Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014547 (focal epilepsy)
1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) Most of the intractable epileptic children showed abnormal EEG and abnormal CT findings. 2) The abnormal side of CT findings of focal epilepsy corresponded with the abnormal side of clinical manifestations and EEG findings. 3) CT findings of the brains of patients with infantile spasms exhibited cerebral cortical atrophy. 4) CT findings of the brains of the other epileptic types were not related to clinical manifestations or EEG findings.
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PMID:Computed tomography of brains of epileptic children. 74 23

Free amino compounds were measured in 16 rapidly frozen epileptogenic foci excised from temporal or frontal cortex of nine patients with focal epilepsy, and in single cortical biopsy specimens obtained from 16 nonepileptic patients. Unlike the findings of a previous study, glutamic and aspartic acids were not diminished in the foci, nor was there a decrease in gamma-aminobutyric acid (GABA) or taurine levels. Glycine content was markedly elevated in two of 16 epileptogenic foci. These results do not suggest that deficiencies of GABA or of taurine, amino acids that may act physiologically as inhibitory neurotransmitters or modulators of inhibition, are causes of focal epilepsy, nor do they provide a logical basis for clinical trials of taurine in treatment of human epilepsy.
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PMID:Amino acids in human epileptogenic foci. 81 Jan 20

Computerized transaxial tomography was carried out on 50 consecutive unselected patients referred to a neurologic practice for evaluation of focal epilepsy. Structural abnormalities were defined in 35.3 percent of these studies: porencephalic cysts in six patients, diffuse cerebral atrophy in five, cerebral hemiatrophy in three, focal cortical atrophy in two, neoplasms in two, hydrocephalus in one patient, and cerebeller hypoplasia in one. Computerized transaxial tomography is a useful outpatient procedure for evaluation and follow-up of patients with focal seizure disorders.
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PMID:Computerized transaxial tomography in the evaluation of patients with focal epilepsy. 81 Jul 37

Among the 1100 patients with convulsive disorders attending out-patient paediatric clinics of the Universities of Vienna and Graz, there are 14 cases of postnatal posttraumatic epilepsy. The characteristic features of this condition, as evidenced even by this small group of patients are focal epilepsy with focal paroxysms in the EEG, often combined with neurological defects and psychological abnormalities, but more seldom with defects of intelligence; resistance to anticonvulsive drugs is a frequent observation. In a retrospective study such as this, the criteria which could predict the development of epilepsy following posttraumatic brain damage are not sufficiently accurately definable; prospective serial studies on brain-damaged children would be of greater prognostic value. The following parameters seem to be important: the kind of brain damage, the duration of unconsciousness, the frequency of initial convulsive attacks and the persistance of the progression of the EEG changes.
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PMID:[Brain damage and epilepsy in childhood (author's transl)]. 81 91

Ninety-one patients operated on for focal epilepsy between 1952 and 1973 have been followed regularly. Nontumoral lesions were found in 68 patients, and tumors in 23. Of the 50 patients without tumor who have been followed for more than 2 years, 30% were seizure-free, 50% improved, while only 20% did not benefit from the operation. There was no operative mortality. Ventricular asymmetry in the pneumoencephalogram was associated with a better prognosis than when there was no or symmetrical enlargement. The time between the onset of seizures and the operation did not affect the prognosis, but early operation is important to achieve better and quicker rehabilitation. There was a positive correlation between the postoperative ECoG and EEG and the clinical results.
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PMID:A follow-up study of 91 patients operated on for focal epilepsy. 81 93

Between 3700 and 3900 children are admitted annually to this children's hospital. During the past four years a total of 455 children with convulsions were admitted for investigation. 255 of these cases were calcified as epilepsy, 202 as febrile convulsions and 28 as neonatal convulsions. A quarter of the epileptic children showed fits of the petit mal type. There were only 5 cases of infantile propulsive petit mal. High frequency of fits and, in particular, status epilepticus, were very rarely seen in the present study. A case of self-induced photosensitive epilepsy, later combined with psychomotor epilepsy, is referred to in detail. Of 149 children with grand mal epilepsy, 36 were classed as idiopathic, and 88 as symptomatic cases. 37 of the symptomatic cases showed focal epilepsy with generalisation. It was concluded from the clinical course and the EEG that the combined effects of familial predisposition towards fits and exogenous cerebral lesions were operative factors in 14 patients. Children with febrile, convulsions possessed an EEG suggestive of a familial predisposition towards fits in slightly more than 50% of the cases. No cause could be found for the seizures in 5 infants with neonatal convulsions, but the mother of one of these infants was an epileptic herself, undergoing treatment with anticonvulsive drugs in high dosage and a withdrawal syndrome was suspected in this particular case. 17 infants with neonatal convulsions were symptomless on leaving hospital and remained so during the first year of life. Of the remaining cases, 10 showed neurological disturbances and one died. There was only one case in which neonatal convulsions progressed directly to epilepsy. The peak incidence of the first appearance of fits occurred during the first year of life (136 children), with 18% of the entire case material presenting within the first 6 months. 108 children presented with fits for the first time during the second year of life. Thereafter, the tendency towards the development of fits for the first time in life declined with increasing age.
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PMID:[Aspects of epilepsy in childhood (author's transl)]. 81 19

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

In cortical areas associated with an epileptic focus, there is, in the majority of cases, a correlation between decreased benzodiazepine (Bz) receptor binding, detectable with 123I-Iomazenil, and decreased blood flow. A patient with focal epilepsy due to a localized abnormality in cortical differentiation is presented who showed a marked focal decrease in Bz receptor binding and a normal 99mTc-HMPAO SPECT. Based on this case the relation between blood flow and Bz receptor binding in epileptic foci is discussed.
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PMID:[Cortical dysplasia as an epileptogenic focus: reduced binding of 123I-iomezanil with barely perceptible 99mTc-HMPAO SPECT]. 132 35


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