Tissue oxygenation and post-covid brain fog: any link?
Many of us are more and more believing that there is a link between poor functioning in patients with long covid and some sort of problems in the use of oxygen from tissues. Either mitochondria struggle to use them, or the endothelial cells can create some sort of problems in the transport of oxygen from red blood cells to tissues. About the latter, this may due to the endothelitis that is documented in long covid, as you can read from previous posts about thromboinflammation and microclots, leading some of us to use enoxaparine or other agents acting on coagulation or platelets to improve this problem.
In this study, using frequency-domain near-infrared spectroscopy (fdNIRS), the authors measured cerebral tissue oxygen saturation (StO2) (a measure of hypoxia) in participants who had contracted COVID-19 at least 8 weeks prior to the study visit and healthy controls. They also conducted neuropsychological assessments and health-related quality of life assessments, fatigue, and depression.
Fifty-six percent of the post-COVID-19 participants self-reported having persistent symptoms, with the most reported symptom being fatigue and brain fog. There was a gradation in the decrease of oxyhemoglobin between controls, and normoxic and hypoxic post-COVID-19 groups (31.7 ± 8.3 μM, 27.8 ± 7.0 μM and 21.1 ± 7.2 μM, respectively, p = 0.028, p = 0.005, and p = 0.081). 24% of convalescent individuals’ post-COVID-19 infection had reduced StO2 in the brain and this was assocaited with reduced neurological function and quality of life.
The authros suggest that with the fdNIRS technology, combined with neuropsychological assessment, clinicians may identify individuals at risk of hypoxia-related symptomology and target individuals that are likely to respond to treatments aimed at improving cerebral oxygenation. Potential options, that of course should be tested in a trial, can be indeed agents acting on the endothelial system, particularly agents like enoxaparine which not only prevents coagulation but also has antiinflammatory and protective roles on the endothelial cess, as I have mentioned here. Other options may be newer agents, hyperbaric oxygen, vasodilators, or other targets switching off inflammation in tissue sanctuaries, like the brain.
Importantly, these data are somehow in line with the existing literature, which showed a link between inflammation and hypoxia, in general but also specifically in covid and post covid, as discussed in several previous posts in my blog.