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

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.
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PMID:Arterial PaO2 and PaCO2 influence seizure duration in dogs receiving electroconvulsive therapy. 366 9

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23

Many patients admitted for observation to the intensive care unit after a drug overdose do not ultimately require intensive care interventions. We retrospectively analyzed data on 209 overdose cases to determine whether clinical assessment in the emergency room could identify patients at risk for complications. Patients were classified as low risk when none of the following high-risk criteria were present in the emergency room: need for intubation; seizures; unresponsiveness to verbal stimuli; arterial carbon dioxide pressure (tension) greater than or equal to 45 mm Hg; any rhythm except sinus; second- or third-degree atrioventricular block; QRS greater than or equal to 0.12 s; or systolic pressure less than 80 mm Hg. Of 151 low-risk patients, none developed a high-risk condition after admission, and none required an intensive care intervention. The use of these predictive criteria in our patient population would have eliminated over half the intensive care days without compromising quality of care.
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PMID:Predicting the clinical course in intentional drug overdose. Implications for use of the intensive care unit. 380 May 15

This article reviews normal acid-base regulation, related laboratory tests, and the potential disorders if the body's ability to compensate is disrupted. Acid derived from the oxidation of proteins and through tissue metabolism must be excreted or neutralized daily by the kidneys and lungs to maintain a proper acid-base balance. Acid-base homeostasis is normally maintained by chemical buffering, changes in renal hydrogen-ion excretion, and alterations in the rate and volume of alveolar ventilation. Metabolic disorders are characterized by disturbances in bicarbonate (HCO3-) concentration, and respiratory disorders develop with primary alterations in the partial pressure of carbon dioxide (Pco2). Metabolic acidosis is characterized by low pH, low serum HCO3- concentrations, and a compensatory decrease in Pco2 with hyperventilation. Bicarbonate administration can correct this disorder, and equations for calculating the necessary amount of HCO3- are presented. Metabolic alkalosis is characterized by a primary increase in HCO3-, compensatory hypoventilation, and an increase in Pco2 (hypercapnia). The drug therapy for this disorder is directed at either saline-responsive alkalosis or saline-resistant alkalosis. Formulas for estimating the volume requirements of patients and appropriate doses of acidifying agents are presented. Respiratory acidosis and alkalosis are also discussed. The initial therapy for the hypercapnia associated with respiratory acidosis requires reversing the underlying pulmonary disease with steroids, bronchodilators, or antibiotics. The increased Pco2 in this conditions must be lowered slowly to avoid precipitating cardiac arrhythmias and seizures. The correction of respiratory alkalosis requires elevating the Pco2 and again treating the underlying disease. Pharmacists should be knowledgeable about acid-base regulation and the disorders that frequently occur with disease because drugs are capable of inducing or exacerbating these disorders and are often key elements in therapy.
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PMID:Simple acid-base disorders. 393 55

The objective of the study was to estimate changes in extracellular pH (pHe) and intracellular pH (pHi) during seizures and in the recovery period following the arrest of seizure activity. Seizures of 5- and 20-min duration were induced in rats by fluorothyl added to the insufflated gas mixture, and recovery for 5, 15, and 45 min was instituted by withdrawal of the fluorothyl supply following 20 min of continuous seizures. Changes in pHe were measured by double-barreled, liquid ion-exchange pH microelectrodes, and in pHi by the CO2 method, following estimation of tissue PCO2 and extracellular fluid (ECF) volume. The animals were either normoxic or rendered moderately hypoxic (arterial PO2 40-50 mm Hg). Upon induction of seizures in normoxic animals, pHe decreased by a mean of 0.36 unit, the values being identical at 5 and 20 min. In moderate hypoxia, seizures sustained for 20 min were accompanied by a further fall in pHe (mean decrease 0.51 unit). The changes in pHe seemed mainly to reflect the nonionic diffusion of lactic acid from cells to the ECF (tissue lactate levels approximately 10 and 15 mumol g-1 during seizures in normoxic and hypoxic animals, respectively). However, the gradual fall in pHe attributable able to lactic acid production was preceded by rapid acidification, sometimes exceeding the steady-state values subsequently attained. This acidification was interpreted to reflect spreading depression and fast transcellular Na+/H+ exchange. Following cessation of seizure discharge, pHe normalized at a surprisingly slow rate, with some acidosis persisting even after 45 min. The difference between cerebrovenous and arterial PCO2 was reduced during seizures and increased in the recovery period, probably reflecting alterations in the blood flow/metabolic rate coupling. Impedance changes were slight, indicating only minor changes in ECF volume. Changes in pHi after 5 min of seizures ranged from 0.20 (normoxic animals) to 0.32 (hypoxic animals) unit, the pHi values after 20 min being 0.07-0.08 unit higher. The results suggest the regulation of pHi during ongoing seizures. Upon arrest of seizure activity, pHi rapidly increased to normal and subsequently to supranormal values. Postepileptic intracellular alkalosis occurred at a time when pHe was still reduced and in spite of the fact that tissue lactate values had not normalized. It is concluded that the rapid normalization of pHi and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H+, and the extrusion of H+ from cells, possibly via a Na+/H+ exchanger, the latter probably delaying normalization of pHe.
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PMID:Extra- and intracellular pH in the brain during seizures and in the recovery period following the arrest of seizure activity. 397 23

The importance of cerebral blood volume (CBV) as a physiological parameter has been well recognized, especially in its relation to the intracranial pressure (ICP). Although various methods have been applied to measure CBV, several problems and difficulties still remain to be settled. In the present study, noninvasive monitoring of CBV on the cortical surface was done with organ reflectance spectrophotometry. Through the cranial window, the cat brain was illuminated by the white light via optical fibers and reflected light was analized by spectrophotometer equipped with microcomputer and image-sensor (Sumitomo Elec. Co., Spectrum analyzer TS-200), which enables to estimate CBV on real time as the absorbance value at the isobestic point of the spectral curve of hemoglobin (Hb). In order to ascertain the reliability and reproducibility, the change of CBV was examined by 5% & 10% CO2 inhalation, 5% O2 inhalation and bilateral jugular vein occlusion. A linear correlation was found between PaCO2 and Hb absorbance value on CO2 inhalation. By the bilateral jugular vein occlusion, Hb increased concomitantly with ICP, while cerebral blood flow (CBF) decreased. On 5% O2 inhalation, absorbance spectral pattern of tissue Hb changed from that of oxy-Hb to deoxy-Hb without change of absorbance value at the isobestic point. Thus, the Hb absorbance value obtained by this spectrophotometer was considered to be reliable for the estimation of CBV on the cortical surface. Using this, the change of CBV was examined on the drug-induced seizure and post-decompression state after sustained intracranial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Continuous monitoring of cerebral blood volume in cats using a reflectance spectrophotometer]. 400 77

Much evidence shows that glia regulates the cation and anion content of brain interstitial space. In rats the pH and bicarbonate (HCO3-) concentration of neurons and glia were derived from carbon 14-labeled HCO3- and dimethyloxazolidinedione uptake into brain and cerebrospinal fluid. Acetazolamide increases the total CO2 concentration in neurons and decreases the pH and HCO3- concentration in glia. Inhibition of glial carbonic anhydrase (CA) reduces conversion of neuronally derived CO2 to HCO3-, glial pH is lowered, and neuronal CO2 accumulates. CA therefore has an essential role in regulating pH in neurons, glia, and interstitial fluid. In audiogenic seizure mice, glial CA activity is increased and glial anion transport is reduced. As the mice age, seizure susceptibility, the increased CA activity, and the defect in anion transport disappear concurrently. The enhanced CA activity in the glial cells of these mice is an adaptive mechanism to overcome the defect in anion transport that results from a deficiency of HCO3- -dependent and Na+- and K+ -dependent adenosine triphosphatase. Pentylenetetrazol stimulates neurons in neonatal rats, but after 10 days of age, when glia is present, it too is stimulated and the seizures are attenuated. Cobalt implantation in the cortex of rats also induces a glial response that ameliorates the focal seizures produced by this procedure.
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PMID:Ionic and acid-base regulation of neurons and glia during seizures. 615 Jun 82

The authors present the results of medical examinations of 444 workers from an aluminum electrolysis plants with occupational exposure to fluorides, polycyclic aromatic hydrocarbons, carbon dioxide, aluminum dust and electromagnetic fields. The concentration of fluorides and polycyclic aromatic hydrocarbons exceeded the accepted levels. Nervous system changes, probably caused by occupational harmful factors, were demonstrated in 123 workers, with neurotic syndromes in 89. Slight pyramidal and cerebellar changes were observed in the remaining 39 workers. In 71 cases EEG investigations were done and 10 were abnormal, including 9 with seizure activity, and one with diffuse changes. The authors stress great difficulties in evaluating the combined action of toxic and physical factors on the nervous system.
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PMID:[Evaluation of the combined effect of various harmful physical and chemical factors on the nervous system]. 641 Feb 97

Seizure duration in unilateral electroconvulsive therapy (ECT) was recorded by means of EEG in an intraindividual comparison under different alveolar O2- and CO2-concentrations. Hypocapnia induced by hyperventilation to an alveolar CO2-concentration of 2% (2 kPa) resulted in a highly significant increase in seizure duration compared to a normal CO2 of 5%, when the alveolar O2-concentration was constant at 92%. Oxygen ventilation to an alveolar O2-concentration of 92% gave no significant increase in seizure duration compared to 15%, obtained by ventilation with air, when the CO2-concentration was kept constant at 5%. Seizure duration seems to augment progressively with decreasing alveolar CO2-concentration.
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PMID:Seizure duration in unilateral electroconvulsive therapy. The effect of hypocapnia induced by hyperventilation and the effect of ventilation with oxygen. 642 4

Eleven women and seven men with moderate to severe chronic hyperventilation and idiopathic seizures refractory to therapeutic serum levels of anticonvulsant medication were given diaphragmatic respiration training with percent end-tidal CO2 biofeedback. The training had a rapid correcting effect on their respiration, making it comparable to that of 18 asymptomatic control subjects. Ten of the seizure-group subjects were in the study at least 7 months and following treatment, 8 showed EEG power spectrum "normalization", restoration of cardio-respiratory synchrony (RSA), and their seizure frequency and severity were significantly reduced.
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PMID:Behavioral control of intractable idiopathic seizures: I. Self-regulation of end-tidal carbon dioxide. 643 47


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