Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pentobarbital-anesthesized cats, bolus i.v. injections of sodium azide produced dose-dependent transient hypotension accompanied by a modest tachycardia and a brief hyperpnea. Intracerebroventricular injections of azide elicited graded effects similar to the i.v. doses, but the responses were slower in onset and could be delayed by occluding the cranial blood supply. This is interpreted to mean that intracerebroventricular azide acts systematically after escaping from the cerebrospinal fluid into the bloodstream. The hypotensive response to i.v. azide was not affected by cholinergic or adrenergic blockade or buffer nerve section. The tachycardia was blocked by sympathetic neural blockade or buffer nerve section indicating that it is a baroreflex response to the vasodepressor effect. Respiratory effects of bolus i.v. azide occurred independently of the hypotensive response and were abolished by peripheral chemodenervation. Infusion of azide facilitated CO2-tidal volume responsiveness in the steady state, an effect that was essentially eliminated by carotid sinus neurotomy. The azide did not affect the tidal volume-respiratory frequency relationship mediated by the pulmonary stretch receptors. Thus, the respiratory stimulant effect of azide in subtoxic doses is attributable to an excitatory action on the arterial chemoreceptors. Toxic doses of azide resulted in centrally mediated hypertension, tachycardia, cardiac arrhythmia, respiratory depression, seizures and death.
 ...
PMID:Peripheral and central actions of sodium azide on circulatory and respiratory homeostasis in anesthesized cats. 643 70

The eyes of infants who were premature or had exposure to increased ambient oxygen from 1979 to 1981 were examined. Of 1012 neonates, 19 were found to have acute retrolental fibroplasia (RLF) grade III or worse in at least one eye. Sixteen also had chronic lung disease (CLD), and when compared to 25 control patients who had CLD but not grade III or more RLF, they were found to consistently have lower blood CO2 tensions (PCO2), lower pH values, higher inspired oxygen concentrations (FIO2S) and a higher incidence of seizure disorders (100% vs. 48%). We could not show that an elevated PCO2 increased the risk for developing RLF. Infants with either chronic lung disease or chronic lung disease and seizures had a high risk for developing RLF grade III (39% and 57%, respectively).
 ...
PMID:Risk factors associated with retrolental fibroplasia. 644 Nov 33

Local blood flow, and partial pressures of oxygen and carbon dioxide were directly monitored in the vulnerable region of Ammon's horn (e.g. CA3) of unanaesthetized, freely breathing rats in which epileptic seizures of 120 min duration were induced by parenteral kainic acid. Blood flow was periodically determined by helium clearance. Partial pressures of oxygen and carbon dioxide were simultaneously and continuously measured by means of mass spectrometry, in order to determine if the neuronal damage occurring during the seizures were due to local hypoxia or if blood flow compensated the metabolic demand. During the wet shakes period, a decrease of 35% in the partial pressure of oxygen occurred, concomitant with an increase of 33% in the partial pressure of carbon dioxide and of 330% in local blood flow in Ammon's horn. During the limbic motor seizures, the partial pressure of oxygen increased progressively to twice its baseline value, while the partial pressure of carbon dioxide returned to its baseline value and blood flow underwent a six-fold increase. Thus the seizures produced by kainate do not lead to a mismatch between oxygen supply and blood flow. Our results provide direct evidence that hypoxia cannot be considered responsible for the damage produced by the seizures in CA3. It is concluded that brain damage in CA3 is due to an enhanced neuronal activity associated with the release of a toxic endogenous substance and an excessive rise of intracellular concentration of calcium.
 ...
PMID:Blood flow compensates oxygen demand in the vulnerable CA3 region of the hippocampus during kainate-induced seizures. 644 98

In twelve patients the EEG was recorded under isoflurane--nitrous oxide inhalation anesthesia. A quiet EEG pattern was registered, without suppressions and seizures of spike activity which are often observed under enflurane. This was the case even when end expiratory CO2 shifted to low values (3-3.6 Vol%). In one patient the induction with N2O/O2 and thiopentone, resulted in spikes and suppression bursts on the EEG. After isoflurane was added, these changes disappeared. In another patient, epileptic EEG patterns were observed prior to the induction (confirmed by the history of the patient). During isoflurane anesthesia the epileptic waves disappeared and remained absent.
 ...
PMID:Absence of electroencephalographic excitation pattern under isoflurane anesthesia. 652 87

Glutamic acid decarboxylase (GAD) activity in cerebrospinal fluid (CSF) was determined in 53 patients with neurological diseases as follows: Epilepsy (n:17), febrile convulsions (n:3), meningoencephalitis (n:17), encephalopathies (n:10), CNS leukemia (n:3), congenital hydrocephalus (n:2) and pseudoileus neonatorum (n:1). Compared with the mean normal value (5.2 +/- 2.5 pmol CO2 formed/hr/ml) reported in Part I, a significant increase of GAD activity in CSF was demonstrated in patients with uncontrolled epileptic seizures (11.4 +/- 3.9 pmol CO2 formed/hr/ml), febrile convulsions (13.5 +/- 8.7), viral meningitis with or without encephalitis (20.3 +/- 13.6), encephalopathies (30.0 +/- 25.9), CNS leukemia (11.1 +/- 5.0), congenital hydrocephalus (20.5 +/- 7.3) and pseudoileus neonatorum (28.6). Markedly high GAD activity was found in patients with CNS leukemia several days after intrathecal injection of methotrexate (39.8 +/- 18.0). On the other hand, significantly low GAD activity was shown in patients with bacterial meningitis or brain abscess (1.3 +/- 1.2). This suggests that some bacterial factors may be inhibitory toward GAD activity in CSF. High GAD activity in CSF may be useful as an indicator of aseptic brain dysfunction, although it was not always correlated with the severity of symptoms.
 ...
PMID:Glutamic acid decarboxylase in cerebrospinal fluid in infancy and childhood Part II. Glutamic acid decarboxylase activity in cerebrospinal fluid of children with neurological diseases. 666 Apr 21

Seizure duration in unilateral electroconvulsive therapy (ECT) was recorded by means of EEG in an intraindividual comparison of etomidate (dissolved in a soy-bean oil emulsion) 0.3 mg/kg and Althesin (alphaxalone 9 mg and alphadolone 3 mg/ml) 0.6 mg/kg with methohexitone 1 mg/kg body weight. The patients were intubated and alveolar CO2- and O2-concentrations kept constant at 3% (3 kPa) and 92% (92 kPa) respectively. Seizure duration was the same when either etomidate or methohexitone were used, whereas Althesin significantly shortened seizure duration in comparison with methohexitone. Local pain on injection and a subsequent superficial thrombophlebitis occurred frequently with methohexitone. This did not occur with etomidate or Althesin.
 ...
PMID:Seizure duration in unilateral electroconvulsive therapy. A comparison of the anaesthetic agents etomidate and Althesin with methohexitone. 674 97

Epileptogenic foci were created by topical application of penicillin to the cerebral cortex in 40 paralyzed and artificially ventilated cats receiving halothane anesthesia. The animals were divided into two equal groups to compare primary and secondary foci. The following variables were recorded at normocapnia, hypocapnia, and hypercapnia prior to and during seizure activity: cerebral blood flow (CBF), determined by clearance of xenon 133; cortical redox states, measured by the fluorescence of reduced pyridine nucleotides (PN); brain pH, measured using a lipid-soluble, pH-sensitive fluorescent indicator; and electroencephalograms (EEG). Mean arterial blood pressure, arterial pH, arterial carbon dioxide tension (PaCO2), and arterial oxygen tension (PaO2) were monitored in each animal. All animals had a normal PaCO2-CBF response prior to the creation of a seizure focus, assuring the presence of autoregulation and normal metabolic function. CBF increased equally with seizures in the primary and secondary hemispheres. The relative increase was related to the PaCO2 but approximated 68% at normocapnia. There was an alteration in the PaCO2-CBF response with seizures, but the ability of the cerebral vasculature to constrict and dilate with hypocapnia and hypercapnia was retained. There was no significant difference in the reduced PN signal with variations in PaCO2 prior to seizures, but there was an apparent 10 to 15% fall with seizures. The "equivalent" intracellular pH fell to 6.94 at normocapnia in the primary focus but remained essentially unchanged from the control value of 7.10 in the secondary focus. These differences in pH were consistent with the greater degree of seizure activity observed in the primary focus. We conclude that a nonhypoxic acidosis existed in the primary focus and that changes in CBF were not related to it because the CBF changed equally in both hemispheres.
 ...
PMID:Correlation of intracellular redox states and pH with blood flow in primary and secondary seizure foci. 678 36

Brain glucose metabolism was studied in paralyzed, ventilated rats given electroconvulsive shock (ECS) under normocapnic and hypercapnic conditions. Brains were obtained with a freeze-blowing apparatus. Rates of glucose utilization were determined with [2-14C]glucose and [3H]deoxyglucose as tracers. In normocapnic rats, ECS caused a large increase in the rate of glycolysis to 5--6 mumol/g/min. Brain lactate levels increased three- to fourfold. The stimulation of glucose metabolism was reflected in decreased brain glucose 6-phosphate concentration as early as 2--3 s after ECS. There were significant decreases in brain glucose and glycogen levels at 20 and 30 s after ECS. The decreases in endogenous brain glucose accounted for most of the increases in glucose utilization measured isotopically, implying that influx of glucose from blood into brain did not increase greatly over these time periods. Animals made hypercapnic by respiration with 10% CO2 for 2 min prior to ECS were different in their metabolic responses to ECS in several ways. The increases in glycolytic rate and lactate content of brain were half of those found in normocapnic rats. Brain glycogen and glucose concentrations did not change significantly in the hypercapnic rats during seizure activity. Thus, hypercapnia lessened the stimulation of glycolysis caused by ECS, but increased net influx of glucose from blood to brain. The mechanisms of these effects of hypercapnia are uncertain, but it is postulated that the effect on glycolytic activity is due to the acidosis and that the effect on glucose transport is due to an increase in capillary surface area.
 ...
PMID:Cerebral metabolic responses to electroconvulsive shock and their modification by hypercapnia. 680 Dec 6

Hyperoxia beyond 1.8 ATA results in a striking reduction of high-pressure neurological syndrome (HPNS) type I convulsion threshold pressures but is without measurable effect on type II convulsions. The synergism is partially or completely reversed by increasing alveolar or tissue CO2 levels. High total pressures (PI) result in striking reductions in the duration of hyperoxic exposure preceding seizure onset (tc). The interaction of hyperoxia and high pressure gives rise to three zones on the PO2-Pt plane. In zone I, Pt less than 30 ATA, the duration of hyperoxia prior to convulsion onset is given by the equation PO2 -- PO2 lim = K/(tc -- tc lim), where PO2 lim and tc lim both decrease with increasing total pressure. Zone II, Pt = 30-50 ATA and PO2 1.8-2.3 ATA, is characterized by a sharp drop in tc, as Pt is increased beyond 30 ATA, to a value near 15 min that is constant within the PO2 limits given. In zone III, Pt greater than 50 ATA and PO2 greater than 0.2 ATA, tc is of the order of 2 min, and the seizures are essentially HPNS seizures only slightly modified by hyperoxia. The data are interpreted as suggesting that zone I represents hyperoxic seizures facilitated by high pressures, whereas zone II represents HPNS type I seizures facilitated by hyperoxia.
 ...
PMID:Synergism of hyperoxia and high helium pressures in the causation of convulsions. 681 23

The EEG of a patient with acute carbon monoxide poisoning was characterized by lateralized sharp waves and a focal electrographic seizure discharge within hours of the exposure. These findings were associated with coma and focal motor seizures. The patient made a full clinical recovery, and the EEG was normal two months after the exposure. The association of a primarily diffuse cerebral insult after CO poisoning, with prominent lateralized epileptiform discharges in the EEG, is a distinctly unusual phenomenon.
 ...
PMID:Localized EEG abnormalities in acute carbon monoxide poisoning. 724 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>