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

The classical view of the function of radial glia in brain development is a supporting function guiding radial neural migration. However, recent evidence indicates that they may play key roles in neurogenesis and gliogenesis, as ubiquitous precursors that generate neurons and glia. Although we previously reported the emergence of radial glia after spinal cord injury in adult rats, their precise function in this process is still unknown. In the present study, we examined emergence of radial glia in rat brain during progression of kindling, by performing immunohistochemical staining for vimentin which is a specific marker of radial glia. Vimentin immunoreactivity was found to be highest at clonus 3 and then decreased at clonus 5 in the hippocampal formation, regions around the third ventricle, caudate putamen and lateral habenular nucleus. Contrast, vimentin immunoreactivity consistently increased with progression of kindling in the cingulum and parietal cortex. These findings indicate dynamic changes in vimentin expression dependent on the kindling stage of seizure-prone state, and suggest that these changes play roles in formation of new circuits following kindling.
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PMID:Regional expression of the radial glial marker vimentin at different stages of the kindling process. 1545 Oct 15

Marked perivascular clustering (PC), i.e., groups and rows of small round cells along white matter vessels, is seen in temporal lobe epilepsy (TLE) specimens obtained by surgery. This study focuses on the constituting cell types and discusses clinical significance and pathogenesis of PC, which are so far unknown. Based on a series of 59 nonlesional TLE surgical specimens, we characterized PC by immunohistochemistry and correlated the amount of PC with clinical parameters. PC cells were variably positive for galactocerebroside, myelin basic protein and S-100 protein, while glial fibrillary acidic protein, vimentin, nestin and neuronal antigens were not expressed. There was no correlation between the amount of PC and any clinical feature, including age at surgery, age at epilepsy onset, duration of epilepsy, preoperative seizure frequency, childhood febrile convulsions, family history of epilepsy, and postsurgical outcome. Our findings suggest oligodendroglial differentiation of PC, while its primary (dysplastic) versus secondary (reactive) pathogenesis remains unresolved.
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PMID:Perivascular clustering in temporal lobe epilepsy: oligodendroglial cells of unknown function. 1548 Jul 11

The amygdala-kindling model is used to study complex partial epilepsy with secondary generalization. The present study was designed to (A) quantify astrocytic changes in the piriform cortex of amygdala-kindled subjects over time and (B) investigate the role that astrocytes might play in maintaining the seizure-prone state. In Study A, once the experimental subjects reached five stage 5 seizures, stimulation was stopped, and both kindled and control rats were allowed to survive for the interval appropriate to their group (7, 18, 30, or 90 days). Following each interval, the kindled and control animals were given 10 intraperitoneal injections of bromodeoxyuridine (BrdU) and sacrificed 24 h following the last injection. Significantly higher numbers of dividing astrocytes (identified by co-labeling for BrdU and to one of the astrocytic intermediate filament proteins glial fibrillary acidic protein or vimentin) were found in the kindled brains. All kindled groups had significantly higher numbers of double-labeled cells on the side contralateral to the stimulation site, except for those in the 90 day survival group. In Study B, rats were implanted with chemotrodes, were kindled as in Study A, and were subsequently infused with either saline or with L alpha-AA (to lesion astrocytes) during a further 25 stimulations (1/day). L alpha-AA infused rats had significantly diminished levels of behavioral seizures, higher after discharge thresholds, lower after discharge durations, and decreased numbers of double-labeled astrocytes in piriform cortex than did saline infused rats. Together, the data indicate that astrocytes may play a role in maintaining the seizure-prone state.
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PMID:Might astrocytes play a role in maintaining the seizure-prone state? 1588 17

A cerebrospinal fluid sample collected from the cerebellomedullary cistern of a 10-year-old Shetland Sheepdog with a recent history of seizures was submitted for fluid analysis and cytologic examination. Key findings included a total nucleated cell count of 520/microL (reference interval 0-5 cells/microL), with a predominance of mononuclear cells, a protein concentration of 51.8 mg/dL (reference interval 0-35 mg/dL), and a glucose concentration of 44.7 mg/dL (reference interval 52-105 mg/dL). There was marked atypia of the mononuclear cells, with abundant eosinophilic cytoplasm, marked anisocytosis and anisokaryosis, occasional binucleated cells, mitotic figures, and rare erythrophagia. The cytologic interpretation was marked, monocytoid-rich, mixed cell pleocytosis with cellular atypia worrisome for neoplasia. In addition to histiocytic neoplasia, differentials included granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and granulomatous inflammation. The dog did not respond to anti-inflammatory and anticonvulsive therapy. At necropsy, a mass involving the meninges and subtending the neuropil of the right temporal lobe of the cerebrum was found. Histologically, the mass was composed of large, bizarre histiocytic cells with multinucleated forms and numerous mitotic figures. Using immunochemistry on cytologic and histologic samples, the pleomorphic histiocytic cells were positive for CD1c, CD11ad, CD45, lysozyme, and vimentin, and were negative for CD3, CD4, CD79a, CD90, and pancytokeratin. These findings supported a diagnosis of primary CNS malignant histiocytosis of dendritic antigen-presenting cell (CD1c+) origin. To our knowledge, this is only the third reported case of primary CNS histiocytic sarcoma in dogs, and the first to demonstrate strong immunochemical evidence for dendritic antigen-presenting cell origin.
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PMID:Cerebrospinal fluid from a 10-year-old dog with a single seizure episode. 1651 5

Three dogs (two Rottweilers and a Flat-coated retriever) showed various neurological signs, including apathy, depression, circling, a partial decrease in functions associated with cranial nerves, seizures, hyperaesthesia, proprioceptive deficits, and increased spinal reflexes. In all three cases, necropsy revealed a solid, distinct, white mass in the brain and multiple, poorly demarcated, firm nodular proliferations in the lung; in one case the liver was also affected. Histopathological examination showed loosely aggregated, pleomorphic cells, with abundant eosinophilic cytoplasm. The neoplastic cells sometimes contained vacuoles or phagocytized cells. Binucleated and multinucleated giant cells, and mitotic figures, were common. Immunohistochemically, the tumour cells reacted strongly for lysozyme and vimentin, but there was no reaction for S-100 protein, cytokeratin, CD3 or CD79a. The histological and immunohistochemical examinations indicated a histiocytic origin of the tumour cells and malignant histiocytosis was therefore diagnosed.
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PMID:Malignant histiocytosis of the brain in three dogs. 1653 81

We report five cases of sporadic meningioangiomatosis, three males and two females, ranging in age from 12 to 36 years at diagnosis. The lesion was found incidentally by MRI after a head trauma in one case; the other four subjects had a seizure disorders, which improved following surgical resection of the cortical lesions. Grossly, the lesionectomy specimens were of a whitish color and firm consistency. Histological examination revealed that the lesions were confined to the cortex with focal involvement of the overlying leptomeninges, and revealed unifying features of meningioangiomatosis, such as proliferating microvessels with perivascular cuffs of spindle-cell proliferation within the cortex. Two cases had numerous calcifications; one was associated with a prominent fibrocalcifying component. Immunostaining results were variable among the cases. Only vimentin was consistently positive. Some of the spindle cells were weak positive for EMA in two cases. Immunoreactions with anti-CD34 detected within the cytoplasm of the spindle cells were observed in three of the five cases. The Ki-67 proliferation index of all the cases was very low, less than 0.1%. Neurofibrillary tangles were identified in only one of the five cases using the Bodian and immunostaining methods. These findings indicate that meningioangiomatosis lesions show a wide range of clinicopathological features, making diagnosis difficult. A histopathological spectrum and differential diagnoses were discussed with a review of the literature. Since this lesion is a distinct clinicopathological entity and hamartomatous in nature, it is important to make a correct diagnosis in order to avoid further aggressive treatment.
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PMID:Histopathological study of five cases with sporadic meningioangiomatosis. 1677 Nov 83

Hippocampal kindling, a model of mesial temporal lobe epilepsy, is developed through repetitive stimulation of the hippocampus and leads to increased after-discharges as measured by EEG and an enduring seizure-prone state. Synthesis of new proteins is thought to form the basis for sustained seizure-induced physiological and/or pathological changes in synaptic reorganization and apoptotic/necrotic neuronal death. Here we examined the effect of kindling on stimulus-induced c-Jun N-terminal kinase (JNK) and p38 phosphorylation, events postulated to lie upstream of seizure-induced changes in gene transcription. We found that stimulus-induced phosphorylation of JNK, but not of p38, is significantly enhanced in kindled animals compared with their naive counterparts in the CA1 subregion of the hippocampus. Immunofluorescent staining confirmed this region-specific pattern of JNK activation and revealed that reactive astrocytes mediate this effect. Astrocyte proliferation and hypertrophy, as well as upregulation of vimentin protein levels, common markers of astrogliosis, were present after 4 d of kindling. Moreover, this reactive astrogliosis was associated with neuronal death as visualized with Fluoro-jade B and anti-active caspase-3 staining. Stimulus-induced phosphorylation of the JNK substrate paxillin was enhanced in kindled animals, but not that of c-Jun. Moreover, a pan-antibody against MAPK/CDK (mitogen-activated protein kinases/cyclin-dependent kinase) substrates indicated the presence of phosphorylated proteins in cytosolic, membrane, and nuclear fractions. The consequence of these phosphorylation events is not completely understood, but these findings suggest a selective astrocytic signaling response to aberrant synaptic activity, signaling that may modulate kindling progression and/or neuronal death.
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PMID:c-Jun N-terminal kinase activation responses induced by hippocampal kindling are mediated by reactive astrocytes. 1689 24

In the adult human brain, the presence of neural stem cells has been documented in the subgranular layer of the dentate gyrus of the hippocampus and in the subventricular zone of the lateral ventricles. Neurogenesis has also been reported in rodent models of ischemic stroke, traumatic brain injury, epileptic seizures, and intracerebral or subarachnoid hemorrhage. However, only sparse information is available about the occurrence of neurogenesis in the human brain under similar pathological conditions. In the present report, we describe neural progenitor cell proliferation in the brain of patients suffering from subarachnoid hemorrhage (SAH) resulting from ruptured aneurysm. Ten cerebral samples from both SAH and control patients obtained, respectively, during aneurysm clipping and deep brain tumor removal were analyzed by reverse transcription followed by polymerase chain reaction (RT-PCR) and/or immunohistochemistry (IHC). In tissue specimens from SAH patients, RT-PCR and IHC revealed the expression of a variety of markers consistent with CNS progenitor cells, including nestin, vimentin, SOX-2, and Musashi1 and -2. In the same specimens, double immunohistochemistry followed by confocal analysis revealed that Musashi2 consistently colocalized with the proliferation marker Ki67. By contrast, no such gene or protein expression profiles were detected in any of the control specimens. Thus, activation of neural progenitor cell proliferation may occur in adult human brain following subarachnoid hemorrhage, possibly contributing to the promotion of spontaneous recovery, in this pathological condition.
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PMID:Activation of endogenous neural stem cells in the adult human brain following subarachnoid hemorrhage. 1745 4

Diffuse cerebellar meningeal carcinomatosis secondary to haematogenous dissemination from an anaplastic solid mammary carcinoma was diagnosed in an old German shepherd dog suffering from seizures and rapidly progressing to stupor. A single computed tomography cerebellar scan identified an unusual homogeneous density area that was considered to be associated with a vascular disorder, in the absence of space-occupying lesions. At necropsy, nodular masses were observed in the mammary gland, lungs, tracheobronchial lymph nodes and adrenals. Cerebellar leptomeninges were affected by diffuse blood effusion. Histology showed a solid mammary tumour, characterised by anaplastic cells with a cytoplasmic keratin-positive and vimentin-negative immunoreaction. The tumour had spread to the lungs, tracheobronchial lymph nodes and adrenals. Cerebellar leptomeninges were diffusely infiltrated by the cytokeratin-positive neoplastic cells. Even though computed tomography scan gave no evidence of meningeal carcinomatosis, it was considered that a cerebellar vascular disorder might be present. This was subsequently confirmed by neuropathological investigation and seen to be associated with a cerebellar leptomeningeal carcinomatosis.
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PMID:Cerebellar leptomeningeal carcinomatosis in a dog. 1760 59

Angiocentric glioma has recently been described as a novel epilepsy associated tumor with distinct clinico-pathologic features. We report the clinical and pathologic findings in 8 additional cases of this rare tumor type and extend its characterization by genomic profiling. Almost all patients had a history of long-standing drug-resistant epilepsy. Cortico-subcortical tumors were located in the temporal and parietal lobes. Seizures began at 3 to 14 years of age and surgery was performed at 6 to 70 years. Histologically, the tumors were characterized by diffuse growth and prominent perivascular tumor cell arrangements with features of astrocytic/ependymal differentiation, but lacking neoplastic neuronal features. Necrosis and vascular proliferation were not observed and mitoses were sparse or absent. MIB-1 proliferation indices ranged from <1% to 5%. Immunohistochemically, all cases stained positively for glial fibrillary acidic protein, vimentin, protein S100B, variably for podoplanin, and showed epithelial membrane antigen-positive cytoplasmic dots. Electron microscopy showed ependymal characteristics in 2 of 3 cases investigated. An analysis of genomic imbalances by chromosomal comparative genomic hybridization revealed loss of chromosomal bands 6q24 to q25 as the only alteration in 1 of 8 cases. In 1 of 3 cases, a high-resolution screen by array-comparative genomic hybridization identified a copy number gain of 2 adjacent clones from chromosomal band 11p11.2 containing the protein-tyrosine phosphatase receptor type J (PTPRJ) gene. All patients are seizure free and without evidence of tumor recurrence at follow-up times ranging from 1/2 to 6.9 years. Our findings support 2 previous reports proposing that angiocentric glioma is a novel glial tumor entity of low-grade malignancy.
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PMID:Angiocentric glioma: report of clinico-pathologic and genetic findings in 8 cases. 1805 28


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