ObjectivesTo determine whether there are differences in the profile and in the care of adult patients with epileptic seizures in emergency department according to age ≥ 75 years, and if this is independently associated with results in the emergency department and 30 days after discharge.Material and methodsACESUR is a multicentre, prospective, observational cohort multipurpose register that was carried out in 2017. The distribution of the variables corresponding to the clinical presentation and care according to age ≥ 75 years were compared. Subsequently, logistic regression models were performed with the objective of evaluating the effect of age ≥ 75 years on the outcome variables.ResultsA total of 541 (81.5%) cases younger than 75 years were analysed compared to 123 adult patients (18.5%) of ≥ 75 years or more. In the group of long-lived it was observed significantly greater probability of dependence, co-morbidity, polypharmacy, a previous visit to the hospital emergency department, arrived by ambulance, first seizures and a symptomatic aetiopathogenic classification. In the multivariate analysis, after adjusting for the above variables, it is observed that age > 75 years is associated independently with a higher incidence of specific supplementary tests (OR: 2.31; 95% CI: 1.21-4.44), but not pharmacological intervention (OR: 1.63; 95% CI: 0.96-2.80), or hospitalisation or extended stay in emergency departments (OR: 1.56; 95% CI: 0.94-2.59). On adjusting for all previous variables, age > 75 years is associated with lower incidence of adverse events at 30 days (OR: 0.43; 95% CI: 0.25-0.77).ConclusionsIn the ACESUR Registry, differences in clinical presentation and in the care of patients with seizures in emergency departments were identified when comparing those patients > 75 years with those < 75 years. Age ≥ 75 years is not independently associated with a higher incidence of intervention in emergency departments, or with more adverse outcomes at 30 days after discharge. 相似文献
d,l-Homocysteine thiolactone (H), a reactive homocysteine metabolite, contributes to total homocysteine pool. The aim of the
present study was to determine the effects of H after acute application in increasing doses to rats. Adult Wistar rat were
intraperitoneally administered saline or H in increasing doses (5.5, 8.0, or 11.0 mmol/kg). For electroencephalographic (EEG)
recordings, three gold-plated screws were implanted into the skull and animals were supervised. We observed H-induced two
types of seizures, the coexistence of convulsive and nonconvulsive epilepsy. Dose-related increase in the number and severity
(0–4) of displaying convulsions was recorded. In H5.5 group, the majority of seizure episodes were grade 1 (62.5 and 0% lethality), in H8 40% grade 2, and in H11 grade 4 in 42.11% (100% lethal outcome). EEGs recordings in convulsive animals showed a high-voltage spike-wave and polyspikes
complexes. The second, absence-like, nonconvulsive seizures were accompanied by the EEGs mostly with 6–8 Hz spikes-and-wave
discharges (SWD). Latency time to the generalized clonic-tonic seizures overlapped with the time of the maximal median number
and median duration of the SWD per 15 min during 90-min observing period. The results show that acute H administration significantly
changes neurons, EEG tracings, and behavioral responses and suggests a possible model for studying petit mal epilepsy. 相似文献
Harmful algal blooms are increasing worldwide, including those of Pseudo-nitzschia spp. producing domoic acid off the California coast. This neurotoxin was first shown to cause mortality of marine mammals in 1998. A decade of monitoring California sea lion (Zalophus californianus) health since then has indicated that changes in the symptomatology and epidemiology of domoic acid toxicosis in this species are associated with the increase in toxigenic blooms. Two separate clinical syndromes now exist: acute domoic acid toxicosis as has been previously documented, and a second novel neurological syndrome characterized by epilepsy described here associated with chronic consequences of previous sub-lethal exposure to the toxin. This study indicates that domoic acid causes chronic damage to California sea lions and that these health effects are increasing. 相似文献
Dravet syndrome (DS), previously known as severe myoclonic epilepsy of infancy, is one of the most severe forms of childhood epilepsy. DS is caused by a mutation in the neuronal voltage-gated sodium-channel alpha-subunit gene (SCN1A). However, 25–30% of patients with DS are negative for the SCN1A mutation screening, suggesting that other molecular mechanisms may account for these disorders. Recently, the first case of DS caused by a mutation in the neuronal voltage-gated sodium-channel beta-subunit gene (SCN1B) was also reported. In this report we aim to make the molecular analysis of the SCN1A and SCN1B genes in two Tunisian patients affected with DS. The SCN1A and SCN1B genes were tested for mutations by direct sequencing. No mutation was revealed in the SCN1A and SCN1B genes by sequencing analyses. On the other hand, 11 known single nucleotide polymorphisms were identified in the SCN1A gene and composed a putative disease-associated haplotype in patients with DS phenotype. One of the two patients with putative disease-associated haplotype in SCN1A had also one known single nucleotide polymorphism in the SCN1B gene. The sequencing analyses of the SCN1A gene revealed the presence of a putative disease-associated haplotype in two patients affected with Dravet syndrome. 相似文献
Triheptanoin, the triglyceride of heptanoate, is anticonvulsant in various epilepsy models. It is thought to improve energy metabolism in the epileptic brain by re‐filling the tricarboxylic acid (TCA) cycle with C4‐intermediates (anaplerosis). Here, we injected mice with [1,2‐13C]glucose 3.5–4 weeks after pilocarpine‐induced status epilepticus (SE) fed either a control or triheptanoin diet. Amounts of metabolites and incorporations of 13C were determined in extracts of cerebral cortices and hippocampal formation and enzyme activity and mRNA expression were quantified. The percentage enrichment with two 13C atoms in malate, citrate, succinate, and GABA was reduced in hippocampal formation of control‐fed SE compared with control mice. Except for succinate, these reductions were not found in triheptanoin‐fed SE mice, indicating that triheptanoin prevented a decrease of TCA cycle capacity. Compared to those on control diet, triheptanoin‐fed SE mice showed few changes in most other metabolite levels and their 13C labeling. Reduced pyruvate carboxylase mRNA and enzyme activity in forebrains and decreased [2,3‐13C]aspartate amounts in cortex suggest a pyruvate carboxylation independent source of C‐4 TCA cycle intermediates. Most likely anaplerosis was kept unchanged by carboxylation of propionyl‐CoA derived from heptanoate. Further studies are proposed to fully understand triheptanoin's effects on neuroglial metabolism and interaction.