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Kleiner wrote:Does anyone know of any correlation between MS (CCSVI) and sleep apnea? I was diagnosed with sleep apnea while going through the million tests to detemine i had MS. I tried the CPAP machine for months but it didn't offer any relief. I am starting to now think that my sleep apnea could have something to do with blood flow and not enough oxygen to the brain and that is what is waking my up constantly not the typical sleep apnea (throat closing). Just a theory and I was wondering if anyone else had any thoughts on this.

Thanks

Hi Kleiner--
Jeff used to wake up gasping for air a few times every night. He'd also thrash and spasm a lot... his doctor thought it was sleep apnea, and he had a sleep test scheduled. We ended up canceling it before he had angioplasty at Stanford. Since the angioplasty, he no longer wakes up gasping, no snoring, no spasms. The change has been remarkable. The only change was the angioplasty and opened jugular veins. We now think that the gasping was his body's way of waking him, so he would sit up and breath.

Here's an interesting study. Doctors here call MS sleep apnea "central sleep apnea" ...meaning it is linked to lesions in the brain, not obstructions in the throat.

We performed polysomnography on eight randomly chosen male patients who met Poser's criteria for definite multiple sclerosis (MS), to obtain an idea of the frequency and severity of sleep apnea (SA) in this population. Ages ranged from 27 to 67 years (mean, 50 years). The mean Kurtzke's disability score was 6.1. Only one complained of awakenings with shortness of breath. Otherwise, none had a history of sleep disorder or significant pulmonary disease. We found that two patients had an apnea index greater than 5, with oxygen desaturation to 60% in one. Two others had apnea indices less than 5, but had oxygen desaturation to 59% and 81% during the apneas. Two patients had apnea indices less than 5 without oxygen desaturation. The apneas were mainly central type, except in one who had a mixed central-obstructive pattern. These preliminary results suggest that SA in MS may be more frequent than suspected, and it can be associated to significant oxygen desaturation in some cases. The potential impact of SA in MS deserves further evaluation. Key Words: Sleep apnea—Multiple sclerosis—Automatic respiration—Central apneas—Apneas with central nervous system lesions.

http://nnr.sagepub.com/content/3/3/133.abstract

I'm sure "central apnea" is what the docs would have called Jeff's apnea...but it resolved the day after his angioplasty. Does this mean the lesions in his brain healed overnight? No. It means he was receiving oxygen.
cheer

But have you noticed: if only jugulars are involved, the only benefits of Liberation occur during sleep. (Or hospitalization.) Conversely, if the jugulars are the only thing blocked, the only problems happen during sleep.

Hmm. But it can't be that binary a matter. My feet turned purple standing up when awake, now (jugulars opened) they don't. Likewise cogfog. Improvement often seems to be immediate and not posture-dependent.
-d

There's a particular sign in the Zamboni ultrasound that counts as an indicator of CCSVI. It's when the jugular's CSA is bigger when you're standing then when you're lying down. I don't get why. But it would be something that if the jugulars were cleared improvements would happen when standing as well.

My take on that one is that there is some flow diverted from the vertebrals when you are upright. It should not be there. I don't know what causes them to collapse in the upright position, but I hears it's pretty dramatic when you are watching it on Doppler.

This sounds like the negative CSA thing. It will go negative if the cross-sectional area (CSA) is relatively smaller (prone minus upright is a negative number). Two things could be at fault: 1 the jugulars fail to grow larger when you lie down; 2 they fail to grow smaller when standing up. It's still relative: Prone is smaller: neg CSA. I think the prone CSA is normally be the larger of the two. P > U is normal. U > P is abnormal.

Sounds like what is happening is when you lie down the flow is normally off-loaded from the vertebrals (maybe because there is no more gravity to move it to or through them). But if there is a blockage, perhaps they fail to inflate when you lie down. So then, blood will be driven by gravity when upright, and maybe goes through collateral veins when you lie down. When upright, there will still be a blockage, so maybe the gravity that normally closes them can't do it because of something stopping it. So an obstruction might actually be keeping them more open when you are upright. I can't remember but I would imagine this is a measurement at the widest part of the vein. I think what can happen is the collapse and disuse when you are upright doesn't happen because the overall capacity is too low (stenosis in vertebrals?) and there is always enough upstream pressure to keep the jugulars patent.

I don't know. I would like to know more about that switchover, the mechanics of it normally. What parts of the brain are involved...

Isn't hemodynamics fun?