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 26 year old man with no previous history of convulsions presented in status epilepticus and severe lactic acidosis. He regained consciousness and the acidosis resolved after several hours of conservative management without intravenous bicarbonate, but he developed severe myalgia associated with marked elevation of creatine kinase and moderate raised plasma creatinine levels which resolved spontaneously after 3 days. Severe lactic acidosis and rhabdomyolysis may accompany status epilepticus, although they appear to be self-limiting without important sequelae.
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PMID:Severe, self-limiting lactic acidosis and rhabdomyolysis accompanying convulsions. 251 19

The authors studied specific and sensitive indicators of neuronal adenosine triphosphate (ATP) depletion--hypoxanthine, xanthine and uridine levels--in the cerebrospinal fluid (CSF) of nine children during non-convulsive status epilepticus. No evidence of ATP depletion was found and CSF pH and creatine kinase levels were similar to those of controls. Hypoxanthine, xanthine and uridine had a tendency to be low, but this was significant only for xanthine. The authors speculatively link this reduction to a reduction in neuronal protein synthesis. This might be a mechanism whereby non-convulsive status epilepticus could lead to intellectual deterioration and dementia.
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PMID:Cerebrospinal fluid nucleotide metabolites following non-convulsive status epilepticus. 273 69

31P NMR studies on the brains of living rabbits were carried out at 32 MHz in a spectrometer having a 200-mm clear bore. Paralyzed pump-ventilated animals under nitrous oxide analgesia were inserted into the 1.89-T field and signals were focused in the brain by using a 4-cm surface coil. Several conventional physiological variables were monitored together with 31P spectra during induction and reversal of insulin shock and hypoxic hypoxia sufficient to abolish the electroencephalogram and during status epilepticus. A reversible decrease in phosphocreatine stores accompanied by an increase in Pi was detected during hypoglycemia and hypoxia. Similar changes were observed in prolonged status epilepticus but were not reversed. ATP levels fell about 50% in hypoglycemia but only slightly in the other two metabolic stresses. Intracellular pH rose in hypoglycemia; in status epilepticus and hypoxia it fell, but only when cardiovascular function was severely impaired. From the measured NMR parameters and the assumptions (i) that creatine kinase was at equilibrium and (ii) that the creatine/phosphocreatine pool was constant, it was possible to calculate the relative changes in cytoplasmic ADP levels associated with these metabolic disturbances.
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PMID:Cerebral metabolic studies in vivo by 31P NMR. 657 78

A 72-year-old woman was referred to hospital for obnubilation with general muscle weakness and hypotonia. Biology showed hypocalcemia, hypophosphatemia, increased serum creatine kinase and alkaline phosphatase levels. Brain CT scan, cerebrospinal fluid examination, and electromyogram were normal. Clinical status and electroencephalogram were consistent with non-convulsive generalized status epilepticus. The treatment included clonazepam and CaCl2 and consciousness returned to normal. A treatment with multivitamin infusion containing vitamin D2 was given for 3 weeks. Muscle weakness improved partially. Serum vitamin D3 level was low and osteomalacic myopathy was diagnosed. A treatment was given with 25OH vitamin D3, 50 micrograms per day. Two months later, serum vitamin D3 and creatine kinase levels were normal and the patient could walk without help. We conclude that vitamin D status should be monitored in elderly patients with muscle symptoms and abnormal calcium status. Osteomalacic myopathy should be considered in critically ill patients with muscle symptoms of an unclear cause.
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PMID:Muscle weakness in intensive care patients: initial manifestation of vitamin D deficiency. 770 75

The aim of the study was to investigate the changes in biochemical mechanisms facilitating cellular damages in the lithium plus pilocarpine treatment and the resulting status epilepticus. The whole brain free fatty acid (FFA) level as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), glutamate dehydrogenase, aspartate-aminotransferase (AST), alanine-aminotransferase, gamma-glutamoyl transferase, alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and creatine kinase in the frontal cortex, cerebellum, hippocampus and pons-medulla region of Hannover-Wistar rats were determined. The control group was intact with no previous experimental history. LiCl (125 mg/kg i.p.) was injected 20 h prior to pilocarpine (30 mg/kg i.p.) and the treated rats were sacrificed 1 or 2 1/2 h after pilocarpine administration. The results show that lithium plus pilocarpine administration and the resulting status epilepticus produced the significant increase of the brain FFA content. Decreased GPX activities were detected in the frontal cortex, cerebellum and hippocampus of the treated rats without the accompanying decrease of SOD activity. Increased AST and LDH activities were observed in the frontal cortex, increased soluble ALP activities in the frontal cortex and pons-medulla region whereas the increased activity of membrane bound ALP was detected in the hippocampus of the rats with status epilepticus. Activities of the other analysed enzymes did not change in the examined brain regions. The presented data indicate clear regional differences of biochemical changes caused by lithium plus pilocarpine treatment and the resulting status epilepticus, frontal cortex being the most affected site.
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PMID:Lithium plus pilocarpine induced status epilepticus--biochemical changes. 1071 13

Episodes of psychogenic nonepileptic status epilepticus (PNESE) characterized by pronounced generalized motor features were compared with those of refractory generalized convulsive status epilepticus. Patients with PNESE were younger, had port systems implanted more frequently, received higher doses of benzodiazepines until seizure termination or respiratory failure, and had lower serum creatine kinase levels.
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PMID:Diagnosis of psychogenic nonepileptic status epilepticus in the emergency setting. 1676 30

A 22-year-old girl presented with convulsive status epilepticus and a previous history of recurrent seizures, myoclonus, ataxia and impaired cognitive functions. Neurological examination revealed rest and action-induced myoclonus, pyramidal signs and opposition hypertonia. Testing revealed severe metabolic acidosis, elevated transaminases and creatine kinase, and respiratory insufficiency. After intubation and ventilation, thiopental was introduced but the patient's condition worsened dramatically with death in a few hours. Autopsy showed profuse periodic acid-Schiff (PAS) positive intracellular inclusions in the CNS (Lafora bodies), most abundant in thalamus, cerebellum, and brainstem, as well as in other organs. Genetic testing revealed a homozygous missense mutation (c.205C > G, P69A) in the EPM2B (NHLRC1) gene, confirming the diagnosis of progressive myoclonic epilepsy Lafora-type.
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PMID:22-year-old girl with status epilepticus and progressive neurological symptoms. 1974 44

We present a case of 32-year-old male with profound mental retardation and autism spectrum disorder who had presented with seizures, rigidity and elevated creatine kinase and was initially diagnosed as neuroleptic malignant syndrome (NMS). The patient subsequently had a complicated clinical course, developing refractory status epilepticus, which lead to the eventual diagnosis of progressive encephalomyelitis with rigidity and myoclonus (PERM). We discuss the clinical similarities and differences between NMS and PERM, and highlight the need to consider alternative diagnoses when the clinical picture of NMS is atypical, particularly in this patient group where the history and clinical examination may be challenging.
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PMID:Progressive Encephalomyelitis with Rigidity and Myoclonus in an Intellectually Disabled Patient Mimicking Neuroleptic Malignant Syndrome. 2835 55