Abstract:Individuals susceptible to high altitude pulmonary edema show altered pulmonary vascular responses within minutes of exposure to hypoxia. We hypothesized that a similar acute-phase vulnerability to hypoxia may exist in the brain of individuals susceptible to acute mountain sickness (AMS). In established AMS and high-altitude cerebral edema, there is a propensity for vasogenic white matter edema. We therefore hypothesized that increased cerebral blood flow (CBF) during acute hypoxia would also be disproportiona… Show more
“…They found a greater degree of rCBF in the forebrain grey matter during acute hypoxia and speculated that this localised response might be ascribed to an acute compensatory mechanism involving regions with increased sensitivity to oxygen deficits, possibly because they would develop reversible neuronal impairment. However, DYER et al [30] found that there was no difference in the percentage change of rCBF in different regions of the brain during acute hypoxia. The discrepant findings might have been due to differences in the degree of hypoxia or differences in the methods used to assess rCBF (fMRI versus single-photon emission computed tomography).…”
This study was designed to investigate the association of perceived dyspnoea intensity with cortical oxygenation and cortical activation during exercise in patients with chronic obstructive pulmonary disease (COPD) and exertional hypoxaemia.Low-intensity exercise was performed at a constant work rate by patients with COPD and exertional hypoxaemia (n=11) or no hypoxaemia (n=16), and in control participants (n=11). Cortical oxyhaemoglobin (oxy-Hb) and deoxyhaemoglobin (deoxy-Hb) concentrations were measured by multichannel near-infrared spectroscopy. Increased deoxy-Hb is assumed to reflect impaired oxygenation, whereas decreased deoxy-Hb signifies cortical activation.Exercise decreased cortical deoxy-Hb in control and nonhypoxaemic patients. Deoxy-Hb was increased in hypoxaemic patients and oxygen supplementation improved cortical oxygenation. Decreased deoxy-Hb in the pre-motor cortex (PMA) was significantly correlated with exertional dyspnoea in control participants and patients with COPD without hypoxaemia. In contrast, increased cortical deoxy-Hb concentration was correlated with dyspnoea in patients with COPD and hypoxaemia. With the administration of oxygen supplementation, exertional dyspnoea was correlated with decreased deoxy-Hb in the PMA of COPD patients with hypoxaemia.During exercise, cortical oxygenation was impaired in patients with COPD and hypoxaemia compared with control and nonhypoxaemic patients; this difference was ameliorated with oxygen supplementation. Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients. @ERSpublications Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients
“…They found a greater degree of rCBF in the forebrain grey matter during acute hypoxia and speculated that this localised response might be ascribed to an acute compensatory mechanism involving regions with increased sensitivity to oxygen deficits, possibly because they would develop reversible neuronal impairment. However, DYER et al [30] found that there was no difference in the percentage change of rCBF in different regions of the brain during acute hypoxia. The discrepant findings might have been due to differences in the degree of hypoxia or differences in the methods used to assess rCBF (fMRI versus single-photon emission computed tomography).…”
This study was designed to investigate the association of perceived dyspnoea intensity with cortical oxygenation and cortical activation during exercise in patients with chronic obstructive pulmonary disease (COPD) and exertional hypoxaemia.Low-intensity exercise was performed at a constant work rate by patients with COPD and exertional hypoxaemia (n=11) or no hypoxaemia (n=16), and in control participants (n=11). Cortical oxyhaemoglobin (oxy-Hb) and deoxyhaemoglobin (deoxy-Hb) concentrations were measured by multichannel near-infrared spectroscopy. Increased deoxy-Hb is assumed to reflect impaired oxygenation, whereas decreased deoxy-Hb signifies cortical activation.Exercise decreased cortical deoxy-Hb in control and nonhypoxaemic patients. Deoxy-Hb was increased in hypoxaemic patients and oxygen supplementation improved cortical oxygenation. Decreased deoxy-Hb in the pre-motor cortex (PMA) was significantly correlated with exertional dyspnoea in control participants and patients with COPD without hypoxaemia. In contrast, increased cortical deoxy-Hb concentration was correlated with dyspnoea in patients with COPD and hypoxaemia. With the administration of oxygen supplementation, exertional dyspnoea was correlated with decreased deoxy-Hb in the PMA of COPD patients with hypoxaemia.During exercise, cortical oxygenation was impaired in patients with COPD and hypoxaemia compared with control and nonhypoxaemic patients; this difference was ameliorated with oxygen supplementation. Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients. @ERSpublications Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients
“…Subsequently, an expansion of the extracellular space occurs (vasogenic edema), which is only observed with more prolonged or severe hypoxic exposure in conjunction with high-altitude cerebral edema. In opposition to this hypothesis, Hunt et al 8 identified no evidence linking cerebral edema to acute mountain sickness susceptibility after 2 days at 3,800 m, although this result is not surprising given the low incidence of high-altitude cerebral edema at altitudes between 2,500 and 5,000 m. 22 Given that a central tenant of the intracellular swelling explanation is disruption of cellular membrane Na þ /K þ ATPase, it should be remembered that global increases in cerebral blood flow 23,24 and maintained or increased global cerebral metabolic rate of oxygen 11,25,26 have been observed. Thus, it is possible that the reduction in white matter water mobility as observed herein is the consequence of regionally reduced white matter blood flow and oxygen delivery because of transient or persistent elevations in intracranial pressure.…”
Elevated brain water is a common finding in individuals with severe forms of altitude illness. However, the location, nature, and a causative link between brain edema and symptoms of acute mountain sickness such as headache remains unknown. We examined indices of brain white matter water mobility in 13 participants after 2 and 10 hours in normoxia (21% O 2 ) and hypoxia (12% O 2 ) using magnetic resonance imaging. Using a whole-brain analysis (tract-based spatial statistics (TBSS)), mean diffusivity was reduced in the left posterior hemisphere after 2 hours and globally reduced throughout cerebral white matter by 10 hours in hypoxia. However, no changes in T 2 relaxation time (T 2 ) or fractional anisotropy were observed. The TBSS identified an association between changes in mean diffusivity, fractional anisotropy, and T 2 both supra and subtentorially after 2 and 10 hours, with headache score after 10 hours in hypoxia. Region of interest-based analyses generally confirmed these results. These data indicate that acute periods of hypoxemia cause a shift of water into the intracellular space within the cerebral white matter, whereas no evidence of brain edema (a volumetric enlargement) is identifiable. Furthermore, these changes in brain water mobility are related to the intensity of high-altitude headache.
“…The first step down the path to brain swelling is hypothesized to be increased cerebral blood flow and associated increased cerebral blood volume, which directly produces brain swelling-leading to increased capillary pressure and cerebral edema. We previously found that increased cerebral blood flow is a common outcome of ascent to high altitude, 17 as is cerebral swelling and reduced CSF volume, 18 but neither was associated with a greater propensity to develop AMS. An alternate hypothesis for brain swelling and symptoms of AMS may relate to compromised cerebral energy status.…”
Section: Diffusion-weighted Mri Changes In Acute Mountain Sickness Jsmentioning
Diffusion magnetic resonance imaging (MRI) provides a sensitive indicator of cerebral hypoxia. We investigated if apparent diffusion coefficient (ADC) and transverse relaxation (T 2 ) predict symptoms of acute mountain sickness (AMS), or merely indicate the AMS phenotype irrespective of symptoms. Fourteen normal subjects were studied in two groups; unambiguous AMS and no-AMS at 3,800 m altitude (intermediate AMS scores were excluded). T 2 relaxation was estimated from a T 2 index of T 2 -weighted signal normalized by cerebrospinal fluid signal. Measurements were made in normoxia and repeated after 2 days sustained hypoxia (AMS group symptomatic and no-AMS group asymptomatic) and after 7 days hypoxia (both groups asymptomatic). Decreased ADC directly predicted AMS symptoms (Po0.05). Apparent diffusion coefficient increased in asymptomatic subjects, or as symptoms abated with acclimatization. This pattern was similar in basal ganglia, white matter, and gray matter. Corpus callosum behaved differently; restricted diffusion was absent (or rapidly reversed) in the splenium, and was sustained in the genu. In symptomatic subjects, T 2,index decreased after 2 days hypoxia and further decreased after 7 days. In asymptomatic subjects, T 2,index initially increased after 2 days, but decreased after 7 days. T 2,index changes were not predictive of AMS symptoms. These findings indicate that restricted diffusion, an indicator of diminished cerebral energy status, directly predicts symptoms of AMS in humans at altitude.
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