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

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

Lithium carbonate appears to inhibit the development of cocaine-induced behavioral sensitization while it does not inhibit the development of amygdala kindling. Lithium chloride did not inhibit kindled seizures. Carbamazepine does not inhibit cocaine-induced motor activity or the development of behavioral sensitization in the rat. Carbamazepine is highly effective in blocking completed amygdala-kindled seizures, but does not block their development in the rat. Lithium carbonate and carbamazepine, two drugs of use in the prophylactic treatment of affective illness, appear to have differential effects on sensitization and kindling.
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PMID:Differential effects of carbamazepine and lithium on sensitization and kindling. 643 80

We have described a 22-year-old woman who manifested clinical seizures after treatment with lithium carbonate was initiated. Serial electroencephalograms showed both nonspecific activation and activation of an epileptiform discharge with serum levels of lithium carbonate maintained within the therapeutic range.
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PMID:Seizures activated by therapeutic levels of lithium carbonate. 643 61

The relationship between neuronal epileptic activity and regional cerebral blood flow was studied by means of hydrogen clearance method (rCBF). Measurements of rCBF in the limbic structure and cerebral cortex were performed during limbic seizures induced by a microinjection of kainic acid to the left amygdala under concurrent monitoring of polygraph. Pentobarbital (35 mg/kg, i.p.) anesthesia was induced and cats were artificially ventilated. Physiological parameters such as blood pressure, body temperature, PaO2, PaCO2 and HCO3 were kept stable. After fixation of the cat's head in a stereotaxic device, stainless screw electrodes were placed over bilateral anterior sigmoid gyrus so as to touch the dura mater for cortical EEG monitoring. Bipolar needle electrodes were stereotaxically placed to both amygdala and the left dorsal hippocampus. Platinum electrodes were stereotaxically placed to the left amygdala, dorsal hippocampus and sensorimotor cortex. After measurements of control rCBF, a microsyringe was stereotaxically inserted into the left amygdala and kainic acid solution (2 micrograms) was injected. Polygraphic monitoring followed. Five to 30 minuted after kainic acid injection, continuous multiple spikes appeared in the left amygdala. Forty to 120 minutes later, continuous multiple spikes transmitted to the left hippocampus. Two to five hours later, limbic seizure occurred. The limbic seizure lasted five to eight hours and interictal discharges appeared. Repeated measurements of rCBF were done. In the left amygdala, rCBF increased about two-fold of the control immediately after development of continuous multiple spikes and remained increased as long as the seizure persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Regional cerebral blood flow in limbic seizures induced by microinjection of kainic acid into amygdala in cats]. 648 36

In a retrospective study involving 680 EEG investigations in 593 patients the effects of various psychopharmaceutical agents were examined by visual interpretation of the EEG. The drugs were given singly in the majority of cases and were combined in others, and special attention was paid to the occurrence of paroxysmal EEG activity. The proportions of abnormal EEGs in the various groups were (in descending order): clozapine 59%, lithium salts 50%, butyrophenone 44%, maprotiline 37%, dibenzepine 32%, laevomepromazine and amitriptyline 31%, imipramine 9% and diazepam 4%. The proportions of paroxysmal discharges (13%) and generalized transient disturbances with groups of slow waves (16%) were also greatest in the clozapine group. During 3.5 years (1973-1974, May 1979-November 1980) we observed drug-induced generalized seizures in 16 inpatients = 0.28% of all inpatients (N = 5785) in that time. The psychotropic drugs given to these patients were either laevomepromazine (Neurocil 4x), perazine (Taxilan 3x), maprotiline (Ludiomil 3x), clozapine (Leponex 2x), lithium carbonate (Quilonum retard 2x) and amitriptyline (Saroten 2x) alone or partly in combination with butyrophenone (3x), fluphenazine (2x) and biperiden (3x). The appearance of paroxysmal EEG activity seems dose dependent and occurs more often during treatment with a combination of psychoactive compounds, than in patients receiving a single drug.
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PMID:Abnormal EEG activities induced by psychotropic drugs. 696 41

The effects of the inhibition of carbonic anhydrase on the manifestation of tonic-clonic seizures were investigated in freely-moving rats. 4-Aminopyridine, a specific blocker of the neuronal K+ channels was used to produce generalized convulsions. After pretreatment of adult male rats with 20 or 40 mg/kg acetazolamide, 3, 5, 7 or 9 mg/kg 4-aminopyridine was injected intraperitoneally and the latencies of the symptoms were measured. Pharmacological inhibition of brain carbonic anhydrase significantly increased the latency of onset of seizures. Bolus administration of acetazolamide decreased the incidence of generalized convulsions and protected against status epilepticus. Chronic acetazolamide treatment for 2 days affected only the generalized convulsions. The results suggested that alterations of the extracellular and intracellular pH by acetazolamide decreased the efficacy of synaptic transmission in several areas of the brain. The possible effects of the HCO3- ions on the sensitivity of synaptic and nonsynaptic neuronal receptors are discussed.
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PMID:Pharmacological inhibition of brain carbonic anhydrase protects against 4-aminopyridine seizures. 788 80

There is little information on the prevalence and clinical presentation of acid-base abnormalities associated with cocaine toxicity. To address these issues, arterial blood gas results were evaluated in 156 cocaine-associated emergency department patient visits. Arterial blood gas results were obtained as part of the patient's clinical assessment. The majority of patients (52%) had a normal pH (7.35 to 7.45). Thirty-three percent of patients were acidotic, with a pH between 6.4 and 7.35. In 33 patients the acidosis was metabolic, with a HCO3- of 14 +/- 6 mmol/L. The acidosis was primarily respiratory in 18 patients, with evidence of hypoventilation. Hypoventilation was generally secondary to chest trauma or decreased mental status. Alkalosis (pH > 7.45) was observed in 15% of patients, and was usually respiratory, as evidenced by tachypnea and a low PCO2. These results indicate that metabolic and respiratory acid-base abnormalities are common during cocaine toxicity. Acidosis and alkalosis were associated with numerous patient presentations, including chest pain, shortness of breath, decreased mental status, trauma, and seizures. Acid-base abnormalities do not appear to be associated with a specific route of cocaine self-administration. Patients with a history of potential cocaine toxicity should be evaluated for acid-base abnormalities.
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PMID:Acid-base abnormalities associated with cocaine toxicity in emergency department patients. 830 47

In order to evaluate the neonatal outcomes of infants who had prolonged fetal heart rate (FHR) deceleration during the second stage of labor, the neonatal outcomes of 24 infants born after vaginal delivery at 37 to 42 weeks of gestation with prolonged FHR deceleration during the second stage of labor were compared with the outcomes of 28 infants of a similar gestational age who had normal FHR patterns. No differences in the Apgar scores, mean umbilical PaCO2, PaO2, HCO3- or base deficit values were observed between the two groups, but the mean pH values differed significantly. The occurrences of a 1-minute Apgar score < 7, umbilical arterial pH < 7.20, presence of meconium and admission to the neonatal intensive care unit were higher in the study group, but were not significantly different. None of the 24 infants with prolonged FHR deceleration experienced birth trauma, meconium aspiration, neonatal seizure or neonatal death, but three were found to have congenital heart disease. We conclude that prolonged FHR deceleration during the second stage of labor without FHR abnormalities during the first stage of labor is not always associated with an adverse neonatal outcome and does not mandate the need for surgical or immediate vaginal delivery. Their appearance on FHR tracings requires the implementation of additional methods to assess fetal well-being and also to diagnose fetal distress.
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PMID:Implications of prolonged fetal heart rate deceleration during the second stage of labor. 885 56

Anticonvulsants have moved into an important position as alternatives and adjuncts to lithium carbonate in the treatment of bipolar illness. Work with the nonhomologous model of kindled seizures helped in the choice of carbamazepine as a potential mood stabilizer and in the study of the mechanisms of action of the second generation anticonvulsants carbamazepine and valproate, as well as the putative third generation psychotropic anticonvulsants lamotrigine and gabapentin. Anticonvulsant neuropeptides such as TRH and nonconvulsant approaches with repeated transcranial magnetic stimulation (rTMS) also appear promising.
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PMID:A history of the use of anticonvulsants as mood stabilizers in the last two decades of the 20th century. 977 4

The aim of this study was to assess whether a drug which combines an antagonistic action at both NMDA and non-NMDA receptors offers advantages for treatment of epileptic seizures compared to drugs which antagonize only one of these ionotropic glutamate receptors. The novel glutamate receptor antagonist LU 73068 (4,5-dihydro-1-methyl-4-oxo-7-trifluoromethylimidazo[1,2a]quinoxal ine-2-carbonic acid) binds with high affinity to both the glycine site of the NMDA receptor (Ki 185 nM) and to the AMPA receptor (Ki 158 nM). Furthermore, binding experiments with recombinant kainate receptor subunits showed that LU 73068 binds to several of these subunits, particularly to rGluR7 (Ki 104 nM) and rGluR5 (Ki 271 nM). In comparison, the prototype non-NMDA receptor antagonist NBQX (2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo[f]quinoxaline) binds with high affinity to AMPA receptors only. Both NBQX and LU 73068 were about equieffective after i.p. injection in mice to block lethal convulsions induced by AMPA or NMDA. In the rat amygdala kindling model of temporal lobe epilepsy, LU 73068 dose-dependently increased the focal seizure threshold (afterdischarge threshold, ADT). When rats were stimulated with a current 20% above the individual control ADT, LU 73068 completely blocked seizures with an ED50 of 4.9 mg kg(-1). Up to 20 mg kg(-1), only moderate adverse effects, e.g. slight ataxia, were observed. NBQX, 10 mg kg(-1), and the glycine/NMDA site antagonist L-701,324 (7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-quinoline-2(1H)one), 2.5 or 5 mg kg(-1), exerted no anticonvulsant effects in kindled rats when administered alone, but combined treatment with both drugs resulted in a significant ADT increase. The data indicate that combination of glycine/NMDA and non-NMDA receptor antagonism in a single drug is an effective means of developing a potent and effective anticonvulsant agent.
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PMID:LU 73068, a new non-NMDA and glycine/NMDA receptor antagonist: pharmacological characterization and comparison with NBQX and L-701,324 in the kindling model of epilepsy. 986 55


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