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)

Two hundred and thirty-seven children have died who were seen in the Division of Neurology, Kanagawa Children's Medical Center from 1975 to 1989. They corresponded to about 11% of the total death in the hospital. A total of 128 cases of 237 deaths (54.0%) were suffering from epilepsies, most of whom were also complicated with other CNS disorders. The causes of death were pneumonia, respiratory failure and suffocation in 60%, whereas status epilepticus or convulsions only in 14%. About 40% of victims died at home or in an emergency room without effective resuscitation. Mortality was considered high in infantile spasms (16 out of 146, 11%) and in severe myoclonic epilepsy in infancy (4 out of 8, 50%). It was note worthy that 3 cases of severe myoclonic epilepsy in infancy died of status epilepticus and 2 died at home. Sixteen cases whose chief problems were partial epilepsies and severe myoclonic epilepsy in infancy, died of status epilepticus in 10 cases, convulsions after tonsillectomy, etc. Causes of death of these 16 cases were related to convulsions except in two cases whose causes were pneumonia in one and unknown in the other. About a half of them (7 cases) died at home. Adequate managements appeared necessary to prevent accidental deaths of children with epilepsies.
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PMID:[Mortality patterns of children with epilepsies in a children's medical center]. 187 50

We report six single-lung transplantations in emphysematous patients with end-stage disease. Compression of the graft or ventilation/perfusion imbalance were not observed. Rejection episodes were generally documented through transbronchial biopsies and the radiological changes related to acute infections or rejections were restricted to the transplanted lung. Three patients died from CMV pneumonia, status epilepticus and fibrosis of the graft following bronchography, respectively. The three remaining patients are well, with documented improvement of pulmonary function tests and arterial blood gases. Bronchial complications were observed in all patients and have in some cases required dilatation or insertion of a stent. Although requiring a longer follow up, single transplantation is feasible and beneficial in patients with end-stage emphysema.
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PMID:Single-lung transplantation in emphysematous patients. 211 18

Immediately after induction therapy for acute lymphoblastic leukemia, a 2 1/2-year-old child developed invasive pulmonary aspergillosis revealed by pneumothorax, an unusual manifestation. Despite treatment with amphotericin B, status epilepticus occurred; this manifestation was related to diffuse ischemic cerebral lesions probably caused by cerebral aspergillosis. Outcome was fatal. Early invasive pulmonary aspergillosis is responsible for non-specific pneumonia. Thoracic CT scan and fiberoptic bronchoscopy are informative investigations. At recovery of bone marrow aplasia, the occurrence of hemoptysis and the discovery of excavated lesions on roentgenograms are suggestive of the diagnosis. Cerebral aspergillosis should be routinely considered whenever neurologic symptoms develop in a patient with agranulocytosis, fever, and pneumonia. The prognosis of invasive aspergillosis depends above all on the promptness of treatment; amphotericin B should be given intravenously whenever broad spectrum antimicrobial therapy fails to induce apyrexia in a patient with agranulocytosis.
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PMID:[Fatal cerebral and pulmonary aspergillosis in acute leukemia in a child]. 226 96

A case of a young man who was a victim of strangulation is presented. He arrived at the hospital in refractory status epilepticus, controlled only with intravenous pentobarbital. The initial CT scan showed mild cortical edema. Two days later, a CT scan showed diffuse cortical swelling and bilateral basal ganglia infarcts. Upon discontinuation of pentobarbital therapy, his neurological examination revealed spontaneous ventilation and a gag reflex. A CT scan 4 weeks after the insult demonstrated hypodensities in both cerebral hemispheres and hydrocephalus. EEG was isoelectric throughout his hospitalization. He survived nearly 5 months and succumbed to pneumonia. Neuropathological examination demonstrated severe encephalomalacia, multiple cystic infarcts and generalized compensatory ventriculomegaly. Microscopic examination was particularly remarkable for a pronounced gemistocytic astrocyte proliferation in the white matter. This case illustrates the long-term neuropathological consequences of severe, global hypoxia/ischemia and the paucity of intact brain required to maintain a persistent vegetative state.
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PMID:Late neuropathological consequences of strangulation. 282 56

I have described an adult patient who had dissecting retropharyngeal abscess complicated by pneumonia, mediastinitis, pericarditis, sepsis, and status epilepticus.
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PMID:Dissecting retropharyngeal abscess due to Fusobacterium necrophorum in an adult. 398 69

At a follow-up study of 385 patients with epilepsy beginning under age 15, 22 (5.7%) had died during the first 10 years after the onset of epilepsy and another 11 (2.9%) between 11 and 24 years. Mortality was significantly high in cases with the following clinical features: (1) epilepsy with onset before the first birthday (mortality being 25.5%), (2) symptomatic epilepsy in etiology (17.2%), (3) infantile spasms (40.7%), tonic epilepsy (33.3%) or myoclonic epilepsy (33.3%) as compared with grand mal (5.9%) in seizure type and (4) developmental retardation at the first visit (25.5%). Seizures were not controlled in 31 out of 33 patients at the time of death. The causes of death were status epilepticus or convulsion in 10, pneumonia in 5, severe emaciation in 3, "cerebral palsy" in 5, and drowning, suffocation, traffic accidents or acute lymphocytic leukemia, in one each, and unknown in 6. Most of the patients died at home.
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PMID:Mortality and clinical features in cases of death among epileptic children. 713 11

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

Clinical characteristics of clonazepam (CZP) discontinuation seizures were clarified from 17 patients who developed seizure exacerbation after rapid discontinuation, including abrupt discontinuation, reduction, or replacement with nitrazepam (NZP). Safe discontinuation rates of CZP were estimated by comparing these patients with 23 patients without CZP discontinuation seizures. The seizures consisted of status epilepticus or frequent attacks of generalized tonic-clonic seizures (GTC) or non-GTC, and the first attack of GTC. Incidence did not differ significantly between CZP-effective cases and CZP-ineffective cases at discontinuation. The reasons for abrupt discontinuation included adverse effects, insufficient efficacy, difficulty in taking CZP owing to pneumonia, or carelessness of the doctors or the families. Seizure exacerbation occurred 1-6 days after CZP discontinuation. Most of the problems improved with readministration of the original or smaller dosages of CZP or of NZP in an amount threefold or more greater than the original CZP dose. Safe discontinuation rates were estimated to be < or = 0.04 mg/kg for abrupt discontinuation, < or = 0.04 mg/kg/week for reduction, and replacement with NZP of 2.5 or more times the original amount of CZP. These safe discontinuation rates were prospectively confirmed by 84 cases of CZP discontinuation in 54 other patients, and no seizure exacerbation occurred with these discontinuation rates.
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PMID:Seizures with clonazepam: discontinuation and suggestions for safe discontinuation rates in children. 824 61

Three children with refractory status epilepticus, unresponsive to intravenous administration of diazepam, phenytoin, and lidocaine, received pentobarbital therapy and were monitored by electroencephalography (EEG). They required mechanical ventilation and vasopressor therapy. Intravenous pentobarbital therapy was successful and without distinct sequelae in all 3 patients, and could be incrementally discontinued without breakthrough seizures after 12-65 hours of a burst-suppression or complete suppression pattern on EEG. Obtaining a suppression pattern was important for controlling status epilepticus in children as well as adults. We suggest that 12 hours after a burst-suppression pattern is obtained, tapering of pentobarbital should be attempted to avoid serious complications of extended pentobarbital anesthesia (e.g., respiratory depression, hypotension, pneumonia).
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PMID:Pentobarbital therapy for status epilepticus in children: timing of tapering. 853 84

A 21-year-old man presented with fever, rash, seizure, stiff neck and rapidly progressive bilateral pulmonary infiltrates. Cerebrospinal fluid (CSF) study revealed pleocytosis with predominant polymorphonuclear cells, and hypo-glycorrhachia. Status epilepticus occurred, followed by acute respiratory distress syndrome with respiratory failure. Blood and CSF cultures for bacteria were negative, but an indirect immunofluorescence assay revealed a fourfold rise in antibody to Rickettsia tsutsugamushi in paired serum and a 1:2560 (+) IgM antibody titer. Severe scrub typhus with meningoencephalitis and extensive pneumonitis was diagnosed. The patient survived after intravenous minocycline therapy and intensive care, including aggressive seizure control, supportive mechanical ventilation and avoidance of fluid overloading. He had a nearly complete recovery. Practicing physicians in Taiwan should be aware of this reportable disease and its potentially serious complications if not promptly diagnosed and treated.
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PMID:Life-threatening scrub typhus with meningoencephalitis and acute respiratory distress syndrome. 908 Jul 62


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