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

A patient with fits of laughter due to a tumorous alteration (hyperplasia) of the floor of the third ventricle is described with electroencephalographic findings indicative of focal epilepsy (complex partial seizures = psychomotor fits). The laughter is interpreted as an inborn emotional expression with structural substrate in the hypothalamus and neighboring brain. With structures remaining intact functional disorders in this area can cause epileptic phenomena with participation of the limbic system.
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PMID:Fits of laughter (gelastic epilepsy) with a tumour of the floor of the third ventricle. A video tape analysis. 6 51

Spreading depression (SD) of EEG activity was elicited by microinjection (5 microliter) of 5% potassium chloride into the caudate nucleus (n = 7) or hippocampus (n = 3) during stereotactic brain surgery in patients with focal epilepsy. An electrode-cannula assembly for eliciting and recording the slow potential waves of SD is described. The parameters of SD in human brain are similar to those in lower mammals. Functional ablation by SD can be used as a diagnostic tool in neurosurgery.
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PMID:Functional ablation by spreading depression: possible use in human stereotactic neurosurgery. 9 40

Nonketotic hyperglycemia has a definite convulsive effect, which may manifest itself in generalized or focal seizures. This report deals specifically with focal convulsive phenomena. Two patients with nonketotic hyperglycemia focal seizures are described. Focal seizures are of motor Jackson, aphasic, adversive or of the 'epilepsia partialis continua' type. Different types of focal seizures may appear in one and the same patient. Focal epilepsy can be the first manifestation of a diabetic disorder. Focal epileptic seizures are linked with moderate nonketotic hyperglycemia with values of 360 mg% sugar and 310 osm. Higher values lead to generalized seizures and coma. The mechanisms are discussed and pertinent literature is reviewed.
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PMID:Moderate nonketotic hyperglycemia--a cause of focal epilepsy. Report of two cases and review of literature. 9 31

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

Preparatory to craniotomy for the relief of medically refractory focal epilepsy, the lateralization of cerebral speech functions was determined by the Wada intracarotid Amytal test in 134 patients with clinical and radiologic evidence of an early left-hemisphere lesion. Their results were compared with those for 262 patients (140 right-handed, 122 left-handed), who were tested in a similar way. One-third of the patients with early lesions were still right-handed, and 81% of these right-handers were left-hemisphere dominant for speech. In the non-right-handers, speech was represented in the left cerebral hemisphere in nearly a third of the group, in the right hemisphere in half the group, and bilaterally in the remainder. Bilateral speech representation was demonstrated in 15% of the non-right-handers without early left-brain injury and in 19% of those with evidence of such early injury, whereas it was extremely rare in the right-handed groups. In addition, nearly half the patients with bilateral speech representation exhibited a complete or partial dissociation between errors of naming and errors in the repetition of verbal sequences after Amytal injection into left or right hemispheres. This points to the possibility of a functionally asymmetric participation of the two hemispheres in the language processes of some normal left-handers. The results of the Amytal speech tests in this series of patients point to locus of lesion as one of the critical determinants in the lateralization of cerebral speech processes after early left-brain injury. It is argued that in such cases the continuing dominance of the left hemisphere for speech in largely contingent upon the integrity of the frontal and parietal speech zones.
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PMID:The role of early left-brain injury in determining lateralization of cerebral speech functions. 10 Nov 16

Histoenzymologic analysis of human and animal epileptogenic foci has shown enzymatic changes in certain reactive astrocytes. Histochemical examination of these astrocytes in animals has led to clear differentiation between the classic, perilesional reactive astrocyte, constituting a medium for cicatrical glioses and the reactive astrocyte present in experimental epileptogenic foci. We have called the latter the "activated astrocyte". Analysis of 154 human cerebral tumours revealed activated astrocytes in the cortex of all patients with epileptic antecedents. No epileptic attacks were observed in patients where the cortex was invaded by the tumour but no activated astrocytes were present. Analysis of ten cases of non tumoral focal epilepsy confirmed the presence of activated astrocytes in the focus in all cases where the scar was resected surgically. The production of epileptogenic foci in animals shows the close relation between activated astrocytes and the epileptogenic focus. It even seems that the enzymatic changes in the astrocytes precedes the first electrical signs. The authors arguse against the hypothesis that the activated astrocytes are the result of attacks. Until the morphological criteria of the epilectic neuron have been defined the activated astrocyte constitutes the only morphological evidence of the epileptogenic focus.
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PMID:[Correlation between epileptogenic nature of a lesional focus and presence of "activated astrocytes". Human and animal investigation (author's transl)]. 10 2

This report is a sequel to our 1958, 1960 and 1968 reports on a series of patients operated upon for focal epilepsy whose surgical specimens unexpectedly showed histological lesions typical of active encephalitis. None of these patients, now 27 in number, exhibited the clinical picture ordinarily associated with encephalitis. With one exception, all showed a severe focal seizure tendency beginning in infancy or childhood, often associated with episodes of epilepsia partialis continua. In addition, all except 2 showed slowly progressive neurological deterioration, usually hemiparesis and mental retardation, which advanced over periods of months or years before the progression became arrested. No infectious agent has yet been identified by standard viral studies carried out in the most recent 14 patients or by investigation for slow viruses in 6 patients operated upon between 1966 and 1971. The clinical course of this condition is outlined and the role, the timing and the results of treatment by craniotomy and cortical excision are discussed.
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PMID:Further observations on the syndrome of chronic encephalitis and epilepsy. 10 97

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

Isolated infantile convulsions were noted in 206 patients (13%) of 1,572 patients who underwent cortical resection for medically refractory focal epilepsy at the Montreal Neurological Institute over the period 1928 through 1977. In 59 patients (29% of the 206), the isolated infantile convulsion was associated with an identifiable febrile systemic or neural illness. In 54 patients (26%), there was a definite history of cerebral birth injury in addition to the isolated infantile convulsions. Twenty patients (10%) had some other potential etiological factor for the later development of seizures, such as postnatal head injury, Sturge-Weber syndrome, etc., in addition to the isolated infantile convulsions. In 95 patients, 6% of the total 1,572 patient series and 41% of those with isolated infantile convulsions, the latter was the sole apparent cause for the later development of recurring seizures. Although this was the case in a small but significant percentage in this series of patients, more frequently, the isolated infantile convulsion represents a manifestation of invasion of the brain by an infectious agent of a systemic or brain disease, or is a harbinger of the later development of a seizure tendency due to some other preexisting etiological factor.
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PMID:Relative significance of isolated infantile convulsions as a primary cause of focal epilepsy. 11 7

In three patients operated on for focal epilepsy small pathological lesions in the functionally important cortical regions were microsurgically extirpated. The neighbouring areas of cortex were preseved, although they showed epileptic activity on electrocorticography. The patients are seizure-free three years, two years, and nineteen months later, respectively. On the bases of these facts and experience with another 35 patients operated on for focal epilepsy the authors speculate on the relations between the pathological lesion, epileptogenic cortical area, and the relative dependence of the extent of cortical resection on the electrocorticographic status.
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PMID:The electrocorticographic status and the extent of the cortical resection in epileptic patients. 11 97


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