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

A conceptual approach to the understanding of the pathogenesis of idiopathic seizures is presented. Hypokalemia and/or alkalosis promotes the elaboration of an alkaline urine, which increases the renal return of ammonia and exposes the brain to chronically higher concentrations of ammonia. In the brain, ammonia is preferentially detoxified to glutamine and therefore depletes the available glutamic acid, which is also a precursor of GABA, the major mediator of central inhibition. Mild chronic elevations of ammonia may also result in long-term nutritional alterations of amino-acid precursors of other brain neurotransmitters. A linkage thus exists for the metabolic basis of seizures: the role of the potassium-ammonia axis may be important in the selective depletion of GABA, the major mediator of central inhibition.
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PMID:The metabolic basis for the genesis of seizures: the role of the potassium-ammonia axis. 671 18

A conceptual approach to the understanding of the pathogenesis of idiopathic seizures is presented. Hypokalemia and/or alkalosis promotes the elaboration of an alkaline urine, which increases the renal return of ammonia and exposes the brain to chronically higher concentrations of ammonia. In the brain, ammonia is preferentially detoxified to glutamine and therefore depletes the available glutamic acid, which is also a precursor of GABA, the major mediator of central inhibition. Mild chronic elevations of ammonia may also result in long-term nutritional alterations of amino-acid precursors of other brain neurotransmitters. A linkage thus exists for the metabolic basis of seizures: the role of the potassium-ammonia axis may be important in the selective depletion of GABA, the major mediator of central inhibition.
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PMID:The metabolic basis for the genesis of seizures: the role of the potassium-ammonia axis. 671 22

Phosphorus magnetic resonance spectroscopic imaging has previously demonstrated localized metabolic abnormalities within the epileptogenic region in patients with temporal lobe epilepsy, including alkalosis, increased inorganic phosphate level, and decreased phosphomonoester levels. We studied 8 patients with frontal lobe epilepsy, finding interictal alkalosis in the epileptogenic region compared to the contralateral frontal lobe in all patients (7.10 +/- 0.05 vs 7.00 +/- 0.06, p < 0.001). Seven patients exhibited decreased phosphomonoester levels in the epileptogenic frontal lobe compared to the contralateral frontal lobe (16.0 +/- 6.0 vs 23.0 +/- 4.0, p < 0.01). In contrast to findings in temporal lobe epilepsy, inorganic phosphate level was not increased in the epileptogenic region. Based on values derived from normal control subjects, 5 patients had elevated pH in the seizure focus and 2 patients had decreased phosphomonoesters while none had abnormalities in the contralateral frontal lobe. These data suggest that magnetic resonance spectroscopy will be useful in the presurgical evaluation of patients with frontal lobe epilepsy.
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PMID:Phosphorus magnetic resonance spectroscopic imaging in patients with frontal lobe epilepsy. 810 2

There is little information on the prevalence and clinical presentation of acid-base abnormalities associated with cocaine toxicity. To address these issues, arterial blood gas results were evaluated in 156 cocaine-associated emergency department patient visits. Arterial blood gas results were obtained as part of the patient's clinical assessment. The majority of patients (52%) had a normal pH (7.35 to 7.45). Thirty-three percent of patients were acidotic, with a pH between 6.4 and 7.35. In 33 patients the acidosis was metabolic, with a HCO3- of 14 +/- 6 mmol/L. The acidosis was primarily respiratory in 18 patients, with evidence of hypoventilation. Hypoventilation was generally secondary to chest trauma or decreased mental status. Alkalosis (pH > 7.45) was observed in 15% of patients, and was usually respiratory, as evidenced by tachypnea and a low PCO2. These results indicate that metabolic and respiratory acid-base abnormalities are common during cocaine toxicity. Acidosis and alkalosis were associated with numerous patient presentations, including chest pain, shortness of breath, decreased mental status, trauma, and seizures. Acid-base abnormalities do not appear to be associated with a specific route of cocaine self-administration. Patients with a history of potential cocaine toxicity should be evaluated for acid-base abnormalities.
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PMID:Acid-base abnormalities associated with cocaine toxicity in emergency department patients. 830 47

The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.
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PMID:[Effect of intravenous lidocaine infusion on arterial baroreflex]. 851 40

A 73-year-old man was admitted to our hospital after convulsive seizures preceded by encephalopathy lasting one week. He had a history of long-standing chronic obstructive pulmonary disease and analysis showed hypokalemia, respiratory alkalosis and toxic levels of theophylline. We discuss the severity of the convulsions and arrhythmias, the high incidence of hypokalemia in theophylline poisoning, as well as the role of hypokalemia in the pathogenesis of the convulsions and the high level of mortality in this type of intoxication. Other possible mechanisms involved in theophylline encephalopathy are mentioned, along with the controversial use of theophylline for continuous treatment of chronic obstructive pulmonary disease.
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PMID:[Encephalopathy, convulsions and hypopotassemia in theophylline poisoning: a case analysis]. 877 34

The present experiments were undertaken to study how preischemic hyperglycemia, which is known to exaggerate ischemic damage and to trigger delayed postischemic seizures affects the bioenergetic state and the intracellular pH (pHi) of brain tissue at early (6 h) and late (18 h) recirculation times. To that end, normo- and hyperglycemic rats were subjected to 10 min of forebrain ischemia, and neocortical tissue was frozen in situ for analyses of labile energy metabolites. Animals with preischemic hyperglycemia failed to show a postischemic reduction of the phosphorylation state of the adenine nucleotide pool, or a rise in tissue lactate content, nor did they show a change in tissue redox state. However, the hyperglycemia led to a rise in phosphocreatine (PCr) content after 6 h of recirculation. Calculations of intracellular pH (pHi) from the creatine kinase (CK) equilibrium showed a rise in pHi above normal, a finding which was supported by a limited number of 5,5-dimethyl[2-14C]oxazolidine-2,4-dione (DMO) measurements. The preischemic hyperglycemia also blunted the postischemic rise in tissue glycogen content, which is usually observed in normoglycemic rats. The results thus fail to reveal that the hyperglycemia-triggered, massive exaggeration of ischemic brain damage, which is heralded by generalized seizures after 18-24 h of recirculation, is preceded by mitochondrial dysfunction of a degree which affects the bioenergetic state or the redox potential of the tissue. However, the results suggest that the hyperglycemia enhances and/or prolongs the postischemic alkalosis. It is discussed whether the rise in pH contributes to the mitochondrial dysfunction which subsequently develops.
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PMID:Changes in labile energy metabolites, redox state and intracellular pH in postischemic brain of normo- and hyperglycemic rats. 883 45

Local cerebral changes of acid-base balance may interfere with neuronal communication. Acidosis enhances and alkalosis suppresses GABAA receptor neurotransmission while there are opposite effects on NMDA receptor transmission. In this study, we determined site-specific effects of acidified solutions of Na-HEPES-artificial cerebrospinal fluid infused into the anterior or posterior area of the substantia nigra pars reticulata (SNR) in rats. Two levels of pH were compared: 6.7 and 7.4. Rats were challenged with flurothyl and the threshold for clonic and tonic-clonic seizures was determined. In the anterior SNR, there were no differences between the effects of the solution with pH 6.7 and 7.4 on flurothyl seizures. In contrast in the posterior SNR, microinfusions with pH 6.7 had proconvulsant effects. The results suggest that local pH changes may have site-specific effects on seizure susceptibility in vivo.
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PMID:Site-specific effects of local pH changes in the substantia nigra pars reticulata on flurothyl-induced seizures. 952 79

In December 1997, more than 680 children developed convulsive seizures while watching a notorious audiovisually provocative TV program, "Pocket Monster." Emotional stimulation via hyperventilation may cause respiratory alkalosis, fall of blood ionized calcium (Ca), and sensitization of the nervous system to excessive emotional stress. A study was therefore undertaken to follow the changes of blood ionized Ca in eight healthy volunteers after watching the "Pocket Monster" and also a quiet program, "Classical Music," as a control for 20min from 4 P.M. Although neither marked hyperventilation nor convulsions developed in any of these adult volunteers, blood ionized Ca showed a significantly more pronounced fall during and after watching "Pocket Monster," and their plasma intact parathyroid hormone (iPTH) was significantly higher 120min after the beginning of "Pocket Monster" than the "Classical Music" program. Plasma total Ca, pH, and albumin were free of detectable changes. Ingestion of 600mg Ca as active absorbable algal Ca (AAA Ca) with high bioavailability completely prevented the fall of ionized Ca and suppressed iPTH. Plama osteocalcin was also significantly suppressed after ingestion of AAA Ca. It may be worthwhile to ingest AAA Ca before anticipated emotional stress such as watching a provocative TV program to prevent possible neuromuscular instability.
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PMID:Fall of blood ionized calcium on watching a provocative TV program and its prevention by active absorbable algal calcium (AAA Ca). 1034 Jun 41

Results regarding the anticonvulsant potency of bromide have been questioned, and the mechanisms of its action are unclear. Using combined rat hippocampus-entorhinal cortex slices we analyzed the effects of NaBr on four types of epileptiform discharges in two different models of epilepsy, the low-Ca2+ and the low-Mg2+ model. NaBr concentration-dependently reduced the frequency and finally blocked the low Ca2+-induced discharges. Low Mg2+-induced short recurrent discharges were also reduced in a concentration-dependent manner. In the entorhinal cortex the frequency of seizure-like events was reduced by 3 and 5 mM and the discharges were blocked by 7 mM NaBr. Also, the late recurrent discharges in the entorhinal cortex which do not respond to most clinically employed anticonvulsants were reduced by concentrations of 10 and 15 mM and completely blocked by 30 mM NaBr. Using pH-sensitive microelectrodes different effects of NaBr were seen than those of acetazolamide on extracellular pH under control conditions and after stimulation. Acetazolamide at 1 mM caused a reversible acidification of delta pH: 0.2+/-0.14 at rest whereas no change on extracellular pH was seen with 5 mM NaBr. Acetazolamide increased the transient alkalosis induced by repetitive stimulation of the stratum radiatum in area CA1 and reduced the subsequent acidosis. NaBr also increased the alkalosis but had no effect on the subsequent acidosis. A significant increase in paired-pulse inhibition was seen in a paired-pulse stimulation protocol used to monitor the efficacy of GABAergic inhibition at concentrations of 5 mM NaBr. This finding was confirmed in whole-cell patch clamp recordings from cultured hippocampal neurons showing an increase in inhibitory postsynaptic current amplitude. In summary, our results suggest a broad-spectrum anticonvulsant activity which is likely to be caused by its effects on membrane excitability, by an increase in GABAergic inhibition and is less likely caused by its effects on extracellular pH.
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PMID:Sodium bromide: effects on different patterns of epileptiform activity, extracellular pH changes and GABAergic inhibition. 1065 Nov 43


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