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Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders
The pathogenesis underlying communicating hydrocephalus has been centered on impaired cerebrospinal fluid (CSF) outflow secondary to abnormal CSF pulsation and venous hypertension. Hydrodynamic theory of hydrocephalus fares better than traditional theory in explaining the possible mechanisms underly...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038869/ https://www.ncbi.nlm.nih.gov/pubmed/24891884 http://dx.doi.org/10.4103/1793-5482.131058 |
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author | Idris, Zamzuri Mustapha, Muzaimi Abdullah, Jafri M. |
author_facet | Idris, Zamzuri Mustapha, Muzaimi Abdullah, Jafri M. |
author_sort | Idris, Zamzuri |
collection | PubMed |
description | The pathogenesis underlying communicating hydrocephalus has been centered on impaired cerebrospinal fluid (CSF) outflow secondary to abnormal CSF pulsation and venous hypertension. Hydrodynamic theory of hydrocephalus fares better than traditional theory in explaining the possible mechanisms underlying communicating hydrocephalus. Nonetheless, hydrodynamic theory alone could not fully explain some conditions that have ventriculomegaly but without hydrocephalus. By revisiting brain buoyancy from a fresher perspective, called microgravity environment of the brain, introducing wider concepts of anatomical and physiological compensatory–decompensatory phases for a persistent raise in intracranial pressure, and along with combining these two concepts with the previously well-accepted concepts of Monro–Kellie doctrine, intracranial hypertension, cerebral blood flow, cerebral perfusion pressure, brain compliance and elasticity, cerebral autoregulation, blood–brain and blood–CSF barriers, venous and cardiopulmonary hypertension, Windkessel phenomenon, and cerebral pulsation, we provide plausible explanations to the pathogenesis for communicating hydrocephalus and its related disorders. |
format | Online Article Text |
id | pubmed-4038869 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-40388692014-06-02 Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders Idris, Zamzuri Mustapha, Muzaimi Abdullah, Jafri M. Asian J Neurosurg Review Article The pathogenesis underlying communicating hydrocephalus has been centered on impaired cerebrospinal fluid (CSF) outflow secondary to abnormal CSF pulsation and venous hypertension. Hydrodynamic theory of hydrocephalus fares better than traditional theory in explaining the possible mechanisms underlying communicating hydrocephalus. Nonetheless, hydrodynamic theory alone could not fully explain some conditions that have ventriculomegaly but without hydrocephalus. By revisiting brain buoyancy from a fresher perspective, called microgravity environment of the brain, introducing wider concepts of anatomical and physiological compensatory–decompensatory phases for a persistent raise in intracranial pressure, and along with combining these two concepts with the previously well-accepted concepts of Monro–Kellie doctrine, intracranial hypertension, cerebral blood flow, cerebral perfusion pressure, brain compliance and elasticity, cerebral autoregulation, blood–brain and blood–CSF barriers, venous and cardiopulmonary hypertension, Windkessel phenomenon, and cerebral pulsation, we provide plausible explanations to the pathogenesis for communicating hydrocephalus and its related disorders. Medknow Publications & Media Pvt Ltd 2014 /pmc/articles/PMC4038869/ /pubmed/24891884 http://dx.doi.org/10.4103/1793-5482.131058 Text en Copyright: © Asian Journal of Neurosurgery http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Idris, Zamzuri Mustapha, Muzaimi Abdullah, Jafri M. Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title | Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title_full | Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title_fullStr | Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title_full_unstemmed | Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title_short | Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
title_sort | microgravity environment and compensatory: decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038869/ https://www.ncbi.nlm.nih.gov/pubmed/24891884 http://dx.doi.org/10.4103/1793-5482.131058 |
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