{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T01:13:00Z","timestamp":1792026780670,"version":"4.4.0"},"reference-count":20,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2017,9,21]],"date-time":"2017-09-21T00:00:00Z","timestamp":1505952000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2017,12]]},"abstract":"<jats:sec><jats:title>Background and purpose<\/jats:title><jats:p>To date, no pathophysiological model has sufficiently accounted for all the findings encountered in patients with idiopathic intracranial hypertension (<jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content>). Intracranial elastance is an index of volume\u2010buffering capacity known to play a role in certain disorders of cerebrospinal fluid (<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>) dynamics, which has not been previously investigated in relation to <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content> patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This was a single\u2010center retrospective cohort study from 1 July 2011 to 1 July 2016. Values for opening pressure (<jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>O<\/jats:sub><\/jats:styled-content>), closing pressure (<jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>C<\/jats:sub><\/jats:styled-content>) and volume (<jats:italic>V<\/jats:italic>) of <jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> removed were collected, as well as demographic and clinical covariates. Intracranial elastance (<jats:italic>E<\/jats:italic>) and pressure\u2212volume index (<jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content>) were calculated according to established equations: <jats:italic>E<\/jats:italic> = (<jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>O<\/jats:sub><\/jats:styled-content><jats:italic>\u2212<\/jats:italic><jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>C<\/jats:sub><\/jats:styled-content>)\/<jats:italic>V<\/jats:italic> and <jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content><jats:italic> = V<\/jats:italic>\/log<jats:sub>10<\/jats:sub>(<jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>O<\/jats:sub><\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\"><jats:italic>P<\/jats:italic><jats:sub>C<\/jats:sub><\/jats:styled-content>), respectively. Those with an alternative central nervous system pathology, including meningitis, encephalitis and normal pressure hydrocephalus were excluded. Eligible patients were subdivided into two groups based on final diagnosis: a control group and an <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content> group.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In our cohort (<jats:italic>n<\/jats:italic> = 49), a significant association of both <jats:italic>E<\/jats:italic> (<jats:italic>P<\/jats:italic> &lt; 0.0001) and <jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.005) with a diagnosis of <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content> was observed. Median <jats:italic>E<\/jats:italic> was 0.45 [interquartile range (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content>) 0.29\u20130.63] in the control group and 1 (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content> 0.59\u20131.29) in the <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content> group, and median <jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content> was 98.07 (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content> 59.92\u2013135.86) in the control group and 64.1 (<jats:styled-content style=\"fixed-case\">IQR<\/jats:styled-content> 42.4\u201391.7) in the <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content> group. Neither <jats:italic>E<\/jats:italic> nor <jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content> were significantly associated with age, gender or body mass index. <jats:styled-content style=\"fixed-case\">PVI<\/jats:styled-content> was independent of opening pressure.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>As calculated by clinically accessible indices, our study provides evidence that intracranial elastance is increased in <jats:styled-content style=\"fixed-case\">IIH<\/jats:styled-content>, reflecting a novel insight into disease pathogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ene.13410","type":"journal-article","created":{"date-parts":[[2017,8,11]],"date-time":"2017-08-11T15:36:39Z","timestamp":1502465799000},"page":"1457-1463","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Intracranial elastance is increased in idiopathic intracranial hypertension"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8527-2475","authenticated-orcid":false,"given":"J. 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