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

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

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.
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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).
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PMID:Risk factors associated with retrolental fibroplasia. 644 Nov 33

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.
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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.
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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.
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PMID:Seizure duration in unilateral electroconvulsive therapy. A comparison of the anaesthetic agents etomidate and Althesin with methohexitone. 674 97

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.
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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.
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PMID:Synergism of hyperoxia and high helium pressures in the causation of convulsions. 681 23

We report the case of a 9-year-old girl with multiple problems due to hypothalamic dysfunction of obscure origin: apnoeic spells, behavioural problems, developmental delay, hypodipsia with bouts of hypernatraemia, episodes of spontaneous hypothermia, obesity, petit-mal seizures, non-progressive precocious puberty, absence of respiratory response to CO2 and probably insensitivity of hyposensitivity to pain. She also had hyperprolactinaemia and decreased human growth hormone secretion. Hypothyroidism of central origin and hyposecretion of cortisol were also present. Multiple brain CT-scans failed to reveal any tumour or other anatomical abnormality. Her clinical course was improved initially by treatment with clomipramine, but she died suddenly, and the autopsy failed to disclose any anatomical lesion. We compare this case with three similar previously reported cases.
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PMID:Hypothalamic dysfunction in a child: a distinct syndrome? Report of a case and review of the literature. 768 46

In order to examine the respiratory effects of tonic-clonic seizures and their treatment with i.v. diazepam or lorazepam, we utilized a spontaneously breathing piglet seizure model. A tracheostomy, arterial catheter, and epidural electrodes were inserted and pigs were maintained under ketamine anesthesia. After baseline recordings, seizures were induced with a pentylenetetrazol (PTZ) bolus and a 20 min infusion (5-6 mg/kg/min). After 10 min of PTZ infusion, randomly assigned animals received diazepam (D; N = 7; 0.5 mg/kg), lorazepam (L; N = 7; 0.2 mg/kg), or 0.9% saline (C; N = 7; controls) by rapid peripheral vein injection. Minute ventilation (Ve), Pa(CO2), and the pressure change in response to airway occlusion at end-expiration (P0.1) were measured at standard intervals. All groups had comparable increases in respiratory drive during untreated seizures. Changes in Ve and P0.1 were reduced to at or below baseline values in groups D and L, but not C, from 2 to 45 min after treatment (P < 0.05). No significant changes were observed in Pa(CO2) after either intervention. Following anticonvulsants, the cumulative duration of seizures was significantly reduced in L and D groups, compared to C (P < 0.05). We conclude that increases in respiratory drive occur during tonic-clonic seizures induced with PTZ. Amelioration of seizure activity with lorazepam or diazepam results in a reduction in respiratory drive, but not respiratory failure, in this tracheostomized model.
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PMID:Respiratory drive during status epilepticus and its treatment: comparison of diazepam and lorazepam. 771 57


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