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The benefits of regular exercise on brain health are undeniable. Long-term exercise increases the production of reactive oxygen species in brain. Therefore, athletes often consume antioxidant supplements to remedy exercise-related damage and fatigue during exercise. The aim of this study is to evaluate the role of ascorbic acid in the effects of different intensities of swimming exercise on the brain susceptibility to experimental epilepsy in rats. Ascorbic acid was administered intraperitoneally (ip) during three different swimming exercise programme for 90 days (15 min, 30 min, 90 min/day). The anticonvulsant activity regarding the frequency of epileptiform activity appeared in the 80 min after 500 units intracortical penicillin injection in 30 min and 90 min/day exercise groups. The administration of ascorbic acid (100 mg/kg, ip) did not alter the anticonvulsant properties seen in the in short-duration (15 min/day) swimming exercise group. The amplitude of epileptiform activity also became significant in the 110 and 120 min after penicillin injection in the moderate (30 min/day) and long duration (60 min/day) groups, respectively. The results of the present study provide electrophysiologic evidence that long-term administration of ascorbic acid causes anticonvulsant activities in the moderate and long-duration swimming exercise. Antioxidant supplementation such as ascorbic acid might be suggested for moderate and long-duration swimming exercise in epilepsy.
Levetiracetam (LEV) is an S-enantiomer pyrrolidone derivative with established antiepileptic efficacy in generalized epilepsy and partial epilepsy. However, its effects on ion currents and membrane potential remain largely unclear. We investigated the effect of LEV on differentiated NG108-15 neurons. In these cells treated with dibutyryl cyclic AMP, the expression level of the KV3.1 mRNA was elevated. With the aid of patch clamp technology, we found that LEV could suppress the amplitude of delayed rectifier K+ current (IK(DR)) in a concentration-dependent manner with an IC50 value of 37 µM. LEV (30 µM) shifted the steady-state activation of IK(DR) to a more positive potential by 10 mV, without shifting the steady-state inactivation of IK(DR). Neither Na+, nor erg (ether-a-go-go-related)-mediated K+ and ATP-sensitive K+ currents were affected by LEV (100 µM). LEV increased the duration of action potentials in current clamp configuration. Simulation studies in a modified Hodgkin-Huxley neuron and network unraveled that the reduction of slowly inactivating IK(DR) resulted in membrane depolarization accompanied by termination of the firing of action potentials in a stochastic manner. Therefore, the inhibitory effects on slowly inactivating IK(DR) (KV3.1-encoded current) may constitute one of the underlying mechanisms through which LEV affect neuronal activity in vivo.
The amygdala is a nuclear complex composed of 13 nuclei and cortical areas and their subdivisions. Tract-tracing studies performed over the past 20 years demonstrate that each nucleus is uniquely connected with other brain areas. Consistent with anatomic heterogeneity, the functions of the amygdala vary from attention to memory to formation of emotional responses to sensory stimuli. Here, we briefly review the principles of amygdaloid neuronal wiring that underlie the computations necessary to perform such complex behavioural functions.
Recent fi ndings in experimental models and in the clinical setting highlight the possibility that infl ammatory processes in the brain contribute to the etiopathogenesis of seizures and to the establishment of a chronic epileptic focus. Prototypical infl ammatory cytokines such as IL-1β and TNF-α are overexpressed in epileptogenic brain areas, prominently by glia and to a lesser extent by neurons and endothelial cells of the blood brain barrier. Cytokine receptors are also upregulated, and the related intracellular signalling is activated, highlighting both autocrine and paracrine actions of cytokines in diseased brain. Cytokines can profoundly affect neuronal network excitability, and the recent demonstration of molecular and functional interactions between cytokines and classical neurotransmitters, such as glutamate and GABA, provides one mechanism by which cytokines affect neuronal activity. These interactions may result in increased tissue excitability leading to seizures and cell loss. These fi ndings describe novel communications between glia and neurons which may contribute to pathological conditions (e.g. seizures, neurodegeneration) characterized by the activation of infl ammatory processes, thus highlighting potential new targets for therapeutic intervention.
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Wavelet mapping of sleep spindles in young patients with epilepsy

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Using the wavelet mapping of sleep spindles we investigated influence of focal epilepsy on spindle generation. We found that the maximum of sleep spindle intensity is usually localized away from the epileptic focus. We discuss the possibility of the application of wavelet mapping for localization of epileptic foci prior to epileptic neurosurgery.
This study examines the effects of ethanol on lindane-induced seizures in rats. The animals were divided into following groups: 1. saline, 2. DMSO (dimethylsulfoxide), 3. lindane dissolved in DMSO in the dose of 4, 6 or 8 mg/kg (L4, L6 and L8 groups, respectively), 4. ethanol 2 g/kg administered 30 min prior to lindane (protected groups AL4, AL6 and AL8) and 5. ethanol alone (2 g/kg). In order to determine ethanol concentration in plasma, blood samples were collected by cardiac puncture 30 and 60 min after ethanol injection. For EEG and power spectra recordings, electrodes were implanted into the skull. The lindane treatment resulted in a dose-dependent increase of seizure incidence and severity. The rats displayed severe seizure patterns characterized by high voltage spike-wave complexes, poly-spikes and sleep-like patterns in EEG, while the power spectra were intensively elevated in comparison to the corresponding controls. Ethanol alone led to increased EEG power spectra, which became dominant in the range of 0-4 Hz. For evaluation of anticonvulsant ethanol action we compared latency to seizure, incidence and seizure severity (scale from 0 to 4) in the examined groups. Ethanol diminished seizure incidence in AL4 and AL6 groups, decreased intensity of convulsions, and prolonged duration of latency period in AL8 group. We observed suppression of the EEG signs of lindane-provoked epileptiform activity in AL4 and AL6, but not in AL8 group. These results suggest that ethanol acted protectively on lindane-induced seizures and suppressed behavioral and epileptic EEG spiking activity.
Ketogenic Diet is effective in the treatment of epilepsy in both children and adults. KD increases the effectiveness of conventional therapies and can be applied for the treatment of other diseases. Simultaneously, KD is cheaper and does not possess as many adverse effects as conventional medicine.
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