FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2045372425> ?p ?o ?g. }

• W2045372425 endingPage "522" @default.
• W2045372425 startingPage "513" @default.
• W2045372425 abstract "purpose: Severe hyponatremia is often associated with permanent brain damage. There has been substantial controversy about whether central pontine myelinolysis (CPM), a rare neurologic disorder of uncertain etiology, can complicate either hyponatremia or its therapy. This study was undertaken to determine how often hyponatremic patients with the clinical diagnosis of CPM actually have the disorder as an integral structural component of their encephalopathy. patients: Analyses were carried out in 20 patients who had severe symptomatic hyponatremia and a presumptive diagnosis of CPM, based on clinical and/or neuroradiologic findings. All had been referred for neuroradiology consultation. The mean age (± SD) was 47 ± 14 years, the lowest serum sodium level was 104 ± 8 mM, and 85% of the patients were female. The etiologies were diverse and included postoperative status, thiazide diuretics, polydipsia, infection, acute renal failure, chronic alcoholism with emesis, and beer potomania. methods: The original and subsequent films of 20 patients were reevaluated retrospectively by two neuroradiologists. The clinical course was also reevaluated, and in eight patients, the postmortem brain findings were reviewed. The diagnosis of CPM was made only on the basis of strict criteria relating to either (1) pathologic findings of CPM on postmortem examination; or (2) computed tomographic scan and/or magnetic resonance imaging findings diagnostic of CPM. results: No pontine lesions were present in 15 of 20 patients in whom the diagnosis of CPM had initially been made. All 15 had extrapontine demyelinating lesions but the pons was normal. Two others had only lateral pontine lesions, so that only three of 20 patients had definite CPM. All but one of the 20 hyponatremic patients had a definite hypoxic event prior to any therapy with intravenous sodium chloride. The involved brain areas included basal ganglia, thalamus, cortical gray matter, and periventricular white matter, areas often affected by hypoxia. Each of the three patients in whom unequivocal findings of CPM were present had long histories of chronic alcoholism and hepatic cirrhosis. conclusions: These results suggest that: (1) Neither hyponatremic encephalopathy nor its therapy is commonly associated with CPM; (2) Patients with chronic alcoholism who also become hyponatremic can develop pontine demyelinating lesions; (3) Most patients with symptomatic hyponatremia who are diagnosed as having CPM in fact have diffuse cerebral demyelinating lesions with a normal pons; (4) The distribution of cerebral demyelinating lesions in patients with hyponatremic encephalopathy is compatible with hypoxic damage." @default.
• W2045372425 created "2016-06-24" @default.
• W2045372425 creator A5017799212 @default.
• W2045372425 creator A5029378373 @default.
• W2045372425 creator A5054963418 @default.
• W2045372425 creator A5057233593 @default.
• W2045372425 creator A5063167945 @default.
• W2045372425 date "1992-05-01" @default.
• W2045372425 modified "2023-10-18" @default.
• W2045372425 title "Hyponatremic encephalopathy: Is central pontine myelinolysis a component?" @default.
• W2045372425 cites W1964838514 @default.
• W2045372425 cites W1967635925 @default.
• W2045372425 cites W1982443888 @default.
• W2045372425 cites W1994541894 @default.
• W2045372425 cites W1996466671 @default.
• W2045372425 cites W1996856941 @default.
• W2045372425 cites W2003695859 @default.
• W2045372425 cites W2004387009 @default.
• W2045372425 cites W2004955229 @default.
• W2045372425 cites W2008127715 @default.
• W2045372425 cites W2012630087 @default.
• W2045372425 cites W2025101749 @default.
• W2045372425 cites W2028342183 @default.
• W2045372425 cites W2032866637 @default.
• W2045372425 cites W2035082043 @default.
• W2045372425 cites W2038614864 @default.
• W2045372425 cites W2039029246 @default.
• W2045372425 cites W2041001201 @default.
• W2045372425 cites W2041231375 @default.
• W2045372425 cites W2041511990 @default.
• W2045372425 cites W2052045246 @default.
• W2045372425 cites W2052943929 @default.
• W2045372425 cites W2054976537 @default.
• W2045372425 cites W2059171327 @default.
• W2045372425 cites W2060854596 @default.
• W2045372425 cites W2069978313 @default.
• W2045372425 cites W2070711858 @default.
• W2045372425 cites W2073429999 @default.
• W2045372425 cites W2076684223 @default.
• W2045372425 cites W2084185101 @default.
• W2045372425 cites W2085680575 @default.
• W2045372425 cites W2088869561 @default.
• W2045372425 cites W2094039977 @default.
• W2045372425 cites W2095288947 @default.
• W2045372425 cites W2107888120 @default.
• W2045372425 cites W2123289589 @default.
• W2045372425 cites W2125460351 @default.
• W2045372425 cites W2130135001 @default.
• W2045372425 cites W2130474752 @default.
• W2045372425 cites W2147491287 @default.
• W2045372425 cites W2157509249 @default.
• W2045372425 cites W2162967708 @default.
• W2045372425 cites W2172327934 @default.
• W2045372425 cites W2295493440 @default.
• W2045372425 cites W2313394348 @default.
• W2045372425 cites W2335702149 @default.
• W2045372425 cites W345056605 @default.
• W2045372425 cites W4294349871 @default.
• W2045372425 cites W4302081968 @default.
• W2045372425 doi "https://doi.org/10.1016/0002-9343(92)90748-z" @default.
• W2045372425 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/1580298" @default.
• W2045372425 hasPublicationYear "1992" @default.
• W2045372425 type Work @default.
• W2045372425 sameAs 2045372425 @default.
• W2045372425 citedByCount "91" @default.
• W2045372425 countsByYear W20453724252013 @default.
• W2045372425 countsByYear W20453724252014 @default.
• W2045372425 countsByYear W20453724252018 @default.
• W2045372425 crossrefType "journal-article" @default.
• W2045372425 hasAuthorship W2045372425A5017799212 @default.
• W2045372425 hasAuthorship W2045372425A5029378373 @default.
• W2045372425 hasAuthorship W2045372425A5054963418 @default.
• W2045372425 hasAuthorship W2045372425A5057233593 @default.
• W2045372425 hasAuthorship W2045372425A5063167945 @default.
• W2045372425 hasConcept C126322002 @default.
• W2045372425 hasConcept C126838900 @default.
• W2045372425 hasConcept C137627325 @default.
• W2045372425 hasConcept C143409427 @default.
• W2045372425 hasConcept C187212893 @default.
• W2045372425 hasConcept C2776703092 @default.
• W2045372425 hasConcept C2778621155 @default.
• W2045372425 hasConcept C2781122673 @default.
• W2045372425 hasConcept C71924100 @default.
• W2045372425 hasConceptScore W2045372425C126322002 @default.
• W2045372425 hasConceptScore W2045372425C126838900 @default.
• W2045372425 hasConceptScore W2045372425C137627325 @default.
• W2045372425 hasConceptScore W2045372425C143409427 @default.
• W2045372425 hasConceptScore W2045372425C187212893 @default.
• W2045372425 hasConceptScore W2045372425C2776703092 @default.
• W2045372425 hasConceptScore W2045372425C2778621155 @default.
• W2045372425 hasConceptScore W2045372425C2781122673 @default.
• W2045372425 hasConceptScore W2045372425C71924100 @default.
• W2045372425 hasIssue "5" @default.
• W2045372425 hasLocation W20453724251 @default.
• W2045372425 hasLocation W20453724252 @default.
• W2045372425 hasOpenAccess W2045372425 @default.
• W2045372425 hasPrimaryLocation W20453724251 @default.
• W2045372425 hasRelatedWork W130481378 @default.

• next