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

Increasing evidence implicates glutamate receptor over-stimulation in the neurotoxicity associated with a host of metabolic insults, including seizures and hypoxia-ischemia. To begin to understand more completely the role of energy metabolism in the mechanism of neuron death following excitatory amino acid exposure, we investigated the effects of kainic acid exposure on metabolic rate in cultured hippocampal cells using a recently developed silicon microphysiometer. The device gives a continual real-time measure of metabolism in relatively small numbers of cells, as assessed by efflux of protons generated at least in part by ATP hydrolysis and lactic acid production. In the first half of this report, we characterize the feasibility of using this device for measuring cellular metabolism in hippocampal cultures. Metabolic rate in both astrocytes and neurons was readily detectable, with a high signal-to-noise ratio. The rate was proportional to the number of cells and was sensitive to metabolic enhancement or depression. We then utilized this device to study metabolic responses to the excitotoxin kainic acid. We observed a receptor-mediated, dose-dependent increase in metabolic rate upon stimulation by kainic acid, with an EC50 of approximately 100 microM. Exposure to toxic levels of kainic acid for 10 min produced an initial elevation (for 2 hr) in metabolic rate and then a gradual decline in metabolism over the next 8 hr that preceded a measurable loss of cell viability. This study further delineates a time window for the onset of kainic acid-induced damage. The results clearly show the feasibility of using silicon microphysiometry for assessing metabolism of brain cultures and for exploring the relationship between metabolism and synaptic activation.
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PMID:Effects of excitotoxin exposure on metabolic rate of primary hippocampal cultures: application of silicon microphysiometry to neurobiology. 154 39

In a prospective study 144 adult patients with chronic subdural hematomas were randomly divided into three treatment groups after burr-hole evacuation. The two commonly used procedures (external closed system drainage and aspiration and irrigation without any drainage) were compared to a modified technique: permanent subdural drain with subcutaneous reservoir. After the hematoma was washed out with saline solution, a silicon catheter with multiple perforations was introduced into the subdural cavity and connected to a Rickham reservoir, fixed in the frontoparietal burr hole. In patients who showed secondary deterioration or enlargement of the residual hematoma as proven by computed tomographic scan, the reservoir was punctured and the subdural fluid aspirated. The great advantage of this method is that it is practicable at the bedside as well as in the outpatient department, thus making it possible to reduce the number of additional operations. The incidence of symptomatic residual or recurrent hematoma was similar in all three groups. The reoperation rate was 4-fold greater in the groups treated with conventional therapy, when compared to the group with the implanted system. At the same time there was no indication that the implantation of the drain was less safe, as judged by the incidence of seizures and infections.
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PMID:Implantation of a reservoir for recurrent subdural hematoma drainage. 1184 42

A miniature multiple thin-film recording sensor was used to measure simultaneously the electrical activity, oxygen content and temperature of brain tissue. The chamber-type potential sensor was an Ag/AgCl electrode covered by an Si3N4 (silicon nitride) chamber. The chamber-type oxygen sensor consisted of an Au-Ag/AgCl two-electrode electrochemical cell embedded in an electrolyte-filled Si3N4 chamber. The temperature sensor was a thin-film germanium resistor. The different sensors were spaced 300 microns apart. Anaesthetics (pentobarbital, chloral hydrate, chlornembutal, halothane) were shown to depress electrical activity and to increase local oxygen tension in the hippocampus. Halothane, but not the other anaesthetics, also increased the current output of the oxygen sensor when tested in saline bath, indicating that the apparent increase in measured oxygen levels during halothane anaesthesia was partly due to an electrochemical effect of halothane on the oxygen sensors. The decrease of tissue oxygen consumption produced by the other anaesthetics is likely to be the result of metabolic depression. Cerebral ischemia, evoked by cauterization of the vertebral arteries and occlusion of the carotid arteries for 30 min, resulted in the disappearance of both spontaneous and evoked electrical activity in the hippocampus and a decrease of both local temperature and oxygen tension. There was a marked overshoot of the oxygen tension to above preocclusion level following the release of the carotid arteries. As soon as electrical activity returned, the oxygen tension fell again, often below the lowest level seen during the ischemic period. This secondary decrease of oxygen level could be reversed by administration of supplementary small doses of anaesthetic. The anaesthetic-induced increase in oxygen tension was accompanied by a marked decrease in electroencephalogram amplitude and frequency. During electrically induced seizures a decrease in hippocampal oxygen content occurred and was accompanied by an increase of local temperature. Since the rectal temperature was kept constant, the changes in temperature are likely to reflect changes in blood perfusion of the recorded area. These findings are in agreement with previous observations made with conventional electrodes. In addition, the miniature size of the chamber-type microelectrode assembly allows a correlated monitoring of parallel physiological changes with high spatial and temporal resolution during anaesthesia, ischemia and epilepsy.
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PMID:Simultaneous recording of local electrical activity, partial oxygen tension and temperature in the rat hippocampus with a chamber-type microelectrode. Effects of anaesthesia, ischemia and epilepsy. 271 Mar 29

In this study, we describe a method for imaging intracerebral electrodes within a three-dimensional reconstructed image of the brain. A three-dimensional image of the brain was reconstructed from serial magnetic resonance images. The locations of intracerebral electrodes were determined from anterior-posterior and lateral skull X-rays performed after intracerebral electrode implantation. The three-dimensional reconstruction of the brain including electrode locations was displayed using IRIS Explorer Software (Silicon Graphics, Mountainview, CA). This method might improve the interpretation of electrical patterns of seizure activity recorded from intracerebral electrodes.
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PMID:A method for imaging of intracranial EEG electrodes using magnetic resonance imaging. 781 97

An increased incidence of seizures and cerebral calcifications, usually bilateral and located in the occipital cortex, has been reported in celiac patients. The histology of cerebral lesions is not well defined, and their pathogenesis is only speculative. We report the autopsy results of a patient with celiac disease, seizures, and cerebral calcifications who died following a cerebral hemorrhage caused by Fisher-Evans syndrome. Calcifications were restricted to the cortical gray matter and composed of aggregates of small calcified spicules. Calcium deposition was present as psammoma-like bodies, along small vessels, and within neurons. X-ray spectroscopy of the calcified areas revealed that calcium (43%) and silica (57%) were present in the lesions. High silica content was also found in the cerebral hemorrhagic fluid. Silica toxicity has to be considered in regard to the pathogenesis of the cerebral lesions and of the seizures.
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PMID:Celiac disease with cerebral calcium and silica deposits: x-ray spectroscopic findings, an autopsy study. 878 97

Between 1990 and 1992 six cases of subdural empyema were surgically treated at the Neurosurgical Division of Emergency Department of Cardarelli Hospital in Naples. Three cases were associated with paranasal sinusitis and three cases with otitis media. Headache and fever were the presenting symptoms in all cases; in only two cases they were associated with seizures and altered mental status. CT scans showed convexity low density collections in five cases and multilocalized pus collection in one; concurrent paranasal or mastoid infections were visualized as well. The organisms responsible for the subdural empyema were Peptococcus in four cases, Streptococcus and anaerobius in the other two cases. In five cases surgical treatment consists in pus drainage by selective burr hole and placement of a subdural small silicon tube for local antibiotic therapy. In one case with a loculated diffuse empyema, craniotomy was performed in order to provide a better access to all the localizations. In all cases drainage of the wound and intravenous antibiotic therapy were used. Paranasal sinus drainage or mastoidectomy performed by the otolaryngologist when a localized collection of pus was present, grave a quicker regression of symptoms. A full recover of the original neurological status was achieved in all cases; a 20 months mean followup confirms the results.
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PMID:Surgical treatment of subdural empyema: a critical review. 891 61

The contribution of the various hippocampal regions to the maintenance of epileptic activity, induced by stimulation of the perforant path or commissural system, was examined in the awake rat. Combination of multiple-site recordings with silicon probes, current source density analysis and unit recordings allowed for a high spatial resolution of the field events. Following perforant path stimulation, seizures began in the dentate gyrus, followed by events in the CA3-CA1 regions. After commissural stimulation, rhythmic bursts in the CA3-CA1 circuitry preceded the activation of the dentate gyrus. Correlation of events in the different subregions indicated that the sustained rhythmic afterdischarge (2-6 Hz) could not be explained by a cycle-by-cycle excitation of principal cell populations in the hippocampal-entorhinal loop. The primary afterdischarge always terminated in the CA1 region, followed by the dentate gyrus, CA3 region and the entorhinal cortex. The duration and pattern of the hippocampal afterdischarge was essentially unaffected by removal of the entorhinal cortex. The emergence of large population spike bursts coincided with a decreased discharge of interneurons in both CA1 and hilar regions. The majority of hilar interneurons displayed a strong amplitude decrement prior to the onset of population spike phase of the afterdischarge. These findings suggest that (i) afterdischarges can independently arise in the CA3-CA1 and entorhinal dentate gyrus circuitries, (ii) reverberation of excitation in the hippocampal-entorhinal loop is not critical for the maintenance of afterdischarges and (iii) decreased activity of the interneuronal network may release population bursting of principal cells.
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PMID:Epileptic afterdischarge in the hippocampal-entorhinal system: current source density and unit studies. 902 78

Thalamocortical circuits are recognized as the main elements involved in the genesis of synchronized oscillations typical of certain generalized seizures. We addressed the capability of thalamic disinhibition to generate synchronized oscillations in neocortex. Microdialysis was used to infuse GABA(A) and GABA(B) receptor antagonists directly into the thalamus of anesthetized rats while recording cortical field potentials from 16 sites aligned perpendicular to the cortical surface, using 100 microm spaced linear array silicon probes. The results demonstrate that block of thalamic GABA(A) receptors induces continuous 3 Hz discharges in neocortex and that thalamic GABA(B) receptors mediate this activity. Also, during thalamic disinhibition sporadic long-lasting discharges at 12 Hz occur that do not depend on GABA(B) receptors. Current source density analysis of these activities revealed that the dynamics of sinks and sources for the 3 and 12 Hz discharges was quite distinct, in a way that suggests a different active involvement of the neocortex. The results indicate that intrathalamic inhibitory processes play an essential role in the generation of neocortical synchronized oscillatory activity that may be related to certain forms of generalized seizures.
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PMID:Neocortical synchronized oscillations induced by thalamic disinhibition in vivo. 1047 20

We used kainic acid in rats as an animal model of temporal lobe epilepsy, and studied the synaptic transmission in hippocampal subfield CA1 of urethane-anesthetized rats in vivo. Dendritic currents were revealed by field potential mapping, using a single micropipette or a 16-channel silicon probe, followed by current source density analysis. We found that the population excitatory postsynaptic potentials in the basal dendrites and distal apical dendrites of CA1 were increased in kainate-treated as compared with control rats following paired-pulse, but not single-pulse, stimulation of CA3b or medial perforant path. In contrast, the trisynaptic midapical dendritic response in CA1 following medial perforant path stimulation was decreased in kainate-treated as compared with control rats. Increased coupling between excitatory postsynaptic potential and the population spike in CA1 was found after kainate seizures. Short-latency, presumably monosynaptic CA1 population spikes following medial perforant path stimulation was found in kainate-treated but not control rats. An enhancement of dendritic excitability was evidenced by population spikes that invaded into or originated from the distal apical dendrites of CA1 in kainate-treated but not control rats. Reverberation of hippocampo-entorhinal activity was evidenced by recurrent excitation of CA1 following CA3b stimulation in kainate-treated but not control rats. Blockade of inhibition by intraventricularly administered bicuculline induced excitatory potentials in CA1 that were stronger and more prolonged in kainate-treated than control rats. The bicuculline-induced excitation was mainly blocked by non-N-methyl-D-aspartate receptor antagonists. We conclude that kainate seizures induced disinhibition in CA1 that unveiled excitation at the basal and distal apical dendrites, resulting in enhancement of the direct entorhinal cortex to CA1 input and reverberations via the hippocampo-entorhinal loop. These changes in the output of the hippocampus from CA1 are likely detrimental to the behavioral functions of the hippocampus and they may contribute to increased seizure susceptibility after kainate seizures.
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PMID:Increased dendritic excitability in hippocampal ca1 in vivo in the kainic acid model of temporal lobe epilepsy: a study using current source density analysis. 1255 15

It has been clearly established that nonsynaptic interactions are sufficient for generating epileptiform activity in brain slices. However, it is not known whether this type of epilepsy model can be generated in vivo. In this paper we investigate low-calcium nonsynaptic epileptiform activity in an intact hippocampus. The calcium chelator EGTA was used to lower [Ca2+]o in the hippocampus of urethane anesthetized rats. Spontaneous and evoked field potentials in CA1 pyramidal stratum and in CA1 stratum radiatum were recorded using four-channel silicon recording probes. Three different types of epileptic activity were observed while synaptic transmission was gradually blocked by a decline in hippocampal [Ca2+]o. A short latency burst, named early-burst, occurred during the early period of EGTA application. Periodic slow-waves and a long latency high-frequency burst, named late-burst, were seen after synaptic transmission was mostly blocked. Therefore these activities appear to be associated with nonsynaptic mechanisms. Moreover, the slow-waves were similar in appearance to the depolarization potential shifts in vitro with low calcium. In addition, excitatory postsynaptic amino acid antagonists could not eliminate the development of slow-waves and late-bursts. The slow-waves and late-bursts were morphologically similar to electrographic seizure activity seen in patients with temporal lobe epilepsy. These results clearly show that epileptic activity can be generated in vivo in the absence of synaptic transmission. This type of low-calcium nonsynaptic epilepsy model in an intact hippocampus could play an important role in revealing additional mechanisms of epilepsy disorders and in developing novel anti-convulsant drugs.
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PMID:Low-calcium epileptiform activity in the hippocampus in vivo. 1453 65


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