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

Extracellular calcium and potassium activities (aCa and aK) as well as neuronal activity were simultaneously recorded with ion-sensitive electrodes in the somatosensory cortex of cats. Baseline aCa was 1.2-1.5 mM/l, baseline aK 2.7-3.2 mM/l. Transient decreases in aCa and simultaneous increases in aK were evoked by repetitive stimulation of the contralateral forepaw, the nucleus ventroposterolateralis thalami and the cortical surface. Considerable decreases in aCa (by up to 0.7 mM/l) were found during seizure activity. A fall in aCa preceded the onset of paroxysmal discharges and the rise in aK after injection of pentylene tetrazol. The decrease in aCa led also the rise in aK during cyclical spike driving in a penicillin focus. It is concluded that alterations of Ca++ dependent mechanisms participate in the generation of epileptic activity.
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PMID:Extracellular free calcium and potassium during paroxsmal activity in the cerebral cortex of the cat. 88 Sep 84

The opposing actions of diphenylhydantoin (DPH) and calcium on the level of [32P]phosphate incorporation into particular rat and human brain proteins have been demonstrated in this study by employing the techniques of acrylamide gel electrophoresis and autoradiography. In the presence of calcium several brain proteins showed a marked increase in the incorporation of [32P]phosphate from [gamma-32P]ATP. The calcium-induced increase in phosphorylation of two proteins, designated proteins DPH-L and DPH-M, was significantly inhibited by DPH. DPH inhibited both the calcium-stimulated initial rate and net level of [32P]phosphate incorporated into proteins DPH-L and DPH-M in homogenate and synaptosomal preparations. The data presented in this study are compatible with the hypothesis that the effect of DPH on protein phosphorylation may play an important role in mediating the stabilizing actions of this anticonvulsant on neuronal tissue and seizure discharge.
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PMID:Antagonistic action of diphenylhydantoin and calcium on the level of phosphorylation of particular rat and human brain proteins. 91 10

Phenytoin, phenobarbital, ethosuximide, and procaine hydrochloride were evaluated for their ability to inhibit Ca2+ flux into isolated presynaptic endings (synaptosomes) prepared from rabbit neocortex. Calcium influx produced by depolarizing concentrations (69 mM) of K+ was inhibited 7% to 63% by phenytoin, phenobarbital, or procaine, whereas ethosuximide was ineffective. Decreased Ca2+ influx was observed with as little as 0.08 mM phenytoin and 0.04 mM phenobarbital. In contrast, 4 mM procaine was needed to produce an effect. These results lead to the conclusion that ability to produce membrane stabilization is not a property of all anticonvulsant drugs; however, this property may be essential for the action of drugs effective in the treatment of major seizures.
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PMID:Anticonvulsant drug mechanisms. Phenytoin, phenobarbital, and ethosuximide and calcium flux in isolated presynaptic endings. 96 45

The authors present the case of a child aged 7 years who suffered from relapsing acute lymphocytic leukemia. Treatment consisting mainly of oral and intrathecal methotrexate and x-ray therapy produced remission of the hematologic symptoms. Three years after the onset of the leukemia, mental deterioration gradually appeared. Radiography of the skull revealed diffuse bilateral calcium deposits in both cerebral and cerebellar hemispheres. Four years after the onset of the disease, a hematologic relapse occurred. Behavioral disorders became more severe and the child died after a period of seizures and unconsciousness. The main pathologic data obtained by the study of a brain biopsy and after a complete postmortem examination consisted of calcifications located bilaterally in the cerebral and cerebellar cortex. No signs of leukemia were present. Cerebral calcification is an extremely rare complication in the course of the therapy of lymphocytic leukemia. Its possible causes are discussed.
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PMID:Intracerebral calcifications appearing during the course of acute lymphocytic leukemia treated with methotrexate and X-rays. 105 35

Cerebral cortex of cat was incubated with 14C-lysine and 3H-glucosamine. Subsequent superfusion of the surface of the cortex resulted in the release into the superfusate of a variety of 14C- and 3H-labeled compounds including proteins, glycoproteins, and gangliosides. The release of 14C- and 3H-labeled macromolecules could be considerably enhanced by topical addition of 40 mM K+, WHICH INDUCED Epileptiform EEG activity. Peaks in efflux could also be correlated with the onset of seizures induced by superfusion with low (0.75 mM) Ca2+ media. Control experiments in which the cortex was prelabeled with 14C-carboxyl-inulin and 3H2O indicate that the release of macromolecules was not a direct consequence of the altered blood flow that may occur during convulsions.
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PMID:Extracellular release of cerebral macromolecules during potassium- and low-calcium-induced seizures. 112 1

A case of giant aneurysm arising from the anterior communicating artery, 24 X 28 X 30 mm in diameter was found in a 30 year old man. About ten years ago he became blind and recently developed right anosmia and diencephalic seizures. No subarachnoid hemorrhage, however, was found. Radiograms and tomograms of the cranium showed a ring-like calcification, but by angiography it couldn't be recognized as a giant aneurysm. The right frontal craniotomy and partial resection, therefore, was performed. A histological study of the resected material revealed that it was a spontaneously thrombosed giant aneurysm. The inner layer of its wall had neither endothelium nor elastic lamina, but had deposits of calcium salt. The outer layer was composed of collagen fibers without cell infiltration. The aneurysm was thrombosed except for its neck but its organization occurred incompletely. We want to emphasize the importance of a correct preoperative diagnosis, as an erroneous operative procedure can result in disaster. Volume, viscosity and tension of flowing blood into the aneurysm as well as the size of its neck and dome regulate dynamic properties. These properties may determine the enlargement rate or growth of the aneurysm. The dynamic characteristics and features of the inner surface of the aneurysmal wall may regulate the formation of thrombosis in the aneurysm. The intraluminal thrombosis and strength of aneurysmal wall, for example, calcium deposits, may prohibit aneurysm from its rupture.
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PMID:[Giant anterior communicating artery aneurysm (author's transl)]. 123 24

The convulsant profile of lindane was investigated in OF1 and NMRI mice lines in relation to other convulsants acting at the GABAA and NMDA receptor complexes. Thus, a specific GABA-gated chloride channel blocker, PTX, a GABAA receptor antagonist, PTZ, and an excitatory amino acid receptor agonist, NMDA, were used. Antagonism of the convulsant effects of each of these drugs was investigated with (+)MK-801, a blocker of the NMDA-operated cation channel, and with nifedipine, a voltage-dependent calcium channel antagonist. While no differences in potency for PTX or PTZ to induce seizures were observed between OF1 and NMRI mice, lindane was approximately 80 and 90% more potent in its ability to induce seizures and lethality, respectively, in OF1 than in NMRI mice. Brain lindane concentrations at the moment of convulsion, measured after ED100 doses of lindane (400 and 200 mg/kg for NMRI and OF1 mice, respectively), did not differ between OF1 and NMRI mice, suggesting that the different potency of lindane between these mouse lines is a consequence of pharmacokinetic factors. Furthermore, (+)MK-801 antagonized seizures induced by either lindane, PTX or PTZ with similar potencies in both mouse lines. These results, coupled with the different pharmacokinetics of lindane in OF1 and NMRI mice, suggest that the distinct effects of lindane in these mice are not mediated by different activities at either NMDA or GABAA receptor complexes. Nonetheless, nifedipine antagonized lindane-induced seizures with a three-fold higher potency in NMRI than in OF1 mice. In contrast, nifedipine failed to antagonize PTX and PTZ convulsions in both OF1 and NMRI mice. These results suggest that besides the GABAA receptor complex other mechanisms related to calcium mobilization may be involved in the convulsant action of lindane.
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PMID:Lindane-induced convulsions in NMRI and OF1 mice: antagonism with (+)MK-801 and voltage-dependent calcium channel blockers. 128 May 23

1. The convulsant activity of the calcium voltage L-channel agonist Bay k 8644 was studied in genetically epilepsy prone DBA/2 mice. 2. Seizures were induced by intracerebroventricular injection of Bay k 8644. 3. These seizures were reversed by some calcium channel blockers such as dihydropyridines, some excitatory amino acid antagonists such as 2-amino-7-phosphonoeptanoate and CPPene, 2-chloro-adenosine, some anticonvulsant drugs such as magnesium valproate, diazepam and clonazepam and two kappa opioid agonists (U-50488H and U-54494A). 4. The remaining antiepileptic drugs (carbamazepine, phenytoin, phenobarbital and trimethadione) were ineffective in this respect. Other anticonvulsant compounds such as dizocilpine (MK 801), ketamine and drugs enhancing GABAergic transmission did not significantly affect the clonic phase of the seizures induced by Bay k 8644. 5. These results show that Bay k 8644 seizures are relatively resistant to some anticonvulsant compounds. The role of some neurotransmitters on seizures induced by Bay k 8644 is discussed.
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PMID:Effects of antiepileptic drugs, calcium channel blockers and other compounds on seizures induced by activation of voltage-dependent L calcium channel in DBA/2 mice. 128 40

Potassium is tightly regulated within the extracellular compartment of the brain. Nonetheless, it can increase 3- to 4-fold during periods of intense seizure activity and 10- to 20-fold under certain pathological conditions such as spreading depression. Within the central nervous system, neurons and astrocytes are both affected by shifts in the extracellular concentration of potassium. Elevated potassium can lead to a redistribution of other ions (e.g., calcium, sodium, chloride, hydrogen, etc.) within the cellular compartment of the brain. Small shifts in the extracellular potassium concentration can markedly affect acid-based homeostasis, energy metabolism, and volume regulation of these two brain cells. Since normal neuronal function is tightly coupled to the ability of the surrounding glial cells to regulate ionic shifts within the brain and since both cell types can be affected by shifts in the extracellular potassium, it is important to characterize their individual response to an elevation of this ion. This review describes the results of side-by-side studies conducted on cortical neurons and astrocytes, which assessed the effect of elevated potassium on their resting membrane potential, intracellular volume, and their intracellular concentration of potassium, sodium, and chloride. The results obtained from these studies suggest that there exists a marked cellular heterogeneity between neurons and astrocytes in their response to an elevation in the extracellular potassium concentration.
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PMID:Effect of elevated potassium on the ion content of mouse astrocytes and neurons. 129 76

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67


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