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

We report a girl 3 years and 6 months old with onset of aphasia at age 3 years and 3 months. There was no evidence of brain damage and there were no seizures. The neuropsychological evaluation showed that the girl tended to be right-handed, that aphasia was global and that other higher cortical functions seemed to be preserved. Isolated spikes and spikes-and-wave were recorded during wake over the right temporal region with rare independent contralateral abnormalities. During polysomnography (PSG), the physiological patterns of sleep were preserved and right temporal epileptiform discharges were significantly increased in all sleep stages. Maximal activation was obtained at sleep onset and during rapid eye movement (REM) sleep periods, when focal abnormalities became continuous and spread contralaterally. Repeat PSGs showed that the activation profile retained this particular trait, although subclinical discharges tended to increase during slow wave sleep (SWS). This pattern of subclinical temporal status epilepticus during REM sleep differs from the characteristic activation profile found in the syndrome of continuous spikes-and-waves during SWS. However, this profile was transient and all epileptiform changes disappeared during clinical recovery at 18 months of follow-up.
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PMID:Continuous focal spikes during REM sleep in a case of acquired aphasia (Landau-Kleffner syndrome). 128 Aug 54

The application of leucin-enkephalin solution (LEU) (2 micrograms/2 microliters) on stimulated region of sensomotor cortex did not influence threshold of direct and transcallosal cortex responses (DR and TCR). On coupling of repeated electrostimulation train (RET) (duration of impulse--0.1 ms; duration of train--10 s; frequency--10/s) with application of LEU (after every odd train) the changes of DR and TCR in course of even trains and latency of afterdischarge appearance were such as in control ones. Simultaneously LEU effectively depressed short posttetanic potentiation of DR and TCR and potentiation of amplitude and duration AD, evoked by RET. It is suggested that LEU released from neurons in the course of RET does not participate in initiation of seizure in sensomotor cortex. A possible role of LEU in sensomotor cortex is limitation of intensity and duration of seizures and prevention of status epilepticus.
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PMID:[The effect of leucine enkephalin on the development of a convulsive afterdischarge in the sensorimotor cortex of rats]. 128 80

Seventy-eight patients with post-stroke seizures were studied retrospectively to determine the clinical, EEG and CT features of these seizures and their prognosis. There were 57 cerebral infarctions and 21 hemorrhages. Twenty-eight (36%) initial seizures occurred within one month after the stroke (0-24 hours in 19 cases) and were classified as early-onset seizures. Fifty (64%) initial seizures occurred more than 3 months after the stroke (3-12 months in 33 cases) and were classified as late-onset seizures. Compared with a population of 1938 strokes admitted during the same period, the proportion of patients with alcohol abuse, infarction in the anterior cerebral artery territory, watershed infarcts and lobar haemorrhages was significantly greater in our series. The proportion did not vary with the nature of the stroke (infarction or hemorrhage), except for early onset seizures in which the proportion of hemorrhages was significantly greater. Nor did it vary with the cause of hemispheric infarctions (cardioembolism or atherothrombosis or others). Ninety-five percent of the lesions affected the cerebral cortex or the subcortical white matter or both. Of all 78 initial seizures, 64% were partial motor (simple or secondarily generalized); 32% were primarily generalized, and 4% were partial not motor; status epilepticus was seen in 14% of the cases. An initial EEG, performed in 76 patients was normal in 7. Among the remaining 69 patients EEG showed focal or diffuse slowing down in 63% and epileptic features in 37% (including 10 cases of PLEDs). Early post-seizure EEG and repeated recordings significantly increased the specificity of EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Epileptic crisis during and after cerebrovascular diseases. A clinical analysis of 78 cases]. 130 71

During a nine-month period we have treated 46 patients with status epilepticus with intravenous application of diazepam or midazolam. The initial doze od diazepam was 10 mg (rate: 2-5 mg/min) and of midazolam 15 mg (rate: 5 mg/min). Diazepam was effective in 26 and ineffective in 15 patients. Midazolam stopped status in 4 out of 7 patients. Both drugs were more effective when they were administered at the beginning of status. After the initial termination of status and recovering of consciousness, seizures returned in 10 patients (22%). In the group treated with diazepam, 4 patients had sudden apnea and 6 respiratory depression (totally 10 out of 41). In the group treated with midazolam, 3 had apnea and 2 respiratory depression (totally 5 out of 7). All patients with apnea or respiratory depression received higher doses of both drugs at the higher rates than the others. We conclude that the efficacy of the therapy is moderate while the frequency of serious complications is high. In status epilepticus, where the life of patient is in danger, drugs with such activity are of limited value.
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PMID:[Efficacy of therapy, recurrence of seizures and respiratory complications in the treatment of status epilepticus by intravenous administration of diazepam or midazolam]. 130 8

Understanding the molecular basis of altered neuronal excitability in epilepsy is a major challenge in neuroscience research. The present study suggests an inverse correlation between changes in neuronal excitability in status epilepticus and the activity of type II multifunctional calcium/calmodulin-dependent kinase II (CaM kinase II), a major Ca(2+)-signal transducing system in brain. 'Continuous' hippocampal stimulation (CHS), a new model of non-convulsive limbic status epilepticus (SE), mimics the progression of electrographic changes characteristic in human SE and allows for quantitation of post-stimulus seizure severity. In the present study, hippocampus and anterior neocortex from CHS-stimulated rats and paired surgical controls were assayed for CaM kinase II activity by incorporation of radiolabeled phosphate from [gamma-32P]ATP into the 50-kDa subunit of the kinase itself (autophosphorylation). In all instances, CHS induced sustained interictal bursting and/or electrographic seizures. Decreased CaM kinase II activity was seen in all preparations from electrically stimulated hippocampus. CaM kinase II activity in CHS animals was diminished by 37% relative to controls (P less than 0.01; Student's paired t-test). The progressive intensity of the EEG discharges correlated directly with the decrement of CaM kinase II activity (P less than 0.05; Spearman's rank correlation test, n = 5). This is the first report of a dynamic modulation of a biochemical system that has been implicated in neuronal excitability in coordination with the characterized developmental stages of SE.
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PMID:Loss of type II calcium/calmodulin-dependent kinase activity correlates with stages of development of electrographic seizures in status epilepticus in rat. 131 99

Lithium is known to potentiate the ability of pilocarpine to induce status epilepticus in rats. The goal of this study was to determine whether lithium could potentiate pilocarpine-induced seizures in developing animals. Behavioral, electroencephalographic (EEG), and histopathological changes induced by systemic administration of lithium (3 meq/kg) followed 20 h later by pilocarpine (3, 10, 30, 60 mg/kg) were studied in 3-30-day-old rats. Lithium followed by pilocarpine (30 and 60 mg/kg) induced hyperactivity, tremor, loss of postural control and scratching but no electrographic seizures in 3-8-day-old rats. In the 7-10-day-old animals pretreatment with lithium and pilocarpine 60 mg/kg induced status epilepticus with sustained myoclonus and continuous bilateral synchronous spike and sharp wave, but doses of pilocarpine lower than 60 mg/kg had no effect. The susceptibility to lithium-pilocarpine-induced status epilepticus increased markedly during the third postnatal week of life. During this time period, rats treated with lithium (3 meq/kg) plus pilocarpine 10 mg/kg exhibited behavioral and EEG manifestations of status epilepticus. The same combination of lithium and pilocarpine failed to induce status epilepticus either before or after the third week of life. Histopathological analysis of the brains of the animals used in these studies failed to demonstrate the widespread damage reported in adult rats that have undergone lithium-pilocarpine-induced status epilepticus.
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PMID:Ontogenic study of lithium-pilocarpine-induced status epilepticus in rats. 132 90

Several experiments were designed to evaluate a secondary humoral response following limbic seizures. After baseline antigen binding capacity (ABC) had been determined for the primary response, a second subcutaneous injection of the antigen (human serum albumin) was accompanied by an injection of either lithium (3 mEq/kg)-pilocarpine (30 mg/kg) or one of two comparator treatments: metrazol (30 mg/kg) or cyclophosphamide (50 mg/kg); other rats served as drug controls. Only the groups that received the lithium-pilocarpine (status epilepticus) or cyclophosphamide (no seizure) displayed significant immunosuppression after 5 but not 10 days. The results support the hypothesis that seizure activity within the amygdaloid-hippocampal complex modulates immunocompetence through corticotropin mechanisms.
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PMID:Transient suppression of a secondary humoral response in rats is evoked by lithium-pilocarpine-induced limbic seizures. 132 17

The influence of seizures on phosphoinositide hydrolysis and protein kinase C activity was measured in rat hippocampus and cerebral cortex, primarily using a model in which generalized convulsive status epilepticus was induced by administration of LiCl (3 mmole/kg) 20 hr prior to pilocarpine (30 mg/kg). A short (5 min) period of seizures reduced phosphoinositide hydrolysis in hippocampal slices stimulated by norepinephrine or ibotenate, but did not alter the responses to carbachol, 50 mM K+, or NaF. Induction of seizures with diisopropylfluorophosphate caused a similar reduction in the response to norepinephrine without altering carbachol-stimulated phosphoinositide hydrolysis. The inhibition of norepinephrine-stimulated phosphoinositide hydrolysis after seizures generated by lithium plus pilocarpine administration was apparently not due to inhibitory influences of quisqualate or activation of protein kinase C since both of these treatments caused similar inhibitions in slices from control and treated rats. Seizures induced by lithium plus pilocarpine or by kainate did not alter the activity of protein kinase C or the distribution of protein kinase C between membrane and cytosolic fractions. Thus, seizures cause a neurotransmitter-selective impairment of phosphoinositide hydrolysis, and this response may play a role in the severity or duration of seizure activity.
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PMID:Seizures selectively impair agonist-stimulated phosphoinositide hydrolysis without affecting protein kinase C activity in rat brain. 133 19

The pattern of hippocampal cell death has been studied following hippocampal seizure activity and status epilepticus induced by 110-min stimulation of the perforant pathway in awake rats. The order of vulnerability of principal cells in the different hippocampal subfields--as determined by silver impregnation--was found to be very similar to the pattern found in ischemia; i.e., dentate hilus greater than CA1, subiculum greater than CA3c greater than CA3a,b greater than dentate granule cells. The hilar somatostatin-containing cells were the most vulnerable cell type, whereas all other subpopulations of nonprincipal neurons--visualized by immunocytochemistry for the calcium binding proteins parvalbumin and calbindin--were remarkably resistant. Pyramidal cells in the CA3 region containing neither of the examined calcium binding proteins were more resistant to overexcitation than CA1 pyramidal cells, most of which do contain calbindin. This indicates that no simple relationship exists between vulnerability in status epilepticus and neuronal calcium binding protein content, and that local and/or systemic hypoxia during status epilepticus may be responsible for the ischemic pattern of cell death.
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PMID:Pattern of neuronal death in the rat hippocampus after status epilepticus. Relationship to calcium binding protein content and ischemic vulnerability. 134 49

The term "status epilepticus" was first coined in 1824 by Calmeil as this condition had such a poor prognosis. Although still commonly misused today, from the beginning this term actually included all kinds of epileptic seizures, since there are as many types of status epileptici as there are seizure types. Status epileptici are usually triggered by a combination of factors including sleep deprivation, alcohol withdrawal, failure to take medication regularly and fever. In status epilepticus epileptic seizures and EEG discharges initially appear to be no different from isolated seizures. The longer the status epilepticus continues, however, the more atypical the seizures and EEG discharges become. Usually status epilepticus ends gradually. Irreversible damage or fatalities may occur especially in infants or under certain conditions (e.g. long status duration, protracted interval between seizure onset and medical treatment and symptomatic etiology). In most cases benzodiazepines and diphenylhydantoine are the preferred drugs used for treatment.
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PMID:[Clinical symptoms and therapy of status epilepticus]. 135 Oct 28


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