Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleomorphic xanthoastrocytoma (PXA) is an uncommon tumor, often seizure-associated and occurring in the temporal lobe of young adults. Although its cells are considered astrocytic in nature, recent studies suggest the presence of neuronal differentiation and a possible relationship to glioneuronal neoplasms. We immunostained 40 cases of PXA, including two composite PXA-gangliogliomas (PXA-GG), with a panel of glial (glial fibrillary acidic protein, S-100 protein) and neuronal markers (class III beta-tubulin, synaptophysin, neurofilament proteins, MAP2, and chromogranin A). Conventional PXAs demonstrated immunoreactivity for glial fibrillary acidic protein (100% of cases), S-100 protein (100%), class III beta-tubulin (73%), synaptophysin (38%), NF proteins (18 and 8%), and MAP2 (8%). Chromogranin A stain was absent in all conventional PXA cases. Neoplastic ganglion cells in both PXA-GGs stained with class III beta-tubulin, synaptophysin, and chromogranin A. Ultrastructural studies, performed in nine cases, demonstrated neuronal features including microtubules, dense core granules, and/or clear vesicles largely limited to cell processes (two PXAs) and in the cytoplasm (PXA component of one PXA-GG). Although the essential nature of PXA is clearly and uniformly glial, the significance of the limited neuronal differentiation is unclear, as it is the relationship between conventional PXA and PXA-GG. We found no evidence that the former is a precursor of the latter.
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PMID:Immunophenotype of pleomorphic xanthoastrocytoma. 1191 26

Neurocytoma is an unusual neuronal tumor especially affecting young people. It commonly arises in the ventricles and has a benign outcome. Herein, we report on a rare case of extraventricular neurocytomas (right parietal lobe) in a young girl admitted to hospital for a cranial trauma subsequent to a seizure. The tumor, radiologically well-circumscribed, cystic and enhancing, was surgically excised. The patient, who received no post surgical treatment, is alive and well after 18 months of follow-up. Pathological examination showed a well-differentiated lesion composed of uniform, round cells with perinuclear halos in a neuropil background and immunohistochemically positive for neuronal markers (synaptophysin, neuron-specific enolase, neurofilaments). The authors emphasize the role of the morphological and immunohistochemical evaluations to recognize this rare tumor.
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PMID:Extraventricular neurocytoma: morphological and immunohistochemical considerations on differential diagnosis. 1244 Jul 86

A female patient started to suffer from transient ischemic attacks when she was 47 years of age, followed by increasing predominantly left-side spastic tetraparesis, generalized seizures and progressive dementia over a period of 11 years. She died when she was 58 years of age. On gross examination the brain showed enlarged ventricles and arteriosclerotic changes of large extracerebral vessels of the circulus arteriosus. Microscopic examination of the atrophic brain showed innumerable incomplete microinfarcts in the white and gray matter throughout all parts of the brain. In the white matter these lesions were characterized by small foci of demyelination and loss of oligodendrocytes while occasionally some scavenger cells were seen. Axons seemed to be unaffected or displayed irregular axonal regeneratory growth. Any inflammatory reaction failed. In the cerebral cortex and subcortical nuclei the lesions showed loss of neurons and decrease in synaptophysin expression. Intracerebral arteries showed fibrosis or fibrohyalinosis of the entire intracerebral small-vessel network. In addition, numerous uncommon clusters of angioma-like telangiectatic vessels were observed. Medium-sized ischemic infarcts were found in the right putamen and adjacent internal capsule region, left-side dorsolateral brain stem and cerebellar hemisphere as well as a left-side pyramidal tract degeneration. Contralateral pseudohypertrophy of the inferior olivary nucleus was seen. The clinical and the neuropathologic observations made in this patient are compatible with small vessel disease characterized by a multicentric special and not yet described type of incomplete mini-infarcts in cerebral cortex and white matter accompanied by some larger ischemic infarcts of the common type in brain stem and cerebellum.
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PMID:Mini-infarct encephalopathy associated with uncommon microvessel convolute formation presenting with presenile dementia. 1280 52

Apoptosis-linked gene-2 interacting protein X (Alix) is thought to be involved in both cell death and vesicular trafficking. We examined Alix expression 2 h, 6 h and 24 h after triggering seizure-dependent neuronal death by i.p. kainic acid injection. In the hippocampus, intense, transient immunolabelling was observed in the strata lucidum, oriens and radiatum, areas of high synaptic activity. The similarity of this distribution to those of synaptophysin and endophilin suggests a presynaptic localisation. Alix labelling was increased in neuronal cell bodies in kainate-sensitive regions before or concomitant with the first signs of oedema and/or neuronal eosinophilia. The increase persisted 24 h after kainate-injection in CA3 and the piriform cortex which are areas with massive swelling and numerous pyknotic neurons. This suggests that Alix may play an early role in the mechanisms leading to cell death. Taken together, our results suggest that Alix may be a molecular link between synaptic functioning and neuronal death.
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PMID:Early increase of apoptosis-linked gene-2 interacting protein X in areas of kainate-induced neurodegeneration. 1475 Dec 82

Desmoplastic infantile ganglioglioma is a very rare supratentorial tumor occurring in the first two years of life. A five-month-old female infant presented with recurrent seizures, large head and loss of acquired milestones. Computerized Tomographic Scan of brain showed a large subarachnoid cyst with a solid intensely contrast enhancing tumor in the right temporoparietal region with severe degree of mass effect. Craniotomy and total excision of the tumor followed subsequently by subduro-peritoneal shunt for the extracerebral fluid collection was done. The child made good recovery. Histopathology revealed features of desmoplastic infantile ganglioglioma, viz., marked desmoplastic component with glial and neuronal elements. Immunohistochemistry showed positive staining for glial fibrillary acidic protein (GFAP) with areas of synaptophysin and chromogranin positivity. Desmoplastic infantile ganglioglioma is a rare tumor of infancy, which has excellent prognosis after total excision. No adjuvant therapy is required. This is the first Indian report of desmoplastic infantile ganglioglioma out of less than fifty cases reported worldwide.
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PMID:Desmoplastic infantile ganglioglioma -- a case report. 1547 36

Subependymal giant cell astrocytomas (SEGAs) are relatively rare tumors but occur commonly in the setting of the familial syndrome of tuberous sclerosis complex (TSC). In view of its varied morphology, i.e. resemblance to astrocytic and ganglion cells, its histogenesis remains controversial. We studied 23 cases of SEGA, 19 from our own institute and 4 from NIMHANS, Bangalore. These 19 cases of SEGAs were collected over a period of 23 years (1979 to 2001), and accounted for 0.16% of intracranial tumors and 0.51% of all gliomas reported at our center. The majority of patients presented with visual disturbances (19/23, 82.6%) in the form of decreased vision (60.8%) and blindness (21.7%), generalized tonic clonic seizures (43.4%) and focal motor seizures (4.37%). Age ranged from 4 to 37 years (mean 13.2 years) with male predominance (M:F 2.2:1), and the duration of symptoms varied from 1 month to 96 months (mean 17.2 months). Lateral ventricular involvement was the most common site (91.3%), followed by the third ventricle (8.6%). Nine patients (39.1%) had stigmata of tuberous sclerosis (6 at the time of diagnosis and 3 in the follow-up period). Two patients died due to surgical complications, while the rest were alive and well in the follow-up period ranging from 3 to 264 months (mean 37.1 months). Two patients experienced recurrences, one two years and another 22 years after surgery. Microscopic examination showed varied histology consisting of sweeping bundles of spindle cells, gemistocyte and ganglion-like cells with interspersed inflammatory cell component. The inflammatory cell component on special staining turned out to be an admixture of mast cells and T lymphocytes. Six cases showed areas of necrosis and/or mitosis, but were not indicative of aggressive nature of this tumor. Immunoreactivity for GFAP, NF, S-100, NSE and synaptophysin indicates that this is a hybrid tumor with glial and neuronal differentiation. None of the tumors was immunopositive for HMB-45. The significance of the presence of T lymphocytes and mast cells is not clear. It could be related to tumor immunology and may indicate a favorable prognosis.
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PMID:Subependymal giant cell astrocytoma--a clinicopathological study of 23 cases with special emphasis on histogenesis. 1561 43

During status epilepticus (SE), GABAergic mechanisms fail and seizures become self-sustaining and pharmacoresistant. During lithiumpilocarpine-induced SE, our studies of postsynaptic GABA(A) receptors in dentate gyrus granule cells show a reduction in the amplitude of miniature IPSCs (mIPSCs). Anatomical studies show a reduction in the colocalization of the beta2/beta3 and gamma2 subunits of GABA(A) receptors with the presynaptic marker synaptophysin and an increase in the proportion of those subunits in the interior of dentate granule cells and other hippocampal neurons with SE. Unlike synaptic mIPSCs, the amplitude of extrasynaptic GABA(A) tonic currents is augmented during SE. Mathematical modeling suggests that the change of mIPSCs with SE reflects a decrease in the number of functional postsynaptic GABA(A) receptors. It also suggests that increases in extracellular [GABA] during SE can account for the tonic current changes and can affect postsynaptic receptor kinetics with a loss of paired-pulse inhibition. GABA exposure mimics the effects of SE on mIPSC and tonic GABA(A) current amplitudes in granule cells, consistent with the model predictions. These results provide a potential mechanism for the inhibitory loss that characterizes initiation of SE and for the pharmacoresistance to benzodiazepines, as a reduction of available functional GABA(A) postsynaptic receptors. Novel therapies for SE might be directed toward prevention or reversal of these losses.
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PMID:Trafficking of GABA(A) receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus. 1676 Oct 75

Several types of glioneuronal tumors are known to induce intractable partial seizures in children and adults. The most frequent are dysembryoplastic neuroepithelial tumors (DNETs) and gangliogliomas. We report here a new clinicopathological entity within the spectrum of glioneuronal tumors observed in 10 children who underwent surgery for refractory epilepsy. These tumors demonstrate a unique, pathognomonic histological pattern and a specific appearance at magnetic resonance imaging (MRI). The most striking neuropathological feature is an angiocentric polarity of the tumor with gliofibrillary acidic protein (GFAP) positive fusiform and bipolar astrocytic cells arranged around blood vessels (perivascular cuffing with tumoral astrocytes). Characteristic MRI findings include involvement of cortical gray and white matter, intrinsically high signal on T1-weighted images, as well as a stalk like extension to the ventricle. Immunohistochemical neuronal markers (neurofilament protein, synaptophysin and chromogranin) confirm the presence of a neuronal cell component. Therefore, the term angiocentric neuroepithelial tumor (ANET) is proposed.
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PMID:Angiocentric neuroepithelial tumor (ANET): a new epilepsy-related clinicopathological entity with distinctive MRI. 1638 40

7beta-Hydroxycholesterol has been previously demonstrated to inhibit astrocytosis in injured cortex or spinal cord of rats. In this study, we explored the inhibitory effects of the liposome containing 7beta-hydroxycholesterol on the reactive astrocytosis caused by the injection of iron into the hippocampus of rats and furthermore evaluated the involvement of reactive astrocytosis in iron-induced epilepsy. Injection of ferric chloride solution unilaterally into the hippocampus of rats induced spontaneous spiking activity ipsilaterally then developed into bilateral hippocampi and generalized convulsive seizures within the first week post-operation, and spontaneous epileptiform activity and generalized seizures lasted as long as 2 weeks post-operation, whereas none of the rats injected with sodium chloride solution unilaterally into the hippocampus developed generalized seizures. With immunohistochemistry and Western blot analyses, apparent reactive astrocytosis in bilateral hippocampi was detected using antibody against glial fibrillary acidic protein 14 days after the injection of ferric chloride solution, but no significant differences were found in the amount of synaptophysin protein, a presynaptic vesicle protein, as compared with the rats injected with sodium chloride solution. Infusion of liposome suspension containing 7beta-hydroxycholesterol into the same site immediately after the injection of ferric chloride solution reduced the extent of the reactive astrocytosis by 50%-55% of the amount of glial fibrillary acidic protein in the hippocampi of both hemispheres, and non-significantly elevated the amount of synaptophysin protein in both sides of hippocampus. However, these effects did not significantly modify the seizure latency and the incidence of generalized seizures in the rats. These findings demonstrate the effects of 7beta-hydroxycholesterol on the inhibition of reactive astrocytosis caused by iron deposition in the hippocampus of rats, and suggest that the reactive astrocytosis may not play a causal role in the development of iron-induced seizures.
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PMID:7beta-hydroxycholesterol reduces the extent of reactive gliosis caused by iron deposition in the hippocampus but does not attenuate the iron-induced seizures in rats. 1644 40

Cannabinoid CB1 receptors are the most abundant G-protein-coupled receptors in the brain. Its presynaptic location suggests a role for cannabinoids in modulating the release of neurotransmitters from axon terminals by retrograde signaling. The neuroprotective effects of cannabinoid agonists in animal models of ischemia, seizures, hypoxia, Multiple Sclerosis, Huntington and Parkinson disease have been demonstrated in several reports. The proposed mechanism for the neuroprotection ranges from antioxidant effects, reduction of microglial activation and anti-inflammatory reaction to receptor-mediated reduction of glutamate release. In the present work, we analyzed the morphological changes induced by a chronic treatment with the synthetic cannabinoid receptor agonist, WIN 55,212-2, in four brain regions where the CB1 cannabinoid receptor is present in high density: the CA1 hippocampal area, corpus striatum, cerebellum and frontal cortex. After a twice-daily treatment for 14 days with the cannabinoid receptor agonist (3 mg/kg sc, each dose) to male Wistar rats (150-170 g), the expression of neurofilaments (Nf-160 and Nf-200), microtubule-associated protein-2 (MAP-2), synaptophysin (Syn) and glial fibrillary acidic protein (GFAP) was studied by immunohistochemistry and digital image analysis. Ultrastructural study of the synapses was done using electron microscopy. After the treatment, a significant increase in the expression of neuronal cytoskeletal proteins (Nf-160, Nf-200, MAP-2) was observed, but we did not find changes in the expression of GFAP, the main astroglial cytoskeletal protein. In cerebellum, there was an increase in Syn expression and in the number of synaptic vesicles, while, in the hippocampus, an increase in the Syn expression and in the thickness of the postsynaptic densities was observed. The results obtained from these studies provide evidences on the absence of astroglial reaction and a sprouting phenomena induced by the WIN treatment that might be a key contributor to the long-term neuroprotective effects observed after cannabinoid treatments in different models of central nervous system (CNS) injury reported in the literature.
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PMID:Neuronal cytoskeleton and synaptic densities are altered after a chronic treatment with the cannabinoid receptor agonist WIN 55,212-2. 1656 7


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