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

The effects of kainic acid (KA)-induced limbic seizures have been investigated on cytochrome c oxidase (COx) activity, COx subunit IV mRNA abundance, ATP and phosphocreatine (PCr) levels in amygdala, hippocampus and frontal cortex of rat brain. Rats were killed either 1 h, three days or seven days after the onset of status epilepticus (SE) by CO2 and decapitation for the assay of COx activity and by head-focused microwave for the determination of ATP and PCr. Within 1 h COx activity and COx subunit IV mRNA increased in all brain areas tested between 120% and 130% of control activity, followed by a significant reduction from control, in amygdala and hippocampus on day three and seven, respectively. In amygdala, ATP and PCr levels were reduced to 44% and 49% of control 1 h after seizures. No significant recovery was seen on day three or seven. Pretreatment of rats with the spin trapping agent N-tert-butyl-alpha-phenylnitrone (PBN, 200 mg kg(-1), i.p.) 30 min before KA administration had no effect on SE, but protected COx activity and attenuated changes in energy metabolites. Pretreatment for three days with the endogenous antioxidant vitamin E (Vit-E, 100 mg/kg, i.p.) had an even greater protective effect than PBN. Both pretreatment regimens attenuated KA-induced neurodegenerative changes, as assessed by histology and prevention of the decrease of COx subunit IV mRNA and COx activity in hippocampus and amygdala, otherwise seen following KA-treatment alone. These findings suggest a close relationship between SE-induced neuronal injury and deficits in energy metabolism due to mitochondrial dysfunction.
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PMID:Alterations in cytochrome c oxidase activity and energy metabolites in response to kainic acid-induced status epilepticus. 1152 Apr 94

Yawning is a normal reflex triggered by arousal, drowsiness, boredom, hunger and emotional conditions and it is associated to several neurological diseases and drug abuse. Its wide presence in the phylogenetic vertebrate scale and even in human fetuses as young as 12 weeks directed the search for the common anatomic and biochemical mechanisms involved. The demonstration that yawning is not connected with high CO2 or low O2 blood levels left aside a prevalent metabolic hypothesis. Its close relationship with the sleep-wake cycle, specially in moments previous to falling asleep and after awaking has been related to changes in personal situation and activity. A single component of this reflex which is to be found exclusively in humans, is the fact that yawning is contagious. Thus, it is considered a component of the adaptative mechanism that is part of the surveillance reflex, becoming a significant paralinguistic evolutive expression aimed at protection and social cohesion. The common anatomical structures and neurochemical systems taking part in yawning, the sleep-wake cycle and the temporal lobe epilepsy may imply that yawning results from a set of protective systems induced by endogenous opiods which intervene in the inhibition and prevention of the temporal lobe epileptic seizures.
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PMID:[Yawning]. 1287 10

Anxiety is a medical mimicker that can imitate both cardiac and neurological symptoms. Anxiety disorder research protocols regularly use hyperventilation or i.v. lactate infusion to trigger panic attacks in susceptible subjects. Susceptible patients experience panic attacks with slight decreases in CO2 or increases in lactate production seen in mild exercise such as stair climbing. To the unsuspecting physician this appears to be dyspnea on exertion. Hyperventilation during rapid eye movement (dream) sleep may trigger panic attacks in patients with panic disorder, mimicking paroxysmal nocturnal dyspnea. Syncope from panic-induced hyperventilation can mimic seizures. When panic-like anxiety is discovered in aircrew it necessitates grounding. The prognosis is frequently good after treatment with psychotherapy, with return to full flying status a strong possibility.
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PMID:You're the flight surgeon. Anxiety. 1292 69

Accumulation of carbon dioxide (CO2) can disturb systemic hemodynamics and increase the seizure threshold in patients receiving electroconvulsive therapy (ECT). The purpose of this study was to investigate the effects of the laryngeal mask on blood gas, hemodynamics, and seizure duration during ECT under propofol anesthesia. Ventilation was assisted using either a face mask (n=23) or laryngeal mask (n=23) and 100% oxygen. There was no significant difference in PaO2 between the two groups. PaCO2 was greater in the face mask group than the laryngeal mask group at 3 minutes (54 +/- 11 mm Hg, 41 +/- 8 mm Hg, respectively) and 5 minutes (52 +/- 11 mm Hg, 43 +/- 15 mm Hg, respectively) after electrical stimulation (p<0.01). Mean blood pressure was higher than the corresponding preanesthesia value at 1 to 5 minutes after electrical stimulation in the face mask group and at 1 to 3 minutes after electrical stimulation in the laryngeal mask group. Mean seizure duration in the face mask group was significantly shorter than that in the laryngeal mask group (33 +/- 11 seconds, 42 +/- 10 seconds, respectively p<0.01). The change in PaCO2 was minor in the laryngeal mask group compared with the face mask group and seizure duration was longer in the laryngeal mask group. Laryngeal mask may be suitable for airway management during ECT anesthesia, especially when fitting a face mask is difficult.
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PMID:Benefits of the laryngeal mask for airway management during electroconvulsive therapy. 1465 73

Hypoxia causes dysfunction of excitatory and inhibitory neurotransmission, often resulting in encephalopathy, seizures or myoclonus. We evaluated the effects of hypoxia on GABAA receptor (GABAAR) function and expression in an in vitro model of neuronal hypoxia. NT2-N cells, derived from the human NT2 teratocarcinoma cell line, were exposed to < or =1% O2 for 8 h and then used immediately for experiments or allowed to recover under normoxic conditions (95% air/5% CO2) for 24, 48 or 96 h. Hypoxic treatment did not cause obvious morphological changes or cell death. In whole-cell patch-clamp recordings, the GABA current EC50 was unchanged, however, maximal GABA-evoked currents changed in a biphasic manner. Maximal GABA currents were significantly increased immediately after hypoxia, but were significantly reduced after 48 h normoxic recovery, and then returned to baseline after 96 h recovery. Maximal potentiation of 10 microM GABA currents by diazepam was increased 48 h after hypoxia, but potentiation by zolpidem was decreased. Barbiturate enhancement and zinc inhibition of GABA currents were unchanged. Semiquantitative reverse transcriptase (RT)-PCR showed decreased alpha1, alpha5, beta2 and gamma2 subunit mRNA after hypoxia. Hypoxic exposure altered GABAAR physiology and subunit mRNA expression, which may correlate with symptoms observed after hypoxia in vivo.
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PMID:Hypoxia alters GABAA receptor function and subunit expression in NT2-N neurons. 1497 87

A patient with a rare variation of fronto-orbital artery (FOA) that developed generalized tonic and clonic seizures is reported. The epilepsy focus was in her left frontal region, where blood was supplied by the contralateral fronto-orbital artery. The region was vulnerable to ischemic changes due to a decrease in blood CO2 gas caused by an increase in endogenous progesterone in the luteal period. The anomaly illustrates an important mechanism of ischemia in epilepsy.
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PMID:Epilepsy and variation in the frontal lobe artery. 1585 Jul 59

Methylmalonic acidemias are metabolic disorders caused by a severe deficiency of methylmalonyl CoA mutase activity, which are characterized by neurological dysfunction, including convulsions. It has been reported that methylmalonic acid (MMA) accumulation inhibits succinate dehydrogenase (SDH) and beta-hydroxybutyrate dehydrogenase activity and respiratory chain complexes in vitro, leading to decreased CO2 production, O2 consumption and increased lactate production. Acute intrastriatal administration of MMA also induces convulsions and reactive species production. Though creatine has been reported to decrease MMA-induced convulsions and lactate production, it is not known whether it also protects against MMA-induced oxidative damage. In the present study we investigated the effects of creatine (1.2-12 mg/kg, i.p.) and MK-801 (3 nmol/striatum) on the convulsions, striatal content of thiobarbituric acid reactive substances (TBARS) and on protein carbonylation induced by MMA. Moreover, we investigated the effect of creatine (12 mg/kg, i.p.) on the MMA-induced striatal creatine and phosphocreatine depletion. Low doses of creatine (1.2 and 3.6 mg/kg) protected against MMA-induced oxidative damage, but did not protect against MMA-induced convulsions. A high dose of creatine (12 mg/kg, i.p.) and MK-801 (3 nmol/striatum) protected against MMA-induced seizures (evidenced by electrographic recording), protein carbonylation and TBARS production ex vivo. Furthermore, acute creatine administration increased the striatal creatine and phosphocreatine content and protected against MMA-induced creatine and phosphocreatine depletion. Our results suggest that an increase of the striatal high-energy phosphates elicited by creatine protects not only against MMA-induced convulsions, but also against MMA-induced oxidative damage. Therefore, since NMDA antagonists are limited value in the clinics, the present results indicate that creatine may be useful as an adjuvant therapy for methylmalonic acidemic patients.
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PMID:Effectiveness of creatine monohydrate on seizures and oxidative damage induced by methylmalonate. 1646 66

Febrile seizures are frequent during early childhood, and prolonged (complex) febrile seizures are associated with an increased susceptibility to temporal lobe epilepsy. The pathophysiological consequences of febrile seizures have been extensively studied in rat pups exposed to hyperthermia. The mechanisms that trigger these seizures are unknown, however. A rise in brain pH is known to enhance neuronal excitability. Here we show that hyperthermia causes respiratory alkalosis in the immature brain, with a threshold of 0.2-0.3 pH units for seizure induction. Suppressing alkalosis with 5% ambient CO2 abolished seizures within 20 s. CO2 also prevented two long-term effects of hyperthermic seizures in the hippocampus: the upregulation of the I(h) current and the upregulation of CB1 receptor expression. The effects of hyperthermia were closely mimicked by intraperitoneal injection of bicarbonate. Our work indicates a mechanism for triggering hyperthermic seizures and suggests new strategies in the research and therapy of fever-related epileptic syndromes.
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PMID:Experimental febrile seizures are precipitated by a hyperthermia-induced respiratory alkalosis. 1730 48

A 60-year-old man without comorbidity underwent a totally extraperitoneal repair of bilateral inguinal hernias under general anesthesia. Forty minutes after the procedure he developed a slow, shallow respiratory pattern with a respiratory rate of 5/min and a self-limiting grand mal seizure lasting 30 seconds. Arterial blood gas analysis indicated significant hypercarbia and acidosis. The total dose of morphine administered was 20 mg intravenously. Naloxone was administered and the respiratory rate improved. The patient was discharged after 24 hours after making a good recovery and has had no further seizures a year after surgery. Although hypercarbia is a well-known complication of laparoscopic surgery when CO2 is used for insufflation, this, to the best of our knowledge, is the first reported case of a patient sustaining a grand mal seizure resulting from CO2 narcosis after laparoscopic surgery. The possible mechanisms are discussed.
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PMID:Carbon dioxide narcosis and grand mal seizure complicating laparoscopic herniorrhaphy. 1731 57

Most seizures stop spontaneously; however, the molecular mechanisms that terminate seizures remain unknown. Observations that seizures reduced brain pH and that acidosis inhibited seizures indicate that acidosis halts epileptic activity. Because acid-sensing ion channel 1a (ASIC1a) is exquisitely sensitive to extracellular pH and regulates neuron excitability, we hypothesized that acidosis might activate ASIC1a, which would terminate seizures. Disrupting mouse ASIC1a increased the severity of chemoconvulsant-induced seizures, whereas overexpressing ASIC1a had the opposite effect. ASIC1a did not affect seizure threshold or onset, but shortened seizure duration and prevented seizure progression. CO2 inhalation, long known to lower brain pH and inhibit seizures, required ASIC1a to interrupt tonic-clonic seizures. Acidosis activated inhibitory interneurons through ASIC1a, suggesting that ASIC1a might limit seizures by increasing inhibitory tone. Our results identify ASIC1a as an important element in seizure termination when brain pH falls and suggest both a molecular mechanism for how the brain stops seizures and new therapeutic strategies.
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PMID:Seizure termination by acidosis depends on ASIC1a. 1942 82


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