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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Children with epilepsy are at risk for developing learning problems. The poor academic achievement shown by children with epilepsy may result from the underlying cognitive deficits. The study of such problems reveals the implication of several factors that determine the nature and degree of the neuropsychological defects. Among the most frequently reported factors are epileptic factors such as age of onset, type of seizures, duration, localization of cerebral dysfunction, frequency, antiepileptic treatment, and etiology.
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PMID:[Neuropsychological involvement in childhood epilepsy]. 898 54

Single gene disorders offer the best opportunity for identification of genetic linkage and of abnormal genes. Epilepsies with single gene inheritance include symptomatic epilepsies where there is associated diffuse brain dysfunction, and idiopathic epilepsies where seizures are the major neurological abnormality. There are over 200 single gene symptomatic epilepsies; most are rare. Gene identification has been achieved in a number of these conditions but these important advances have not yet led to a better understanding of epileptogenesis, because of the associated brain disease. Idiopathic single gene epilepsies include benign familial neonatal convulsions, where genetic linkage to chromosomes 20q and 8q has been found in different families, and benign familial infantile convulsions where linkage is presently unknown. Recently, four autosomal dominant partial epilepsies have been described. In autosomal dominant nocturnal frontal lobe epilepsy a genetic defect in the alpha 4 subunit of the nicotinic acetylcholine receptor was found in one family. This is the first genetic defect described in an idiopathic epilepsy. The other three syndromes are autosomal dominant partial epilepsy with variable foci, autosomal dominant rolandic epilepsy with speech dyspraxia, and familial temporal lobe epilepsy. In the latter condition, linkage to chromosome 10q has been reported in one family, but the genetic defect is unknown. It is likely that other idiopathic single gene epilepsies will be identified. Molecular genetic study of these disorders is likely to lead to discovery of other epilepsy genes. This will lead to an improved understanding of human epileptogenesis with implications for clinical diagnosis, genetic counselling, pharmacological therapy and possibly prevention of epilepsy.
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PMID:Epilepsies with single gene inheritance. 907 84

We report a 12-year-old boy with unilateral meningoencephalitis due to non-herpes simplex virus. He experienced secondarily generalized partial seizures of the left extremities with loss of consciousness. In contrast with normal neuroimaging findings, interictal electroencephalograms (EEGs) showed prolonged slowing in the right hemisphere. This laterality agreed with the right brain dysfunction verified on neuropsychological examination. Follow-up EEG is important in such a subtle case with normal neuroimaging.
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PMID:Unilateral meningoencephalitis with hemispheric slowing on EEG. 907 95

The relationship between the number of cortical tubers observed by magnetic resonance imaging (MRI) and the severity of cerebral dysfunction of tuberous sclerosis patients has been examined in a meta-analysis of the published literature. The literature review has identified five independent studies for examining the association. These studies consistently reveal that the cortical tuber count detected on MRI scans is increased among those with more severe cerebral disease. Severity of the cerebral dysfunction is measured by the seizure status and its control and by the developmental status and the level of mental retardation. Meta-analysis demonstrates that within a study population, the MRI-detected cortical tuber count is six times more likely to be above the median count for tuberous sclerosis patients with severe cerebral dysfunction (poor seizure control or moderate-severe retardation or both) than more mildly affected tuberous sclerosis patients. Similarly, across studies, moderately to severely affected patients are five times more likely to have greater than seven MRI-detected cortical tubers than those more mildly affected. These associations are both statistically significant and strong. The cortical tuber count is a biomarker that reasonably predicts the severity of cerebral dysfunction of tuberous sclerosis. Cortical tubers of tuberous sclerosis form in the early gestational period. The embryologic disruption determining the clinical severity of the cortical dysfunction of tuberous sclerosis is set in the early gestational period.
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PMID:Cortical tuber count: a biomarker indicating neurologic severity of tuberous sclerosis complex. 907 14

Echographia is a phenomenon in which a patient continuously translates verbal stimuli into writing. We encountered a patient with epilepsy who developed visual echographia during interictal periods. In this case, echographia was observed during two different periods, namely the period of disturbed consciousness after the epileptic seizure and the period of clear consciousness after suppression of the seizures. Disinhibition due to disturbance of the consciousness is considered to have been the cause of echographia in the former period. In the latter period, it is considered that echographia was caused by the release of lower function from suppression of upper function by brain dysfunction, as the after effect of status epilepticus. As echographia can be observed in epileptic patients, attention and careful observation by epileptologists is needed.
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PMID:Echographia as a symptom of interictal state in an epileptic patient: a case report. 907 57

In order to identify the brain lesions of symptomatic/cryptogenic partial epilepsies (S/CPEs) in infants and children, magnetic resonance imaging (MRI) studies, thorough encephalographic (EEGic) studies, and detailed clinical and neurologic evaluations were obtained in 300 infants and children who were diagnosed to have S/CPEs with onset before the age of 13 years during the past 7 years. The overall detection rate of brain lesions by MRI was 41.7% (125/300). Congenital malformations (18 cases), vascular malformations (9 cases), neurocutaneous syndromes (13 cases), and space-taking lesions (20 cases) constitute a large percentage of SPEs in infants and children. A variety of insults such as infection, ischemia, hemorrhage, trauma and metabolic disorders can result in destructive parenchymal loss lesions including porencephaly, focal atrophy, hemiatrophy, and diffuse brain atrophy (20 cases). Major etiologic factors leading to infarction, encephalomalacia, leukomalacia, included trauma, hvpoxicischemic encephalopathy (HIE), systemic lupus erythematosus (SLE), encephalitis, vasculitis, venous thrombosis, vasculopathies, and heart problems (22 cases). Mesial temporal sclerosis (MTS) could be evidenced in around 20% (18/95) of cases with temporal lobe epilepsy (TLE), which was strongly associated with past histories of febrile seizures and encephalitis complicated by status epileptics. However, cases with porencephaly, global atrophy or delayed myelination of unilateral temporal lobe on MRI were more related to HIE. With the advent of neuroimaging techniques, particularly MRI, a wide variety of underlying pathology can be detected as a cause of symptomatic partial epilepsies in pediatric patients. The occurrence of S/CPE indicates the presence of localized brain dysfunction, and many of the causes are potentially treatable. An orderly and thorough clinical and laboratory investigations, as well as neuroimaging studies should be made to diagnose and treat any underlying conditions.
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PMID:Magnetic resonance imaging in symptomatic/cryptogenic partial epilepsies of infants and children. 915 66

Eclampsia accounts for a third of maternal mortality in developing countries. The neurological manifestations of eclampsia consist of seizures and alteration of sensorium or coma on a background of pre-eclampsia. Occasionally there can be focal neurological deficits too. Recent studies with CT scan and MRI have demonstrated the presence of cerebral edema and/or cerebral hemorrhage in eclampsia. EEG in patients with eclampsia has revealed evidence of diffuse cerebral dysfunction (delta waves) and epileptiform transients (spikes or sharp waves). There is also evidence of extensive vasculopathy within the brain parenchyma. A variety of mechanisms have been suggested to explain these changes, the most important being failure of autoregulation of cerebral blood flow that leads to cerebral edema and hemorrhage. There is considerable controversy regarding the treatment of seizures in eclampsia. Recent studies have shown that magnesium sulfate is superior to phenytoin or diazepam in the treatment of eclamptic seizures and prevention of eclamptic seizures in women with pre-eclampsia.
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PMID:Neurological aspects of eclampsia. 956 20

Epileptic seizures are a principal brain dysfunction with important public health implications, as they affect 0.8% of humans. Many of these patients (20%) are resistant to treatment with drugs. The ability to anticipate the onset of seizures in such cases would permit clinical interventions. The view of chronic focal epilepsy now is that abnormally discharging neurons act as pacemakers to recruit and entrain other normal neurons by loss of inhibition and synchronization into a critical mass. Thus, preictal changes should be detectable during the stages of recruitment. Traditional signal analyses, such as the count of focal spike density, the frequency coherence or spectral analyses are not reliable predictors. Non-linear indicators may undergo consistent changes around seizure onset. Our objective was to follow the transition into seizure by reconstructing intracranial recordings in implanted patients as trajectories in a phase space and then introduce non-linear indicators to characterize them. These indicators take into account the extended spatio-temporal nature of the epileptic recruitment processes and the corresponding physiological events governed by short-term causalities in the time series. We demonstrate that in most cases (17 of 19), seizure onset could be anticipated well in advance (between 2-6 minutes beforehand), and that all subjects seemed to share a similar 'route' towards seizure.
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PMID:Epileptic seizures can be anticipated by non-linear analysis. 1261 50

Possible sex differences in the pattern of interictal hypometabolism were investigated, and also seizure spread in patients with mesial temporal lobe epilepsy (n=48) and hippocampal sclerosis (MTLE). Male patients (n=21) more often had a frontal lobe hypometabolism ipsilateral to the seizure onset (p<0.0001) and a spread of epileptiform activity to this region (p=0.001). By contrast, female patients more often exhibited hypometabolism (p=0.0052) and an ictal spread to the contralateral temporal lobe (p=0.0097). These findings suggest sex differences in spatial distribution of brain dysfunction in MTLE, perhaps reflecting sexual dimorphism in regional cerebral connectivity.
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PMID:Sex differences in patients with mesial temporal lobe epilepsy. 985 69

Complex developmental venous anomalies (DVAs) represent variations of normal cerebral venous drainage and consist of dilation of the superficial and/or deep venous system. These rare anomalies can occur unilaterally or bilaterally, supratentorially or infratentorially, focally or they can affect the entire hemisphere. Some DVAs are associated with cervicofacial venous malformations or facial lymphatic malformations. Anomalies of this type are generally clinically silent, and cerebral dysfunction is usually absent. Symptoms, when they occur, are most commonly headache or mild seizure disorders. The angiographic findings are striking, with well-formed but enlarged transcerebral medullary and deep and/or superficial cortical veins. Opacification of these venous structures occurs within the same time frame as a normal angiographic venous phase. The authors report the case of a 33-year-old man in whom a large inoperable arteriovenous malformation had been previously diagnosed and who presented with seizures. Repeated magnetic resonance imaging and angiography demonstrated abnormally dilated transcerebral, superficial, and deep venous structures involving the entire right hemisphere with no identifiable nidus. Additionally, multiple bilateral benign facial hemangiomas were present in this patient. It is important to recognize this rare venous appearance as a developmental variant and not mistake it for an arteriovenous malformation or a partially thrombosed vein of Galen malformation. Because these venous anomalies are extreme variants of the normal venous system, hemorrhage rarely, if ever, occurs and the patient can be reassured that no interventional or surgical therapy is necessary or warranted.
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PMID:Complex right hemisphere developmental venous anomaly associated with multiple facial hemangiomas. Case report. 1019 23


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