Preoperative contaminated wound management using short-term negative pressure wound therapy with instillation.

Background: The short-term application of negative pressure wound therapy with instillation and dwell time (NPWTi-d) enables the delivery of topical wound solutions, the solubilisation of debris and cleansing of the wound bed. The application of NPWTi-d may support the transition of the wound to a more manageable state and minimises the use of more invasive techniques.

Method: In this case series, we describe the process of applying NPWTi-d early as part of a contaminated wound treatment plan.

Monitoring and antiepileptic drug safety.

Treatment of patients with epilepsy strives for complete seizure control without intolerable drug side effects. Independent of blood drug levels, toxic effects allow titration to efficacy; however, allergic reactions, metabolically or genetically determined drug-induced illnesses, and idiosyncratic effects of drugs, while rare, may be life-threatening.Monitoring is an attempt to detect serious systemic toxic reactions of antiepileptic drugs in time to intervene and protect patients.

Hippocampal gene expression profiling in a rat model of posttraumatic epilepsy reveals temporal upregulation of lipid metabolism-related genes.

Traumatic brain injury occasionally causes posttraumatic epilepsy. To elucidate the molecular events responsible for posttraumatic epilepsy, we established a rodent model that involved the injection of microliter quantities of FeCl3 solution into the amygdalar nuclear complex. We previously compared hippocampal gene expression profiles in the traumatic epilepsy model and normal rats at 5 days after brain injury (acute phase) to determine the role of inflammation.

Posttraumatic Epilepsy: What's Contusion Got to Do With It?

Text of Abstract Liability to develop posttraumatic epilepsy (PTE) correlates in a general way with trauma dose. While contusion of the brain produces an admixture of extravasated blood, edema fluid and necrotic tissue at the site of skull trauma and in regions remote from the direct force, an unpredictable cascade of shearing injury, torsion and rotation and a myriad of physiological changes occur in structures subject to the mechanical pressure wave. Animal models mimic components of injury, some more thoroughly than others.

Role of endoplasmic reticulum stress in the amygdaloid kindling model of rats.

Endoplasmic reticulum (ER) is an organelle responsible for correct folding and sorting of proteins contributing to neurogenesis and neuronal cell death. We used rapid kindling to analyze specific ER stress marker expression underlying focal epileptogenesis. Seven-week-old rats were divided into three groups: sham (n = 6), partially kindled (n = 8), and over-kindled rats (n = 9).

Differential molecular regulation of glutamate in kindling resistant rats.

Using pentylenetetrazol (PTZ) kindling, we collected hippocampal tissue from standard response and kindling resistant animals, measuring hippocampal mRNA with real-time PCR of glutamate transporters GLAST, GLT-1, and EAAC1 and the sodium-coupled neutral amino acid transporter (SNAT) 1, SNAT2, and SNAT3. In addition, we measured mRNA of glutamine synthetase (GS), phosphate-activated glutaminase (PAG), glutamic acid decarboxylase (GAD) 1, GAD2, and vesicular inhibitory amino acid transporter (VIAAT). Fully kindled animals had decreased expression of mRNA in the hippocampus for GLAST and GAD2 compared with saline injected control.

Use of a new antiepileptic drug or an old one as first drug for treatment of absence epilepsy.

Treatment of absence epilepsy requires understanding the efficacy and side effects of several drugs, one of which first became available more than 50 years ago. Methods for drug development and procedures for evaluating their safety and efficacy over that time have changed dramatically. Observational studies of the efficacy of ethosuximide, a drug developed in the 1950s, reported complete seizure control in 40-60% of patients.

Levetiracetam enhances endogenous antioxidant in the hippocampus of rats: in vivo evaluation by brain microdialysis combined with ESR spectroscopy.

We have attempted to explore the neuroprotective effectiveness of levetiracetam (LEV) by measuring its in vivo antioxidant effect in the hippocampus of rats in a freely moving state. Male Wistar rats were used for the estimation of the in vivo antioxidant effect of LEV through microdialysis combined with electron spin resonance spectroscopy. The antioxidant effect was examined using the principle by which a systemically administered blood-brain barrier-permeable nitroxide radical (PCAM) decreases in an exponential decay manner that is correlated with the amount of antioxidant in the brain.

Vigabatrin: 2008 update.

Unlabelled: Vigabatrin (VGB) is a structural analogue of gamma-aminobutyric acid (GABA) that irreversibly inhibits GABA-transaminase (GABA-T), increasing brain levels of GABA. VGB is under assessment for treatment of infantile spasms (IS) and refractory complex partial seizures (CPS). Response can be rapid with spasm cessation following approximately 2 weeks of therapy.

Role of glutamate and GABA transporters in development of pentylenetetrazol-kindling.

Kindling is a form of epileptogenesis that can be induced with pentylenetetrazol (PTZ). We undertook this study to evaluate the contribution of glutamate and GABA transporters to the process of PTZ kindling. Rats were injected i.

In vivo EPR estimation of bilateral hippocampal antioxidant ability of rats with epileptogenesis induced by amygdalar FeCl3 microinjection.

Purpose: To measure the neural antioxidant function in the hippocampus of rats with epileptogenesis induced by microinjection of FeCl3 into the amygdala using the decay rate of the nitroxide radical as estimated by L-band electron paramagnetic resonance (EPR) spectroscopy.

Materials And Methods: Region-selected intensity determination (RSID) was used for the estimation of the nitroxide decay ratio. It is possible to estimate the in vivo hippocampal antioxidant ability using the half-life of the EPR signal of the blood-brain barrier-permeable nitroxide radical.

Functional role for redox in the epileptogenesis: molecular regulation of glutamate in the hippocampus of FeCl3-induced limbic epilepsy model.

We used western blotting to measure the quantity of glutamate and gamma-aminobutyric acid (GABA) transporters proteins within hippocampal tissue obtained from rats who had undergone epileptogenesis. Chronic seizures were induced by amygdalar injection of FeCl(3). We found that the glial glutamate transporters GLAST and GLT-1 were down-regulated at 60 days after initiation of chronic and recurrent seizures.

Effect of levetiracetam on molecular regulation of hippocampal glutamate and GABA transporters in rats with chronic seizures induced by amygdalar FeCl3 injection.

Enhancement of the glutamatergic excitatory synaptic transmission efficacy in the FeCl3 induced epilepsy model is associated with changes in the levels of glutamate and GABA transporter proteins. This study examined the effect of levetiracetam (LEV) on glutamate overflow and glutamate/GABA transporters expression in rats with epileptogenesis induced by the amygdalar injection of 1.0 microl of 100 mM FeCl3 (epileptic rat) and in control rats receiving amygdalar acidic saline injection (non-epileptic rat).

Zonisamide - a review of experience and use in partial seizures.

Zonisamide is a modern antiepileptic drug (AED) that is distinguished from other AEDs by its unique structure and broad mechanistic profile. Preclinical studies have reported a range of potential mechanisms of action for zonisamide, such as blocking voltage-gated sodium channels, reduction of T-type calcium channel currents, and enhancement of gamma-aminobutyric acid (GABA)-mediated inhibition, which are indicative of its broad antiseizure effects. Zonisamide has a favorable linear pharmacokinetic profile, a long half-life, and a low incidence of protein-binding interactions with other AEDs.

Molecular regulation of glutamate and GABA transporter proteins by clobazam during epileptogenesis in Fe(+++)-induced epileptic rats.

To assess the molecular effects of the antiepileptic drug clobazam (CLB, 1,5-benzodiazepine), a benzodiazepine effective in the management of epilepsy, we performed a series of experiments using rats with chronic, spontaneous recurrent seizures induced by amygdalar injection of FeCl(3). Experimental animals were treated for 14 days with CLB. We then measured the expression of glutamate and GABA transporter proteins and evaluated the changes that occurred in these proteins using both experimental and control animals.

Antiepileptic drugs and neuroprotection: current status and future roles.

There has been a growing interest in the use of antiepileptic drugs (AEDs) for neuroprotection, and in the possible role of AEDs in disease modification (i.e., antiepileptogenesis).

Natural antioxidants may prevent posttraumatic epilepsy: a proposal based on experimental animal studies.

Head injury or hemorrhagic cortical infarction results in extravasation of blood and breakdown of red blood cells and hemoglobin. Iron liberated from hemoglobin, and hemoglobin itself, are associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS have been demonstrated to be involved in the mechanism of seizures induced by iron ions in the rat brain, an experimental animal model for posttraumatic epilepsy (PTE).

MRI-based high-dimensional hippocampal mapping in mesial temporal lobe epilepsy.

MRI-based evaluation of the hippocampus is important in the assessment and treatment of patients with mesial temporal lobe epilepsy (MTLE). Using MRI-based large-deformation high-dimensional mapping (HDM-LD), which allows structural evaluation of regions of the hippocampus, we document the HDM-LD-defined pattern of hippocampal deformation in MTLE patients compared with matched controls. In 30 subjects with MTLE and confirmed medial temporal lobe sclerosis (MTS), we performed measurements of intracranial area, brain parenchymal volume and deformation-based hippocampal segmentations, and then grouped patients into right and left MTS groups (resulting in 15 subjects in each group).

Divalproex and epilepsy.

Valproic acid, a branched chain carboxylic acid, has a broad spectrum of action as an antiepilepsy drug. While effective in myoclonus syndromes and absence epilepsy, the drug has efficacy for patients with generalized convulsive and partial seizures as well. Mechanisms of action are similar to other drugs used to treat epilepsy, in that valproate limits sustained repetitive firing by actions on the voltage sensitive sodium channel.

Effect of zonisamide on molecular regulation of glutamate and GABA transporter proteins during epileptogenesis in rats with hippocampal seizures.

Epileptiform discharges and behavioral seizures may be the consequences of excess excitation associated with the neurotransmitter glutamate, or from inadequate inhibitory effects associated with gamma-aminobutyric acid (GABA). Synaptic effects of these neurotransmitters are terminated by the action of transporter proteins that remove amino acids from the synaptic cleft. Excitation initiated by the synaptic release of glutamate is attenuated by the action of glial transporters glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1), and the neuronal transporter excitatory amino-acid carrier-1 (EAAC-1).

Molecular biology and genetics of epilepsy.

Genetic and molecular biological methodologies are being applied to the study of patients with epilepsy at an ever-increasing pace. Accurate classification of epilepsy within large families has allowed identification of genes through linkage analysis and then isolation of gene products. Mutations causing ion channel abnormalities coupled with clinical patterns of focal epilepsy syndromes are beginning to change our thinking about the etiology of recurrent seizures in all patients.