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

Why do the epileptogenic foci appear hypometabolic on interictal glucose metabolism positron emission tomography (PET) in a substantial proportion of patients with focal epilepsy but appear normo- or even hyper-metabolic in others? Such observations on interictal PET have not been fully explained by the frequency of interictal spike discharges alone. In the present study using digital electrocorticography monitoring system with high-frequency sampling, we determined how well regression models using spectral ECoG measures and spike frequency derived from 651 intracranial electrode sites explained cortical glucose metabolic patterns in six children with nonlesional focal epilepsy. Univariate regression analysis demonstrated that spectral amplitudes at gamma ranges (32-64, 64-100, and 100-200 Hz) were tightly correlated with interictal glucose uptake in the given electrode site in all children. Spike frequency was negatively correlated with interictal glucose uptake in three patients, whose epileptogenic focus appeared hypometabolic and interictal epileptiform discharge often consisted of a spike followed by a subsequent delta-wave. Conversely, spike frequency was positively correlated with interictal glucose uptake in the other three patients, whose epileptogenic foci appeared more hypermetabolic compared to the surrounding regions and associated with frequent interictal spike bursts. The spatial pattern of interictal glucose metabolism in nonlesional focal epilepsy may be better explained by gamma-oscillations derived from epileptiform and physiological neuronal activities rather than the frequency of interictal epileptiform discharges alone.
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PMID:Cortical glucose metabolism positively correlates with gamma-oscillations in nonlesional focal epilepsy. 1865 2

Temporal lobe epilepsy is the most common type of focal epilepsy diagnosed in adult patients. According to the location of seizure generation it is classified as mesial temporal lobe epilepsy and neocortical lateral lobe epilepsy. Diagnosis of temporal lobe epilepsy can be proved by the combination of the clinical manifestation of partial complex seizures, scalp-video EEG monitoring, results of magnetic resonance imaging (MRI) and imaging of interictal fluoro-deoxy-glucose positron emission tomography. Mesial temporal sclerosis is the most common finding on MRI. Temporal lobe epilepsy is the most surgically amenable diagnosis and results of surgery treatments are clearly superior to the prolonged medical therapy; surgical treatment of the mesial temporal epilepsy with mesial temporal sclerosis has the best clinical results. Except for standard microsurgical approaches such as anterior temporal resection and selective amygdalo-hippocampectomy, stereotactic thermocoagulation amygdalo-hippocampectomy is provided in our epilepsy centre. This alternative approach has comparable clinical outcome to the standard surgery approaches in 2 years clinical follow-ups. MRI is important not only in diagnostic procedures, but also in neuronavigation of surgery approaches, per operation control of the extent of resections and postoperative follow-ups, especially in failed epilepsy surgery.
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PMID:[Temporal lobe epilepsy in adults and possibilities of neurosurgical treatment: the role of magnetic resonance]. 2163 5

The antiseizure efficacy and safety of levetiracetam (LEV) is well documented; however, few clinical studies have investigated the predictability of patient responsiveness to LEV, especially when the drug is first administered. The aim of this study was to ascertain the utility of clinical, electrophysiological, and neuroimaging parameters for assessing the early response to LEV treatment in focal epilepsy patients. Twelve confirmed focal epilepsy patients were included who had never taken LEV before. At baseline and 1 month after LEV administration, all subjects underwent 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) and electroencephalography (EEG), and completed the Quality of Life in Epilepsy questionnaire (QOLIE-31). Participants were divided by drug response: good versus poor. The good response group (seven subjects) was defined by a >50% decrease in seizure frequency compared to baseline (3 months before LEV intake). The other five participants with a <50% decrease in seizure frequency were placed into the poor response group. We compared the differential changes in brain glucose metabolism on FDG-PET, power spectrum on the EEG, and QOLIE-31 results between the two groups after a 1-month LEV trial. In the good response group, it was possible to identify brain regions with increased glucose metabolism, including the bilateral caudate nuclei and both frontal and left parietal regions (uncorrected P<0.005). In the poor response group, FDG-PET did not reveal any areas with significantly increased glucose metabolism. In the good response group, spectral EEG analysis revealed decreased delta power (1-3 Hz, P<0.05) in the parietal region and increased beta1 power (13-19 Hz, P<0.05) in the frontal region, whereas no significant changes were observed in the poor response group. There were no significant changes on the QOLIE-31 in either group after a 1-month LEV trial. Our results suggest that LEV-induced glucose metabolism and EEG spectral changes may be indicative of initial drug responsiveness as early as 1 month following treatment initiation. These parameters may be useful prognostic markers of antiseizure effects caused by LEV medication or may indicate an epiphenomenon of LEV-induced changes in glucose metabolism and EEG frequency. Further studies with larger sample sizes are warranted.
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PMID:Changes in background electroencephalography and regional cerebral glucose metabolism in focal epilepsy patients after 1-month administration of levetiracetam. 2565 85

Brain glucose transport is dependent on glucose transporter 1 (GLUT1), encoded by the solute carrier family 2 member 1 (SLC2A1) gene. Mutations in SLC2A1 cause GLUT1 deficiency which is characterized by a broad spectrum of neurological phenotypes including generalized epilepsy, motor disorders, developmental delay and microcephaly. Recent case reports suggest SLC2A1 mutations can contribute to non-acquired focal epilepsy (NAFE) but interrogation of a large patient cohort has not been reported. We studied 200 patients with NAFE (126 with temporal lobe epilepsy) comprising 104 females and 96 males with a mean age of onset of 18 years. Polymerase chain reaction (PCR) and Sanger sequencing was performed to detect variants in all 10 coding exons and splice site regions of the SLC2A1 gene. We did not detect any pathogenic mutations in SLC2A1 in this cohort. Our data suggests that the frequency of GLUT1 mutations in NAFE is low. Limitations of this study include the mean age of onset and cohort size. Future research should focus on subpopulations of focal epilepsy with lower age of seizure onset particularly with co-existent movement disorders in which GLUT1 mutations may play a more important role.
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PMID:Evaluation of GLUT1 variation in non-acquired focal epilepsy. 2841 80


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