Desmond Connolly, Indran Davagnanam, Marzena Wylezinska-Arridge, Dermot Mallon, Stephen Wastling, Vivienne M Lee
{"title":"脑磁共振成像对非缺氧低压减压的反应","authors":"Desmond Connolly, Indran Davagnanam, Marzena Wylezinska-Arridge, Dermot Mallon, Stephen Wastling, Vivienne M Lee","doi":"10.3357/AMHP.6445.2024","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.</p><p><strong>Methods: </strong>Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m). Research magnetic resonance imaging sequences, conducted on the days preceding and following decompression, evaluated subcortical WM integrity, cerebral blood flow, neuronal integrity (fractional anisotropy), and neurometabolite concentrations.</p><p><strong>Results: </strong>No subcortical lesions were evident on diffusion weighted imaging and WM fractional anisotropy was unaffected. Mean WM blood flow was upregulated by 20% to over 25 mL · 100 g-1 · min-1. Gray matter flow was unchanged. There were no changes in gray matter or cerebellar neurometabolites. In parietal subcortical WM, levels of γ-aminobutyric acid (GABA) fell from (mean ± SD) 1.68 ± 0.2 to 1.35 ± 0.3 institutional units while glutathione (GSH) fell from 1.71 ± 0.4 to 1.25 ± 0.3 institutional units. Lactate increased postexposure in five subjects.</p><p><strong>Conclusions: </strong>Postexposure decrements in GABA and GSH imply WM insult with loss of neuroprotection and oxidative stress. An association between decrements in GABA and GSH support a common origin, while GSH decrements also correlate with WM blood flow responses. WM lactate increments are prone to error but suggest dysregulation of subcortical microvascular flow. WM neurometabolite and blood flow indices did not normalize by 24 h postexposure. Connolly D, Davagnanam I, Wylezinska-Arridge M, Mallon D, Wastling S, Lee VM. Brain magnetic resonance imaging responses to nonhypoxic hypobaric decompression. Aerosp Med Hum Perform. 2024; 95(10):733-740.</p>","PeriodicalId":7463,"journal":{"name":"Aerospace medicine and human performance","volume":"95 10","pages":"733-740"},"PeriodicalIF":0.9000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Brain Magnetic Resonance Imaging Responses to Nonhypoxic Hypobaric Decompression.\",\"authors\":\"Desmond Connolly, Indran Davagnanam, Marzena Wylezinska-Arridge, Dermot Mallon, Stephen Wastling, Vivienne M Lee\",\"doi\":\"10.3357/AMHP.6445.2024\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.</p><p><strong>Methods: </strong>Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m). Research magnetic resonance imaging sequences, conducted on the days preceding and following decompression, evaluated subcortical WM integrity, cerebral blood flow, neuronal integrity (fractional anisotropy), and neurometabolite concentrations.</p><p><strong>Results: </strong>No subcortical lesions were evident on diffusion weighted imaging and WM fractional anisotropy was unaffected. Mean WM blood flow was upregulated by 20% to over 25 mL · 100 g-1 · min-1. Gray matter flow was unchanged. There were no changes in gray matter or cerebellar neurometabolites. In parietal subcortical WM, levels of γ-aminobutyric acid (GABA) fell from (mean ± SD) 1.68 ± 0.2 to 1.35 ± 0.3 institutional units while glutathione (GSH) fell from 1.71 ± 0.4 to 1.25 ± 0.3 institutional units. Lactate increased postexposure in five subjects.</p><p><strong>Conclusions: </strong>Postexposure decrements in GABA and GSH imply WM insult with loss of neuroprotection and oxidative stress. An association between decrements in GABA and GSH support a common origin, while GSH decrements also correlate with WM blood flow responses. WM lactate increments are prone to error but suggest dysregulation of subcortical microvascular flow. WM neurometabolite and blood flow indices did not normalize by 24 h postexposure. Connolly D, Davagnanam I, Wylezinska-Arridge M, Mallon D, Wastling S, Lee VM. Brain magnetic resonance imaging responses to nonhypoxic hypobaric decompression. 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Brain Magnetic Resonance Imaging Responses to Nonhypoxic Hypobaric Decompression.
Introduction: The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.
Methods: Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m). Research magnetic resonance imaging sequences, conducted on the days preceding and following decompression, evaluated subcortical WM integrity, cerebral blood flow, neuronal integrity (fractional anisotropy), and neurometabolite concentrations.
Results: No subcortical lesions were evident on diffusion weighted imaging and WM fractional anisotropy was unaffected. Mean WM blood flow was upregulated by 20% to over 25 mL · 100 g-1 · min-1. Gray matter flow was unchanged. There were no changes in gray matter or cerebellar neurometabolites. In parietal subcortical WM, levels of γ-aminobutyric acid (GABA) fell from (mean ± SD) 1.68 ± 0.2 to 1.35 ± 0.3 institutional units while glutathione (GSH) fell from 1.71 ± 0.4 to 1.25 ± 0.3 institutional units. Lactate increased postexposure in five subjects.
Conclusions: Postexposure decrements in GABA and GSH imply WM insult with loss of neuroprotection and oxidative stress. An association between decrements in GABA and GSH support a common origin, while GSH decrements also correlate with WM blood flow responses. WM lactate increments are prone to error but suggest dysregulation of subcortical microvascular flow. WM neurometabolite and blood flow indices did not normalize by 24 h postexposure. Connolly D, Davagnanam I, Wylezinska-Arridge M, Mallon D, Wastling S, Lee VM. Brain magnetic resonance imaging responses to nonhypoxic hypobaric decompression. Aerosp Med Hum Perform. 2024; 95(10):733-740.
期刊介绍:
The peer-reviewed monthly journal, Aerospace Medicine and Human Performance (AMHP), formerly Aviation, Space, and Environmental Medicine, provides contact with physicians, life scientists, bioengineers, and medical specialists working in both basic medical research and in its clinical applications. It is the most used and cited journal in its field. It is distributed to more than 80 nations.