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

Prolonged neonatal seizures are often accompanied or exacerbated by hypoxemia. To determine the effects of hypoxemia on neonatal status epilepticus, we determined cerebral blood flow and cerebral metabolic state in groups of neonatal dogs subjected to hypoxia, to seizures during normoxia, or to seizures during hypoxia. The compensatory increase in cerebral blood flow was greatest in animals subjected to seizures during normoxia and somewhat less pronounced in animals made hypoxic. However, blood flow failed to increase in forebrain structures when animals were subjected to the combination of seizures and hypoxia. Accordingly, levels of adenosine triphosphate in forebrain (measured both by in vitro enzymatic analysis and by in vivo phosphorus-31 nuclear magnetic resonance spectroscopy) were depleted to the greatest degree in animals who were seizing while hypoxic. In addition, brain glucose was significantly reduced only in the seizure-hypoxia group. Systemic factors such as hypoxemia may play a critical role in the disruption of cerebral energy balance during neonatal status epilepticus.
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PMID:31P nuclear magnetic resonance study of the effect of hypoxemia on neonatal status epilepticus. 372 54

A series of sulfur-containing congeners have been prepared from alpha-ethyl-alpha-methyl-gamma-butyrolactone, beta-ethyl-beta-methyl-gamma-butyrolactone, and alpha,alpha,beta,beta-tetramethyl-gamma-butyrolactone as potential neuropharmacologic agents. The lactones were treated with benzyl mercaptide anion to form 4-(benzylthio)butyric acid, which, on treatment with trifluoroacetic acid, cyclized to yield thiololactones. The thiono- and dithiolactones were prepared by treating the corresponding lactones either with Lawesson's reagent or with phosphorus pentasulfide, respectively. As had been observed previously for the lactones, the beta-substituted and alpha,beta-substituted congeners were potent convulsants that caused generalized clonic and tonic seizures in mice. The alpha-substituted congeners were effective in inhibiting pentylenetetrazole-induced seizures in mice. alpha-Ethyl-alpha-methylthiolo-gamma-butyrolactone showed an increase in potency over the congeneric alpha-ethyl-alpha-methyl-gamma-butyrolactone and, additionally, was effective against maximal electroshock seizures. In no cases was a convulsant converted to an anticonvulsant or vice versa by sulfur-for-oxygen substitution.
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PMID:Alkyl-substituted thiolo-, thiono-, and dithio-gamma-butyrolactones: new classes of convulsant and anticonvulsant agents. 376 17

In vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy was used to evaluate changes in cerebral high-energy phosphate compounds in 8 infants with seizures. During the study 4 babies had seizures that caused a 50% decrease in the phosphocreatine to inorganic phosphate (PCr/Pi) ratio. Focal seizures caused lateralized decreases in the PCr/Pi ratio; generalized seizures caused bilateral decreases. Postictal spectra had increased PCr/Pi ratios, presumably due to postictal inhibition. Interictal 31P NMR spectra were normal. One patient's seizures were successfully treated with intravenously administered phenobarbital during NMR data acquisition, causing an immediate increase in the PCr/Pi ratio from 0.7 to 1.2. These studies indicate that cerebral PCr concentration decreases by approximately 33% and that oxidative metabolism increases by approximately 45% during neonatal seizures. Five babies had PCr/Pi ratios of less than 0.8 during seizures and subsequently developed long-term neurological sequelae, which suggests that neonatal seizures may cause or exacerbate cerebral injury by increasing cerebral metabolic demands above energy supply.
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PMID:Cerebral metabolic effects of neonatal seizures measured with in vivo 31P NMR spectroscopy. 378 67

The effects of prolonged bicuculline-induced seizures on cerebral blood flow and metabolism were determined in paralyzed, mechanically ventilated neonatal dogs. Transient changes occurring early in the course of status epilepticus included significant arterial hypertension, hypocarbia, elevation of plasma norepinephrine levels, and decline in brain glucose concentration. Cerebral blood flow remained elevated throughout the 45 minutes of seizure. Determination of cerebral metabolite values by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy and by in vitro enzymatic analysis of frozen brain samples showed significant decreases in the level of phosphocreatine and relatively less change in ATP values. Progressive intracellular acidosis occurred, coincident with elevation of brain lactate concentrations. We conclude that the physiological and metabolic alterations that occur during prolonged seizures are not uniform, but change with time. Any hypothesis advanced to explain the mechanism of neuronal injury during prolonged seizures must take into account these temporally related changes.
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PMID:31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog. 403 47

A series of phosphorus compounds, designed as analogues of gamma-aminobutyric acid (GABA) in that they possess a P = O moiety separated by three atoms from an amino or acetamido group, was synthesized and tested by using in vitro GABAA and GABAB receptor binding, GABA uptake assays, and was examined for anticonvulsant activity. Weak GABAB receptor affinity was noted for one agent, whereas six compounds displayed moderate to high potencies as inhibitors of electroshock- and pentylenetetrazol-induced seizures. The best anticonvulsant effect was found with the (m-aminophenyl) phosphinic acid compounds, with members of this class selected for further study.
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PMID:Phosphorus analogues of gamma-aminobutyric acid, a new class of anticonvulsants. 632 92

Bicuculline-induced status epilepticus was studied in paralyzed rabbits ventilated with an oxygen and nitrous oxide mixture. An Oxford Instruments TMR 32-200 spectrometer was used to record phosphorus 31 nuclear magnetic resonance spectra of the in vivo brain. An array of conventional physiological variables including the electroencephalogram was simultaneously recorded. Several features were consistently observed during status epilepticus: (1) Phosphocreatine levels fell to about two-thirds of their control values and remained at that level despite a gradual decline in seizure activity; (2) intracellular pH declined and then remained constant, whereas seizure discharges declined; (3) adenosine triphosphate levels remained constant at their control values. These new, lower levels of brain phosphocreatine and intracellular pH were largely unaffected by increases in seizure activity brought about by elevation of blood pressure from levels too low to support adequate cerebral perfusion, by waning of anticonvulsant drug effect, or by repeated doses of bicuculline.
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PMID:In vivo phosphorus nuclear magnetic resonance spectroscopy in status epilepticus. 647 92

Essential thrombocythemia is a clonal myeloproliferative disorder, characterized predominantly by a markedly elevated platelet count without known cause. We report a case that was recognized during investigation of a transient ischemic attack, and review the neurologic findings in 33 patients with unequivocal essential thrombocythemia under prospective study by the Polycythemia Vera Study Group. Twenty-one patients had neurologic manifestations at some point during their course, including headache (13 patients), paresthesiae (10), posterior cerebral circulatory ischemia (9), anterior cerebral circulatory ischemia (6), visual disturbances (6) and epileptic seizures (2). All patients with neurologic symptoms responded satisfactorily to treatment, although continuous or repeated treatment was often required. Therapeutic recommendations include plateletpheresis for major thrombo-hemorrhagic phenomena, or megakaryocyte suppression with radioactive phosphorus, alkylating agents (such as melphalan), or hydroxyurea; minor symptoms may respond to platelet antiaggregating agents.
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PMID:Neurologic manifestations of essential thrombocythemia. 668 92

Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
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PMID:Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome. 677 12

Magnesium deficiency was induced in a setting of an otherwise adequate diet in adult beagle dogs. Despite the development of severe hypomagnesemia (from 1.5 +/- 0.2 to 0.5 +/- 0.2 meq/liter) during the 10-wk study, Mg content of skeletal muscle fell only modestly (from 3.8 +/- 0.2 to 3.1 +/- 0.4, P less than 0.005, at 7 wk and 3.5 +/- 0.4 mM/100 g FFDS, NS, at 10 wk). The most pronounced muscle compositional changes were a loss of phosphorus (from 29.5 +/- 1.8 to 22.0 +/- 1.6, P less than 0.001, at 7 wk and 24.8 +/- 2.8 mM/100 G FFDS, P less than 0.001, at 10 wk) and gains of calcium (from 0.64 +/- 0.11 to 0.93 +/- 0.17, P less than 0.05, at 7 wk, and 0.85 +/- 0.26 mM/100 g FFDS, P less than 0.05, at 10 wk), sodium (from 13.2 +/- 2.6 to 22.9 +/- 4.7, P less than 0.001 at 7 wk and 17.8 +/- 2.0 meq/100 g FFDS, P less than 0.005, at 10 wk), and chloride (from 5.8 +/- 0.8 to 8.2 +/- 1.6, P less than 0.001, at 7 wk and 6.8 +/- 0.6 meq/100 g FFDS, P less than 0.05, at 10 wk). Cellular potassium content did not change (from 35.9 +/- 1.9 to 33.0 +/- 4.1, NS, at 7 wk and 36.3 +/- 2.0 meq/100 g FFDS, NS, at 10 wk). Muscle cell electrical hyperpolarization developed after 10 wk of Mg depletion. Convulsive seizures developed in three animals. Frank rhabdomyolysis in three animals and focal necrosis in four animals were present on terminal biopsy, with only four animals having completely normal histology.
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PMID:Skeletal muscle injury after magnesium depletion in the dog. 711 11

Bone mineral status was assessed by direct photon absorptiometry on 140 children and adolescent hospital outpatients receiving long-term anticonvulsant drug therapy and on 132 institutionalized mentally retarded subjects, 74 of whom were receiving anticonvulsant drugs. Serum calcium, phosphorus and alkaline phosphatase concentrations were determined for the hospital outpatients. Average deviations of bone mineral content (%BMC) ranged from 8.4-16.2% of normal values predicted from regression analysis. A trend toward increased demineralization was associated with length of anticonvulsant drug therapy. Mentally retarded subjects and hospital subjects with seizures accompanied by other serious disorders showed significantly greater osteopenia than hospital subjects with seizures alone. A lack of association of BMC with presence of anticonvulsant drug therapy in the mentally retarded population suggested that their low %BMC values were due to other factors related to the nature of the sample and the condition of institutionalization. Biochemical values showed a lack of association with osteopenia. A comparison of the present results on compact bone with results of others involving osteoid of trabecular bone suggests that anticonvulsant drug therapy affects these tissues differently and that the chemistry of the blood more closely reflects the osteoid proliferation of the trabecular bone rather than the changes related to the osteopenia of compact bone.
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PMID:Bone status of children receiving anticonvulsant therapy. 712 Dec 54


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