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

The most important premise for a successful surgical treatment of epilepsy lies in an accurate diagnosis of the focus location. The hitherto employed methods for this purpose are meticulous analysis of seizure contents and scalp EEGs, but spatial localization of the focus sites is far beyond the capacity of these diagnostic measures. With the advent of positron emission tomography (PET), in vivo observation of human brain metabolism has become possible. The indices of brain metabolism such as cerebral blood flow (rCBF), cerebral metabolic rate of glucose or oxygen (CMRG, CMRO2) are noninvasively measured by PET offering priceless information for diagnosing brain dysfunction such as ischemia, degeneration, psychosis, or epilepsy. Kuhl et al. first employed PET in assessment of epileptic foci, in which interictal foci were beautifully detected as discrete "hypometabolic zones". Many researchers have confirmed this invaluable finding, and nowadays PET seems to have acquired the citizenship as one of the most capable diagnostic measures in focus localization. We have hitherto applied PET study in 72 epileptic patients. The main contents of their seizures consists of complex partial in 32, elementary partial in 32, generalized in 6, and others in 3 cases. We administered perorally 10 mCi glucose labeled with C11 produced in the JSW Baby Cyclotron for the study of CMRG. The continuous inhalation method of CO2 and O2 labeled with O15 produced in the same cyclotron was also employed for measurement of rCBF and CMRO2. In both studies, epileptic foci were shown as well demarcated hypometabolic zones with decreased CMRG, rCBF or CMRO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of convexity focal epilepsy--based on diagnosis of PET and subdural EEG]. 310 88

The study is part of a series of investigations performed with the ultimate goal of obtaining an objective evaluation of the ethical aspects and the narcotic efficiency of CO2 inhalation used as pre-slaughter anaesthesia for swine. Six Yorkshire swine were exposed twice to 80% CO2 for 1 min during simultaneous recording of the EEGs from the frontal neocortex, the dorsal hippocampus, and the amygdaloid region via permanently implanted electrodes. In five of the animals myoclonic jerks started at 28 +/- 1 s of CO2 exposure and lasted for 6 +/- 2 s. Neocortical slow wave (delta) activity and increased amplitude of the hippocampal theta (5-7 Hz) waves (i.e. EEG changes seen during the second stage of barbiturate anaesthesia) had developed before the brief period of myoclonic jerks. After this period the EEG activity gradually declined, resulting in neocortical EEG silence at the end of the exposure. This apparent isoelectricity lasted for on average 1 min. The return of the neocortical EEG activity exhibited a pattern reverse to its disappearance, but was much prolonged in comparison to the EEG extinction. Pre-exposure neocortical EEG pattern was not regained until 3-5 min post-exposure. In eight out of 11 experiments the CO2 inhalation also induced hippocampal EEG silence lasting for on average 30 s. EEG flattening was further obtained when recording from the amygdaloid nuclear complex and the adjacent pyriform cortex. The observed changes in the neocortical and hippocampal EEGs suggest that the present swine were unconscious already when they exhibited motor reactions. This does not exclude the possibility that CO2-independent stress/arousal factors present in a slaughterhouse environment may facilitate the development of motor phenomena similar to seizures, with the result that such reactions become manifest before the neocortical EEG exhibits an anaesthesia pattern. The duration of the observed EEG silence implies that, from the ethical point of view, exsanguination might safely be performed within 1 min after the moment when the animal is removed from the high concentration CO2. However, the slow return to a pre-exposure neocortical EEG pattern suggests that the swine remains unconscious for at least another minute.
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PMID:Transient neocortical, hippocampal and amygdaloid EEG silence induced by one minute inhalation of high concentration CO2 in swine. 310 10

The influence of end-expired carbon dioxide concentration (E'CO2) on seizure duration was studied in 30 depressed patients undergoing electroconvulsive therapy (ECT) on three separate consecutive occasions. Unpremedicated patients breathed 100% oxygen before the induction of anaesthesia with methohexitone and the provision of partial neuromuscular blockade with suxamethonium. They then received no further ventilation, 10 breaths, or 20 breaths of hyperventilation with 100% oxygen from a non-rebreathing system with a high fresh gas flow. Transcutaneous oxyhaemoglobin saturation (SaO2) was monitored continuously and E'CO2 was measured before and after the seizure. Observation of an isolated forearm was used to time the seizure duration. SaO2 remained greater than 90% in all patients. Passive hyperventilation with 20 breaths significantly reduced E'CO2 and prolonged seizure duration. E'CO2 before the seizure and change in E'CO2 during the seizure did not correlate significantly with seizure duration.
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PMID:Effect of passive hyperventilation on seizure duration in patients undergoing electroconvulsive therapy. 312 11

Cerebral blood flow was sequentially determined (every 2-3 min) with helium clearance in two "vulnerable" structures: the hippocampus and the frontoparietal cortex during bicuculline (n = 11) and kainic acid (n = 9)-induced seizures in unanaesthetized, spontaneously breathing rats. Tissue partial pressures of oxygen and carbon dioxide were continuously and simultaneously evaluated in the same brain areas. All these variables were measured by mass spectrometry with a single gas sampling cannula previously implanted in each structure. The systemic variables, arterial blood pressure, arterial partial pressures of oxygen and carbon dioxide, pH, and bicarbonate concentration were also determined. Arterial and venous catheters were chronically implanted several days prior to the definitive experiments. Bicuculline induced short (about 15 min), recurrent, generalized seizures, with an abrupt rise in arterial blood pressure, an arterial metabolic acidosis and comparable blood flow increases (4-fold) in the hippocampus and the neocortex. A marked increase in tissue partial pressure of oxygen was always preceded by an increase in tissue partial pressure of carbon dioxide. After the seizures, in the 5 rats that survived, cerebral blood flow was significantly lowered; tissue partial pressure of oxygen and partial pressure of carbon dioxide also decreased, but to a lesser extent. Histological examination revealed two types of lesions: predominantly selective chromatolysis but also ischaemic cell change. Kainic acid first induced a decrease in arterial pressure and then hypertension during status epilepticus, with a return of arterial pressure towards basal levels during the recovery period (4 h after the injection). Respiratory alkalosis occurred throughout the experiment. Cerebral blood flow increased progressively to become maximal during status epilepticus. This vasodilatation was greater in the hippocampus (x 8) than in the neocortex (x 4). During recovery, cerebral blood flow tended to decrease but remained significantly elevated. In both structures, tissue partial pressure of oxygen was first lowered while tissue partial pressure of carbon dioxide was elevated; with the occurrence of the wet dog shakes, tissue partial pressure of O2 increased and tissue partial pressure of CO2 decreased. The changes in tissue gases were maximal during status epilepticus and tended to return to their basal levels thereafter, but no decrease in tissue partial pressure of O2 was observed, even 4 h after kainic acid administration. Histological analysis demonstrated ischaemic cell changes, particularly in the limbic system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Continuous determination of the cerebrovascular changes induced by bicuculline and kainic acid in unanaesthetized spontaneously breathing rats. 312 92

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

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

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

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