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It is characterized by the absence of detectable cerebrospinal fluid (CSF) outflow obstructions and often with increased CSF pulsatility measured in the cerebral aqueduct (CA). We hypothesize that the cardiac-related pulsatile flow over the CA, with fast systolic outflow and slow diastolic inflow, can generate net pressure effects that could source the ventriculomegaly in these patients. This would require a non-zero cardiac cycle averaged net pressure difference (\u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>net<\/jats:italic><\/jats:sub>) over the CA, with higher average pressure in the lateral and third ventricles.<\/jats:p>\n<\/jats:sec><jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>We tested the hypothesis by calculating \u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>net<\/jats:italic><\/jats:sub> across the CA using computational fluid dynamics based on prospectively collected high-resolution structural (FIESTA-C, resolution 0.39\u2009\u00d7\u20090.39\u2009\u00d7\u20090.3\u00a0mm<jats:sup>3<\/jats:sup>) and velocimetric (2D-PCMRI, in-plane resolution 0.35\u2009\u00d7\u20090.35\u00a0mm<jats:sup>2<\/jats:sup>) MRI-data from 30 patients investigated for communicating hydrocephalus.<\/jats:p>\n<\/jats:sec><jats:sec>\n<jats:title>Results<\/jats:title>\n<jats:p>The \u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>net<\/jats:italic><\/jats:sub> due to CSF pulsations was non-zero for the study group (p\u2009=\u20090.03) with a magnitude of 0.2\u2009\u00b1\u20090.4\u00a0Pa (0.001\u2009\u00b1\u20090.003\u00a0mmHg), with higher pressure in the third ventricle. The maximum pressure difference over the cardiac cycle \u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>max<\/jats:italic><\/jats:sub> was 20.3\u2009\u00b1\u200911.8\u00a0Pa and occurred during systole. A generalized linear model verified an association between \u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>net<\/jats:italic><\/jats:sub> and CA cross-sectional area (p\u2009=\u20090.01) and flow asymmetry, described by the ratio of maximum inflow\/outflow (p\u2009=\u20090.04), but not for aqueductal stroke volume (p\u2009=\u20090.35).<\/jats:p>\n<\/jats:sec><jats:sec>\n<jats:title>Conclusions<\/jats:title>\n<jats:p>The results supported the hypothesis with respect to the direction of \u0394<jats:italic>P<\/jats:italic><jats:sub><jats:italic>net<\/jats:italic><\/jats:sub>, although the magnitude was low. Thus, although the pulsations may generate a pressure difference across the CA it is likely too small to explain the ventriculomegaly in communicating hydrocephalus.<\/jats:p>\n<\/jats:sec>","DOI":"10.1186\/s12987-019-0159-0","type":"journal-article","created":{"date-parts":[[2019,12,23]],"date-time":"2019-12-23T00:02:10Z","timestamp":1577059330000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Can pulsatile CSF flow across the cerebral aqueduct cause ventriculomegaly? 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