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

Postictal symptoms can be disabling in themselves, but their underlying substrates may endure, giving rise to epilepsy-induced interictal behavioral disorders. Chronic temporal lobe epilepsy is reported to be associated with a variety of interictal behavioral changes which often take the form of affective disturbances. Depression, among the more common interictal psychological dysfunctions suffered by patients with temporal lobe seizures, could reflect epilepsy-induced alterations in normal opioid peptide mechanisms. In experimental animal models, certain postictal behaviors have been shown to be opioid-mediated. Furthermore, an experimental model of interictal behavioral disturbance resembles stimulation-induced defensive rage, which can be relieved by intracerebral administration of opioid peptides. Defensive rage is a species-specific behavior encountered in cats. Its correlate in humans would be difficult to predict in view of the stronger cortical control; however, it may manifest rather as insecurity, irritability, and perhaps depression. Extrapolation of animal experiments would suggest that depression and certain other common postictal and interictal affective disturbances seen in patients with temporal lobe seizures reflect mechanisms more related to opiate withdrawal, than to direct opiate actions. The activity-induced plasticity associated with recurrent temporal lobe seizures, therefore, should result in changes in opioid function that predispose to withdrawal phenomena. Limbic seizures induce enhanced enkephalin synthesis lasting for up to 2 weeks. Recurrent seizures in experimental animals, however, cause paradoxical up-regulation of mu opiate receptors. Patients with temporal lobe epilepsy demonstrate enhanced mu receptor binding in the neocortex of the epileptogenic temporal lobe on PET. The reasons for this enduring interictal effect are not clear. Nevertheless, if animals or patients become dependent on enhanced endogenous opioid activity as a result of seizures, and also have up-regulation of mu receptors, then severe withdrawal effects, such as defensive rage in cats or depression in humans, might be expected when seizures do not recur frequently. Plotting the time course of mRNAenk and enkephalin expression after seizures, and the time course of symptoms of interictal behavioral disturbances, may demonstrate a temporal relationship that supports this hypothesis. For instance, depression or other withdrawal symptoms might only occur when the interval between seizures is greater than the duration of seizure-induced enkephalin synthesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interictal behavioral disturbances: a search for molecular substrates. 133 48

Intracerebral microdialysis combined with electrocorticographic recordings was used in a patient subjected to epilepsy surgery. The patient developed a series of partial seizures during an 8 min period. Marked elevations of aspartate (79-fold), glycine (21-fold), glutamate (16-fold) and serine (8-fold) dialysate concentrations occurred in association with onset of the period with seizures. Recurrent seizures occurred, in spite of normalizing amino acid levels. Other amino acids analyzed (aspargine, threonine, arginine, alanine, taurine, tyrosine, phenylalanine, isoleucine and leucine) showed less pronounced changes (1-5 times the basal levels).
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PMID:Seizure related elevations of extracellular amino acids in human focal epilepsy. 140 96

Generalized tonic-clonic seizures are the most common type of convulsive disorders in children. They are always a sign of an epileptogenic cerebral dysfunction and present either acutely, predominantly as a single event with detectable origin, or chronically, recurring as an epileptic syndrome. In view of the etiology and classification of convulsions it is important to differentiate between primarily and secondarily generalized seizures. This distinction is first of all based on an exact description of the very beginning and of the course of the seizures, on the EEG findings and on any connection between the seizures and a particular time of day. Primarily generalized tonic-clonic seizures with and without associated petit mal seizures are manifestations of an idiopathic epilepsy and are most probably genetically determined, secondarily generalized seizures on the other hand are often signs of a central nervous lesion or of another symptomatic form of epilepsy. Benign idiopathic partial seizures, however, take the from of secondarily generalized convulsions during the morning sleep. Prolonged tonic-clonic seizures of any origin require vigorous treatment with anticonvulsants, if necessary in an intensive care unit. Recurrent seizures are treated with long-term anticonvulsant medication. The first-line treatment is valproic acid or phenobarbitone (or if necessary, a bromide) in primarily generalized seizures and carbamazepine or phenytoin in secondarily generalized convulsions. The recommended duration of this therapy and the risk of recurrence of seizures vary widely with the underlying etiology and the type of epilepsy.
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PMID:[Grand mal epilepsy in childhood]. 143 12

Seizures persist or recur in 20-60% of patients after resective surgery for intractable partial epilepsy. Further information about the natural course of these seizures is lacking in the literature. During one decade of epilepsy surgery at a single institution, we identified 72 patients with recurrent postoperative seizures after resective procedures for epilepsy. Prospectively compiled seizure diaries, hospital records, and outpatient office records were reviewed and supplemented by telephone communications to assess subsequent seizure frequency. Follow-up data was available ranging from 6 months to 7 years 5 months (mean 3 years 5 months). The likelihood of persistent seizures and recurrent intractability was examined with life-tables. Seizures recurred within the first postoperative year in 86% of patients and were similar to preoperative events in 74% of patients. After the first seizure recurrence, there was 80% likelihood of persistent seizures in the next 6 years and 40% likelihood of intractability (more than one seizure a month despite optimal medical therapy). The interval until recurrence within the first postoperative year did not affect the likelihood of subsequent seizures or intractability. Late seizure recurrence (after the first year) was not associated with any instances of subsequent intractability. Recurrent seizures after extratemporal resections were more likely to become persistent and intractable than seizures recurring after temporal resections. This information provides rational prognostication and assists in counseling patients with recurrent seizures after resective surgery for intractable epilepsy.
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PMID:Natural history of recurrent seizures after resective surgery for epilepsy. 174 56

Seizure-induced plasticity, in the form of either changes in cellular morphology or changes in neurochemistry, could have a profound impact upon regional excitability in brain. There is now ample evidence that in genetically 'normal' animals, seizure activity stimulates alterations in neuronal gene expression which could lead to changes in levels of excitability and, hence, to changes in the susceptibility for further seizures. Here we describe the influence of limbic seizures upon the expression of nerve growth factor (NGF), 2 related neurotrophic factors, brain derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3), and several neuropeptides (enkephalin, dynorphin, and neuropeptide Y) in the rat forebrain. Using 35S-labeled riboprobes and in situ hybridization methods, the effects of recurrent limbic seizures and of individual hippocampal paroxysmal discharges have been evaluated. Recurrent seizures are found to increase levels of mRNAs for NGF and BDNF and to decrease levels of mRNA for NT3 within select hippocampal neurons. Temporally distinct increases in the expression of mRNAs for NGF and BDNF are also observed across broad fields of neocortex, paleocortex (entorhinal, piriform, and cingulate cortices), and the amygdala. As little as one 20-sec paroxysmal discharge is sufficient to stimulate large changes in neurotrophic factor mRNA content of hippocampal neurons. The time courses and cellular specificities of these alterations in neurotrophic factor expression are discussed and contrasted with seizure-induced changes in neuropeptide expression. Mechanisms by which seizure-induced increases in hippocampal neuropeptide and neurotrophic factor synthesis could lead to both short- and long-term changes in regional excitability, and thereby could contribute to susceptibility for further seizure activity, are considered.
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PMID:Seizures and the regulation of neurotrophic factor and neuropeptide gene expression in brain. 181 5

We present our surgical experience with second operations in 15 patients with recurrent intractable partial seizures after resection for epilepsy. The interval from the first operation until the first recurrence of seizures ranged from 1 day to 7 months (mean, 62 days). The interval between the first and second operations ranged from 3 months to 12 years (mean, 38 months). Detailed video-electroencephalographic interictal and ictal recording was performed in all patients (invasive electrodes were used in 11 patients). Ictal onset was shown to be remote from the zone of previous resection in 3 of 15 cases (all 3 extratemporal and in the ipsilateral hemisphere). Recurrent seizures arose from the area of previous extratemporal resection in 2 of 15 patients, and from the area of previous temporal resection in 10 of 15 patients. Both cases of extratemporal recurrences and 3 of the 10 cases of temporal lobe recurrences in the area of previous resection were associated with residual unresected structural lesion. Of the 10 patients with local temporal recurrence, 6 had proven epileptogenicity in the residual mesial structures, and 4 had residual epileptogenicity in the unresected lateral temporal lobe. The patients have been monitored for 8 to 82 months (mean, 18 months) after the second operation: 7 patients (47%) have remained seizure-free and another 5 (33%) have achieved a reduction in seizure frequency of more than 90%. There was no mortality or significant morbidity in this series. We conclude that the extent and distribution of residual epileptogenicity after failed epilepsy surgery are highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Second operation after the failure of previous resection for epilepsy. 203 44

During a scheduled visit to the school physician, the number of children with a history of febrile seizures was determined in 3570 children attending primary schools in the suburban area of the city of Rotterdam. At the age of 6 years, 140 had experienced at least one febrile seizure (3.9%, 95% confidence interval 3.3% to 4.5%). Of these, 19 (14%) had experienced a recurrent seizure during the same febrile illness. Recurrent seizures in subsequent fever episodes occurred in 26%. The median age at onset was 18 months. One-third of the children had visited the hospital directly after the seizure, and 6% had used anticonvulsant drugs for at least 6 months. Of all the children, 5.4% had a positive first-degree family history of febrile seizures. Children with a positive family history were at a 4.5-fold increased risk of experiencing febrile seizures. Since in this study a generally accepted definition of febrile seizures was used, the estimated prevalence in Dutch school-children may well be compared with prevalence rates found in the United States and Great Britain.
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PMID:Prevalence of febrile seizures in Dutch schoolchildren. 205 80

Recent studies have demonstrated that the regulation of neuropeptide expression in forebrain neurons is responsive to external influences including changes in physiological activity. This has been demonstrated most clearly in studies of hippocampus where the synthesis and resting levels of several neuropeptides, localized within well-characterized components of hippocampal circuitry, have been shown to be selectively influenced by seizure activity. In studies described here, we examined the influence of recurrent limbic seizures on the expression of enkephalin, dynorphin, cholecystokinin, and neuropeptide Y (NPY) in rat and mouse hippocampus using immunohistochemical, in situ hybridization and blot hybridization techniques. The data demonstrate that seizures differentially influence the expression of each peptide as a part of a broader cascade of changes in genomic expression within individual hippocampal neurons. In particular, seizures increase preproenkephalin mRNA and enkephalin peptide but decrease dynorphin peptide in the dentate gyrus granule cell/mossy fiber system. Seizure-induced decreases in the concentration of preprodynorphin mRNA in the granule cells have been reported by others. Immunoreactivity for CCK, which is codistributed with the opioid peptides in the mossy fiber system of mouse, is also dramatically reduced in the granule cell axons by seizure. Recurrent seizures induce two temporally distinct changes in NPY expression in hippocampus. First, there is an increase in hybridization to preproNPY mRNA within scattered, probable local circuit neurons in all subfields. This is followed by the seemingly novel appearance of preproNPY mRNA within the dentate gyrus granule cells and pyramidal cells of field CA1. Clues about mechanisms of neuropeptide regulation have come from observations of other, more rapid, transcriptional events induced by seizure. Most notably, our results and those of others demonstrate that seizures increase the expression of messenger RNAs from immediate-early genes (c-fos, c-jun, and NGFI-A) which encode proteins that may mediate neuropeptide gene regulation. In addition, mRNA for nerve growth factor is dramatically increased in the dentate gyrus granule cells by seizure; increased production of this trophic factor might mediate the more delayed changes in genomic expression and growth responses observed to occur in hippocampus and other forebrain areas following seizure activity.
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PMID:Seizures, neuropeptide regulation, and mRNA expression in the hippocampus. 220 4

Recurrent seizures are a significant cause of childhood morbidity. Often the underlying pathogenesis is unknown. Studies from several laboratories have suggested a relationship between perturbations of humoral immunity and clinical epilepsy. Brain-specific antigens have been observed in the systemic circulation after brain injury. This can be followed by the appearance of antibodies to neuronal tissues in both serum and cerebrospinal fluid. Moreover, there appears to be disproportionate representation of persons with coexisting humoral immune deficiencies among patients with chronic epilepsy. Interestingly, a potent immunosuppressant, adrenocorticotropic hormone, has long been the principal treatment for infantile spasms. Given this body of information associating humoral immunity with recurrent seizures, several investigators have recently attempted to treat intractable childhood epilepsy with high-dose intravenous immune globulin. Although the number of patients treated is small and it is not possible to make comparisons between individual studies, nevertheless the results have been encouraging. Five patients with intractable seizures who failed to respond to conventional therapy were treated with an outpatient regimen of intravenous immune globulin (1 gm/kg/day) for 2 days. Two patients showed significant clinical improvement while a third had an equivocal response. Immunologic analysis of these patients before therapy revealed a surprisingly high incidence of immune abnormalities. We conclude that intravenous immune globulin may be useful in the treatment of selected patients with chronic epilepsy unresponsive to anticonvulsants.
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PMID:Use of intravenous immune globulin in the treatment of seizure disorders. 279 1

1. A method was developed to quantify paired-pulse depression of population spikes in the CA1 region of the hippocampus of urethane-anesthetized rats with paired stimuli to the contralateral CA3 region at various states of excitability of pyramidal cells. This method was applied to measure changes following recurrent seizures, a single seizure, or long-term potentiation (LTP). 2. In naive animals paired-pulse depression was highly variable at low stimulus intensities, but constant above a certain "threshold" stimulus intensity. The potency of paired-pulse depression also depended on the time between paired stimuli, being maximal at an interpulse interval of 20 ms. The general relationships of paired-pulse depression to stimulus intensity and to interpulse interval were unaltered after LTP, after a single seizure, and after recurrent seizures, but there were quantitative changes in the last two cases. 3. A variety of pharmacologic agents known to interact with GABAergic inhibition were studied for their effect on paired-pulse depression. These agents affected earlier phases of paired-pulse depression (interpulse intervals less than or equal to 100 ms). The GABA agonist muscimol and the benzodiazepine diazepam enhanced paired-pulse depression whereas the GABA antagonist bicuculline decreased it. 4. Repeated seizures elicited by trains (50-Hz, 10-s durations every 5 min) of electrical stimuli to the hippocampus were associated with progressive lengthening of afterdischarges. 5. Recurrent seizures caused a statistically significant reduction in the potency of earlier phases of paired-pulse depression. There was an increase in the potency of later phases of paired-pulse depression after recurrent seizures, but this was not statistically significant. These changes were present for at least 2 h after the last seizure. 6. An antidromic-orthdromic paired-pulse protocol was used to exclude slow conductance changes as the cause of paired-pulse depression. Paired-pulse depression measured with this method was also decreased by recurrent seizures. 7. A single seizure caused a small reduction in paired-pulse depression that dissipated in less than an hour. 8. A single seizure caused LTP of stimulus intensity versus population spike curves whereas recurrent seizures attenuated or even reversed the potentiation, leading to a rightward shift of the curves relative to control curves. When LTP was produced by a less intense stimulus train (50-Hz, 400-ms duration), there were no associated seizures nor was there any change in paired-pulse depression.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evidence that repetitive seizures in the hippocampus cause a lasting reduction of GABAergic inhibition. 291 63


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