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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the astrocytic cytoskeleton were examined in amygdala kindled rats using immunocytochemical techniques. One week following kindling, there was a dramatic increase in immunoreactivity to glial fibrillary acidic protein and vimentin in astrocytes throughout amygdala, pyriform cortex and hippocampus bilaterally. Since these changes occurred in anatomical sites involved in the propagation of kindled seizures, the observed cytoskeletal reorganization in astrocytes may signify important functional alterations in the kindled brain.
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PMID:Kindling causes changes in the composition of the astrocytic cytoskeleton. 128 May 20

The first and second child of a family died from neonatal seizures with no detectable brain malformation, metabolic, infectious, or chromosomal etiology. Neuropathological examination of the brain of the second child who died at 11 days revealed a widespread spongy state and a selective vulnerability of the astrocytes characterized by numerous enlarged bare astrocytic nuclei and different forms of astrocyte degeneration. The glial cells were strongly positive for glial fibrillary acidic protein and vimentin immunocytochemical reaction. Cortical measurement of Na+/K(+)-ATPase revealed very low enzyme activity. We hypothesize that a defect of Na+/K(+)-ATPase of the astrocytes could be the common pathogenetic factor for the congenital status convulsivus and for the spongy state.
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PMID:Neonatal status convulsivus, spongiform encephalopathy, and low activity of Na+/K(+)-ATPase in the brain. 131 Feb 85

Tissues from three cases of hemimegalencephaly (HME) causing intractable seizures treated by cortical resection were studied using immunohistochemical, ultrastructural, and morphometric techniques. Severe cortical dysplasia was seen in all cases and included lesions best characterized as hemilissencephaly and polymicrogyria. Blurring of the cortex-white matter junction, the presence of large neuronal heterotopias, and neuronal cytomegaly were frequent observations. Immunohistochemical analysis demonstrated cellular colocalization of astrocytic markers glial fibrillary acidic protein and vimentin in one case of hemilissencephaly. Morphometric data showed significant increases over controls in neuronal profile area in all cases of HME. Neuronal cell density was increased significantly above controls in one of the cases. The study shows that HME results from severe cortical dysplasia which may be caused by multiple insults, manifest in one of several ways, and reflects abnormal or altered signals that regulate cortical morphogenesis.
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PMID:Neuropathologic findings in surgically treated hemimegalencephaly: immunohistochemical, morphometric, and ultrastructural study. 141 79

We report an autopsy case of tuberous sclerosis. A 19-year-old Japanese man had shown facial adenoma sebaceum, intractable convulsive seizures and severe mental retardation. Gross inspection of the brain showed a cortical tuber from the orbital frontal lobe to the rhinencephalon of the left side and a few subependymal nodules. Histological examination revealed many cortical tubers in the cerebral hemispheres, a few subependymal nodules with calcification and multifocal clusters of heterotopic cells in the white matter (white matter nodules). In these lesions, massive giant cells with abundant eosinophilic cytoplasm and without Nissl substances were found. Although the size and shape of the giant cells were variable, the majority of them were gemistcytic, ovoid or polygonal. Immunohistochemistry was employed in these lesions using antibodies against neurofilament protein (NFP), glial fibrillary acidic protein (GFAP), vimentin (VM) and myelin basic protein (MBP). In the cortical tuber, the majority of the giant cells were positive for both NFP and VM, but a few were positive for GFAP. All of them were negative for MBP. In the subependymal nodule and white matter nodule, the majority of the giant cells were positive for NFP, but a few were positive for VM, and none were positive for either GFAP and MBP. These findings suggest that the majority of the giant cells may be immature cells toward neuronal series and a few may be those toward astroglial series. These findings also indicate that the giant cells in the subependymal nodule and white matter nodule may be more differentiated than those in the cortical tuber. The nature of the giant cells in tuberous sclerosis is discussed.
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PMID:An autopsy case of tuberous sclerosis. Histological and immunohistochemical study. 145 92

We report two cases of oligodendroglioma-like meningioma revealed by symptoms of increased intracranial pressure, progressive hemiparesia and partial epileptic seizures. Brain CT-scan or scintigraphy and carotid arteriography were suggestive of a convexity meningioma. One patient had received radiation treatment for scalp tinea capitis 25 years previously. In spite of complete surgical removal, the tumor recurred in both cases respectively 17 years and 18 months later. The two patients were operated again, and one underwent a complementary radiotherapy. Pathologic diagnosis was particularly difficult in the first case where the pattern at conventional histologic technics was that of oligodendroglioma. On the occasion of recurrence, immuno-histochemistry and ultrastructural studies were performed. The tumor was positive for epithelial membrane antigen (E.M.A) and cytokeratin, but was negative for glial fibrillary acidic (G.F.A.) protein, S 100 protein (S 100), neuron-specific enolase (N.S.E.), vimentin, anti-LEU-7 (N.H.K.1), and neurofilaments (N.F.). Electron microscopy showed closely adjacent cells with tonofilaments and numerous desmosomes. These findings permitted to establish the diagnosis of oligodendroglioma-like meningioma instead of oligodendroglioma. In the second case, the histologic pattern was also reminiscent of oligodendroglioma, but presence of few cellular whorls in some part of the tumor permitted the correct diagnosis. The pathogenesis of this atypical form of meningioma, its tendency for recurrence, and usefulness of radiotherapy are discussed and literature is reviewed.
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PMID:[Pseudo-oligodendrogliomatous meningioma. Report of 2 cases and review of the literature]. 178 19

The rare case of a meningioma with pulmonary metastases in a dog is described. Clinically, the ten-year-old boxer bitch showed generalized seizures, strabismus and deficient proprioception. The post-mortem examination revealed a basically localized meningeal tumor, having the light- and electron-microscopic appearance of a malignant meningotheliomatous meningioma. Immunohistochemically, the tumor cells did not show any positive reaction with antibodies to GFAP, S-100 protein, NSE, vimentin, cytokeratin, desmin, and von Willebrand factor (factor VIII related antigen). Immunohistochemical examination of seven other canine meningiomas showed an identical pattern. The results and the relevant literature are discussed.
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PMID:[Malignant meningioma with lung metastases in a Boxer]. 188 46

We have reported the clinical and autopsy findings in a case with generalized seizures, myoclonus, blindness and deafness which was accompanied by stroke-like episodes. This case was diagnosed as mitochondrial encephalomyopathy, lactic acidosis & stroke-like episodes (MELAS) from these findings. Solitary and continuous lesions of softening were distributed in both hemispheres, more severely in the frontal and occipital poles. These lesions did not correspond to a vascular supply. The pulvinar, lateral and medial geniculate body of the thalamus, cerebellar vermis and dentate nucleus had small lesions of softening. The cortical lesions occurred mainly in layer 4, and the most prominent lesions among them appeared cystic, involving the subcortical white matter, but nerve cells in layer 1 and 2 were preserved. Proliferation of small blood vessels was seen around the softening areas. Electron microscopy revealed increased mitochondria in endothelial cells of these vessels, abnormal dense bodies in skeletal muscle cells and tightly packed mitochondria in choroid plexus epithelial cells. Immunohistochemical study suggested that vimentin positive cells were seen around lesions and proliferated vessels are different from those seen in the intact tissues.
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PMID:[An autopsy case of generalized seizures, myoclonus, blindness and deafness]. 220 39

Originally described and most frequently reported in association with the kidney, the malignant rhabdoid tumor (MRT) is a highly aggressive neoplasm with distinctive morphologic features. Extrarenal sites reported for this neoplasm include the liver, thymus, and various soft tissue sites. Young infants are affected with rare exceptions. We report the case of a 3-month-old boy who presented with hyperirritability and increasing head size over several weeks. The patient died following a two-week hospital stay marked by development of seizures, paralysis, and apnea. At autopsy, significant findings were limited to the central nervous system. The subarachnoid space contained neoplasm throughout, with multiple areas of parenchymal invasion. A predominating intraparenchymal mass was present in the inferior cerebellum contiguous with the neoplasm in the subarachnoid space and probably represented the site of origin. Microscopically, the neoplasm was composed of a highly cellular monomorphic population of polygonal cells with roughly ovoid vesicular nuclei and conspicuous nucleoli. Variable amounts of cytoplasm were present, and many cells contained a single, well-demarcated eosinophilic hyaline globule adjacent to the nucleus. Ultrastructurally, the cytoplasmic globules were composed of whorled aggregates of intermediate filaments. Immunoperoxidase studies confirmed that the filaments were composed, at least in part, of vimentin. The morphologic and immunohistochemical features are diagnostic of MRT, an entity of unknown histogenesis that has not been reported previously as a primary neoplasm of the CNS.
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PMID:Malignant rhabdoid tumor of the central nervous system. 303 Sep 22

Reactive gliosis is a response of astrocytes to a variety of insults that is characterized by hypertrophy of the cell bodies and processes and an increase in the expression of glial fibrillary acidic protein (GFAP). The signal that regulates the transition to the reactive state and the role of vimentin in reactive gliosis are unknown. The experiments here used a model of repeated seizures in the hippocampal-parahippocampal circuits to determine the extent and time course of reactive gliosis, including the appearance of vimentin, in response to seizures. Reactive gliosis, detected by immunohistochemistry for the presence of GFAP and vimentin, was present 2-7 days after the repeated seizures. At least 9 seizures, or at least 250 s of seizure discharge, were needed to induce reactive gliosis. After seizures, cells staining for vimentin were found in the dentate gyrus molecular layer and hilar region, as well as in the molecular layer of CA1. Fewer cells were stained in the CA3 region. These experiments demonstrate that repeated discrete seizures of the hippocampal-parahippocampal circuits can cause reactive gliosis and localized induction of a glial protein (vimentin) that is not normally expressed in the adult brain.
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PMID:Repeated seizures increase GFAP and vimentin in the hippocampus. 873 64

The issue of whether neuronal degeneration is a primary factor in activation of astrocytes during epileptogenesis was addressed using the kindling model of epilepsy. No degenerative changes specific to the kindling process were observed in brain sections from kindled animals, sampled from the olfactory bulbs through to cerebellum and processed with the degeneration-sensitive cupric silver stain. Also, examination of lectin-stained sections did not reveal any reactive microglia. At the same time, reactive astrocytes, as judged by an increase in glial fibrillary acidic protein immunoreactivity and a de novo vimentin immunoreactivity, were prominent in amygdala, piriform cortex, entorhinal cortex and hippocampus. These results suggest that loss of neurones is not a prerequisite for establishment of epilepsy-prone state, that seizures of short duration do not necessarily result in neuronal death, and that in kindling, astrocytes are activated by factors that are not related to neuronal degeneration, but which are likely associated with abnormal neuronal activity.
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PMID:Activation of astrocytes during epileptogenesis in the absence of neuronal degeneration. 898 6


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