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

Neuronal firing during experimental convulsions triggered a large increase in brain eicosanoid synthesis. Mature astrocytes are an important source of cerebral prostanoids. Endogenously formed prostaglandins possess anticonvulsive properties of biological relevance. These conclusions suggest new ideas that might explain the formation and functions of prostanoids in the brain. First, as augmented neuronal discharge is a prerequisite for enhanced prostanoid synthesis during seizures, a functional coupling between firing neurons and prostanoid-forming astrocytes may be expected. Second, the anticonvulsive effects of endogenous prostanoids suggest that astroglia-derived substances might regulate neuronal activity. The phenomenon of convulsion-induced prostanoid synthesis may, therefore, represent a new example of neuron-glia interaction. Neither K+-induced membrane depolarization nor receptor activation by drugs with affinity to alpha or beta adrenoceptors, dopamine, serotonin, muscarine, histamine, GABA, glutamate, aspartate, adenosine, and opioid receptors evoked eicosanoid synthesis in astrocytes. The only physiologically relevant ligand that induced prostanoid synthesis concentration dependently in astrocytes was ATP and related nucleotide triphosphates, as well as nucleotide disphosphates. In peripheral nerves ATP serves as a cotransmitter. The effect of the P2 agonists was reduced by pertussis toxin. The mechanism by which eicosanoids regulate neuronal activity remains to be elucidated.
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PMID:Formation and function of eicosanoids in the central nervous system. 267 46

Neuronal GABAergic sensitivity was assessed using electrophysiological, biochemical and behavioral techniques following the continuous release and maintenance of relatively constant brain levels of diazepam for greater than or equal to 21 days. Our studies indicate that long-term exposure to diazepam results in: (1) a decrease in iontophoretic sensitivity to GABA in the dorsal raphe nucleus, (2) an increase in the affinity of the GABA recognition site in brain tissue and (3) an increase in susceptibility to bicuculline-induced seizures in the intact animal. Since the decrease in GABAergic responsiveness was observed in the presence of measurable levels of diazepam, it was concluded that this subsensitivity phenomenon is associated with tolerance and not with withdrawal effects of the benzodiazepines.
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PMID:Continuous release of diazepam: electrophysiological, biochemical and behavioral consequences. 299 22

A child with AB variant GM2 gangliosidosis who had progressive intellectual deterioration and seizures commencing at the age of 12 months is described. Neuronal loss, and neuronal and astrocytic inclusions characteristic of the gangliosidoses, were seen on cortical biopsy. GM2 ganglioside was detected in the CSF. As CNS ganglioside accumulation in this condition occurs in the presence of normal leukocyte hexosaminidase A and B levels, spinal fluid assay for GM2 ganglioside may serve as a valuable aid in diagnosis.
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PMID:AB variant GM2 gangliosidosis: cerebrospinal fluid and neuropathologic characteristics. 308 32

This study addresses the question of whether the cyclooxygenase inhibitors indomethacin and diclofenac and the glucocorticosteroid dexamethasone ameliorate neuronal necrosis following cerebral ischemia. In addition, since these drugs inhibit the production of prostaglandins and depress phospholipase A2 activity, respectively, the importance of free fatty acids (FFAs) on the development of ischemic neuronal damage was assessed. Neuronal damage was determined in the rat brain at 1 week following 10 min of forebrain ischemia. The cyclooxygenase inhibitors, whether given before or after ischemia, failed to alter the brain damage incurred. Animals given dexamethasone were divided into three groups and the drug was administered at a constant dosage of 2 mg/kg: (a) 2 days, 1 day, and 3 h intraperitoneally before (chronic pretreatment), (b) 3 h intraperitoneally before (acute pretreatment), and (c) 5 min intravenously and 6 h and 1 day intraperitoneally after (chronic posttreatment) induction of ischemia. Acute pretreatment did not affect the histopathological outcome. Chronic posttreatment of animals with dexamethasone ameliorated the damage inflicted on the caudate nucleus, but had no effect on other brain areas investigated. Unexpectedly, the chronic pretreatment aggravated the brain damage and caused seizures following ischemia. Histopathological data showed massive neuronal damage in these brains. The accumulation of FFA levels during ischemia was markedly suppressed, and the decrease in the energy charge was curtailed by chronic pretreatment with dexamethasone. However, brain glucose levels in control animals and lactic acid concentrations following 10 min of ischemia were significantly higher both in the cerebral cortex and in the hippocampus of dexamethasone-treated animals. These results suggest that aggravation of neuronal necrosis by chronic dexamethasone pretreatment could be ascribed to lactic acidosis due to hyperglycemia in combination with an action of dexamethasone on glucocorticoid receptors in the brain.
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PMID:Chronic dexamethasone pretreatment aggravates ischemic neuronal necrosis. 309 61

A newborn is reported with diffuse gliomatosis involving the cerebral hemispheres, the brainstem and the cerebellum. The presenting signs were paucity of spontaneous movements except for multifocal clonic seizures, absent response to sensory stimuli and optic atrophy. A CT scan suggested agyria. The child expired on the seventh day. Autopsy disclosed diffuse gliomatosis affecting both cerebral hemispheres, the brainstem and the whole cerebellum, but excluding the spinal cord. Neuronal loss was unusually severe in all the affected areas. The genitals were ambiguous, an association not explained by the cerebral pathology. The karyotype was 46XY (male pseudohermaphroditism). This is probably the first reported instance of gliomatosis cerebri in a newborn.
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PMID:Gliomatosis cerebri in a newborn. 320 77

Fifty patients underwent superficial temporal lobectomy for intractable temporal lobe epilepsy. Total cure rate was 52%, and significant improvement was achieved in 88%. Cytoarchitectural changes in gray and white tissue were analyzed under light microscopy. Neuronal dysgenesis was correlated with the duration of seizure disorder, age of onset, and other etiologic factors, and with clinical outcome. Temporal lobes from 33 neurologically normal autopsy brains which were age- and sex-matched with patients were examined as controls. Severe neuronal ectopia (greater than 8 neurons/2 mm2 white matter) was present in 42% of patients with epilepsy and in none of controls. There was neuronal clustering in 28% of those with epilepsy, and Chaslin's (subpial) gliosis in 38%. Controls did not have these changes. The presence of severe neuronal ectopia and clustering was predictive of a favorable clinical outcome following surgery (p less than 0.05). No correlation was found between microdysgenesis and other factors. These findings suggest that the presence of neuronal dysgenesis may be of significance in the clinical outcome following surgery, and that the abnormal tissue may be important as a morphologic substrate for seizures in some patients.
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PMID:Microdysgenesis in resected temporal neocortex: incidence and clinical significance in focal epilepsy. 338 20

The effect of L-homocysteine and selected derivatives on the high-affinity uptake of the inhibitory neuroeffectors, GABA and taurine, was investigated in synaptosomes, and in cultured neurons and astrocytes. High-affinity uptake of taurine into synaptosomes was inhibited most effectively by L-homocysteine, DL-homocysteine and homocystine whereas neuronal uptake was unaffected by any of the compounds tested. The high affinity uptake of taurine into astrocytes was markedly inhibited by L-homocysteine, L-homocysteic acid and L-homocystine. High-affinity GABA uptake into astrocytes was notably inhibited by L-homocystine, none of the other compounds tested causing appreciable inhibition below a concentration of 5 mM. Neuronal and synaptosomal high-affinity uptake of GABA was not significantly affected by any of the test compounds at concentrations below 5 mM. The implication of these results to the study of the mechanism of homocysteine-induced seizures and their relevance to the genetic disorder homocystinuria is discussed.
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PMID:Effect of L-homocysteine and derivatives on the high-affinity uptake of taurine and GABA into synaptosomes and cultured neurons and astrocytes. 368 29

Neuronal necrosis in the brain resulting from status epilepticus of 15 to 120 minutes duration in ventilated and well-oxygenated rats was assessed. Seizures were induced by inhalation of the convulsant gas flurothyl, and terminated by withdrawal of flurothyl and a single injection of thiopental. The animals were allowed to recover for one week, and neuronal damage was assessed by cell counts following subserial sectioning of the brain and microscopical examination of the sections. Infarction of the pars reticulata of the substantia nigra occurred in 5 of the 6 animals with seizure duration of 30 minutes, and in all animals with longer seizure durations. There also was a common affectation of the central parts of the globus pallidus. The pars compacta of the substantia nigra was never affected. After 45 to 120 minutes of seizures, moderate neuronal necrosis was observed in the neocortex (layers 3 and 4), and after 60 to 120 minutes was seen in amygdaloid and thalamic nuclei, as well as in CA4 and CA1 hippocampal pyramidal cells. Notably, CA3 neurons were not damaged nor were dentate granule cells affected. After 120 minutes of seizures, damage regularly affected the neocortex and the ventral-posterior nuclei of the thalamus. A conspicuous feature was the localization of neuronal necrosis at sites close to the ventricles.
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PMID:Status epilepticus in well-oxygenated rats causes neuronal necrosis. 405 57

Neuronal recordings from occipital cortex and hippocampus during a seizure originating in the occipital lobe of a patient with an occipito-temporal tumor demonstrated that the visual aura resulted from neuronal activation of medial peristriate and possibly other occipital lobe neurons while the psychomotor automatisms followed 10-20 sec later and were caused by recruitment of hippocampal neurons bilaterally. This confirmed that the complex seizure symptoms were caused by propagation from an occipital lobe focus. The psychomotor symptoms have not recurred for the 6 months since interruption of occipito-temporal connections; however, the spared medial occipital neurons still produce visual auras.
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PMID:Neuronal firing patterns during the spread of an occipital lobe seizure to the temporal lobes in man. 616 74

Neuronal mechanisms responsible for a vertical restriction of focal seizure activity in the motor cortex were analysed. For this purpose intracellular recording from neurones in superficial (50-300 microns below cortical surface), middle (300-800 microns) and deep cortical layers (800-1300 microns) was performed. As a model of foci of various vertical extensions the spread of seizure activity from superficial to deeper cortical laminae following epicortical penicillin application was used. The appearance of characteristic epileptiform potentials in the surface record with a focus restricted to upper cortical laminae was accompanied (i) in superficial neurones by the development of paroxysmal depolarization shifts (PDS), (ii) in middle neurones by depolarization often followed by hyperpolarization, and (iii) in deep neurones by a sequence of membrane potential changes. The latter consisted of an initial depolarization, an early hyperpolarization, an intermediate depolarization, a late hyperpolarization and a final depolarization. The hyperpolarizing components led to complete suppression of action potentials (vertical inhibition). The early hyperpolarization and the first part of the late hyperpolarization were reduced in amplitude when the intracellular chloride activity was elevated. The intermediate depolarization was replaced by PDS with the enlargement of the epileptic focus into the cortex. The actual effect of the vertical inhibition may in part be responsible for the variability in epileptic motor phenomena coinciding with epileptiform potentials in the surface EEG.
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PMID:Penicillin-induced epileptic foci in the motor cortex: vertical inhibition. 619 79


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