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

There is no definite agreement on the localization of the PEAL generators. However, some authors have claimed that the temporal auditive cortex plays a role. Based on these assumptions we searched for the eventual changes developing in PEALs in patients who applied for temporal epilepsy, where the temporal cortex activity is somehow impaired. Altogether 19 patients were explored. The results were compared with 17 matched healthy controls and 4 patients with focal epilepsy who, at the time of the study, received the same treatment as the temporal epileptic subjects. In every case PEATs and PEALs were studied. One thousand Hz less than time monoaural stimulation, 50 db and 50 ms duration was employed for evoking PEALs. Recording was done with surface electrodes located at Cz, F3 and F4 coupled with an electrode placed at the contralateral mastoid; 500 ms sweep were averaged. Band-pass was set up between 1 and 125 Hz and latencies and amplitudes were studied for both types of evoked responses, PEATs and PEALs. No statistical difference was found between patients and both control groups when PEATs mean parameters were analyzed. For further PEALs results, patients were divided into 3 groups; a) Those with right temporal epilepsy (n = 6) (R); b) Those with left temporal epilepsy (n = 7) (L); c) Those in whom the affected side could not be determined (n = 7) (N). In R it was observed, when stimulating the left ear, a delay in the arrival of P1 (F4 mea 87 +/- 10.4 ms) and N1 (F4 mean 122.33 +/- 6.1 ms; Cz mean 170.75 +/- 18.8 ms) waves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of the temporal cortex in long-latency auditory evoked potentials]. 248 30

There is a tendency to call benign focal epilepsy of childhood with centrotemporal origin rolandic epilepsy for the sake of brevity. Martinus Rulandus, a 16th-century medical author, deserves this homage far more than Rolando. Attention is drawn to this 1597 description of the disease, which has become the subject of many publications since 1952. Many characteristics of the disease were already noticed about four centuries ago.
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PMID:A tribute to Martinus Rulandus. A 16th-century description of benign focal epilepsy of childhood. 249 86

Penicillin is well known as a potent convulsive agent. A cortical topical, intracerebral or systemic administration of penicillin produces abnormal and paroxysmal activity which may lead to seizure, and has been used in the investigation of the mechanisms of epilepsy. This is a report on the studies of an acute effect of potassium penicillin G on two models of experimental focal epilepsy: a) amygdaloid kindling model, and b) kainic acid-induced limbic seizure model. Twelve adult cats for amygdaloid kindling model (kindling group), six for KA-induced limbic seizure model (KA group) and four for a control group were prepared for this study. In kindling group, after completion of kindling procedure, 40-60 X 10(4) unit/kg of potassium penicillin G (PC), dissolved in sterilized normal saline, was injected intraperitoneally during an interictal period. In KA group, 1 micrograms of KA was injected into the left amygdala. Limbic seizures occurred frequently during the initial 5 hours but subsided completely within 3 days. After a latent period, spontaneous secondarily generalized convulsion occurred from 30 to 60 days after KA injection. The cats were completely normal in their behavior during the interictal period. During the interictal stage after the first generalized convulsion has been observed, 15-20 X 10(4) unit/kg of PC was injected intraperitoneally. In the control group, 40-60 X 10(4) unit/kg was injected intraperitoneally. Electroclinical observations were continued until 5 hours after PC injection in three groups. In the control group, no cats developed generalized convulsion. In the kindling group, 4 of 12 cats developed focal amygdaloid seizures with secondary generalization by nearly the identical doses required in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute effect of penicillin G on feline models of focal epilepsy]. 250 15

This article has three goals: (1) to review the evidence that bears upon the occurrence of secondary epileptogenesis in man, (2) to set forth the criteria that distinguish secondary epileptogenesis from multifocal epilepsy--both clinically and by pharmacologic means--and (3) to indicate the importance of an understanding of the pathophysiology of secondary epileptogenesis to clinical decision making in the care of epileptic patients. In Section I, the three different developmental stages of secondary epileptogenesis defined in experimental preparations are outlined, and particular emphasis is placed on the remarkable similarity in the electrographic manifestations reported from animal species ranging from reptile to baboon. The clinical manifestations differ depending, within species, on exactly where in the brain the primary focus is situated and, between species, on the different organizations of the neural substrate within which epileptiform discharge is engendered. Section II is devoted to a review of three separate series of patients whose presenting symptom was epilepsy and in whom the etiology proved to be a histologically verified brain tumor or malformation. The choice of patient material was dictated by the conclusion that the main barrier to acceptance of human secondary epileptogenesis is the difficulty of distinguishing between multiple primary lesions maturing at different rates and those secondarily induced by an already existing single one. In the vast majority of patients where trauma, infection, anoxia, and vascular disease represent the most common etiologies, multiple primary structural injury is an ever-present possibility. Restricting our analysis to tumors of neural, glial, or vascular origin eliminates, as far as practicable, the issue of multiple primary lesions. A significant number of patients with focal epilepsy develop secondary epileptogenic lesions. The evidence presented shows that a primary epileptogenic lesion in man may induce a trans-synaptic and long-lasting alteration in nerve cell behavior characterized by paroxysmal electrographic manifestations and clinical seizures. Furthermore, the more frequent the seizures, the more likely is a secondary focus to become permanent. These observations underscore the importance of rigorous seizure control (electrographic as well as behavioral) and raise the question of earlier surgical intervention where medicinal therapy fails.
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PMID:Varieties of human secondary epileptogenesis. 250 38

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

Adrenergic mediated phosphatidylinositol (PI) hydrolysis was measured in tissues obtained from 21 patients immediately following surgery for focal epilepsy. Accumulation of [3H]inositol monophosphate (IP1) was significantly reduced (21%, P less than 0.01) in actively spiking neocortex (n = 15) versus samples from non-spiking regions (n = 9). Epileptic discharges may blunt alpha 1-adrenoceptor stimulated transmembrane signalling in human neocortical epileptic foci.
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PMID:Adrenergic mediated phosphatidylinositol metabolism is modulated by epileptic discharges in human neocortex. 256 33

Characteristic of the intimate relationship between sleep and epilepsy are an increase in IEA in nonREM sleep and a decrease in REM sleep, in both generalized and partial epilepsies. The morphology of epileptiform discharges may also be affected by sleep, with a change or breakdown of the generalized pattern in generalized epilepsy, but a better definition of sharp waves in partial epilepsy, during nonREM sleep. One notes a predilection for certain types of epilepsy to occur in sleep, such as benign focal epilepsy of childhood, or to occur shortly after awakening (juvenile myoclonic epilepsy). Epilepsy may disrupt the sleep architecture with an increase in light sleep and a decrease in deep sleep, and an increase in awake time after sleep onset. Sleep is an important activator of IEA and is of value both in the routine EEG evaluation of epilepsy as well as in more prolonged studies used in epilepsy monitoring units.
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PMID:Sleep and pediatric epilepsy. 265 14

About 300,000 people in the United States suffer from medically uncontrolled focal epilepsy. It is estimated that about 40,000 of these patients are candidates for surgery. Underuse of surgical treatment of epilepsy is reflected by the fact that only about 1% of these candidates are operated on. Candidates for ablative surgery (ie, removal of seizure focus) must have a focus demonstrated by either extracranial or intracranial electrode recordings. Nearly half of the patients who have ablative surgery become seizure-free, and nearly two thirds have no seizures or only rare ones. Candidates for corpus callosotomy are those patients with multiple seizure types and nonfocal EEG abnormalities. Almost half of these patients have at least a 50% reduction in seizure frequency. Patients with infantile hemiplegia and seizures may have marked improvement in seizure control after physiologic hemispherectomy.
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PMID:Surgical management of epilepsy. 266 Feb 91

A case of late onset focal epilepsy in a mentally and neurologically normal girl in which the MRI showed a focal heterotopia is presented. The efficacy of this new procedure in detecting migratory disorders is discussed and the scanty literature reviewed. This case suggests that in the future more cases of epilepsy previously classified as "cryptogenetic" will be demonstrated as secondary to developmental abnormalities.
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PMID:[Finding of focal heterotopy with magnetic resonance. Description of a case associated with late onset epilepsy]. 271 92

Previous studies have shown that a loss of GABAergic neuronal somata is associated with a loss of GABAergic terminals at chronic cortical epileptic foci in monkeys. The present study was undertaken to determine whether GABAergic neuronal loss occurs prior to the onset of clinical seizures in monkeys that were treated with alumina gel but did not display seizures. Seven adolescent (Macaca mulatta) monkeys received alumina gel implants into the left pre- and post-central gyri, specifically centered in hand-face regions of sensorimotor cortex. Three other monkeys were used as controls. Two of these were surgical controls and the third was a normal animal. Three monkeys (pre-seizing) were sacrificed 2-4 weeks after the alumina gel implant but prior to clinically active seizures. Three other monkeys with chronic seizure activity (chronically seizing) were sacrificed 3-6 months after the implant. Tissue sections were taken from an area adjacent to the alumina gel granuloma (focus), from a site distal to it (parafocus) and from the non-epileptic contralateral side. Sections from all monkeys were processed for glutamate decarboxylase (GAD) immunocytochemistry and then examined with a light microscope. In addition, adjacent sections were stained with a Nissl stain and the total number of neurons was counted in these sections. Statistical analysis showed a significant decrease in the number of GAD-positive cells in the pre-seizing and chronic animals. The pre-seizing monkeys showed a significant loss of 23-44% at the focus in contrast to the total number of neurons which did not change significantly. The loss of GAD-positive cells was greater in the chronic animals that showed significant losses at both the focus and parafocus, 42-61% and 15-26%, respectively. It is important to note that the chronic monkeys displayed an 11-61% significant loss of total neurons at the epileptic focus. The surgical control animals showed no seizure activity and no significant loss of total neurons or GAD-positive cells. The main finding of this study indicates that a selective loss of GAD-positive neuronal somata occurs in pre-seizing monkeys with alumina gel implants. This finding is consistent with the previously reported loss of GABAergic terminals in pre-seizing monkeys. Since virtually all monkeys treated with alumina gel develop seizures, the results of this study add further support to the hypothesis that GABA neuronal loss plays a causal role in focal epilepsy.
Epilepsy Res
PMID:A selective decrease in the number of GABAergic somata occurs in pre-seizing monkeys with alumina gel granuloma. 279 67


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