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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous study showed a strong relationship between human focal epilepsy and the presence in the cortex of "activated" astrocytes characterized by an intense activity of dehydrogenases (DH) involved in glucose metabolism and of glutamate DH. Using the semi-chronic model of cobalt-induced experimental focal epilepsy in the rat, we investigated a possible correlation between astrocyte modifications and the chronological development of the epileptic manifestations on the ECoG. After a few days the cobalt-implanted rats present spikes, then sharp waves followed by an electrical crisis and ultimately motor seizures. Activated astrocytes were found in each phase of this evolution. Their number increases with the intensity of the manifestations. There is a close relationship between activated astrocytes and focal epileptic phenomena. At this stage of our study it is clear that the presence of activated astrocytes is not a consequence of seizures. However, it is impossible to say whether the activation is secondary to the hyperactivity of the neurons or directly responsible for the constitution of the epileptic focus. In any case, activated astrocytes provide a new means of localizing an epileptogenic focus.
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PMID:Histochemical study of cobalt-induced focal epilepsy. 9 27

The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of delta 9-tetrahydrocannabinol (delta 9-THC) were investigated electrophysiologically with conscious, unrestrained cobalt epileptic rats. The well-known antiepileptics, trimethadione (TMO), ethosuximide (ESM), and phenytoin (PHT), were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials, but PHT and CBD exerted no such effect. Although CBD did not suppress the focal abnormality, it did abolish jaw and limb clonus; in contrast, delta 9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes, and produced frank convlusions. 11-OH-delta 9-THC, the major metabolite of delta 9-THC, displayed only one of the excitatory properties of the parent compound: production of bursts of polyspikes. In contrast to delta 9-THC and its 11-OH metabolite, CBD, even in very high doses, did not induce any excitatory effects or convulsions. The present study provides the first evidence that CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy, and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.
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PMID:The influence of cannabidiol and delta 9-tetrahydrocannabinol on cobalt epilepsy in rats. 11 6

The authors made 11 adult cats epileptic by implanting cobalt powder on the left sensorimotor cortex. Some of the animals were treated with the immunodepressant drug, cyclophosphamide (Endoxan), before and after surgery, and others were not. Then the two groups of animals were compared in terms of EEG and histopathological findings. The treatedanimals showed a definite reduction of focal electrical activity both primary and secondary, and a much milder perifocal parvicellular infiltration and cerebral edema. In view of these findings, the authors suggest that in addition to other well-known factors, the pathogenesis of cobalt-induced experimental epilepsy involves immunological mechanisms triggered by the release of nerve tissue antigens as a result of tissue injury caused by cobalt. This would result in the formation of antibodies directed against several brain constituents. Last, the authors submit that a similar autoimmune mechanism may be at play also in the pathogenesis of some forms of focal epilepsy of traumatic origin.
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PMID:Cobalt-induced experimental epilepsy in cats pharmacologically immunodepressed. An EEG and histological study. 103 31

Although the importance of neuronal synchrony in epilepsy has not been disputed, few attempts have been made to examine quantitatively the relationship between this parameter and seizure occurrence. The specific objective of the present investigation was to determine how the amount and type of synchrony between EEG and single-unit activity in an experimental model of focal epilepsy are related to the occurrence of seizures. This was accomplished by examining EEG/single unit relationships in two types of cobalt-induced epileptogenic focus: (1) foci that initiated seizures, and (2) foci that exhibited only interictal spike activity. These relationships were examined during slow-wave sleep, a time when synchronous neuronal activity is thought to be augmented. In control rats and rats that had seizures, the majority of units exhibited a non-random relationship between unit discharge and the EEG. In cobalt-treated rats that were not observed to have seizures, however, the percentage of units exhibiting EEG/single unit relationships was significantly less than that in either controls or rats that had seizures. This observation, paired with observations of the details of the EEG/single unit relationships, led to the hypothesis that cobalt treatment produces a shift from an inhibition dominated synchrony (observed in controls) to an excitation dominated synchrony (observed in rats that had seizures). Intermediate between these two types of synchrony is a less synchronized state (observed in seizure-free, cobalt-treated rats), which probably results from a loss of inhibition dominated synchrony without a concomitant increase in excitation dominated synchrony.
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PMID:Relationship between single-unit activity and the electroencephalogram in a neocortical, cobalt-induced epileptogenic focus. 244 19

The distribution of GABA-immunoreactive cell bodies and terminals was studied using an anti-GABA serum during the development of chronic focal epilepsy induced by cobalt deposits onto the motor cortex of the rat. Cell counts of GABA-positive neurons were carried out in the epileptogenic area and correlated with the electrophysiological activity of the cobalt focus. In normal control rats, we identified GABA-immunoreactive somata and processes in the motor agranular cortex; they were multipolar or bipolar but never pyramidal and were present in all layers, especially in layer II. GABA-immunoreactive terminals were widely scattered in the neuropil and surrounded the unlabelled cell bodies. In the cobalt-treated animals, changes in the GABAergic innervation were observed during the development of the epileptic focus: decreases in the GABA-positive cell density and in the number of GABA-positive terminals were present before the onset of epileptic discharges and became more marked during the period of maximal spiking activity; a progressive return to normal values of GABA-positive cell density (except in the deep layers) as well as the reappearance of GABA positive terminals were associated with the extinction of the epileptic syndrome. Our observations suggest that the impaired inhibitory neurotransmission mediated by GABA plays a role in the development of the cobalt-induced epilepsy; moreover the recovery of GABAergic function which occurs during the extinction of the epileptic syndrome might imply a capacity for axonal regeneration of the GABAergic neurons.
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PMID:Changes in GABA-immunoreactive cell density during motor focal epilepsy induced by cobalt in the rat. 250 15

The lysosome-associated cathepsins B and D were localized by means of immunocytochemistry (peroxidase-antiperoxidase technique) in glial cells of rat brain. A specific reaction pattern of hippocampal neuroglia could be observed after intracerebroventricular application of the neurotoxin kainic acid. After the induction of a focal epilepsy in rats by the implantation of cobalt pellets there was a pronounced immunoreaction of glia near the primary focus as well as the mirror focus. It is concluded that both cathepsins are useful immunocytochemical markers to trace functionally activated glia.
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PMID:Cathepsins B and D in rat brain glia during experimentally induced neuropathological defects. An immunocytochemical approach. 310 45

In former investigations on human focal epilepsy and on experimental epilepsy by cobalt implantation, the authors have demonstrated the signaletic importance of "activated astrocytes": cortical astrocytes endowed with a modified metabolism and an accelerated turnover. The present study concerns the results of the intra-amygdaloid injections of kainic acid, a strong excitatory and neurotoxic amino acid. Injections in semi-chronic conditions in the rat lead to electrical and motor seizures and to the production of activated astrocytes not only in regions that might trigger off epileptic seizures (cerebral cortex, amygdala, possibly hippocampus), but also in the neostriatum. Stimulation of this last region results in a Huntington chorea-like syndrome. Thus, the importance of activated astrocytes must be extended to include other conditions of intense hyperactivity of neurons than epilepsy.
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PMID:[Histochemical study of central nervous system lesions in experimental epilepsy caused by kainic acid]. 732 58

Bursting activities were investigated under conditions of reduced outward K+ currents in neocortical slices obtained from rats presenting the gamma-aminobutyric acid (GABA)-withdrawal syndrome (GWS), a focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion into the somatomotor cortex. These bursts were induced by intracellular depolarizing current injection and/or by white matter stimulation. Tetraethylammonium (TEA) at doses which did not change input resistance, spike duration or first interspike time interval abolished the burst terminating process and induced plateau-like potentials (up to 500 ms) which were tetrodotoxin-resistant and blocked by Ca2+ antagonists Cd2+ and Co2+. Therefore, it appears that bursts during GWS are generated by Ca(2+)-dependent plateau potentials which are terminated by a K+ current highly sensitive to TEA.
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PMID:A potassium current controls burst termination in rat neocortical neurons after GABA withdrawal. 760 12

Based on experimental research, since 1982 until 1991 a series of 11 patients diagnosed as suffering from idiopathic focal epilepsy have been treated with stereotactic radiosurgery. Focus location was determined with cortical electrodes and confirmed by stereotactically placed deep electrodes. Stereotactic radiosurgery was performed with photons from a cobalt source with a dose of 10 to 20 Gy, except in two cases in whom a betatron was used. The results were: complete cessation of seizures in four cases and a significant reduction in the number of seizures in five additional cases. Seizures began to decrease gradually after a period of three months of one year, except in two cases in whom there was an immediate response after treatment. In two cases there was no change. No complication related to the irradiation was recorded. The gradual and delayed effect, obtained with low doses, may favour the hypothesis that non-descructive permanent structural changes, possibly related to the neuronal plasticity phenomenon, constitute the mechanism underlying these facts. Although the number of cases so far is too small, the absence of side-effects may make this bloodless method the one of choice specially in those cases in whom eloquent areas are involved.
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PMID:Radiosurgery of epilepsy. Long-term results. 771 26

1. The aim of the present study was to determine the role of noradrenergic neurotransmission in neuronal activities intracellularly recorded in neocortical slices obtained from rats presenting the gamma-aminobutyric acid (GABA) withdrawal syndrome (GWS), a focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion into the somatomotor cortex. Neurons recorded in the epileptic focus area (n = 52) were bursting or nonbursting cells. Intrinsic bursting (IB, n = 20) cells presented bursts of action potentials (APs) to an intracellular depolarizing current injection and paroxysmal depolarization shifts (PDSs) to white matter stimulation. Synaptic bursting (SB, n = 22) cells presented only PDSs. Nonbursting (NB, n = 10) cells presented no burst after either synaptic stimulation or depolarizing current injection. Results were compared with those obtained from NB neurons (n = 4) recorded in slices from saline-infused rats. 2. In all of the recorded neurons, bath application of norepinephrine (NE, 10 and 100 microM) provoked a depolarization (1-5 mV) associated with a decrease in input K+ conductance having a mean reversal potential at -90 to -102 mV, not significantly different for bursting and nonbursting cells. This reversal potential differed from that of Cl(-)-mediated inhibitory postsynaptic potentials (-70 mV) elicited in NB cells by electrical stimulation of the white matter. 3. In IB cells, the NE-induced depolarization replaced the intrinsic bursts by a sustained repetitive discharge of single APs and caused intrinsic bursts to appear during previously subthreshold depolarizing current pulses. These NE-increased activities were abolished by dihydropyridine nitrendipine (1 microM) and by Cd2+ (0.5 mM) or Co2+ (2 mM), thus confirming that Ca2+ currents contribute to burst generation in IB cells. 4. In both NB and SB cells recorded in slices from GWS rats, NE provoked the appearance of intrinsic bursts of APs during steps of depolarizing current injections. In addition, in NB cells, NE caused synaptic bursts to appear after white matter stimulation. These NE-induced bursts were dihydropyridine (nitrendipine, 1 microM)- and Cd2+ (0.5 mM)- or Co2+ (2 mM)-sensitive and were related to an increased AP-afterdepolarization. The fast AP-afterhyperpolarization was not affected by NE. In NB cells recorded in slices from saline-infused rats (n = 4) NE did not provoke the appearance of bursts even when stimulation intensity was increased up to three times.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Noradrenaline mediates paradoxical effects on rat neocortical neurons after GABA withdrawal. 820 8


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