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

It was discovered in 1966 that the senegalese baboon (Papio papio) exhibits a photosensitive epilepsy. This finding has led, among other work, to the neurophysiological study of this epilepsy. Although in some characteristics the baboon's photosensitive epilepsy differs from that of man, it can be considered that this animal presents a real model of essential epilepsy, for the study of the human disease. 2. In the baboon, the EEG disturbances triggered by intermittent light stimulation at 25 Hz appear first at the level of the frontal cortex (area 6). At this level, recordings of single unit discharges show an activation of cortical neurones similar to that observed in human patients with focal epileptic lesions ; at the occipital level, the only modification observed is a change in the resting membrane potentials, in the direction of disinhibition. 3. The analysis of cortical visual evoked responses demonstrated the presence of short latency visual afferents at the frontal cortex level, as well as a high level of hyperexcitability for the visual modality. The most photosensitive animals can be distinguished by a more marked frontal hyperexcitability and by slight differences in the form of both the occipital evoked responses (decrease in amplitude of the early part of the response, frequent absence of wave IV) and the frontal ones (higher amplitude of the later part of the responses). In some of the animals, whether they were photosensitive or not, we found high amplitude frontal visual evoked responses resembling spikes and waves. 4. Certain observations in both man and the photosensitive baboon suggested the possible involvement of periocular somatic afferents in the triggering of paroxysmal manifestations. The study of these cortical projections in the baboon showed that they possess certain specific characteristics which distinguish them from the other somatic projections (short latency, large frontal spread and ipsilateral responses of higher amplitude than contralateral). It seems, however, that if they play a role in the epileptic manifestations, these periocular projections are not required to trigger this behaviour. 5. The baboon frontal lobes seem therefore to be an area receiving multimodal projections, possessing a particular sensitivity to visual afferents, and functionally equivalent to a zone of focal epilepsy as might be met with in man or animals. 6. The results are discussed in the light of observations made on the same or other species, or on other types of epilepsy. In particular, the totality of the visual afferents arriving at the occipital level appears to be necessary to trigger epileptic manifestations. Finally, these results present several arguments in favour of the cortical theory of generalised epilepsies, as well as substantiating the value of the baboon as an animal model for photosensitive epilepsy in man.
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PMID:[Frontal cerebral cortex and photic epilepsy of the baboon Papio papio (author transl)]. 81 47

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

Hippocampal-based epileptiform activity may reach the basal ganglia via the nucleus accumbens. Previous data suggested that caudate nucleus is able to influence hippocampal epilepsy, probably sending a projection to the septum. In order to test the hypothesis of a retrograde activation of accumbens-caudate pathway in hippocampal regulation, we electrically stimulated both caudate nucleus and nucleus accumbens and studied modifications of hippocampal EEG in the feline focal epilepsy model. We also performed bilateral electrolytic lesion of nucleus accumbens and repeated caudate stimulation. Results showed that nucleus accumbens stimulation was ineffective in modifying hippocampal epilepsy; on the contrary, caudate stimulation caused a statistically significant decrease of hippocampal spike frequency and amplitude. On the other hand, in accumbens-lesioned animals caudate activation consistently reduced hippocampal epilepsy to a significant degree. As the caudate nucleus influences hippocampal activity and the septum may constitute a relay station of this functional relation, a possibility was tested concerning a GABAergic mediation. To this end, after a stable caudate-induced effect was reached, an intraseptal microinjection of picrotoxin (GABA receptor antagonist) was made and caudate stimulation repeated at the same parameters. Such a study showed that after intraseptal picrotoxin, caudate stimulation failed to elicit any type of modification of hippocampal activity. Experimental findings support the notion that the striatal modulation on hippocampus is mediated by an anterograde rather than a retrograde pathway, and underline the possibility of a GABAergic caudate-septal influence.
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PMID:Accumbens-caudate-septal circuit as a system for hippocampal regulation: involvement of a GABAergic neurotransmission. 131 94

The authors review some of their experimental data on the contribution of Na(+)- and K(+)-dependent adenosine triphosphatase (Na+,K(+)-ATPase) to focal epilepsy. It has been previously demonstrated that high extracellular K+ concentration increases glial Na+,K(+)-ATPase specific activities in normal conditions while this was not observed in neuronal preparations. At this time, it was hypothesized that this molecular mechanism could play a role in removing K+ released in the extracellular space during neuronal firing. These results have therefore been investigated in acute and chronic epileptogenic lesions of cats with freeze lesion. It was demonstrated that within the primary (F) and the secondary or 'mirror' (M) focus the K+ activation of the glial Na+,K(+)-ATPase dramatically decreased compared to both control animals (C) and the perifocal (PF) non epileptogenic area. Similar results were observed in man when using specimens of anterolateral temporal neocortex obtained during temporal lobectomies in patients with intractable temporal lobe epilepsy, compared with postmortem human specimens or control brain tissues. The modifications of the level of phosphorylation of partially purified Na+,K(+)-ATPase was also investigated in the epileptic cortex in these two experimental conditions. The catalytic subunits were resolved by sodium dodecylsulfate (SDS) gel electrophoresis and their phosphorylation levels were measured in the presence of various concentrations of K+ ions which dephosphorylate the catalytic subunit. K(+)-induced dephosphorylation was decreased in primary and secondary foci of acutely lesioned cats. Those alterations, due to a decreased affinity for K+, were limited to the alpha (-) subunit. In cats with chronic lesions, the dephosphorylating step of the Na+,K+-ATPase catalytic subunit recovered to normal affinity for K+.(ABSTRACT TRUNCATED AT 250 WORDS)
Epilepsy Res 1992 Jul
PMID:Contribution of Na+,K(+)-ATPase to focal epilepsy: a brief review. 132 44

Sequential topographic mapping was performed to differentiate "epileptic" from "non-epileptic" rolandic spikes. Twenty-four children without any indication of organic brain lesion were divided into a group with epilepsy and a group without epilepsy. The group with epilepsy was subdivided into "classical BECT" (benign focal epilepsy of childhood with centro-temporal spikes) and "non-classical BECT." Sequential mapping of the rolandic spikes revealed two different topographic patterns: a pattern of stationary potential fields and a pattern of non-stationary potential fields. The topographic pattern of stationary potential fields was morphologically represented by a single spike-and-wave complex whereas that of non-stationary potential fields was morphologically represented by a "double" spike-and-wave complex. Among the non-stationary topographic patterns represented by a "double" spike, one specific sequence of changes of potential fields was found. This sequence started with a dipolar field, with the negative pole in the frontal region and the positive pole in the centro-temporal region, morphologically represented by the small first spike of the "double" spike-and-wave complex. This dipolar field, changes to a unipolar or dipolar field, with a negative potential field in the centro-temporal region and, sometimes, a simultaneous positive potential field in the frontal region, morphologically represented by the prominent rolandic spike. This characteristic pattern was found to be significantly related to classical BECT.
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PMID:Sequential EEG mapping may differentiate "epileptic" from "non-epileptic" rolandic spikes. 137 47

The GABA withdrawal syndrome (GWS) is a new model of focal epilepsy in which paroxysmal activity is induced through the interruption of a chronic, intracortical infusion of GABA. Preliminary studies have shown extraordinary resistance of this epileptogenic activity to classic anticonvulsants including diazepam, the most effective agent for treating status epilepticus. However, GWS can be inhibited by GABA itself. The rat with petit mal-like seizures is a genetic model of generalized non-convulsive epilepsy (GNCE), with behavioral characteristics and electrical (spike-and-wave discharges) signs resembling absences. Moreover, GABAmimetics aggravate this type of seizure. Rats with GWS induced by cessation of a localized GABA infusion (50 micrograms/microliters/h for 24 h), and the rat model of GNCE, were treated with HEPP, a new anticonvulsant agent. In the case of GWS, the drug produced a significant decrease of focal spike activity in animals which started discharging at low frequencies while in rats with higher frequency discharge, HEPP was without effect. HEPP administered on the second day of the GWS in naive rats had no effect. In rats with GNCE, doses of 50 and 100 mg/kg i.p. blocked the spike-and-wave discharges. The higher dose produced sedation in this absence seizures model. Although the mechanism of action of HEPP is still unknown, its unique antiepileptic profile deserves further studies.
Epilepsy Res 1992 May
PMID:Effects of 3-hydroxy,3-ethyl,3-phenylpropionamide (HEPP) on rat models of generalized and focal epilepsy. 139 31

The clinical correlates of Rolandic spikes were studied in 47 children to determine the significance of this EEG finding to the diagnosis and classification of epilepsy. The children were classified into 'functional' and 'organic' groups, with and without epilepsy. Children with epilepsy were further subdivided into those with Rulandic and those with non-Rulandic seizures. In children without neurological abnormalities, the EEG finding of Rolandic spikes plays a decisive role in the diagnosis of an epileptic syndrome as benign focal epilepsy of childhood with centro-temporal spikes (BECT), a diagnosis with an excellent prognosis. Neurological and neuroradiological examinations of the 'functional' group revealed that the Rolandic spike may occur as a true 'functional' spike. The frequency of a family history of epilepsy among neurologically normal children with Rolandic spikes suggests, in addition to the inheritance of BECT and the EEG trait, the existence of a hereditary susceptibility to epilepsy.
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PMID:Rolandic spikes in the inter-ictal EEG of children: contribution to diagnosis, classification and prognosis of epilepsy. 139 29

We have described the occurrence in freely moving gerbils of slow potential changes (SPC) in two different models of experimental epilepsy: 1) maximal electroshock and 2) bilateral epileptic foci induced by penicillin. SPC is considered a by-product of epileptiform activity in both models and correlates to the SPC which occurs during spreading depression. In the first model there develops a cortical SPC simultaneous with a depression of EEG activity, although there is no propagation of the wave. We suggest that a non-propagated multifocal depression (MD) occurs in the MES model. In the model of focal epilepsy, all requirements are fulfilled, and the SPC is characterized as the one which occurs during spreading depression propagating with an average velocity of 8 mm/min.
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PMID:Cortical slow potential changes during convulsions induced by maximal electroshock or penicillin focus. 152 70

Surgical management of uncontrolled focal epilepsy is most commonly carried out in young adults with good results, but there has been some doubt about the effectiveness of cortical resection in older individuals. We assessed the outcome of temporal lobectomy done after age 45 years in 20 patients with intractable epilepsy followed for more than 2 years after surgery. During a mean follow-up of 5 years, six patients (30%) were seizure-free following surgery and seven (35%) had greater than 90% reduction in seizure frequency. This compares with an outcome of 40% seizure-free and 44% with greater than 90% seizure reduction in 68 younger patients aged 17 to 45 years; the differences do not achieve statistical significance. The outcome was better for complex partial seizures than for secondarily generalized seizures. Complications were no greater than in the younger patients. The findings indicate that surgery is an effective treatment alternative for intractable temporal lobe epilepsy in older patients since two of three of these patients will obtain satisfactory seizure control.
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PMID:Temporal lobectomy for intractable epilepsy in patients over age 45 years. 154 33

A limited cortical resection including the rolandic fissure and the pre- and postcentral cortical regions was carried out in a patient suffering from epilepsia partialis continua resistant to antiepileptic drugs. The histological examination revealed several foci of very large neurons distributed with no laminar organization in the depth of the rolandic fissure and in the crown of the primary motor and primary somatosensory areas; these lesions were consistent with focal cortical dysplasia. In addition, decreased numbers of neurons, astrocytosis and proliferation of capillaries, compatible with chronic tissue necrosis, were found in the inferior regions of the banks of the rolandic fissure. Subpopulations of local-circuit neurons were examined with parvalbumin, calbindin D-28k and somatostatin immunocytochemistry. Focal areas of cortical dysplasia contained abnormal immunoreactive neurons. Huge parvalbumin-immunoreactive cells were distributed at random and resembled axo-axonic (chandelier) and basket neurons. Abnormal calbindin D-28k-immunoreactive cells were reminiscent of double-bouquet neurons and multipolar cells. Very large somatostatin-immunoreactive cells were seldom observed in the dysplastic foci. On the other hand, areas of tissue necrosis displayed massive reduction of immunoreactive cells and fibers. Abnormalities in the morphology and distribution of local-circuit (inhibitory) neurons observed here for the first time in focal cortical dysplasia may have a pivotal role in the appearance and prolongation of electrical discharges and continuous motor signs in human focal epilepsy.
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PMID:Abnormal local-circuit neurons in epilepsia partialis continua associated with focal cortical dysplasia. 163 80


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