Recent imaging studies in hypoxic volunteers

Progress in magnetic resonance imaging (MRI) technology have allowed for accurate determinations of brain volume and of the vasogenic and cytotoxic components of brain edema in hypoxic studies with and without AMS symptomatology. Hackett et al. reported on an intense transverse relaxation rate (T2) signal in white matter, mainly in the splenium of the corpus callosum, and no grey matter abnormalities in 7 of 9 patients with high altitude cerebral edema, investigated after evacuation from high-altitude locations [7].

Figure 2a. Typical recordings of blood pressure (BP) and middle cerebral artery blood flow velocity (Vmca) in a subject in normoxia (upper panel) and in hypoxia (lower panel). Arrows indicate the onset of BP drop.
Figure 2b. Autoregulation index (ARI) calculations in normoxia (upper panel) and in hypoxia (lower panel).

A typical case is illustrated in Figure 4. Similar images were reported by Matsuzawa et al. in the sickest four of 7 subjects with severe AMS after 24 hours of altitude exposure [20]. These results are in keeping with previous CT scan demonstrations of cerebral edema in severe AMS [16].

However, more recently, Morocz et al. imaged the brains of 11 healthy volunteers before and after 32 hours of hypobaric hypoxic exposure to an altitude equivalent to 4572 m, and the majority of whom developed significant AMS scores [21]. The volumes of the brains increased by 2 to 3% (corresponding on average to 24 to 37 ml, with extremes at of 2.5 ml and 71 ml) due to an increased volume of cortical and subcortical grey matter and no change in the white matter and without correlation to AMS scores. The T2 signals in the white matter, which are normally increased in focal

Figure 3. Blood pressure and blood pressure (BP) versus middle cerebral artery velocity (CBFV) in a subject in normoxia and in hypoxia. A cerebral closing pressure (CCP) is estimated by the extrapolation of a linear approximation describing pressure-flow plots. Hypoxia decreased CCP.

Figure 3. Blood pressure and blood pressure (BP) versus middle cerebral artery velocity (CBFV) in a subject in normoxia and in hypoxia. A cerebral closing pressure (CCP) is estimated by the extrapolation of a linear approximation describing pressure-flow plots. Hypoxia decreased CCP.

Figure 4. Left, Axial T2-weighted magnetic resonance image of a patient with high altitude cerebral edema showing markedly increased signal in corpus callosum (arrows), including both the genu and the splenium, as well as increased signal of periventricular and subcortical white matter. Right, Axial T2-weighted magnetic resonance image of the same patient 5 weeks after original presentation, demonstrating no residual abnormality in splenium (arrow). (From reference 7, with permission).

Figure 4. Left, Axial T2-weighted magnetic resonance image of a patient with high altitude cerebral edema showing markedly increased signal in corpus callosum (arrows), including both the genu and the splenium, as well as increased signal of periventricular and subcortical white matter. Right, Axial T2-weighted magnetic resonance image of the same patient 5 weeks after original presentation, demonstrating no residual abnormality in splenium (arrow). (From reference 7, with permission).

brain edema, remained unchanged. Fischer et al. reported on MRI of the brains of 10 subjects exposed to a simulated altitude of 4500 m for 10 hours after the administration of either a placebo, theophylline or acetazolamide [5]. Although 8 of the 10 subjects presented with moderate to severe AMS, there was no MRI of cerebral edema, irrespective of the medication taken. However, there was a moderate swelling of the brain, as indicated by a significant reduction of the inner cerebral fluid volume.

Most recently, Bailey et al. combined molecular and neuroimaging techniques to investigate whether hypoxia-induced release of oxygen free radicals might account for vasogenic edema and increased intracranial pressure in AMS [2]. Twenty-two subjects were exposed for 18 hours to 12% oxygen breathing, with sampling of blood and spinal fluid for oxygen free radicals measurements, lumbar puncture to estimate intracranial pressure, and MRI at the end of the hypoxic exposure. A clinical AMS was diagnosed in 50% of the subjects. Electron paramagnetic resonance spectroscopy identified a clear increase in blood and spinal fluid oxygen free radicals. Intracranial pressure remained normal. There was a slight increase in brain volume, by an average of 7 ml (0.6%) with no evidence of edema. There was tendency for greater increase in brain volume in the sickest subjects, without relationship to oxidative stress or intracranial pressure.

The experiment was repeated by Kallenberg et al., who applied T2- and diffusion-weighted MRI to 22 subjects exposed during 12 hours to a 12% oxygen, corresponding to the altitude of 4500 m [12]. A clinical AMS was diagnosed in 50% of the subjects. Hypoxia was associated with an increase in brain volume, increased T2 and a general trend towards an increase in the diffusion coefficient, indicating both vasogenic and cytotoxic edema. While thus there was cerebral edema as a cause of increased volume of the brain, only the diffusion coefficient (cytotoxic edema) was correlated to AMS symptomatology. The authors concluded that a tightly-fitting brain caused by both vasogenic and cytotoxic edema may prove of pathophysiological importance in AMS.

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