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      Differentiation between anatomical slenderness and acquired stenosis of the internal jugular veins

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          Abstract

          Background and Purposes

          Differentiating between acquired stenosis (pathologic) and anatomical slenderness (physiologic) of internal jugular vein (IJV) remain ambiguous. Herein, we aimed to compare the similarities and differences between the two entities.

          Methods

          Patients who underwent head and neck computer tomography (CT) and brain magnetic resonance imaging (MRI) were enrolled in this case‐control study from January 2016 through October 2021.

          Results

          1487 eligible patients entered final analysis totally. 803 patients had bilateral IJVs imaging without IJV stenosis‐related symptoms and presented in three ways: right IJV slenderness (10.5%, n = 85), left IJV slenderness (48.4%, n = 388), and symmetric IJVs (41.1%, n = 330). In patients with asymmetric IJVs, their bilateral jugular foramina were also asymmetric. All involved asymmetric IJVs presented as slenderness without surrounding abnormal collaterals and credible cloudy‐like white matter hyper‐intensity (WMH). Their cerebral arterial perfusion statuses on brain MR‐PWI maps were normal.

          In contrast, the major patients with IJV stenosis presented with signs and symptoms such as headaches, head noise, etc. In CE‐MRV maps, local stenosis of the IJV was surrounded by abnormal venous collaterals in contrast to the lack of abnormal venous collaterals for patients with IJV slenderness. And in CTV maps, the caliber of jugular foramina was mismatched with the transverse diameter of IJV. Moreover, in MRI maps of most of these patients, a cloudy‐like WMHs were distributed symmetrically in bilateral periventricular and/or centrum semi vales. These patients also had symmetrical cerebral arterial hypo‐perfusion. Seven patients underwent stenting of the IJV stenosis correction, their WMHs attenuated or disappeared subsequently.

          Conclusions

          Imaging features in addition to clinical symptoms can be used to differentiate between physiologic IJV slenderness and pathologic IJV stenosis. Notable imagine‐defining features for IJV stenosis include local stenosis surrounded by abnormal venous collaterals, cloudy‐like WMHs, and mismatch between the transverse diameter of IJV and the caliber of the jugular foramina.

          Abstract

          This study mainly illustrated the categories of anatomic modalities of internal jugular vein and the difference and similarity on neurological imaging and symptoms between slenderness and stenosis of internal jugular vein. Additionally, the effect of demographic data included gender, age and BMI and diameter of jugular foramen on slenderness of internal jugular vein were also analyzed.

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          Most cited references34

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          Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis.

          To determine the prevalence and nature of sinovenous obstruction in idiopathic intracranial hypertension (IIH) using auto-triggered elliptic-centric-ordered three-dimensional gadolinium-enhanced MR venography (ATECO MRV). In a prospective controlled study, 29 patients with established IIH as well as 59 control patients underwent ATECO MRV. In a randomized blinded fashion, three readers evaluated the images. Using a novel scoring system, each reader graded the degree of stenosis seen in the transverse and sigmoid sinuses of each patient. There was excellent agreement across the three readers for application of the grading system. Substantial bilateral sinovenous stenoses were seen in 27 of 29 patients with IIH and in only 4 of 59 control patients. Using ATECO MRV and a novel grading system for quantifying sinovenous stenoses, the authors can identify IIH patients with sensitivity and specificity of 93%.
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            Neuropathologic correlates of white matter hyperintensities.

            White matter hyperintensities (WMH) are commonly seen on neuroimaging scans, but their underlying histopathologic substrate is unclear. The aim of this work was to establish the pathologic correlates of WMH in unselected elderly cases using two study designs. To avoid potential bias from comparisons of different anatomic regions, study 1 compared, region-by-region, the severity of WMH determined in vivo with measures of each of the major white matter (WM) components. Study 2 compared the histopathology of WMH with normal WM. Study 1: The periventricular and deep WM regions of three lobes in 23 brains with in vivo MRI scans were investigated using histologic and immunohistochemical stains. The severity of each pathologic measure was correlated with WMH severity determined using the Scheltens scale. Study 2: Lesioned and nonlesioned areas identified by postmortem MRI in the frontal WM of 20 brains were examined histologically and immunohistochemically. No single pathologic variable correlated with the severity of WMH; however, a multiple stepwise regression analysis revealed that vascular integrity predicted total Scheltens score (beta = -0.53, p = 0.01). Comparison of lesioned and nonlesioned areas demonstrated that vascular integrity was reduced in WMH [t(18) = 3.79, p = 0.001]. Blood-brain barrier integrity was also found to be reduced in WMH [t(5) = -5.31, p = 0.003]. White matter hyperintensities (WMH) involve a loss of vascular integrity, confirming the vascular origin of these lesions. This damage to the vasculature may in turn impair blood-brain barrier integrity and be one mechanism by which WMH evolve.
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              Long-Term Blood-Brain Barrier Permeability Changes in Binswanger Disease.

              The blood-brain barrier (BBB) is disrupted in small vessel disease patients with lacunes and white matter hyperintensities (WMHs). The relationship of WMHs and regional BBB permeability changes has not been studied. We hypothesized that BBB disruption occurs in normal appearing WM and regions near the WMHs. To test the hypothesis, we repeated BBB permeability measurements in patients with extensive WMHs related to Binswanger disease.
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                Author and article information

                Contributors
                victor65@126.com
                Journal
                CNS Neurosci Ther
                CNS Neurosci Ther
                10.1111/(ISSN)1755-5949
                CNS
                CNS Neuroscience & Therapeutics
                John Wiley and Sons Inc. (Hoboken )
                1755-5930
                1755-5949
                02 August 2022
                November 2022
                : 28
                : 11 ( doiID: 10.1002/cns.v28.11 )
                : 1849-1860
                Affiliations
                [ 1 ] Department of Neurology, Xuanwu Hospital Capital Medical University Beijing China
                [ 2 ] Advanced Center of Stroke Beijing Institute for Brain Disorders Beijing China
                [ 3 ] National Center for Neurological Disorders, Xuanwu Hospital Capital Medical University Beijing China
                [ 4 ] Department of China‐America Institute of Neuroscience, Xuanwu Hospital Capital Medical University Beijing China
                [ 5 ] Department of Neurosurgery Wayne State University School of Medicine Detroit Michigan USA
                Author notes
                [*] [* ] Correspondence

                Ran Meng, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.

                Email: victor65@ 123456126.com

                Author information
                https://orcid.org/0000-0003-1376-4213
                https://orcid.org/0000-0003-0293-2744
                http://orcid.org/0000-0003-1190-4710
                Article
                CNS13924 CNSNT-2022-077.R3
                10.1111/cns.13924
                9532925
                35919952
                fe132c4e-e02e-4e7a-9795-b86798a794bf
                © 2022 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 05 July 2022
                : 09 February 2022
                : 07 July 2022
                Page count
                Figures: 7, Tables: 5, Pages: 12, Words: 6078
                Funding
                Funded by: Beijing Natural Science Foundation , doi 10.13039/501100004826;
                Award ID: 7212047
                Funded by: National Natural Science Foundation Grants
                Award ID: 82171297
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                November 2022
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.0 mode:remove_FC converted:05.10.2022

                Neurosciences
                internal jugular vein slenderness,internal jugular vein stenosis,jugular foramina,neuroimaging features

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