Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old woman had uterine bleeding and hypotension after delivery. Hyponatremic seizures and a mild headache prompted early neuroimaging, which disclosed an enlarged nonhemorrhagic pituitary gland with subsequent involution consistent with pituitary apoplexy (Sheehan syndrome). Endocrinologic investigation confirmed a partial pituitary insufficiency with subsequent improvement to almost normal status.
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PMID:MR of nonhemorrhagic postpartum pituitary apoplexy. 869 99

This study was conducted to better define the pathophysiology, risk factors, and therapeutic approach to exercise-associated hyponatremia. Medical records from all participants in the 1998 Suzuki Rock 'N' Roll Marathon who presented to 14 Emergency Departments (EDs) were retrospectively reviewed to identify risk factors for the development of hyponatremia. Hyponatremic patients were compared to other runners with regard to race time and to other marathon participants seen in the ED with regard to gender, clinical signs of dehydration, and use of nonsteroidal anti-inflammatory drugs (NSAIDs). An original treatment algorithm incorporating the early use of hypertonic saline (HTS) was evaluated prospectively in our own ED for participants in the 1999 marathon to evaluate improvements in sodium correction rate and incidence of complications. A total of 26 patients from the 1998 and 1999 marathons were hyponatremic [serum sodium (SNa) < or =135 mEq/L] including 15 with severe hyponatremia (SNa < or = 125 mEq/L). Three developed seizures and required intubation and admission to an intensive care unit. Hyponatremic patients were more likely to be female, use NSAIDS, and have slower finishing times. Hyponatremic runners reported drinking "as much as possible" during and after the race and were less likely to have clinical signs of dehydration. An inverse relationship between initial SNa and time of presentation was observed, with late presentation predicting lower SNa values. The use of HTS in selected 1999 patients resulted in faster SNa correction times and fewer complications than observed for 1998 patients. It is concluded that the development of exercise-associated hyponatremia is associated with excessive fluid consumption during and after extreme athletic events. Additional risk factors include female gender, slower race times, and NSAID use. The use of HTS in selected patients seems to be safe and efficacious.
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PMID:Exercise-associated hyponatremia in marathon runners: a two-year experience. 1139 89

Dysnatremia may cause life-threatening encephalopathy in marathon runners. Hypernatremia and exercise-associated hyponatremia (EAH) may manifest with mental status changes and, if untreated, progress to coma and death. We reviewed the on-site blood sodium testing and treatment in collapsed runners at the finish-line medical tent at the Boston marathons from 2001 through 2008. Dysnatremia was diagnosed in 429 (32.5%) of 1,319 collapsed runners. Hypernatremia was present in 366 (27.7%) and hyponatremia in 63 (4.8%). Hypernatremic runners unable to drink fluids were treated with intravenous normal (0.9%) saline. Hyponatremic runners with seizures or coma received intravenous hypertonic (3%) saline. Sixteen runners with EAH able to drink a concentrated oral hypertonic solution recovered within 30 minutes. Based on on-site sodium testing, dysnatremic runners were treated with appropriate intravenous fluids according to validated standards of care. Hyponatremic runners able to drink an oral hypertonic solution recovered promptly.
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PMID:Exertional dysnatremia in collapsed marathon runners: a critical role for point-of-care testing to guide appropriate therapy. 1968 9

Status epilepticus (SE) is a dreaded neurological emergency. A reignited interest in SE has resulted in a more adaptive use of treatment protocols. More knowledge on SE of various aetiologies is therefore needed. We are interested in treatment of SE under hyponatremia, and have here evaluated whether SE induced by systemic kainic acid could be a suitable platform for such studies. Acute hyponatremia was induced in C57/BL6 mice by intraperitoneal injection of dDAVP and water loading. Hyponatremic mice displayed an increased frequency of epileptiform spikes on EEG and 5/9 hyponatremic mice displayed electrographic seizures. After kainic acid (20mg/kg) treatment, hyponatremic mice displayed significantly longer time with electrographic seizure activity, which was also seen after treatment with diazepam (20mg/kg). We conclude that hyponatremia augments kainic acid-induced SE, This model might be a valuable platform for studies on treatment of SE in hyponatremia.
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PMID:Hyponatremia augments kainic-acid induced status epilepticus in the mouse: a model for dysmetabolic status epilepticus. 2379 Sep 65