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

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

One hundred patients suffering from focal epilepsy with complex partial seizures refractory to medical treatment and showing no abnormality at CT were explored by MRI with an 0.5 Tesla magnet. MRI detected an abnormality in 25 patients with, in 17 of them, good correlation between MRI and clinical as well as electroencephalographic findings. Abnormal morphology and signal was found in 5 patients, with positive CT results on reexamination of previous CT images or on new CT scans in 4 of them. There was a diffuse temporal lobe high-intensity signal in 3 cases and a localized high-intensity signal in 9 cases (temporal lobe 4, occipital lobe 3, frontal lobe 1, fronto-parietal and parietal lobes 1). Thus, in 13% of the cases MRI demonstrated a lesion that had not been detected at CT, and the location of the lesion was concordant with clinical and electroencephalographic data.
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PMID:Magnetic resonance imaging in refractory focal epilepsy with normal CT scans. 251 40

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

The inhibition of seizure activity by behavioural methods is becoming more popular. Lockhart's monkey model of focal epilepsy suggests a theoretical approach to behavioural seizure inhibition. Behaviour, by changing the pattern of excitation and inhibition surrounding a focus, is thus able to inhibit seizure activity. This article describes single case studies in which the behavioural methods of cued arousal, covert desensitization and relaxation have brought about a decrease in seizure frequency.
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PMID:Evoked and psychogenic epileptic seizures: II. Inhibition. 261 81

In this report 17 patients with long-standing non-focal epilepsy underwent callosotomy (this was total in two patients and performed in two stages, and anterior-subtotal in the remaining patients). In all patients the atonic-hypertonic seizures with sudden falls were the most disabling epileptic fits. Callosotomy proved efficient in controlling atonic fits in 10 out of 15 patients in whom surgical results are evaluated. In 3 additional patients the frequency of atonic fits was reduced by more than 50%. In the remaining two patients, no therapeutic effect was observed. Callosotomy was less effective on seizures which were not atonic. Therefore, this procedure appears to be indicated in patients in whom atonic fits are predominant. The main effect of callosotomy is to transform drug-resistant seizures into drug-sensitive ones. Neuropsychological sequels are insignificant unless the splenium is severed. However, considerable psychic and behavioral improvement was nearly always observed after surgery. Despite the fact that on a therapeutic level results were often satisfactory, a number of practical problems still remain. These concern the full spectrum of indications for callosotomy, the extent of corpus callosum section, choice of methods in severely mentally retarded patients and, finally, the age at which the operation should be carried out.
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PMID:[Remarks on callosotomy in the treatment of drug-resistant epilepsy]. 262 17

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

The precipitation of seizures by external stimulation (evoked seizures) is well known. Less well known is the precipitation of seizures by a change in the patient's thinking or feelings. This artick uses Lockhart's monkey model of focal epilepsy to propose that there is a close relationship between seizures and ongoing brain activity. Thus, seizures precipitated by both voluntary and spontaneous changes in behaviour and thinking must commonly occur. Clinical examples of such seizure precipitation is described.
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PMID:Evoked and psychogenic epileptic seizures. I. Precipitation. 269 27

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


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