular malformations (CVMs) are lesions with an abnormal vessel phenotype that predisposes patients to hemorrhagic strokes, seizures, focal neurological deficits, and other clinical manifestations (4,22). They include arteriovenous malformations (AVMs) and cerebral cavernous malformations (CCMs) and have distinct clinicopathological radiological profiles (14,30).…”

Section: Introductionmentioning

confidence: 99%

Differential Gene Expression in Human Cerebrovascular Malformations

et al. 2003

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OBJECTIVE-We sought to identify genes with differential expression in cerebral cavernous malformations (CCMs), arteriovenous malformations (AVMs), and control superficial temporal arteries (STAs) and to confirm differential expression of genes previously implicated in the pathobiology of these lesions. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript METHODS-Total ribonucleic acid was isolated from four CCM, four AVM, and three STA surgical specimens and used to quantify lesion-specific messenger ribonucleic acid expression levels on human gene arrays. Data were analyzed with the use of two separate methodologies: gene discovery and confirmation analysis. RESULTS-The gene discovery method identified 42 genes that were significantly up-regulated and 36 genes that were significantly down-regulated in CCMs as compared with AVMs and STAs (P = 0.006). Similarly, 48 genes were significantly up-regulated and 59 genes were significantly down-regulated in AVMs as compared with CCMs and STAs (P = 0.006). The confirmation analysis showed significant differential expression (P < 0.05) in 11 of 15 genes (angiogenesis factors, receptors, and structural proteins) that previously had been reported to be expressed differentially in CCMs and AVMs in immunohistochemical analysis. CONCLUSION-We identify numerous genes that are differentially expressed in CCMs andAVMs and correlate expression with the immunohistochemistry of genes implicated in cerebrovascular malformations. In future efforts, we will aim to confirm candidate genes specifically related to the pathobiology of cerebrovascular malformations and determine their biological systems and mechanistic relevance. KeywordsArteriovenous malformations; Cavernous malformations; Gene arrays; Gene expression Cerebrovascular malformations (CVMs) are lesions with an abnormal vessel phenotype that predisposes patients to hemorrhagic strokes, seizures, focal neurological deficits, and other clinical manifestations (4,22). They include arteriovenous malformations (AVMs) and cerebral cavernous malformations (CCMs) and have distinct clinicopathological radiological profiles (14,30). The AVMs are tangled complexes of tortuous vessels representing fistulous connections between arteries and veins, and they lack an intervening capillary bed. They reveal preserved features of mature vessel wall phenotype altered by high flow and hemodynamic stress, including arterial, nidal, and venous aneurysms (5,6,28). The CCMs are characterized by caverns filled with blood or thrombus and are lined with a single layer of endothelial cells. These low-flow lesions are associated with brittle vasculature and repetitive oozing (5,6). The CCMs lack inter-endothelial cell tight junctions and mature vessel wall angio-architecture (8, 37).Little is known about the mechanisms of genesis or the progression of these lesions. Several proteins are abnormally expressed in AVMs and CCMs. Our group and others have demonstrated by performing immunohistochemical analysis that vascular endoth...

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“…Pathologically, AVMs are complexes of some curved vessels directly connect between the arteries and veins, lacking the intervening capillaries [2]. For this feature, the high-pressure blood flow from the arteries drains directly into venous system, leading to venous engorgement which resulting in edema and irritating the surrounding brain tissue, consequently causing clinical symptoms [3,4]. Previously, AVMs is treated as a kind of congenital disease.…”

Section: Introductionmentioning

confidence: 99%

Human brain arteriovenous malformation: an analysis of differential expressed genes

Liu

Meng

et al. 2016

Chin Neurosurg Jl

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Background: Much still remains unknown about the pathogenesis of brain arteriovenous malformations (AVMs). Previous studies have revealed the abnormal expression of various angiogenesis-related genes in AVMs. To further understand this disease, we sought to identify genes differently expressed in AVMs by means of the gene microarray technique. Methods: Nine AVMs specimen and nine samples of normal vessels are collected. Total RNA isolated from these specimen is hybridized with Oligonucleotide array and gene analysis was conducted. Analyzing data with the help of significance analysis of microarrays (SAM) and a free web-based molecular annotation system 3.0 (MAS 3.0). Results: The SAM method identify 37 gene significantly up-regulated and 10 genes down-regulated in AVMs.

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Pathology of Epilepsy

Cited by 24 publications

References 152 publications

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Differential Gene Expression in Human Cerebrovascular Malformations

Human brain arteriovenous malformation: an analysis of differential expressed genes

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