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      Dilatation of the bridging cerebral cortical veins in childhood hydrocephalus suggests a malfunction of venous impedance pumping

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          Abstract

          Dogs with a naturally occurring form of hydrocephalus have an elevated transmural venous pressure leading to cortical vein dilatation. The purpose of this study is to discover if there is vein dilatation in childhood hydrocephalus and to estimate the pressure required to maintain any enlargement found. Children with hydrocephalus between the ages of 4 and 15 years were compared with a control group. Magnetic resonance venography (MRV) and flow quantification were performed. The arterial inflow, sagittal sinus and straight sinus venous outflow were measured and the outflow percentages compared to the inflow were calculated. The cross-sectional area of the veins were measured. There were a total of 18 children with hydrocephalus, compared to 72 age and sex matched control MRV’s and 22 control flow quantification studies. In hydrocephalus, the sagittal sinus venous return was reduced by 12.9%, but the straight sinus flow was not significantly different. The superficial territory veins were 22% larger than the controls but the vein of Galen was unchanged. There is evidence of a significant increase in the superficial vein transmural pressure in childhood hydrocephalus estimated to be approximately 4 mmHg. An impedance pump model is suggested to explain these findings.

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          The pathophysiology of idiopathic normal pressure hydrocephalus: cerebral ischemia or altered venous hemodynamics?

          Many theories of normal pressure hydrocephalus (NPH) stress the importance of ischemia in the deep white matter. Alternate theories stress a reduction in superficial venous compliance and changes in pulse-wave propagation. An overlap in the cerebral blood flow volumes measured between NPH and controls suggests that ischemia may not be a prerequisite for this condition. This study sought to compare blood flow and compliance measures in a cohort of patients with NPH selected for having arterial inflows above the normal range to see if deep brain ischemia or superficial hemodynamic changes contribute to the pathophysiology of NPH. Twenty patients with NPH and arterial inflows above the normal range were selected. They underwent MR imaging with flow quantification measuring the total blood inflow, sagittal/straight sinus outflow, aqueduct stroke volume, and arteriovenous delay (AVD). Patients were compared with 12 age-matched controls. The deep outflow volumes were normal. The superficial venous outflow was reduced as a percentage of the inflow by 9% (P = .04). The sagittal sinus compliance as measured by the AVD was reduced by 50% (P = .0001), and the aqueduct stroke volume was elevated by 192% (P = .02). Ischemia in the deep venous territory is not a prerequisite for NPH. Patients with high-inflow NPH show alterations in superficial venous compliance and a reduction in the blood flow returning via the sagittal sinus. These changes together suggest that an elevation in superficial venous pressure may occur in NPH.
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            Amplitude and phase of cerebrospinal fluid pulsations: experimental studies and review of the literature.

            A recently developed model of communicating hydrocephalus suggests that ventricular dilation may be related to the redistribution of pulsations in the cranium from the subarachnoid spaces (SASs) into the ventricles. Based on this model, the authors have developed a method for analyzing flow pulsatility in the brain by using the ratio of aqueductal to cervical subarachnoid stroke volume and the phase of cerebrospinal fluid (CSF) flow, which is obtained at multiple locations throughout the cranium, relative to the phase of arterial flow. Flow data were collected in a group of 15 healthy volunteers by using a series of images acquired with cardiac-gated, phase-contrast magnetic resonance imaging. The stroke volume ratio was 5.1 +/- 1.8% (mean +/- standard deviation). The phase lag in the aqueduct was -52.5 +/-16.5 degrees and the phase lag in the prepontine cistern was -22.1 +/- 8.2 degrees. The flow phase at the level of C-2 was -5.1 +/- 10.5 degrees, which was consistent with flow synchronous with the arterial pulse. The subarachnoid phase lag ventral to the pons was shown to decrease progressively to zero at the craniocervical junction. Flow in the posterior cervical SAS preceded the anterior space flow. Under normal conditions, pulsatile ventricular CSF flow is a small fraction of the net pulsatile CSF flow in the cranium. A thorough review of the literature supports the view that modified intracranial compliance can lead to redistribution of pulsations and increased intraventricular pulsations. The phase of CSF flow may also reflect the local and global compliance of the brain.
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              Pulse wave encephalopathy: a spectrum hypothesis incorporating Alzheimer's disease, vascular dementia and normal pressure hydrocephalus.

              The disorders of Alzheimer's disease, vascular dementia and normal pressure hydrocephalus are all causes of dementia in the elderly population. It is often the case that it is clinically very difficult to tell these diseases apart. All three forms of dementia share the same risk factors, which for the most part are vascular risk factors. This paper proposes that there is an underlying vascular pathophysiology behind these conditions, which is related to the strength of the pulse waves induced in the craniospinal cavity by the arterial vascular tree. It is proposed the manifestation of the dementia in any one patient is dependant on the way that the pulsations interact with the brain and its venous and perivascular drainage. This interaction is predominately dependant on the compliance of the craniospinal cavity and the chronicity of the increased pulse wave stress.
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                Author and article information

                Contributors
                grant.bateman@health.nsw.gov.au
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                29 July 2022
                29 July 2022
                2022
                : 12
                : 13045
                Affiliations
                [1 ]GRID grid.414724.0, ISNI 0000 0004 0577 6676, Department of Medical Imaging, , John Hunter Hospital, ; Locked Bag 1, Newcastle Region Mail Center, Newcastle, NSW 2310 Australia
                [2 ]GRID grid.266842.c, ISNI 0000 0000 8831 109X, Newcastle University Faculty of Health, ; Callaghan Campus, Newcastle, NSW Australia
                [3 ]GRID grid.1005.4, ISNI 0000 0004 4902 0432, School of Mechanical Engineering, , University of New South Wales, ; Sydney, NSW Australia
                [4 ]GRID grid.414724.0, ISNI 0000 0004 0577 6676, Department of Paediatric Neurology, , John Hunter Hospital, ; Newcastle, NSW Australia
                Article
                17465
                10.1038/s41598-022-17465-9
                9338310
                35906407
                ea1f51ba-22f8-47a5-aefa-82cdec941259
                © Crown 2022

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 24 January 2022
                : 26 July 2022
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                © The Author(s) 2022

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                biomedical engineering,experimental models of disease
                Uncategorized
                biomedical engineering, experimental models of disease

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