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

Hyperbaric oxygen (HBO2) is associated with a recognized risk for clinical central nervous system (CNS) toxicity. The risk for oxygen convulsions during routine hyperbaric treatment of most routine conditions is extremely low. Previous observations have suggested that the incidence of CNS toxicity during HBO2 treatment for carbon monoxide (CO) poisoning may be increased, both because of CNS injury caused by the poisoning and because higher treatment pressures are often utilized for this condition. This study reviews data from 900 CO-poisoned patients treated with HBO2 at Virginia Mason and Duke University Medical Centers from 1987 to 1996. One-third of the patient population was treated at each of the three HBO2 treatment pressures most commonly utilized for CO intoxication in North American multiplace chambers. Patient characteristics were similar in all groups. Among the 300 consecutive patients treated at each pressure, there was one seizure at 2.45 atm abs (0.3%), nine seizures at 2.80 atm abs (2.0%), and six seizures at 3.00 atm abs. This difference is statistically significant (P = 0.032; Fisher's Exact Test). The potential difference in seizure risk should be considered when selecting the HBO2 treatment pressure for CO poisoning.
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PMID:Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning. 898 51

Long-term potentiation (LTP), a model of activity-dependent synaptic plasticity and of certain forms of memory, comprises the persistent enhancement of excitatory neurotransmission that results from high-frequency activation. A presynaptic component of LTP is thought to be modulated by a retrograde messenger generated by the postsynaptic neuron. Arachidonic acid, nitric oxide, carbon monoxide and PAF have each been proposed as retrograde messengers in LTP, but arachidonic acid, unlike PAF, requires NMDA receptor activation. A PAF antagonist (BN 52021) that provides neuroprotection in ischemia-reperfusion displaces [3H] PAF bound to presynaptic membranes, blocks PAF-induced glutamate exocytosis and inhibits LTP. An antagonist selective for the intracellular PAF binding site (BN 50730) did not affect LTP, nor did BN 52021 modify NMDA currents. LTP was induced with weak synaptic stimulation coupled with postsynaptically administered enzyme resistant mcPAF. Theta-burst stimulation (10 min) after bath applications of mcPAF (1 microM) induced APV-independent LTP that was blocked by 5 microM BN 52021. When this antagonist was infused into the hippocampus before or immediately after training, it impaired memory of inhibitory avoidance training in the rat. Memory was not altered if the antagonist is infused 30 or 60 min after training. Moreover, mcPAF enhances memory on retention test performance of step-down inhibitory avoidance habituation and learning in rats. Also, memory was studied using a caudate nucleus-dependent cued water maze task. Rats received an 8 trial (30 s intertrial interval) training session in which a visible cued escape platform was located in a different quadrant of the maze of each trial. Following trial 8, the rats received a unilateral post-training intra-caudate injection of mcPAF (1 microgram/0.5 microliter), BN 52021 (0.5 microgram/0.5 microliter) or vehicle. On a retention test session 24 h later, latency to mount the escape platform was used as a measure of memory. The retention test escape latencies of rats given mcPAF were significantly lower than those of the vehicle-injected controls, indicating a memory enhancing effect of mcPAF. Injection of mcPAF did not affect retention when administered 2 h post-training, indicating a time-dependent effect of mcPAF on memory. The latencies for animals injected with BN 52021 were significantly higher than those of the controls, indicating that antagonism of endogenous PAF impairs memory. The findings show that PAF plays a role in memory formation in a caudate-mediated cued discrimination task. Administration of BN 52021 2 h post-training had no affect on retention, indicating a time-dependent effect of endogenous PAF on memory formation. PAF, the most potent bioactive lipid known, modulates excitatory synaptic transmission, neuronal plasticity and memory. When PAF production is overstimulated as in seizures or ischemia, it becomes neurotoxic.
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PMID:Bioactive lipids in excitatory neurotransmission and neuronal plasticity. 901 70

The purpose of this study was to determine whether mild hypothermia after a moderate hypoxic-ischemic insult reduces the extent of brain damage. Hypoxia was achieved in newborn piglets (n = 24; age, 14-72 h) by abrupt reduction of the inspired oxygen concentration (FiO2) to the maximum concentration (approximately 6%) giving low amplitude (< 7.0 microV) EEG. FiO2 was temporarily increased if heart rate, blood pressure, or end expiratory partial pressure of alveolar CO2 (PAco2) were markedly reduced. This intermittently resulted in EEG amplitude greater than 7 microV, the EEG traces were therefore later examined to determine the duration of low amplitude EEG. After 45 min of hypoxia, the animals were randomized to normothermia (39 degrees C) or hypothermia (35 degrees C) for 3 h. Hypothermia was achieved by applying packs containing ice water. Neurologic assessments and EEG recordings were performed regularly until 3 d when the brains were perfusion fixed. Histologic damage in cortex/white matter, cerebellum, hippocampus, basal ganglia, and thalamus was graded by a pathologist blind to treatment allocation. We found that the severity of brain damage (by histopathologic and neurologic evaluation) was not significantly different when the piglets were normothermic after hypoxia compared with the group made hypothermic. Increased duration of low amplitude EEG and seizure activity were associated with increased damage. When controlling for duration of hypoxia and excluding seizures, piglets undergoing hypothermia had approximately 50% less severe histopathologic damage in cortex/white matter, cerebellum, and hippocampus than those kept normothermic. Thalamus and basal ganglia had no or minor damage. It was concluded that there was no general beneficial effect of postinsult hypothermia. However, when controlling for the duration of the insult and occurrence of seizures, hypothermia reduced the severity of brain damage. This indicates a significant neuroprotective effect of 3 h of mild hypothermia on moderate, but not severe, hypoxic-ischemic insults.
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PMID:Posthypoxic hypothermia in newborn piglets. 909 52

A series of studies was undertaken to determine whether CO2 can be used as a humane as well as practical agent for euthanasia or anesthesia of rats. Human volunteers rated the degree of discomfort associated with breathing 50 to 100% CO2 mixed with oxygen. Increasing concentrations of CO2 were judged as progressively more noxious, from "highly unpleasant" for 50% CO2 to "painful" for 100% CO2. The practical aspects of anesthesia and euthanasia with 50 to 100% CO2 were studied, using male Sprague Dawley rats. Time to anesthesia and death were inversely related to CO2 concentration, as were the frequency and severity of adverse reactions, including seizures and hemorrhaging from the nose. The severity of edema and hemorrhage, which were observed on histologic examination of the lungs of all rats euthanized with CO2, were greatest in the animals exposed to the lowest concentrations. There were no significant effects of CO2 concentration on time to recumbency or recovery, and there were no significant effects of precharging versus not precharging the chamber on any of the parameters studied. It was concluded that, although CO2 can be used in a humane manner, the concentrations that are least likely to cause pain and distress are associated with the longest times to anesthesia and death, highest incidence of unwanted side effects, and most severe histologic changes in the lungs. Acceptably humane and reasonably practical euthanasia or anesthesia can be achieved using a nonprecharged chamber and a low gas flow rate so that conscious animals are never exposed to CO2 concentrations > 70%.
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PMID:Humane and practical implications of using carbon dioxide mixed with oxygen for anesthesia or euthanasia of rats. 930 11

The involvement of the L-arginine-nitric oxide (NO) pathway in the pathogenesis of hyperoxia-induced seizures was studied by using agents controlling NO levels. We selected two inhibitors of nitric oxide synthase, the systemic inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) and the novel cerebral-specific inhibitor 7-nitroindazole, and two generators of NO, the NO donor S-nitroso-N-acetylpenicillamine and the physiological precursor L-arginine. Rats with chronic cortical electrodes were injected intraperitoneally with different doses of one of the agents or their vehicles before exposure to 0.5 MPa O2 and O2 with 5% CO2 at an absolute pressure of 0.5 MPa. The duration of the latent period until the onset of electrical discharges in the electroencephalogram was used as an index of central nervous system O2 toxicity. The two nitric oxide synthase inhibitors L-NAME and 7-nitroindazole significantly prolonged the latent period to the onset of seizures on exposure to both hyperbaric O2 and to the hypercapnic-hyperoxic mixture. Pretreatment with the NO donor S-nitroso-N-acetylpenicillamine significantly shortened the latent period, whereas L-arginine, the physiological precursor of NO, significantly prolonged the latent period to onset of seizures. Our results suggest that the L-arginine-NO pathway is involved in the pathophysiology of hyperoxia-induced seizures via various regulating mechanisms.
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PMID:L-arginine-NO pathway and CNS oxygen toxicity. 957 10

Seizures are generally regarded as a manifestation of extreme, generally near-fatal carbon monoxide poisoning. A case is described in which a seizure attributable to carbon monoxide poisoning occurred in a small child at a level not thought to be associated with serious neurologic toxicity. A literature review of the occurrence of seizures in carbon monoxide poisoning found that no particular degree of carboxyhemoglobin was correlated with the presence of seizures. A seizure with no other apparent cause occurring in circumstances in which carbon monoxide toxicity would be suspected can be attributed to carbon monoxide poisoning.
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PMID:Carbon monoxide poisoning presenting as an isolated seizure. 961 Sep 72

Altered postictal cerebral blood flow dilatory responses may contribute to brain injury following neonatal seizures. We developed an initial series of experiments to characterize the effects of seizure activity on cerebral vascular dilatory responses during the immediate postictal period. Significant attenuation of postictal hypoxic cerebral vasodilation was noted. We hypothesize that this diminished cerebral dilator response to hypoxia involves depletion of adenosine (Ado) activity resulting from seizure ictus. Additional experiments were designed to evaluate whether the altered postictal responses were related to a depletion of Ado stores or a decreased response to Ado in the postictal state. Farm-bred piglets were equipped with closed cranial windows. Responses to hypercapnia (10% CO2), hypoxia (fractional inspired O2 = 0.10), and topical sodium nitroprusside (10(-6) M) were compared before and after bicuculline-induced seizures (1 mg/kg). Hypoxia-induced cerebral vasodilation was significantly attenuated in the first 90 min postictal (control: 56.5 +/- 6%, 10 min postictal: 6.3 +/- 2%, 60 min postictal: 21.7 +/- 6%, and 90 min postictal: 21.6 +/- 5%; P < 0.01), whereas the dilator responses to hypercapnia and topical sodium nitroprusside remained intact. In a separate group of piglets, both a dilating (10(-5) M) and a nondilating concentration of Ado (10(-11) M) were topically administered postictally to measure their effects on pial vessel dilatory response to hypoxia. Dilation to topical Ado (10(-5) M) was not altered postictally compared with control. Ado (10(-11) M) restored hypoxia-induced vasodilation to preseizure control values in the immediate postictal period (control: 51.0 +/- 8%, postictal: 46.7 +/- 8%, P > 0.05). Postictal administration of Ado will restore hypoxia-induced cerebral vasodilation in piglets even when a nondilating concentration is employed. This suggests that depletion of Ado with seizure activity is a mechanism for the loss of postictal cerebral vasodilation to hypoxia, and the role of Ado in hypoxic cerebral vasodilation is permissive.
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PMID:Adenosine depletion alters postictal hypoxic cerebral vasodilation in the newborn pig. 961 55

In a randomized crossover study, the influence of the anesthetics methohexital and propofol on EEG seizure parameters, seizure-quality measures, vital signs, and oxygen saturation (SpO2) and end-tidal carbon dioxide tension (ETCO2) was investigated; 146 treatments of 31 patients were analyzed. Significant differences were observed between agents for mean postictal pulse and blood pressure values. With methohexital, there was a clear postictal increase of mean blood pressure from 126/78 mm Hg to 161/102 mm Hg, whereas there was no increase with propofol (p = 0.00), and with methohexital, a postictal increase of the mean pulse rate from 81 to 90 beats/min and a slight decrease with propofol (79 to 78 beats/min). There were no differences in the SpO2 and ETCO2. The mean seizure duration for unilateral treatments was significantly longer with methohexital (52.7 s) compared with propofol (34.1 s; p = 0.000), but there was no difference for the seizure-quality measures: postictal suppression index (propofol 79.7%, methohexital 77.4%) and mean integrated amplitude (30.2/31.8) were the same for both anesthetic agents. The results show that differences in seizure duration are unrelated to seizure-quality measures.
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PMID:Propofol and methohexital as anesthetic agents for electroconvulsive therapy (ECT): a comparison of seizure-quality measures and vital signs. 966 Oct 91

Carbon monoxide (CO) is an endogenously produced gas sharing many properties with nitric oxide (NO), notably activating soluble guanylate cyclase and relaxing blood vessels. The brain can generate high quantities of CO from a constitutive enzyme, haem oxygenase (HO-2). To determine whether CO is involved in the regulatory mechanisms of cerebral blood flow (CBF), two conditions associated with a reproducible CBF increase were studied in rats: epileptic seizures induced by kainate, and hypercapnia. The HO inhibitor tin protoporphyrin (Sn-PP) did not modify the basal level of CBF, significantly reduced the increase in CBF during status epilepticus, and did not affect the cerebrovascular response to hypercapnia. It is concluded that CO participates in the regulation of CBF in specific conditions, notably those associated with glutamate release.
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PMID:Carbon monoxide regulates cerebral blood flow in epileptic seizures but not in hypercapnia. 969 25

During sevoflurane anaesthesia cerebral blood flow is preserved or slightly decreased. Cerebral oxygen consumption is reduced to 50% under 1 MAC sevoflurane. Autoregulation of cerebral blood flow and responsiveness of cerebral blood flow to changes in Pa CO2 are widely preserved. Sevoflurane produces a dose dependent increase in intracranial pressure and a decrease in cerebrovascular resistance that can not be observed under hypocapnic conditions. Central stimulus processing, the electroencephalogram and sensory evoked potentials are suppressed under sevoflurane in a dose dependent fashion. The electrophysiological data indicate that intraoperative awareness phenomena should be suppressed with sevoflurane 1.5-2.0 vol.%. Recovery of cognitive and psychomotor functions seems to be faster and more complete after sevoflurane than after isoflurane anaesthesia. In inducing seizure like EEG or muscle activity, sevoflurane seems to be comparable with isoflurane. There is no limitation of sevoflurane use in patients with concomitant psychiatric or neurological diseases, and sevoflurane may be valuable addition in neurosurgery or carotid surgery.
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PMID:[Sevoflurane and the nervous system]. 989 79


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