Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 16-year-old patient who had a history of complex partial seizures, had frequent episodes of status epilepticus with diffuse slow-wave discharges. The clinical manifestations were apparently insignificant due to the fact that vigilance, orientation and behaviour were unimpaired. Neuropsychological investigations showed that the cognitive processes were selectively impaired during such episodes. The electroclinical pattern was interrupted by break-off of contact concomitant with high-frequency spike discharges. Cognitive impairment is believed to represent the specific feature peculiar to this type of status epilepticus.
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PMID:Status epilepticus with cognitive symptomatology in a patient with partial complex epilepsy. 727 12

Status epilepticus (SE) is a condition wherein epileptic seizure discharges are sufficiently prolonged or repetitive so as to produce persistent alterations in neurologic function and in the underlying physiologic and neurochemical activities of the brain. Thus, the definition of SE now includes any disorder in which there is sustained and prolonged excitation of neurons. Electroencephalographic (EEG) patterns associated with specific types of SE are important components in their classification. Like epileptic seizures, SE can be divided into partial onset SE and primarily generalized SE. Partial onset SE includes secondarily generalized convulsive SE (GCSE), complex partial SE (CPSE), simple partial SE (SPSE), and the syndromes of epilepsia partialis continua (EPC) and rolandic SE (RSE). Primarily generalized SE includes primarily GCSE, absence SE, atypical absence SE, generalized myoclonic SE, generalized clonic SE, generalized tonic SE, atonic SE, and the syndromes of electrical SE of sleep (ESES) and minor epileptic SE of Brett. SE is a dynamic disorder. Behavioral and electrical manifestations change over time if seizure activity is allowed to persist without successful treatment A progression from overt to subtle convulsive activity occurs in secondarily GCSE and there is also a progression of predictable EEG changes in prolonged GCSE. CPSE begins as discrete complex partial seizures but also progresses behaviorally and electrically through a sequence similar to that observed in GCSE. Progressive behavioral and electrical changes have not been reported in primarily generalized forms of SE. EEG is an important tool for verifying successful treatment of SE if the patient does not immediately recover neurologic function. EEG recordings also contribute substantially to understanding the mechanisms of, and development of better treatments for, human SE through their use in the study of experimental SE in the laboratory.
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PMID:Electroclinical features of status epilepticus. 756 22

The systemic administration of a potent muscarinic agonist pilocarpine in rats promotes sequential behavioural and electrographic changes that can be divided in three distinct periods: (a) an acute period that built up progressively into a limbic status epilepticus and that lasts 24 h, (b) a silent period with a progressive normalization of EEG and behaviour which varies from 4 to 44 days, and (c) a chronic period with spontaneous recurrent seizures (SRSs). The main features of the SRSs observed during the long-term period resemble those of human complex partial seizures and recurs 2-3 times per week per animal. Therefore, this novel and unique experimental approach may serve as a model of epilepsy mimicking the human condition.
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PMID:The pilocarpine model of epilepsy. 764 49

Pilocarpine (PILO) induces in rats limbic seizures that become secondarily generalized and evolve to status epilepticus (SE). Spontaneous recurrent seizures are registered during the long-term period following the systemic administration of PILO in rats. EEG, behavioral, and pathological features resemble those of complex partial seizures. The antiepileptic drugs (AEDs) diazepam, phenobarbital (PB), valproic acid (VPA) and trimethadione protect against PILO-induced SE while phenytoin (PHT) and carbamazepine (CBZ) are ineffective. Studies with AEDs on spontaneous seizures (chronic period) of this model have not yet been established. We now report the effects of different AEDs on spontaneous seizures. Male Wistar rats were subjected to PILO-induced SE. Following recovery from SE animals were daily observed in order to detect spontaneous seizures and to establish the baseline seizure frequency. PB 40 mg/kg, PHT 100 mg/kg, CBZ 120 mg/kg, VPA (450 mg/kg and 600 mg/kg) and ethosuximide (ETX) 400 mg/kg were given daily to epileptic rats for two weeks during the spontaneous recurrent seizures period. PB, CBZ and PHT were effective against spontaneous seizures. VPA was also effective against spontaneous seizures at the dose of 600 mg/kg and ETX was inactive against these seizures. Such pharmacological profiles correlate well with complex partial seizures. The results indicate that spontaneous recurrent seizures after PILO-induced SE may be a useful model for finding new AEDs with better efficacy against complex partial seizures. The use of animal models that share both pharmacological and phenomenological features with human epilepsy might improve their predictive value for specific types of human epilepsy.
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PMID:Effects of conventional antiepileptic drugs in a model of spontaneous recurrent seizures in rats. 775 May 14

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46

MB suffered an episode of status epilepticus of febrile origin at the age of 20 months. This was followed at two years by complex partial seizures of temporal lobe origin and at eight years he had learning difficulties arising from the dominant hemisphere. Subsequent symptoms included auditory, visual and olfactory hallucinations which were not controlled by antipsychotics or antiepileptics. EEG and MRI were unhelpful and alternating diagnoses of schizophrenia and temporal lobe epilepsy were made. Now aged 17 years, he has a diagnosis of schizophreniform psychosis with temporal lobe abnormality from status epilepticus in childhood, and is managed by an adult psychiatrist. His symptoms persist.
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PMID:Psychosis or epilepsy--a diagnostic and management quandary. 789 50

Non-convulsive status epilepticus (NCS) is rarely encountered and may appear with a psychiatric mask. As clouding of consciousness is the major ictal manifestation, the condition may easily be overlooked in the mentally retarded. We have studied 11 mentally retarded patients with NCS. Since NCS with a focal onset may have a generalized ictal EEG pattern, a classification of NCS solely based on the seizure classification may be misleading. In some patients, it is impossible, both clinically and on the basis of EEG recordings, to distinguish between continuous complex partial seizures and atypical absences. We therefore propose a revised classification of NCS based on the ictal EEG pattern and the epilepsy syndrome diagnosis (I) NCS in generalized epilepsy syndromes, (II) NCS in localization-related epilepsy, (a) with localized EEG features, (b) with generalized EEG features, and (c) with transitional EEG features, and (III) undetermined NCS. Four of our patients were classified as Group I, two as Group IIa, one as Group IIb, one as Group IIc, and three as Group III. Benzodiazepines at small or standard doses may be ineffective in terminating NCS, particularly in the Lennox-Gastaut Syndrome. The identification of trigger factors is essential. Drugs seemed to be the most important precipitants in our patients; in three, NCS was induced by recurrent rectal diazepam over-administration. This complication of rectal diazepam treatment in epilepsy has not been addressed previously.
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PMID:Non-convulsive status epilepticus in the adult mentally retarded. Classification and role of benzodiazepines. 790 89

Acute catatonic syndrome is a condition that can be caused by a variety of metabolic, neurological, psychiatric, and toxic conditions, including neuroleptic malignant syndrome. Although ictal catatonia as a manifestation of non-convulsive status epilepticus has been described, reference to the occurrence of seizures in patients with acute catatonic syndrome is anecdotal. Twenty nine patients with acute catatonic syndrome were reviewed to identify patients with seizures after the onset of acute catatonic syndrome. Patients were divided into four diagnostic groups: affective (15), schizophrenic (eight), toxic (two), and organic (four). Seizures occurred in four patients (13.8%): two patients with dystonic seizures had viral encephalitis and schizophrenic disorder respectively; one patient with complex partial seizures had viral encephalitis and one patient with absence status had neuroleptic malignant syndrome. The results indicate the value of EEG in detection of epileptic activity in patients with acute catatonic syndrome, both at onset and in the course of such disturbance, particularly to provide a differential diagnosis between pseudo-seizures and neuroleptic-induced acute dystonia.
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PMID:Epileptic seizures in patients with acute catatonic syndrome. 796 25

A 32-month-old child presented in status epilepticus (SE) involving the left side of the body. Fast spin-echo magnetic resonance imaging (FSE-MRI) with hippocampal volumetry performed < or = 24 h after the seizure showed increased T2 signal of the right hippocampus, but no atrophy. Complex partial seizures (CPS) appeared at age 33 months, and three more episodes of SE occurred between 33 and 37 months of age. Follow-up FSE-MRI at 34 and at 45 months of age demonstrated progressive hippocampal atrophy with resolution of the increased T2 signal. Her CPS became intractable and, at age 51 months, she underwent right temporal lobectomy. In the ensuing 5 months, she has had only one major motor seizure. This case demonstrates that acute increased hippocampal T2 signal intensity can occur soon after SE and hippocampal sclerosis (HS) may become evident within months in the setting of recurrent early childhood SE. This observation may support the hypothesis that early childhood SE can lead to HS. Furthermore, this case suggests that years of temporal lobe CPS may not be necessary for development of HS.
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PMID:Magnetic resonance imaging evidence of hippocampal sclerosis in progression: a case report. 798 29

An apparent discrepancy exists between the remarkable language competence of the isolated right cerebral hemisphere in some split-brain patients and the lack of language competence in some aphasic patients in whom only the left cerebral hemisphere has been damaged. This has led to a revival of the idea that the dominant cerebral hemisphere inhibits the potential functioning of its partner. We tested this model of interhemispheric inhibition in four patients with unilateral limbic seizures (three left-sided, one right-sided). While seizure activity was monitored with bilaterally implanted stereotactic EEG depth electrodes or bilateral foramen ovale EEG electrodes, the patients were tested in lateralized hemisphere-specific tachistoscopic recognition experiments. In two patients performance was correlated with the electrical pattern during prolonged unilateral subclinical limbic status epilepticus, and in two patients performance and intracranial electrical activity were compared before, immediately after and during the recovery phase of left limbic complex partial seizures with postictal aphasia. Three main findings were obtained. (i) Focal unilateral limbic seizure activity in the depth interferes with cognitive functions, even when unnoticed clinically or undetectable on the surface EEG, provided that epileptiform EEG activity lasts for several seconds. (ii) This interference is specific to the cognitive functions associated with the 'dominant' processing of the discharging hemisphere. (iii) Seizure-induced impairment of the 'dominant' functions of the discharging hemisphere is associated with improvement of performance of the same function by the other hemisphere. Although each patient's clinical and experimental situation differed, the converging results support the hypothesis of hemispheric interaction based upon functional inhibition for verbal processing in patients with a left hemispheric focus. The reverse situation, namely facial processing in a single case with a right hemisphere focus, remains inconclusive.
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PMID:The dynamics of cerebral dominance during unilateral limbic seizures. 814 16


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