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

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)
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PMID:Contribution of Na+,K(+)-ATPase to focal epilepsy: a brief review. 132 44

Estimation of autospectra and coherence and phase spectra of seizure EEG, using the FFT technique, will cause "smearing" of the rapid dynamic changes which occur during the seizure. This is inherent to FFT spectral estimation, due to the averaging process which is necessary in order to get consistent spectral estimates. A different approach suggested in the present study is to carry out multivariate autoregressive modeling of the multichannel seizure EEG, combined with adaptive segmentation. In order to obtain good estimates in cases of short record length, the vectorial AR modeling was based on residual energy ratios. The method has been tested on multichannel seizure EEG recordings from rats with focal epilepsy, caused by intracerebral administration of Kainic acid, and in depth EEG recordings in patients with temporal lobe epilepsy.
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PMID:On the tracking of rapid dynamic changes in seizure EEG. 147 24

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

Penfield's observations in the 1930s provided the first systematic evidence of changes in regional cerebral blood flow (rCBF) associated with focal seizures. Further studies in humans and animals confirmed increases in cerebral blood flow and metabolism during generalised seizures, but the interictal, ictal, and postictal changes in focal epilepsy have begun to be elucidated in the last decade with the advent of in vivo imaging techniques such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) and, in the case of animal studies, of autoradiography. Most studies have been of temporal lobe epilepsy. Interictally, the characteristic finding has been reduced blood flow and/or metabolism in the affected temporal lobe, or more extensively in the ipsilateral hemisphere. The few studies to date of ictal or postictal changes have been of rCBF using SPECT. They show hyperperfusion of the whole temporal lobe ictally, hyperperfusion of the hippocampus, combined with hypoperfusion of lateral structures in the immediate postictal period. Later in the postictal period, hypoperfusion alone is seen. Studies of focal seizures in animals have shown hyperperfusion and hypermetabolism at the site of the focus often with widespread depression of both parameters in the ipsilateral neocortex. Limited studies of coupling between blood flow and metabolism in humans have suggested that flow during seizures is adequate for metabolic demand, although some animal studies have suggested localised areas of uncoupling. The results of modern in vivo imaging of ictal and postictal changes in blood flow and metabolism have correlated well with Penfield's observations, and these changes are now being used to help localise epileptic foci, allowing wider use of the surgical treatment he pioneered.
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PMID:Epilepsy, cerebral blood flow, and cerebral metabolic rate. 162 38

Wilder Penfield's development of surgical methods for treating focal cerebral seizures, beginning with his early work in Montreal in 1928, is reviewed. The reliance on seizure pattern and focal brain pathology was enormously enhanced by the advent of EEG and direct electrical recording from the cortex during surgery. The recognition in the early 1950's of mesial temporal structures in the pathogenesis of temporal lobe epilepsy with automatism lead to more rational and successful surgical treatment. Positron emission tomography and especially magnetic resonance imaging have recently added to the essential diagnostic information of focal epilepsy provided by EEG.
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PMID:Development of surgical therapy of epilepsy at the Montreal Neurological Institute. 177 66

Immunocytochemical studies have identified alterations in GABA neurons in several models of seizure disorders. However, the changes have varied among different epilepsy models, and these variations presumably reflect the diversity of mechanisms that can lead to seizure disorders. In models of cortical focal epilepsy, there is strong evidence for decreases in the number of GABAergic elements, and the changes closely parallel the time course of seizure development. By contrast, in some genetic models of epilepsy, increases in the number of immunocytochemically-detectable neurons have been observed in selected brain regions. In several models of temporal lobe epilepsy, there presently is little immunocytochemical evidence for alterations of GABA neurons within the hippocampal formation despite physiological demonstrations of decreased GABA-mediated inhibition in this region. However, it remains possible that certain types of GABA neurons could be differentially affected in some seizure disorders while other types are preserved. Thus, distinguishing between different classes of GABA neurons and determining their functional roles represent major challenges for future studies of GABA neurons in seizure disorders.
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PMID:GABA neurons in seizure disorders: a review of immunocytochemical studies. 178 31

Following kainate lesions of hippocampal subfield CA3, the remaining CA 1 pyramidal cells become hyperexcitable. This lesion is of interest because, morphologically, it resembles the damage often seen in cases of temporal lobe epilepsy; it may provide insight into the consequences of such cell loss in humans. The hyperexcitability in CA 1 is associated with a loss of both early and late IPSPs. At long postlesion latencies (2-4 months) inhibition shows partial recovery and the hyperexcitability subsides. The intent of the present work was to determine if alterations in CA 1 excitability and functional inhibition postlesion are correlated with changes in morphologic and physiologic indicators of inhibitory interneuron function or with alterations in binding sites for inhibitory transmitters. Using GAD immunocytochemistry, we found no acute or chronic lesion-induced decrease in numbers of CA 1 interneurons or in qualitative characteristics of the pericellular distribution of their terminals in CA 1 stratum pyramidale. Intracellular recordings from identified cells in CA 1 indicated that putative interneurons were viable in hyperexcitable tissue. It was further observed that "recovery" in tissue studied 2-4 months postlesion primarily involved the early IPSP; the late IPSP failed to reappear. Quantitative in vitro autoradiographic analysis of 3H-flunitrazepam--a marker for the early IPSP associated GABAA receptor complex--indicated that hyperexcitability was associated with an increase in GABAA receptor number in CA 1; receptor binding returned to normal at long postlesion latencies as the early IPSP returned and hyperexcitability subsided. Finally, hyperexcitable pyramidal cells were found to retain their responsivity to exogenously applied GABA. These data indicate that much of the cellular machinery necessary for inhibition is retained in CA 1, despite lesion-induced hyperexcitability. We suggest that the acute loss of the IPSP after kainate lesion is due to a transient disconnection between inhibitory and excitatory elements in CA 1 and/or to a loss of normal afferent drive from CA3 onto some CA 1 interneurons. We further suggest that incomplete recovery can be explained by abnormalities that occur as neuroplastic rearrangements in response to deafferentation of CA 1. The relevance of these studies to human hippocampal necrosis and to other models of focal epilepsy is discussed.
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PMID:Inhibition in kainate-lesioned hyperexcitable hippocampi: physiologic, autoradiographic, and immunocytochemical observations. 283 91

Psychiatric morbidity was assessed in a sample of 88 adult epileptic patients drawn from general practices in South London. Using the Clinical Interview Schedule, 48% emerged as psychiatric cases. When either total CIS score or caseness status was used for comparison, group differences were evident; patients with temporal lobe epilepsy and focal non-TLE did not differ, but each was significantly more impaired than those with primary generalised epilepsy. The groups also differed in their psychiatric symptom profiles. The results suggest that the increased prevalence of interictal psychopathology commonly associated with TLE may also be a feature of other forms of focal epilepsy.
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PMID:Relationship between interictal psychopathology and the type of epilepsy. Results of a survey in general practice. 311 98

Following acute meningitis associated with severe convulsions in childhood, two patients had chronic, drug-resistant, temporal lobe epilepsy. This disorder was preceded by an entirely natural development, in one case extending for nine years and in the other case for eight years. Each patient was treated with right anterior temporal lobectomy. Classic mesial temporal sclerosis (Ammon's horn sclerosis) was found in both patients. Relief of the epilepsy was associated with remission of the concomitant social and psychiatric handicaps. At least ten years of follow-up are required in the evaluation of the treatment of early brain infections. Chronic focal epilepsy after childhood meningitis with febrile convulsions merits neurosurgical consideration.
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PMID:Focal epilepsy with mesial temporal sclerosis after acute meningitis. 393 14

In an epileptic focus there is a three-fold increase of the regional cerebral metabolism and blood flow. This has been shown with the 133 Xenon technique and with positron emission tomography. Such studies suggest that, in temporal lobe epilepsy, the pathways from the deep temporal structures to the frontal lobes do not function normally. The temporal 'gate' to the frontal lobes may be closed. This may explain symptoms of psychopathology in this common type of focal epilepsy.
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PMID:Epilepsy related to cerebral blood flow and metabolism. 642 5


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