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 retrospective study was carried out on 261 patients with various epilepsies who had undergone convulsive status epilepticus prior to the subsequent onset of epileptic seizures. 1. Convulsive status epilepticus was found more in partial epilepsy and secondary generalized epilepsy at about the same rate, and evidently less in primary generalized epilepsy. On the average, three-fourths commenced their convulsive disorders with initial status epilepticus. 2. There were free intervals of years following initial status and preceding subsequent epilepsy. The interval was evidently shorter, less than two years, in a majority of patients with secondary generalized epilepsy, whereas the interval was mostly longer, more than six years, in patients with partial epilepsy. 3. The permanent deficient sequelae resulting from initial status were most closely associated with secondary generalized epilepsy. This was also exemplified by the higher rate of atrophic change on CCT. On the contrary, such permanent sequelae were less marked in partial epilepsy especially of complex seizure. 4. It was concluded that secondary generalized epilepsy resulted in cases with more severe brain damage within a relatively shorter interval, whereas complex partial seizure resulted from less severe damage with an obviously longer interval following convulsive status epilepticus.
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PMID:Status epilepticus in childhood: a retrospective study of initial convulsive status and subsequent epilepsies. 52 Sep 50

We previously described a model of spontaneous "sleep epilepsy" in kindled kittens with temporal lobe epilepsy (TLE). We now describe the postkindling course of this model from preadolescence to maturity and suggest pathophysiologic mechanisms. Spontaneous epilepsy, particularly generalized tonic-clonic convulsions (GTCs), developed 1h to 4 months after amygdala kindling and persisted to adulthood. At first, GTCs were detected only in sleep; later, convulsions also occurred during wakefulness. Two factors were consistently associated with the sequential onset of sleep and waking GTCs: seizure clusters and anatomic seizure localization. (1) Seizure clusters. Cats with infrequent or unclustered GTCs continued to exhibit "sleep epilepsy," defined by convulsions occurring exclusively during sleep. In contrast, cats with frequent seizure clusters developed recurrent or terminal convulsive status in conjunction with GTCs during waking and sleep. Severe seizure manifestations therefore appeared to contribute to the dissociation of convulsions from the sleep-wake cycle. (2) Anatomical seizure localization. Focal seizure origin appeared to differentiate sleep from waking GTCs. Onset during sleep was first recorded in the kindled amygdala, whereas onset during waking was initially detected outside the temporal lobe. Findings thus suggest secondary "kindling" of multifocal epilepsy. Secondary epileptogenesis is consistent with "transsynaptic" kindling effects. This phenomenon is defined in mature animals by rapid secondary site kindling (transfer) and subtle morphologic changes distal to the stimulating electrode. Transfer may be accentuated by youth, because kittens developed spontaneous seizure foci in previously unstimulated tissue. Moreover, multifocal interactions and diffuse cell loss were implicated as possible mechanisms. Collectively, the findings indicate complications with early onset TLE in kindled cats. Onset during youth can have an unfavorable prognosis, reflected by recurrent status epilepticus and multifocal epilepsy with convulsions distributed throughout the sleep-wake cycle.
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PMID:Ontogeny of feline temporal lobe epilepsy, II: Stability of spontaneous sleep epilepsy in amygdala-kindled kittens. 139 18

While working as a physician in Tanzania in the early 1960s, Dr. Louise Jilek-Aall founded an outpatient clinic for epilepsy among the Pogoro people of Mahenge mountains where epilepsy (locally termed Kifafa) had brought misery and death to an unusually high percentage of the population. With local assistance and overseas donations of phenobarbital (PB), this clinic treated approximately 200 patients for less than or equal to 10 years. The area was revisited 30 years later to trace these patients. Of the 164 patients who had started treatment, 86 (52.4%) achieved complete seizure suppression, 59 (36.0%) experienced reduction in seizure frequency, 13 (7.9%) experienced no change, and in 1 (0.6%) seizures were worse. The effect of treatment could not be assessed in 5 (3.0%) patients. After 30 years, only 36 (21.9%) of the 164 patients were known to be alive. Of the patients, 110 (67.1%) had died, and the whereabouts of 18 (11%) could not be traced. The causes of death were epilepsy related (status epilepticus, drowning, burns, dying in or after a seizure) in greater than 50% of the patients. Epilepsy-related deaths were proportionately higher after drug supply was stopped and among patients who were receiving drugs irregularly or who had only partial seizure control. Patients with epilepsy showed an increased mortality rate, which was twice that of the general rural Tanzanian population of similar age. Management of epilepsy in rural Africans should also emphasize methods to prevent epilepsy-related causes of death among patients with epilepsy.
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PMID:Prognosis of epilepsy in a rural African community: a 30-year follow-up of 164 patients in an outpatient clinic in rural Tanzania. 162 78

In order to test the GABA hypothesis of kindling, GABA-complex antagonists were administered in a dose-response paradigm to rats that had been implanted with indwelling forebrain electrodes, but not kindled. Focal seizures were then elicited from either the cortex or the amygdala to see whether kindling-like secondary generalization would occur. Norharmane, a benzodiazepine inverse agonist, failed to promote secondary generalization from either the cortex or the amygdala. Bicuculline, a GABAA receptor antagonist, and picrotoxin, a chloride ionophore antagonist, enhanced generalization from both sites and, in amygdala-implanted subjects, appeared to produce a significant acceleration of kindling as well. Aminophylline, an adenosine antagonist tested for purposes of comparison, also enhanced secondary generalization from both sites, and in amygdala-implanted subjects produced long electrographic discharges which sometimes developed into status epilepticus.
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PMID:Secondary generalization in non-kindled rats following acute administration of GABA-complex and adenosine antagonists. 169 79

Epilepsy is the commonest manifestation of neurocysticercosis. Epilepsy was observed in 127 of 150 cases (84.7%) of neurocysticercosis seen over a period of 17 years. The basis of diagnosis was clinical presentation and concomitant evidence of extraneural cysticercosis in the pre-computed tomography (CT) scan era, and typical CT findings in later years. Eighty one cases (54%) who primarily presented as epilepsy without any neurological deficit have been analysed in detail. In the pre-CT period the occurrence of epilepsy as a presenting feature in neurocysticercosis was 43.5% whereas in later years it was 61.4%. Primary generalised seizure (49 cases) was more common than partial seizure (29) and partial complex seizure (3). Status epilepticus was seen in 6 cases. Magnetic resonance imaging, done in 8 cases, proved to be more sensitive in demonstrating various stages in the development of noncalcified cysticercosis. The new larvicidal drugs offer a potential cure and cysticercosis should be entertained as a cause of epilepsy especially in endemic areas.
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PMID:Epilepsy as a manifestation of neurocysticercosis. 162 33

Among 630 patients with human immunodeficiency virus infection, 70 patients with new-onset seizures were studied. Generalized seizures occurred in 66 patients (94%): they occurred as the initial seizure in 56 patients (80%) and during follow-up in another 10 patients (14%). Partial seizures (18 patients), status epilepticus (10 patients), and recurrent seizures (38 patients) were also noted. Identified processes included cerebral toxoplasmosis in 11 patients, cerebral lymphoma in 8, metabolic derangement in 8, cryptococcal meningitis in 7, and vascular infarction in 4. In 32 patients (46%) seizures were not associated with identifiable brain lesions and were believed to result from human immunodeficiency virus cerebral infection. Phenytoin treatment was associated with adverse drug reactions in 16 of 62 patients who received it. Our results suggest that the majority of patients with human immunodeficiency virus and seizures do not have secondary focal brain lesions as the cause of the seizures and that human immunodeficiency virus infection alone can, and often does, cause seizures.
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PMID:Seizures in human immunodeficiency virus infection. 234 90

We reviewed retrospectively a series of 100 inpatients with onset of epileptic seizure after the age of 60. All of them were investigated by EEG and 96 by CT scan. The most frequent cause of seizure was previous stroke, with 25 cerebral infarcts and 5 hemorrhages. Neoplastic lesions were present in 18 cases, with glioma (high grade), meningioma and metastases in the same proportion. Other etiologies included toxico-metabolic (18 cases), post-traumatic (9 cases), cerebral atrophy (4 cases) and miscellaneous (14 cases). The causes of seizure remained unknown in 7 patients, of whom 6 had focal signs in either clinical examination or EEG. Focal seizures (with or without secondary generalization) accounted for 65% of all cases and generalized seizures for 35%. The EEG was normal in 12 patients and abnormal in 88, with diffuse slowing in 55 patients and focal signs in 70 (some patients had both diffuse slowing and focal signs). Fourteen patients presented status epilepticus. Ten died during hospitalization. We conclude that epileptic seizure with onset after age 60 is nearly always symptomatic, and neuroradiologic investigations are necessary in the search for cerebral lesions. In our study, the prevalence of "idiopathic epilepsy" is lower than previously described.
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PMID:[Initial epileptic crisis after the age of 60: etiology, clinical aspects and EEG]. 234 61

Complex partial status epilepticus (CPSE) has rarely been reported in children. We experienced a 5-year-old girl having had an abrupt onset of complex partial seizure with a fluctuating state of consciousness and aphasia. Electroencephalogram revealed repetitive epileptiform discharges originating from bilateral temporal and parieto-occipital regions over the background of diffuse continuous slow activity. Computerized tomography of the brain showed mild atrophy without focal lesions. All the other studies including bacteriology, virology, toxicology and metabolic screening were unremarkable. Intravenous administration of diazepam was ineffective for recovery of consciousness level and cease of seizure activity. A lasting control of the status was not achieved until intravenous phenytoin and oral carbamazepine were added for one more weeks. Paroxysmal attacks of periodic apnea with subsequent hyperpneic movements occurred the fourth month after the onset of illness. She regained language on rehabilitation program. Unfortunately, the patient had recurrence four months later despite medication. Finally, she died of aspiration pneumonia and status epilepticus eleven months after the onset of the disease. Compared with the other previously documented cases of prolonged complex partial status epilepticus, this case is notable for its unusual, complicated and severe symptomatology and long duration (three more months) with poor prognosis.
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PMID:Complex partial status epilepticus: report of one case. 263 6

Three patients developed prominent neurologic symptoms and signs associated with Schoenlein-Henoch purpura. A 7 1/2-year-old boy was seen with status epilepticus after a 2-week history of generalized headaches, irritability, and intermittent colicky abdominal pain. A left hemiparesis and a left homonymous hemianopia with a right gaze preference that were present on initial examinations gradually resolved, but a mild left arm paresis persisted. Cutaneous, renal, and joint involvement followed initial CNS manifestations. The second patient, a 7-year-old girl, had a complex partial seizure with secondary generalization and a postictal hemiparesis seven days after presentation with classic signs of Schoenlein-Henoch purpura. Behavioral changes were noted during the acute phase of the illness. The third patient, a 13-year-old boy, developed signs of a left brachial plexopathy and transient weakness of his right leg during a complicated course of Schoenlein-Henoch purpura. Review of the world literature indicates that headaches and mental status changes are the most frequent neurologic complications of Schoenlein-Henoch purpura, followed by seizures, focal neurologic deficits, mononeuropathies, and polyradiculoneuropathies. The vasculitis of Schoenlein-Henoch purpura can involve the nervous system and may add significantly to the morbidity of the illness.
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PMID:Neurologic manifestations of Schoenlein-Henoch purpura: report of three cases and review of the literature. 298 37

202 cases of children with shunted hydrocephalus of congenital or acquired origin were studied and the incidence of seizure disorder was found to be 39%. However in only 17% of cases was the seizure disorder found to be persistent. Focal seizures were rarer than expected. If focal seizures were present they did not appear to be related to shunt site. 9.4% of children suffered an episode of status epilepticus. A large number of incidents of seizures could be shown to have a specific precipitant, usually CSF infection or shunt related problems. No aspect of birth history or development or treatment of the hydrocephalus was related to the occurrence or seizure disorder or type of fit experienced. Children with persistent seizure disorder were found to be more likely to be of low IQ, physically handicapped and at Special School.
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PMID:The incidence of seizure disorder in children with acquired and congenital hydrocephalus. 381 21


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