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

One hundred patients with focal epilepsy (44 were children) were evaluated with extraoperative electrocorticography via epidural electrode arrays. Localization of the epileptogenic focus was derived predominantly from recordings made during spontaneously occurring seizures. All resection procedures were carried out under general anesthesia. During anesthesia, the recording of sensory evoked responses made it possible to readily identify the sensorimotor region. Of the 100 patients, 72 underwent resection of an epileptogenic focus, and 33 of these were children. Those who did not have a resection either exhibited a diffuse seizure focus, failed to show an electrical seizure discharge in association with the clinical seizure, failed to have a seizure during the period of monitoring, or failed to exhibit conclusive changes for identifying a focus in the interictal record. Fifty-seven patients (29 children and 28 adults) who had a resection have been followed for between 1 and 12 years. Eighteen (62%) of the 29 children and 18 (64%) of the 28 adults enjoyed a good result. Twenty of the 100 patients reported here had temporal lobe epilepsy. They were candidates for recordings with depth electrodes to identify their focus, but they were evaluated instead with epidural recordings; the method is described. In 15 of them, a unilateral focus was identified and they underwent an anterior temporal lobectomy. Pathological changes were found in every case and, in 11 patients, the epidural recordings distinguished between a medial and a lateral focus. Ten of these patients have been followed for 9 months to 3 1/2 years, and seven have had a good result. The observations suggest that epidural electrodes may be used in lieu of depth electrodes for identifying the symptomatic temporal lobe.
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PMID:Surgical management of epilepsy using epidural recordings to localize the seizure focus. Review of 100 cases. 669 89

Retrospective analysis of the psychiatric diagnoses in a group of patients surgically relieved of medically intractable epilepsy tested the hypothesis that patients with left-sided temporal lobe epileptogenic lesions are at greater risk for the development of a so-called schizophrenic-like psychosis than are those with right-sided temporal lobe epileptogenic lesions. The data confirmed the hypothesis and also demonstrated an increased prevalence of sinistrals in the psychotic group. Thus, epilepsy involving the dominant hemisphere at the inception of the seizure disorder is the significant risk factors. The data also indicated that a psychosis is unlikely to develop in patients with other (nontemporal) forms of focal epilepsy. On the basis of these data and data from other studies, the prevalence of psychosis in patients with poorly controlled temporal lobe epilepsy was estimated to be approximately 10% to 15%.
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PMID:Prevalence of psychosis in epilepsy as a function of the laterality of the epileptogenic lesion. 681 52

When a focal epilepsy proves refractory to medical therapy, surgical treatment is increasingly used. Most interventions consist in cortical resections, and by far the most common operation is a temporal lobectomy. The presurgical evaluation is a multi-disciplinary one, and includes history and examination, neuropsychological testing, neuro-imaging techniques, functional studies (functional imaging and intracarotid amobarbital procedure), and neurophysiologic data (EEG-video monitoring). When non-invasive EEG does not succeed in localizing the epileptogenic zone with sufficient accuracy, several invasive techniques are available. Each has its own advantages and disadvantages. In appropriately selected cases, postoperative outcome is excellent, especially in temporal lobe epilepsy. In general, outcome is slightly less successful in extra-temporal cases.
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PMID:[Temporal lobectomy: indications and role in the surgery of epilepsy]. 756 37

When a focal epilepsy proves refractory to medical therapy, surgical treatment is available and increasingly used. Most interventions consist of focal cortical resections, and by far the most common operation is a temporal lobectomy. The presurgical evaluation is complex and multidisciplinary. It includes clinical evaluation, EEG-video monitoring, neuropsychological testing, and structural as well as functional imaging. When surface EEG fails to identify the epileptogenic zone with sufficient confidence, several invasive methods are available, each with its advantages and limitations. In addition to neurophysiologic data, when there is convergence of structural imaging (MRI) and functional testing (Wada test, neuropsychological evaluation, nuclear imaging), a single focus can be identified, and a focal resection is likely to be successful. Surgery is a well-accepted and effective therapeutic modality for patients with refractory epilepsy. When surgical candidates are selected appropriately, results are excellent, especially for temporal lobe epilepsy.
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PMID:Evaluation for surgical treatment of partial epilepsy: an overview. 757 98

The respective contribution of interictal HMPAO-SPECT and FDG-PET to the imaging of the epileptogenic zone in intractable temporal lobe epilepsy is not known. Ten consecutive patients with drug resistant focal epilepsy of temporal lobe origin were studied with prolonged noninvasive video-EEG monitoring, magnetic resonance imaging, interictal FDG-PET and HMPAO-SPECT. Five patients demonstrated unitemporal and 5 patients bitemporal interictal and/or ictal EEG epileptiform abnormalities. We developed a 3-dimensional semiquantitative method for interpretation and comparison of FDG-PET and HMPAO-SPECT using a 15-compartment model of the temporal lobe. In all 5 patients with unilateral epileptogenicity, interictal hypometabolism and hypoperfusion were recorded on the side of the EEG abnormalities without discrepancy between PET and SPECT. The severity and the extent of focal abnormalities were consistently greater on PET than on SPECT, in agreement with previously well documented better 'sensitivity' of PET. Among the 5 patients with bitemporal epileptogenicity, results of SPECT and PET were convergent in only 2 cases. In this group, SPECT abnormalities appeared more profound but either SPECT or PET were not constantly correlated with the side of predominant EEG epileptogenicity. Abnormalities on PET and SPECT were more frequently limited to mesiobasal structures among cases with unilateral epileptogenicity and tended to involve neocortical structures in bitemporal cases. We conclude that interictal FDG-PET and HMPAO-SPECT provide the same type of information on the side of the epileptogenic zone in cases with clearly unilateral epileptogenicity, with abnormalities more intense and more extensive on PET.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison and spacial correlation of interictal HMPAO-SPECT and FDG-PET in intractable temporal lobe epilepsy. 810 81

Volumetric measurement of the hippocampus is of use in localisation of lesions causing focal epilepsy and in lateralisation of epilepsy due to mesial temporal sclerosis. However, it is time consuming and requires specialised equipment. Hence, we compared volumetric measurement with visual detection of hippocampal asymmetry by five trained observers. MRI studies of 19 neurologically normal subjects and of 34 consecutive patients with epilepsy and hippocampal volume ratios below the lowest normal value were employed. Agreement between visual and quantitative diagnoses was 59% for all subjects (kappa = 0.38) and 65% for those with volumetric hippocampal asymmetry. Disagreements in visual and volumetric lateralisation of hippocampal asymmetry were relatively uncommon. Visual estimates of the extent of hippocampal involvement and the observers' confidence in the diagnosis influenced the accuracy of visual inspection. However, discordance in diagnoses occurred even when confidence in the visual diagnosis was high. Reliable visual detection occurred for hippocampal volume ratios below 0.7, suggesting that visual determination of hippocampal asymmetry is of greatest clinical value in the lateralisation of seizure foci in patients already selected for the presence of intractable temporal lobe epilepsy. Volumetric measurements are particularly important if hippocampal asymmetry is used for seizure localisation in groups of patients with temporal or extratemporal epilepsy.
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PMID:Reliability of visual inspection for detection of volumetric hippocampal asymmetry. 874 Nov 91

The etiology of epilepsy remains in most cases an enigma. Based on the finding of a genetically dependent immune dysfunction in focal epilepsies, brain specimens from 16 patients, ranging in age from 6 to 39 years and operated on for therapy-resistant focal, mainly temporal lobe epilepsy were analyzed for the presence of viral DNA. The PCR technique was used for detection of viral DNA from the herpes virus group. HSV-1 was found in 44% CMV in 50%, and HHV-6 in 25%. Three patients were positive for more than one of these viruses. The control material, consisting of only 4 brain tissue samples, showed DNA from HSV-1 in one case. Until more brain samples from controls have been examined, caution must be taken before a viral etiology is applied to focal epilepsy.
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PMID:Epilepsy etiology with special emphasis on immune dysfunction and neurovirology. 888 74

A variety of clinical observations suggest that certain forms of epilepsy are due to long-term, progressive changes in neural networks that eventually provoke spontaneous and recurring seizures. This process of network transformation, known as epileptogenesis, is a potentially important therapeutic target and also serves as an extremely interesting model of central nervous system plasticity. This article reviews some of the significant, recent advances in our understanding of mechanisms underlying epileptogenesis in different forms of epilepsy. The most substantial progress has been made in work related to temporal lobe epilepsy (TLE), where the biochemical, electrophysiological and anatomical changes in the hippocampus have been intensively studied. This has led to a number of cogent and testable hypotheses, including the concept that dentate granule cell hyperexcitability in TLE is due to a selective loss of hilar neurons that renders inhibitory cells 'dormant.' Studies of other forms of focal epilepsy suggest that a seizure focus may develop as a result of axonal reorganization or immune-mediated effects on membrane channels. Epileptogenesis in generalized epilepsies remains poorly understood, although recent work using models of absence epilepsy point to the critical role of GABAB or T-type calcium channels in the thalamus. Also, new transgenic mouse lines with epilepsy phenotypes have introduced candidate genes, such as those encoding the serotonin 5-HT2C receptor or the alpha subunit of calcium/calmodulin kinase II, that may be responsible for epileptogenesis. Finally, a large amount of investigation has focused on seizure-induced gene expression and it is now clear that seizures can cause a cascade of changes in the expression of gene products that are likely to play a role in network plasticity. Progress in developing 'anti-epileptogenic' therapies will require further advances in understanding the mechanistic roles of these various biochemical and anatomical changes in the transformation of normal to hyperexcitable neural networks.
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PMID:Recent advances related to basic mechanisms of epileptogenesis. 929 27

The limbic/mesial temporal lobe epilepsy syndrome has been defined as a focal epilepsy, with the implication that there is a well defined focus of onset, traditionally centered around the hippocampus. The pathology of the hippocampus in this syndrome has been well described and a number of physiological abnormalities have been defined in this structure in animal models and humans with epilepsy. However, anatomical and physiological abnormalities have also been described in other limbic sites in this form of epilepsy. Previous studies have shown broadly synchronized or multifocal seizure onset within the limbic system of the animal models and human patients. We hypothesized that the epileptogenic circuit for the initiation of seizures was distributed throughout the limbic system with a possible central synchronizing process. In vitro studies showed that multiple limbic sites in epileptic animals (hippocampus, entorhinal cortex, piriform cortex and amygdala) have epileptiform changes with prolonged depolarizations and multiple superimposed action potentials. In vivo studies revealed that thalamic stimulation yields short latency excitatory responses in the entorhinal cortex and hippocampus. In addition, in epileptic animals, thalamic stimulation caused epileptiform responses in the hippocampus. Based on the findings of this study and on previous anatomy and physiology reports, we hypothesize that the process of seizure initiation involves broad circuit interactions involving multiple independent limbic structures, and that the midline thalamus may act as a physiological synchronizer. We offer a new proposal for the functional anatomy of limbic epilepsy that takes widespread hyperexcitability in the limbic system and the potential for thalamic synchronization into consideration.
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PMID:Functional anatomy of limbic epilepsy: a proposal for central synchronization of a diffusely hyperexcitable network. 976 20

We report postictal nose wiping as a postictal symptom of localizing and lateralizing significance in focal epilepsy. We reviewed videotapes of 444 focal seizures in 101 patients who underwent prolonged video and EEG monitoring during presurgical epilepsy evaluation, and observed postictal nose wiping in 51.3% of 76 patients with temporal lobe epilepsy. The hand used to perform postictal nose wiping was ipsilateral to the side of seizure origin in 86.5% of all seizures and in 97.3% of all patients. We conclude that postictal nose wiping is a common, easily assessed symptom after focal seizures of temporal lobe origin that provides reliable lateralizing information on the side of seizure onset.
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PMID:Postictal nose wiping: a lateralizing sign in temporal lobe complex partial seizures. 1033 19


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