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

Electrical induction of seizure activity profoundly impairs hippocampal long-term potentiation (LTP) in rats. A similar effect may account for the memory dysfunction observed after electroconvulsive stimulation in humans and other species. The co-administration of ketamine with the induction of electroconvulsive seizures (ECS) was evaluated as a possible method for reducing the impact of ECS on hippocampal synaptic plasticity in rats. Electrophysiological studies in vivo showed that both the enhancement of the EPSP slope and the subsequent reduction of experimentally induced LTP in the dentate gyrus by repeated, spaced ECS were significantly attenuated by ketamine anaesthesia. The findings suggest that ketamine may protect against ECS-induced memory impairment and thus prove useful in reducing the transient cognitive impairment following electroconvulsive therapy (ECT).
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PMID:Ketamine prevents ECS-induced synaptic enhancement in rat hippocampus. 781 17

Neuropsychological dysfunction in children and adults with epilepsy is common and has several possible interrelated causes, including the underlying pathophysiology, possible cerebral pathology, the effects of subclinical discharges, sleep disorders, status epilepticus and drug therapy. Of these factors the effects of subclinical discharges and those of medication are potentially remediable. In up to 50% of patients with subclinical epileptiform EEG discharges, these are associated with transitory cognitive impairment. When the discharges are focal, the cognitive deficits usually reflect the normal neuropsychological functions of the affected brain region. Most antiepileptic drugs, with the exception of the benzodiazepines (which themselves adversely affect cognition) and lamotrigine, do not suppress inter-ictal discharges. Although well-designed clinical trials of the effects of antiepileptic drugs are difficult to perform, there is convincing evidence that phenobarbitone and phenytoin cause cognitive impairment. Drugs which control both the seizures and inter-ictal discharges should improve cognitive function, provided the drugs themselves do not have a cognitive penalty. Lamotrigine provides effective control of both overt and subclinical seizures, without adversely affecting cognition.
Seizure 1994 Dec
PMID:Cognitive impairment--is it inevitable? 789 46

Patients with epileptic seizures frequently complain of long-lasting cognitive impairment after a seizure. We evaluated this issue in 31 patients with epileptic seizures of a frontal (n = 8) or temporal lobe origin [right temporal lobe (RTL) n = 8/left temporal lobe (LTL) n = 15]. Seizures were secondarily generalized in 18 patients. Computerized testing of verbal and nonverbal recognition memory was performed before the seizure, directly after postictal reorientation, and 30 min and 1 h later. Repeated testing of 14 healthy persons served as control. The following results were obtained: Depending on seizure generalization, postictal reorientation times were 1-45 min. Frontal lobe seizures showed no effect on postictal memory performances, but verbal and visual recognition memory was significantly decreased after temporal lobe seizures. Decrease in either verbal or visual memory and time of recovery were related to lateralization of seizure onset. Functional recovery after reorientation lasted 30 min to 1 h. The decrease in performance was more severe after generalized seizures. Decision times during memory performance were not significantly affected by the seizures. Temporal lobe seizures lead to circumscribed and long-lasting memory deficits, which can be assumed to affect patients' capabilities seriously. Pre- and postictal testing is a useful tool for determining postictal cognitive impairment and in determining the site of seizure onset.
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PMID:Postictal courses of cognitive deficits in focal epilepsies. 792 54

The benign nature of febrile seizures (FS) has been well documented by large prospective population-based studies published between 1976 to 1987. However, many paediatricians still treat FS as though it is a serious condition which may cause brain damage, and epileptologists and neurosurgeons continue to debate the role of FS in causing temporal lobe epilepsy. The efficacy of long-term anticonvulsant therapy has recently been questioned and the possibility of permanent cognitive impairment after long-term phenobarbital has caused public alarm. This article attempts to review the areas of controversy and suggest a rational approach to the investigation and management of FS.
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PMID:Febrile seizures: a new look at an old controversy. 794 56

Sixteen patients (8 female, 8 male) with primary angiitis of the CNS (PACNS), were followed prospectively in a vasculitis clinic. Diagnosis was by angiography in patients without underlying disease. Median age at diagnosis was 36.5 years, and median duration of follow-up was 28 months. Onset was acute in 14 patients (88%), with 3.5 weeks (median) from onset symptoms to diagnosis. Three women developed symptoms within 3 weeks postpartum. The most frequent symptoms were severe headaches (12, 75%), stroke (6, 30%), transient ischaemic attack (TIA) (4, 28%), seizures (7, 44%), visual aberration (3, 19%), and cognitive impairment (5, 31%). Laboratory data included high ESR (2, 13%), leucocytosis (8, 80%), thrombocytosis (1, 6%), positive antinuclear antibody titre (3, 15%), and high levels of complement (5, 31%). Lumbar puncture was performed in 12 patients (75%). CSF analysis was abnormal in five patients (42%). EEG was abnormal in 5/9 patients. The major CT/MRI scan findings were cerebral haemorrhage (4, 25%), brain infarcts (5, 31%), brain atrophy (2, 13%) and non-specific lesions (2, 13%). Four patients had normal studies. All patients received corticosteroids (CS), and five were treated with oral cyclophosphamide. Two patients relapsed despite CS and cyclophosphamide therapy. All patients are alive, and at the last assessment, eight had a permanent neurological deficit, which included paresis (3, 19%), neurocognitive abnormalities (2, 13%), visual loss (2, 13%) and seizure activity (5, 31%). Our data suggest a non-progressive, non-fatal course in those PACNS patients diagnosed angiographically and treated with CS with or without cyclophosphamide.
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PMID:Primary angiitis of the CNS diagnosed by angiography. 804 67

The development is described of a new stimulus electrode placement for electroconvulsive therapy (ECT) from expectations that relate the location and volume of induced seizure foci to side effects and efficacy, respectively. These expectations are that cognitive side effects would be minimized by avoiding induction of seizure foci in brain regions associated with neuropsychological function, and that greater efficacy would be associated with a larger volume of seizure foci. These considerations led to placement on the right temple and on the left forehead. This placement was used in an open trial on 10 consecutive female inpatients suffering from mania, depression, or mixed manic-depressive state, 9 of whom showed severe cognitive impairment, psychosis, or both. All patients achieved remission, indicating efficacy as likely above 93.3% as below it, and above 74% (p < 0.05); 6- to 10-week follow-up was essentially unchanged. No cognitive morbidity was observed. Post-ECT mini-mental status score averaged 28.4 out of 30, with an average improvement of 17.3 points, substantially better than reported after bifrontotemporal ECT. These results justify further consideration of this placement.
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PMID:Asymmetric bilateral right frontotemporal left frontal stimulus electrode placement for electroconvulsive therapy. 804 43

Experience with prolonged seizures in animal models and humans teaches that cellular injury and cognitive impairment can occur in epilepsy. Status epilepticus probably causes cerebral injury and cognitive dysfunction if it is of long duration; however, studies of electroconvulsive therapy do not support the idea that repeated seizures alone produce a decline in cognitive function. Although many factors related to seizures may correlate with cognitive impairment in certain groups of patients with epilepsy, prospective studies do not support the premise that cognitive impairment develops or progresses in a population of epilepsy patients. When impairment is present, its origin appears to be multifactorial. In addition to the seizures and associated seizure variables (including anticonvulsant medications), interictal epileptiform discharges and the perceptions of the patients and others also may play major roles.
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PMID:Epilepsy and mental decline. 818 4

The incidence of epileptic seizures is high in childhood, but shows regression during adult life until the age of 65 when there is again a marked, age-dependent increase in frequency. The specific problems of anticonvulsive therapy in the elderly are discussed in the light of the sparse literature on this subject. Pathophysiological influences of aging on the pharmacodynamics and pharmacokinetics of antiepileptic drugs have to be taken into account, such as changes in the renal, hepatic and intestinal functions as well as increased neuronal receptor sensitivity, among other factors. The optimal time to start therapy is controversial. In selecting the antiepileptic drug, particular attention must be paid on cognitive dysfunction and impairment of impulse conduction. Moreover, age-dependent side effects, as well as possible additive effects due to interaction with other medication have to be taken into consideration. In view of the high rate of relapses great caution has to be taken to withdraw the antiepileptic drugs in completion of the therapeutic regimen.
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PMID:[Therapy of epilepsy in the elderly]. 821 1

Paralysis induced by neuromuscular blocking agents facilitates ventilation of seriously ill patients but may preclude clinical recognition of seizures. We describe the occurrence of severe cognitive impairment in a 14-year-old girl in whom status epilepticus was recognized only when pancuronium was withdrawn after 14 hours of paralysis. This patient emphasizes a potential danger of paralysis from drugs in patients with acute cerebral dysfunction.
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PMID:Failure to recognize status epilepticus in a paralysed patient. 822 90

Early onset Familial Alzheimer's Disease (FAD) is an autosomal dominant disease with apparent complete penetrance. It is genetically heterogeneous with some families carrying mutations in the amyloid precursor protein (APP) gene which segregate with the disease. In addition, there is allelic heterogeneity with four mutations associated with FAD. Three mutations have been reported at APP 717, just distal to the C-terminus of the beta-amyloid domain, APP 717 val-ile, APP 717 val-phe, and APP 717 val-gly, which are associated with autopsy-proven Alzheimer's disease (AD). APP 670/671 lies at the N terminus of the beta-amyloid domain and is associated with clinically diagnosed FAD in two Swedish families. FAD tends to have prominent myoclonus and this is shared by the cases with APP mutations. In two unrelated UK families with APP 717 val-ile mutations there was early prominent memory impairment with dyscalculia proceeding to generalized cognitive impairment with a lack of insight. There was a late development of a gait disturbance with extrapyramidal features in some members. Positron emission tomography (PET) with fluorodeoxyglucose demonstrated posterior bitemporal biparietal hypometabolism in one case. Magnetic resonance imaging (MRI) showed generalized cerebral atrophy particularly affecting the temporal lobes and hippocampus. At autopsy, a single case showed extensive beta-amyloid deposition with congophilic angiopathy and widespread senile plaques and neurofibrillary tangles. The cytoskeletal pathology associated with abnormally phosphorylated tau was similar to cases of sporadic AD. In addition, there were widespread cortical and subcortical Lewy bodies. A single family with the APP 717 val-gly mutation also showed prominent myoclonus, lack of insight, and seizures, PET, in a single case, showed classical biparietal bitemporal hypometabolism. Autopsy, in a single case, showed diffuse deposits of beta-amyloid throughout the cortex with frequent neuritic plaques and neurofibrillary tangles. No other inclusion bodies were seen. There was severe congophilic angiopathy. The age at onset of APP mutations is around 50 years of age by contrast to other early onset FAD pedigrees.
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PMID:Alzheimer's disease families with amyloid precursor protein mutations. 823 83


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