Here's the link and podcast
For those who have been following my writings on hypoxic injury to the brain, slowed perfusion and slowed mean transit time as studied in pwMS, you'll know that there are many studies in the literature showing that there is a slower transit of blood in the brains in MS. It takes longer for blood to get out of the MS brain (venous stenosis, anyone?) This means it takes longer for oxygenated blood to get into the brain. This slowed transit of blood leads to lower oxygenation of brain tissue.
Interestingly enough, those with hypoxic injury show atrophy of the hippocampus and hyperactive HPA axis. JUST LIKE pw MS
Here are some studies to back this up:
Several reports suggest that the activity of the hypothalamo-pituitary-adrenal axis (HPA-axis) is increased following hypoxia/ischaemia and that this might be associated with increased neuronal vulnerability
Hypoxia damages multiple organ systems especially those with high oxygen utilization such as the central nervous system. The purpose of this study was to compare the neuropathological and neuropsychological effects of hypoxia in patients with either carbon monoxide poisoning or obstructive sleep apnea. Neuroimaging revealed evidence of hippocampal atrophy in both groups...
I talked about this at length with Dr. Haacke last year. I know that he and Dr. Hubbard are looking at oxygenation levels in pwMS before and after angioplasty using fMRI BOLD technology, and they are finding that patients indeed have lower oxygen levels in their brains before, and better oxygenation after.
This chronic, low-level hypoxic injury is what I believe caused my husband's first MS flare. He was at high altitude for a week, and came home with a numb left side. His brain just couldn't take the additional low oxygen situation. That's when he got an MS diagnosis. I believe this is why people who live in Colorado (and other high elevation locations) have higher MS rates.
The pieces fit together when we look at MS as a disease of chronic venous insufficiency.