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Impaired glymphatic function in idiopathic intracranial hypertension

Idiopathic intracranial hypertension is a brain disease incorporating cerebrospinal fluid disturbance, increased intracranial pressure and visual failure, but with unknown cause. This study examined a hypothesis that glymphatic function is impaired in idiopathic intracranial hypertension patients. T...

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Autores principales: Eide, Per Kristian, Pripp, Are Hugo, Ringstad, Geir, Valnes, Lars Magnus
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253298/
https://www.ncbi.nlm.nih.gov/pubmed/34235434
http://dx.doi.org/10.1093/braincomms/fcab043
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author Eide, Per Kristian
Pripp, Are Hugo
Ringstad, Geir
Valnes, Lars Magnus
author_facet Eide, Per Kristian
Pripp, Are Hugo
Ringstad, Geir
Valnes, Lars Magnus
author_sort Eide, Per Kristian
collection PubMed
description Idiopathic intracranial hypertension is a brain disease incorporating cerebrospinal fluid disturbance, increased intracranial pressure and visual failure, but with unknown cause. This study examined a hypothesis that glymphatic function is impaired in idiopathic intracranial hypertension patients. The MRI contrast agent gadobutrol was utilized as a cerebrospinal fluid tracer following intrathecal administration. Consecutive standardized T1 MRI acquisitions over 48 h were done to assess tracer distribution within brain of 15 idiopathic intracranial hypertension patients and 15 reference individuals who were comparable in age and gender distribution. Using FreeSurfer software, we semi-quantified tracer level in multiple brain regions as T1 MRI signal change. The tracer enriched the entire brain of idiopathic intracranial hypertension and reference subjects. In idiopathic intracranial hypertension, tracer enrichment was increased and clearance of tracer delayed from a wide range of brain regions, including both grey and white matter. Differences were most evident in frontal and temporal regions. The pulsatile intracranial pressure was measured overnight and tracer propagation in brain compared between individuals with pathological and normal pulsatile intracranial pressure. In individuals with pathological pulsatile intracranial pressure, tracer enrichment was stronger and clearance from brain delayed, particularly in regions nearby large artery trunks at the brain surface. The present in vivo observations provide evidence for impaired glymphatic function in several brain regions of idiopathic intracranial hypertension patients. Glymphatic failure may imply altered clearance of metabolic byproducts, which may precede neurodegeneration. Further studies are needed to characterize glymphatic failure in idiopathic intracranial hypertension.
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spelling pubmed-82532982021-07-06 Impaired glymphatic function in idiopathic intracranial hypertension Eide, Per Kristian Pripp, Are Hugo Ringstad, Geir Valnes, Lars Magnus Brain Commun Original Article Idiopathic intracranial hypertension is a brain disease incorporating cerebrospinal fluid disturbance, increased intracranial pressure and visual failure, but with unknown cause. This study examined a hypothesis that glymphatic function is impaired in idiopathic intracranial hypertension patients. The MRI contrast agent gadobutrol was utilized as a cerebrospinal fluid tracer following intrathecal administration. Consecutive standardized T1 MRI acquisitions over 48 h were done to assess tracer distribution within brain of 15 idiopathic intracranial hypertension patients and 15 reference individuals who were comparable in age and gender distribution. Using FreeSurfer software, we semi-quantified tracer level in multiple brain regions as T1 MRI signal change. The tracer enriched the entire brain of idiopathic intracranial hypertension and reference subjects. In idiopathic intracranial hypertension, tracer enrichment was increased and clearance of tracer delayed from a wide range of brain regions, including both grey and white matter. Differences were most evident in frontal and temporal regions. The pulsatile intracranial pressure was measured overnight and tracer propagation in brain compared between individuals with pathological and normal pulsatile intracranial pressure. In individuals with pathological pulsatile intracranial pressure, tracer enrichment was stronger and clearance from brain delayed, particularly in regions nearby large artery trunks at the brain surface. The present in vivo observations provide evidence for impaired glymphatic function in several brain regions of idiopathic intracranial hypertension patients. Glymphatic failure may imply altered clearance of metabolic byproducts, which may precede neurodegeneration. Further studies are needed to characterize glymphatic failure in idiopathic intracranial hypertension. Oxford University Press 2021-03-21 /pmc/articles/PMC8253298/ /pubmed/34235434 http://dx.doi.org/10.1093/braincomms/fcab043 Text en © The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Eide, Per Kristian
Pripp, Are Hugo
Ringstad, Geir
Valnes, Lars Magnus
Impaired glymphatic function in idiopathic intracranial hypertension
title Impaired glymphatic function in idiopathic intracranial hypertension
title_full Impaired glymphatic function in idiopathic intracranial hypertension
title_fullStr Impaired glymphatic function in idiopathic intracranial hypertension
title_full_unstemmed Impaired glymphatic function in idiopathic intracranial hypertension
title_short Impaired glymphatic function in idiopathic intracranial hypertension
title_sort impaired glymphatic function in idiopathic intracranial hypertension
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253298/
https://www.ncbi.nlm.nih.gov/pubmed/34235434
http://dx.doi.org/10.1093/braincomms/fcab043
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