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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

The incidence of neurological residuals following anatomical correction of transposition of the great arteries (d-TGA) has not been described so far. Clinical examination, EEG recordings, and computed tomography (CT) scans were carried out in a consecutive series of 38 children with d-TGA surviving anatomic corrective surgery. The patients were classified into one of three groups according to the type of operation: 15 patients after two-stage approach (TSA) (Stage 1: pulmonary artery banding+aortopulmonary shunt; Stage 2: anatomic correction); 12 patients with primary anatomic correction within the first 2 weeks of life (early switch, ES); 11 patients with primary anatomic correction later in infancy (later switch, LS). In 26 patients (68%) we found no abnormalities on neurologic examination, CT scan, or EEG. Four patients suffered from spastic hemiplegia, 3 of these had cortical brain damage visible on CT scan, and 3 had focal epilepsy as well. In 2 otherwise clinical normal patients cortical infarction could be seen on a CT scan. Thus, in 5 cases (13% of 38 patients) cerebral infarcts were diagnosed by CT scan. The cortical vascular infarction was seen in 4 patients after TSA and in 1 after LS. In 6 patients we found other neurological abnormalities. Early anatomic correction in patients with d-TGA reduces the risk of cortical vascular infarction.
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PMID:Improved neurological outcome following early anatomical correction of transposition of the great arteries. 137 55

Sequential topographic mapping was performed to differentiate "epileptic" from "non-epileptic" rolandic spikes. Twenty-four children without any indication of organic brain lesion were divided into a group with epilepsy and a group without epilepsy. The group with epilepsy was subdivided into "classical BECT" (benign focal epilepsy of childhood with centro-temporal spikes) and "non-classical BECT." Sequential mapping of the rolandic spikes revealed two different topographic patterns: a pattern of stationary potential fields and a pattern of non-stationary potential fields. The topographic pattern of stationary potential fields was morphologically represented by a single spike-and-wave complex whereas that of non-stationary potential fields was morphologically represented by a "double" spike-and-wave complex. Among the non-stationary topographic patterns represented by a "double" spike, one specific sequence of changes of potential fields was found. This sequence started with a dipolar field, with the negative pole in the frontal region and the positive pole in the centro-temporal region, morphologically represented by the small first spike of the "double" spike-and-wave complex. This dipolar field, changes to a unipolar or dipolar field, with a negative potential field in the centro-temporal region and, sometimes, a simultaneous positive potential field in the frontal region, morphologically represented by the prominent rolandic spike. This characteristic pattern was found to be significantly related to classical BECT.
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PMID:Sequential EEG mapping may differentiate "epileptic" from "non-epileptic" rolandic spikes. 137 47

Thirty cases of benign focal epilepsy of childhood were reported. The seizures were partial or generalized motor ones in all cases. One patient had episodes of visual hallucination with motor seizures. No objective examination has demonstrated cerebral lesions in all cases. The most characteristic in the present study was that the attacks were in relation to the sleep in 90% of cases, 56.7% of all patients had nocturnal seizure only. The characteristic EEG patterns were the spike or sharp discharges in Rolandic area in 29 cases, and occipital sharps or sharp wave complexes in one patient on normal background activities. The discharge rate of Rolandic spikes or sharps were significantly higher during sleep than during the awake stage, and 12 cases had Rolandic discharges only during sleep. Sleep EEG recordings is suggested when children were suspected of having such kind of seizure type but having a normal EEG pattern when awake. Brief induced sleep is usually adequate.
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PMID:[Benign focal epilepsy of childhood (BFEC)]. 139 39

The GABA withdrawal syndrome (GWS) is a new model of focal epilepsy in which paroxysmal activity is induced through the interruption of a chronic, intracortical infusion of GABA. Preliminary studies have shown extraordinary resistance of this epileptogenic activity to classic anticonvulsants including diazepam, the most effective agent for treating status epilepticus. However, GWS can be inhibited by GABA itself. The rat with petit mal-like seizures is a genetic model of generalized non-convulsive epilepsy (GNCE), with behavioral characteristics and electrical (spike-and-wave discharges) signs resembling absences. Moreover, GABAmimetics aggravate this type of seizure. Rats with GWS induced by cessation of a localized GABA infusion (50 micrograms/microliters/h for 24 h), and the rat model of GNCE, were treated with HEPP, a new anticonvulsant agent. In the case of GWS, the drug produced a significant decrease of focal spike activity in animals which started discharging at low frequencies while in rats with higher frequency discharge, HEPP was without effect. HEPP administered on the second day of the GWS in naive rats had no effect. In rats with GNCE, doses of 50 and 100 mg/kg i.p. blocked the spike-and-wave discharges. The higher dose produced sedation in this absence seizures model. Although the mechanism of action of HEPP is still unknown, its unique antiepileptic profile deserves further studies.
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PMID:Effects of 3-hydroxy,3-ethyl,3-phenylpropionamide (HEPP) on rat models of generalized and focal epilepsy. 139 31

The clinical correlates of Rolandic spikes were studied in 47 children to determine the significance of this EEG finding to the diagnosis and classification of epilepsy. The children were classified into 'functional' and 'organic' groups, with and without epilepsy. Children with epilepsy were further subdivided into those with Rulandic and those with non-Rulandic seizures. In children without neurological abnormalities, the EEG finding of Rolandic spikes plays a decisive role in the diagnosis of an epileptic syndrome as benign focal epilepsy of childhood with centro-temporal spikes (BECT), a diagnosis with an excellent prognosis. Neurological and neuroradiological examinations of the 'functional' group revealed that the Rolandic spike may occur as a true 'functional' spike. The frequency of a family history of epilepsy among neurologically normal children with Rolandic spikes suggests, in addition to the inheritance of BECT and the EEG trait, the existence of a hereditary susceptibility to epilepsy.
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PMID:Rolandic spikes in the inter-ictal EEG of children: contribution to diagnosis, classification and prognosis of epilepsy. 139 29

We attempted to lateralize the epileptogenic focus (seven temporal lobe hippocampal foci, one frontal lobe focus) in medically refractory unilateral complex partial seizures, using noninvasive 31P magnetic resonance spectroscopic imaging (MRSI) blindly and interictally to compare hippocampal or frontal regions. The seizure foci were more alkaline (intracellular pH = 7.17 +/- 0.03) compared with the contralateral region (7.06 +/- 0.02, p < 0.01) in all eight cases; the inorganic phosphate was relatively increased (240 +/- 50% of contralateral, seven of eight cases, p < 0.01); and phosphomonoesters were relatively reduced (68 +/- 9% of contralateral, seven of eight cases, p < 0.01). Other phosphorus metabolites were symmetric (+/- 10%). 31P MRSI correctly lateralized the seizure focus in all eight cases. By comparison, imaging correctly lateralized four cases and SPECT, two cases. In conclusion, 31P MRSI is a useful tool for the noninvasive clinical assessment of focal epilepsy and can accurately lateralize the epileptogenic focus.
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PMID:Lateralization of human focal epilepsy by 31P magnetic resonance spectroscopic imaging. 140 85

Fifty-four cases with intractable convexity focal epilepsy were analyzed with regard to surgical treatment. To acquire satisfactory results, preoperative precise localization of focus and selection of relevant operative methods are indicated.
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PMID:Surgical treatment for convexity focal epilepsy. 143 56

Sixteen epileptic patients suffering from focal epilepsy who underwent antiepileptic drug treatment with carbamazepine (CBZ) for the first time were studied. The EEG was recorded at rest with eyes closed, during blocking reaction (BR), fixation (FIX) and mental arithmetic tasks. The computerized EEG study, performed before and after CBZ therapy, utilized spectral analysis. Data underwent statistical evaluation through Anova and correlation analysis. The parameters evaluated were the mean frequency and the mean absolute and relative power. The results have shown that after CBZ treatment there is a decrease in the alpha reactivity during BR and FIX, while a significant increase in beta activity was observed during all tasks. The effect of CBZ therapy on EEG activity during cortical activation patterns are discussed.
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PMID:Effect of carbamazepine treatment on EEG changes induced by different cortical activation patterns in newly referred epileptic patients. 145 64

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


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