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Effects of emotional stress on E1-mouse convulsions, and their biochemical background.

Emotional stress markedly inhibited E1 mouse convulsions. Norepinephrine and dopamine levels in E1 mouse brain were hardly affected by stress, though a marked decrease in norepinephrine and dopamine levels was observed in the ddY mouse brain. The serotonin levels decreased in the E1 mouse brain in the same degree as in the ddY mouse brain. These findings suggest that the serotonergic system is involved in the inhibition of E1 mouse convulsions, through an enhanced serotonin release in the brain brought on by the emotional stress. Noradrenergic and dopaminergic systems may also be involved.

3,4-Dihydroxyphenylacetic Acid↗

An analysis of the epileptogenic potency of CO2+- its ability to induce acute convulsive activity in the isolated frog spinal cord.

The action of Co2+ on the isolated frog spinal cord was studied by extracellular application of the ion in the superfusing solution. A complete and reversible blockade of chemical synaptic transmission by Co2+ (3 mmol/l) could be achieved after a superfusion period of 20-30 min. During continued Co2+ application (greater than 60 min) the following effects upon the motoneuron membrane, dorsal root and ventral root fibres were observed. Motoneurons and ventral root fibers: 1. prolongation of initial segment action potential to a maximum of 30 ms, 2. blockade of the long afterhyperpolarization, 3. abolition of adaptation, 4. increased duration of fibre action potential in the ventral root, 5. backfiring after ventral root stimulation. Dorsal root fibres: 1. prolongation of the extraspinal fibre action potential, 2. marked prolongation of the action potential of the terminal region, 3. backfiring of multiple action potentials after dorsal root stimulation. Even in the presence of Co2+, when synaptic transmission was completely blocked, strong convulsive reactions of the isolated spinal cord were observed. Intracellular injection of Co2+ into motoneurons did not affect the action potential, but led to a shift of the EIPSP towards the membrane potential. The results indicate that the induction of convulsive reactions by Co2+ is mainly due to a prolongation of action potentials. The plateau-like deformation of the action potential of the initial segment membrane and presumably of the terminal region of nerve endings results in retrograde propagation of action potentials and in some cases induces oscillatory discharge of single neurons.

Action Potentials↗

Partial protection against hyperbaric oxygen induced convulsions by dopaminergic agents in mice: possible involvement of autoreceptors?

In the present report we have investigated the effects of apomorphine, (-)3-PPP, L-DOPA and haloperidol on the elicitation of convulsions induced in mice by exposure to oxygen at high pressure (HBO) (5 ata O2). It was found that the administration of apomorphine (0.025-0.1 mg X kg-1 s.c.), (-)3-PPP (4 mg X kg-1 i.p.) L-DOPA (200-400 mg X kg-1 i.p.) as well as haloperidol (0.25-2.0 mg X kg-1 i.p.) produced a significant protection against HBO-induced convulsions. Haloperidol was the only drug to produce a dose-dependent decrease in respiration, and this effect does probably explain the anticonvulsant effects observed. The low doses at which apomorphine was effective, and the effects produced by (-)3-PPP, indicate an effect mediated via DA autoreceptors. Alternatively, and more likely taking the effects of L-DOPA into account, the DA receptors involved are sensitive enough to disclose postsynaptic agonist properties of apomorphine and (-)3-PPP at the doses employed.

Animals↗

Changes in brain dopamine, norepinephrine and serotonin associated with convulsions induced by pinealectomy in the gerbil.

In three separate experiments, adult male gerbils 10 weeks of age were pinealectomized (PX), observed for convulsions, and sacrificed at various intervals after PX. Norepinephrine (NE), dopamine (DA) and serotonin (5-HT) in selected brain parts were determined by fluorometric procedures. No changes in DA were observed. Serotonin levels were shown to be elevated in sham-operated and PX animals, possibly due to stress phenomena associated with anesthesia or surgical procedures. Norepinephrine was significantly depressed over control and sham-operated animals by 1 hour after surgery with a post-operative duration of at least 12 hours. Results in this study did not indicate whether the decreased NE was the cause or an effect of the PX-induced convulsive activity.

Animals↗

Spider toxin (JSTX-3) inhibits the convulsions induced by glutamate agonists.

The effect of a spider toxin (JSTX-3)--a specific blocker of glutamate receptors--on the behavior of mice was studied using an intracerebroventricular (i.c.v.) injection technique. At higher doses (more than 12 nmol/brain), JSTX-3 increased motor activities and induced characteristic symptoms. JSTX-3 at a dose of 4.7 nmol/brain which per se did not produce any abnormal behavior, specifically antagonized quisqualate-induced convulsions but not NMDA- or kainate-induced convulsions. These results indicate that JSTX-3 is a selective antagonist of the quisqualate receptors in the mammalian central nervous system.

Animals↗

Convulsion following intrathecal cephaloridine.

Following therapeutic intrathecal administration of cephaloridine to an 11-day-old premature infant with suspected meningitis, a generalized tonic convulsion was observed. Symptoms continued to subside over the next six hours, followed by postictal sleep. That convulsion and other symptoms were due to cephaloridine was confirmed when the second intrathecal administration produced the same symptom. Because of its possible damaging effect on CNS, it is strongly suggested that cephaloridine should not be administered directly into the cerebrospinal fluid space.

Cephaloridine↗

Benign infantile familial convulsions.

Five infants, three girls and two boys, first had convulsions between the ages of 4 and 6 months. Although the aetiology of the attacks was unknown, all the infants had a family history of similar convulsions occurring at the same age and having a benign outcome. The attacks, which always occurred in a cluster, were promptly controlled, in four cases with phenobarbital and in one case with valproate. Seizures were partial with secondary generalization and were characterized by head and eye deviation (not always the same side in each attack) diffuse hypertonia and then bilateral limb jerks. The interictal EEG was normal. The ictal EEG showed diffuse discharge with onset in the central-occipital region. Laboratory, radiological and neurological findings were normal. A history in at least one paternal relative (the father in four cases) of similar seizures, occurring at the same age suggested a genetic predisposition. No seizures or EEG anomalies were observed during the follow up.

Electroencephalography↗

The effect of pyridoxal phosphate-induced convulsive seizures on rat brain phospholipid metabolism.

The intraventricular injection of pyridoxal phosphate (PLP; 1 mumole/brain) to rats causes convulsive seizures beginning 3 min after injection and lasting for about 20 min. The incorporation of [2-3H] glycerol into rat brain glycerides has been studied to ascertain whether treatment with PLP affects the incorporation of label into various lipid classes. The labeling pattern of glycerides is changed by the administration of PLP. The observed alterations begin a few min after injection, together with the convulsive seizures. 1 h after the injection the pattern of labeling of brain glycerides returns to normal. Different glycerides are differently affected by PLP. This work demonstrates that the labeling of diglyceride increases whereas that of phosphatidylethanolamine decreases following PLP administration.

Animals↗

Effect of generalized seizures on the structure of the sleep-waking cycle and the EEG in rats with an inherited predisposition to audiogenic convulsions.

Data are presented on the effects of generalized tonic-clonic seizures on the structure of the one-day sleep-waking cycle in Krushinskii-Molodkina (KM) rats, which have a genetic predisposition to audiogenic convulsions. Spectral and correlation analysis of EEG activity in the hippocampus, caudate nucleus, medial central nucleus of the thalamus, and in the somatosensory, visual, and auditory regions of the cortex of these animals was carried out for time intervals before and after convulsions. After seizures, rats showed a prolonged (up to 3.5 h) reduction in fast-wave sleep (FWS) with no subsequent compensatory increase in this phase in the sleep-waking cycle, while a disturbance in slow-wave sleep (SWS) was minor and short-lived (not more than 2 h). It is suggested that generalized paroxysmal attacks predominantly involve disorganization of the function of the systems regulating FWS, while the synchronizing mechanisms of the brain, responsible for SWS, are affected to a lesser extent.

Acoustic Stimulation↗

Platelet-activating factor and polyunsaturated fatty acids in cerebral ischemia or convulsions: intracellular PAF-binding sites and activation of a fos/jun/AP-1 transcriptional signaling system.

Platelet-activating factor (PAF) is a lipid mediator formed in the early response of the central nervous system to ischemia or convulsions. Free polyunsaturated fatty acids and arachidonic and docosahexaenoic acids are accumulated along with PAF. Antagonists of PAF have been found to improve cerebral blood flow and partially block the rise in free fatty acids, an effect that may arise by way of inhibition of PAF receptors or stimulation of the reacylation of free fatty acids released upon insult. Three intracellular PAF-binding sites have been identified in rat cerebral cortex. These very high-affinity binding sites are inhibited by PAF antagonists, with certain antagonists exhibiting specificity for a particular binding site. This specificity indicates heterogeneity in these binding sites. Ischemia or stimulation also leads to protooncogene transcriptional activation. Here, we discuss studies with cells in culture showing that PAF promotes transcriptional activation of immediate-early genes. PAF activates the transcription of the immediate-early genes fos and jun, whose gene products are regulators of the transcription of other genes. Transcription of fos is also activated by convulsion or ischemia in the central nervous system. The activation of these genes by PAF can be inhibited by PAF antagonists, and is apparently accomplished by way of an AP-1 transcription regulatory sequence in the promoter region of the target genes. Studies with deletion mutants show that PAF can also exert its activating properties by way of cyclic adenosine-3',5'-monophosphate-(cAMP) and Ca(2+)-responsive elements, and suggest that PAF is involved in an interconnected network of cell signaling that may coordinate short-term and long-term responses of cells to stimulus and injury.

Animals↗

Oral flunitrazepam in the prevention of local anaesthetic-induced convulsions in mice.

The present study determined whether oral flunitrazepam was effective reducing CNS toxicity of lidocaine and bupivacaine. Pretreatment of mice with flunitrazepam, 0.065-0.25 mg X kg-1, significantly reduced or prevented convulsions and mortality induced by lidocaine 106 and 209 mg X kg-1 or bupivacaine 58 and 90 mg X kg-1 injected intraperitoneally. The doses of flunitrazepam used did not cause measurable sedation in mice. The efficacy of oral flunitrazepam in preventing local anaesthetic-induced convulsions is similar to that previously reported by intraperitoneal or intramuscular injections in mice. Flunitrazepam could be useful for oral premedication of patients before regional anaesthesia.

Administration, Oral↗

A major role of viruses in convulsive status epilepticus in children: a prospective study of 22 children.

UNLABELLED: A group of 22 previously healthy children with their first convulsive status epilepticus (SE), treated at Kuopio University Hospital, Finland, were prospectively studied. Eleven children had febrile and 11 afebrile SE. Polymerase chain reaction was used to detect specific DNA from CSF, enzyme immunoassays and immunofluorescence assays to detect specific antibodies in serum and CSF, viral cultures were obtained from CSF, throat and stool and antigen detection from throat specimens. Viral infection was identified in 10 of 11 children with febrile SE (91%) and in 7 of 11 with afebrile SE (64%). Human herpes virus 6 infection was identified in 12 children (55%), and in at least six of them the infection was primary. Single cases of human herpes virus 7, parainfluenza 3, adenovirus 1, echovirus 22, rota, influenza A and Mycoplasma pneumoniae infection were diagnosed. CONCLUSION: Viruses, human herpes virus 6 in particular, seem to be major associated factors in convulsive status epilepticus, both febrile and afebrile. Human herpes virus 7 and Mycoplasma pneumoniae are novel agents associated with status epilepticus.

Antigens, Viral↗

Bilateral intertrochanteric fractures after surgical treatment of bilateral femoral neck fractures secondary to hypocalcemic convulsions with chronic renal failure: a case report and review of the literature.

There have been no reports of bilateral femoral neck fractures followed by bilateral femoral intertrochanteric fractures. A 28-year-old man presenting with bilateral femoral neck fractures due to generalized convulsions was diagnosed with chronic renal failure and treated with percutaneous screw osteosynthesis and hemodialysis. During rehabilitation, the patient again had convulsions resulting in bilateral femoral intertrochanteric fractures 2 months after the operation. He was treated with a compression hip screw on the right side and conservatively on the left side. This is the first well-documented report on bilateral femoral neck fractures followed by bilateral femoral intertrochanteric fractures.

Adult↗

Neonatal convulsion revealing maternal hyperparathyroidism: an unusual case of late neonatal hypoparathyroidism.

Neonatal convulsion is a very alarming manifestation of underlying sinister problem. As an important cause, neonatal hypocalcemia usually occurs soon after birth and reflects abnormal maternal calcium regulation. We report an unusual case of late neonatal hypocalcemia presented with intractable seizures after two-month-old. Further investigations revealed maternal hyperparathyroidism secondary to parathyroid adenoma, which was missed during antenatal checkup. High index of suspicion is necessary in early detection and prompt treatment of neonatal hypocalcemia. Screening of maternal calcium level is mandatory in unexplained late neonatal hypocalcemia as mother with primary hyperparathyroidism could be asymptomatic and first manifest as late-onset neonatal convulsion. Early detection and appropriate intervention could avoid serious maternal and fetal morbidity.

Adenoma↗

Non convulsive status epilepticus after replacement of valproate with lamotrigine.

PURPOSE: Lamotrigine (LTG) and valproate (VPA) are widely used in the treatment of generalized epilepsies. Nevertheless seizure aggravation with LTG has been reported in juvenile myoclonic epilepsy and epilepsy with myoclonic absences. The aim of this study was to describe clinical features and EEG findings in patients with non convulsive status epilepticus (NCSE) after replacement of VPA with LTG. METHOD: Retrospective analysis of three identified patients in a large university hospital. RESULTS: We describe three adult patients aged 39, 50 and 75 years, who developed non-convulsive status epilepticus (NCSE) after replacement of VPA with LTG. The episodes of NCSE presented as an acute confusional state with mild myoclonus. Ictal EEG showed generalized spike-wave or polyspike wave activity. The clinical symptoms and the EEG responded promptly to IV benzodiazepines and patients remained well controlled with dose reduction of LTG (in one patient) or discontinuation of LTG (in two patients). CONCLUSION: The reported episodes of NCSE in these patients with generalized epilepsy may be either due to a possible paradoxical reaction to LTG or due to a withdrawal effect of VPA.

Adult↗

Association of infantile convulsions with paroxysmal dyskinesias (ICCA syndrome): confirmation of linkage to human chromosome 16p12-q12 in a Chinese family.

We have studied one family of Chinese origin, in which benign infantile convulsions and paroxysmal choreoathetosis (of the dystonic form) were co-inherited as a single autosomal dominant trait. This association is specific to ICCA syndrome, which we have recently described in four French families. Some patients in the new family also exhibit recurrence of epileptic seizures at a much later age, making the ICCA syndrome in this family atypical. DNA samples isolated from this family of 22 members (9 affected) have been tested with genetic markers at chromosome 16p12-q12, in which region the ICCA syndrome has previously been linked. Confirmation of linkage to this pericentromeric region of human chromosome 16 has been obtained and no critical meiotic recombination event has been detected in the ICCA region. This result suggests that, in contrast to marked clinical heterogeneity, the association of infantile convulsions with paroxysmal dyskinetic movements could be genetically homogeneous.

China↗

Cefepime-induced non-convulsive status epilepticus in a peritoneal dialysis patient.

Non-convulsive status epilepticus related to cefepime has not been reported in childhood dialysis patients, although several adult cases have been reported. We report a state of acute confusion in a 15-year-old boy on continuous ambulatory peritoneal dialysis (CAPD) receiving cefepime that was diagnosed as status epilepticus by electroencephalography (EEG). The EEG improved after anticonvulsive therapy. All clinical symptoms disappeared dramatically within 24 h of discontinuation of cefepime. The differential diagnosis of confusional states and the mechanisms of the convulsive effects of antimicrobials in chronic renal failure are discussed. The importance that the clinician is aware of the rare side effects of antimicrobials is emphasized.

Adolescent↗

Non-convulsive status epilepticus and generalised tonic-clonic seizures persisting in old age in a patient with idiopathic generalised epilepsy: a long-term observation.

Persisting non-convulsive status epilepticus in a man with idiopathic generalised epilepsy is reported. After a first generalised tonic/clonic seizure on awakening one day at the age of 20, the patient experienced rare non-convulsive status epilepticus until the age of 73, when the frequency of the episodes increased, in spite of the initiation of treatment with antiepileptic drugs. No significant cognitive decline was documented when the patient was 83. The existence of such conditions in the context of idiopathic generalised epilepsy shows the problems of syndromic diagnosis and of age dependency of some epileptic phenomena over the course of life with potential bidirectional influences between epileptic manifestations and senile processes.

Aged, 80 and over↗