Can CPAP treatment reverse damage to brain cells?

[rested gal]

The poster nicknamed split_city raised some interesting questions on page 6 of this topic:

Jul 10, 2007 subject: You can't die from Sleep Apnea

split_city wrote: "So there are studies out there which is looking at the effect of hypoxia. I have no doubt there are other studies which look at the effect of hypoxia on cell death in mice.

The question is, does hypoxia cause irreversible damage to cells in OSA patients? If so, how does this effect cognitive function?"


I think many of us who are using CPAP treatment have wondered, "If damage has been done to my brain cells during so many untreated years of not getting enough oxygen while I slept, how much of the damage can be repaired by consistent CPAP treatment now?"


There were some interesting links about the possibility of residual damage in this topic:

Jul 21, 2005 subject: Brain Fog topic started by DCTom

One of the links (which unfortunately no longer works) was to this:

Editorial in Journal of Sleep 2004 titled "Residual Sleepiness in Patients with Optimally Treated Sleep Apnea: a Case for Hypoxia-Induced Oxidative Brain Injury"

Excerpt from the editorial:

"Thirdly, chronic exposure to the features of OSA, such as repetitive intermittent hypoxia, arousals from sleep, or both, could cause neuronal dysfunction. The increased cell apoptosis, which occurs in the hippocampus and cortex of rats chronically exposed to intermittent hypoxia, supports this latter suggestion.[9] Indeed, in these animals, the neuronal dysfunction has been shown to be in the C1A hippocampal region, an area known to be associated with spatial memory and susceptible to hypoxic damage. Interestingly, in this study, the impaired ability to perform spatial memory tasks was only partially reversed after 14 days of normoxia, suggesting residual damage.
In patients with OSA, focal lesions have been detected in the left hippocampus[10] and in more diffuse areas of the brain[11]; as yet, these changes have not been linked to functional consequences. Further research will doubtless explore these tantalizing links between changesin brain morphology and the neurocognitive functional consequences."

_______________


A couple of other links, which do still work (so far):

High Altitude Study
(There are little forward/backward arrows above the article to "turn" pages.) Below is an excerpt from page 439:

"Interestingly, a few studies have even reported that some of the changes in performance after exposures to extreme altitudes persist for up to a year or longer after return to lower altitudes, although much debate surrounds this issue (Bahrke and Shukitt-Hale, 1993)."



"Cause or Effect? Gray Matter Loss in OSA Patients" Article from Pulmonary Reviews

From the article:
LOS ANGELES — The brains of patients with obstructive sleep apnea (OSA) appear to have decreased amounts of cerebral gray matter, researchers have found.[1] Whether the loss of gray matter contributes to OSA or vice versa is not known, but reduced gray matter may perpetuate the dysfunction of upper airway muscles.
Investigators from the Department of Neurobiology at the University of California in Los Angeles used magnetic resonance imaging (MRI) to compare the brain morphologies of 21 men who had documented OSA and 21 healthy controls. The control group also underwent sleep studies to verify the presence or absence of breathing disturbances.
The MRI scans were analyzed using morphometry designed to detect regional gray matter volume changes. Volume measurements were calculated for white matter, gray matter, the two combined, and cerebrospinal fluid.

DIFFERENCES IN GRAY MATTER

The OSA patients had significantly less gray matter than did the control group. The extent of gray matter loss increased with the severity of OSA. Differences in gray matter between the two groups varied from 2% to 18%, depending on which region of the brain was examined.
There were no between-group differences in white matter or cerebrospinal fluid. Because of the decrease in gray matter in the OSA patients, however, the ratio of total gray-to-white matter volume was significantly greater in the control group. In this group, but not in the OSA patients, the ratio of gray-to-white matter volume declined significantly with age.

WHICH CAME FIRST?

According to the researchers, the results of this study suggest two possibilities. The first is that gray matter loss is a consequence of apnea, and the second, that preexisting gray matter abnormalities contribute to the emergence or maintenance of OSA.[1] Damage to certain areas of the brain may play a role in the cognitive deficits that sometimes accompany OSA.
The investigators noted that at least some changes in the brains of patients with OSA may have resulted from the hypoxia that, along with hypercapnia and elevated blood pressure, occurs during episodes of OSA. Peripheral tissue oxygen saturation during apneic episodes in severe OSA can fall to 70% or less. Repeated episodes of hypoxia can damage gray matter, and patients with OSA have reduced cerebral blood flow.[1]
Conversely, reduced regional gray matter may have preceded OSA and contributed to its development. Reductions in gray matter can be congenital or acquired. This study found gray matter loss with age in the control group but not the OSA group, suggesting that damage to gray matter occurs early in OSA patients. Additionally, in a number of medical conditions, cerebellar damage results in a high incidence of sleep-disordered breathing.
We are left with the question of whether brain changes are a result of OSA or whether they precede it. In an editorial, David Gozal, MD, asked, “Is it the chicken or is it the egg?”[2] For now, he wrote, we can only speculate.

—Gale Jurasek

References
1. Macey PM, Henderson LA, Macey KE, et al. Brain morphology associated with obstructive sleep apnea. Am J Respir Crit Care Med. 2002;166:1382-1387.
2. Gozal D. The brain in sleep-disordered breathing: is it the chicken or is it the egg? Am J Respir Crit Care Med. 2002;166:1305-1306.

[Goofproof]

I don't believe damaged brain cells can be repaired. Someone I know has had 47 Electro Shock Therapies, the brain has sucessfully rerouted all the bad things the EST was done for, the Treatments worked, but only for a short time (under 3 months), then the beast rears it ugly head again.

BTW: Most EST treatments used normally are under 13. We only use a small portion of our brains, some use less than others. It seems that the memories can be shifted from one location to another within the brain, that's why stroke patients can recover some use. Jim

[Snoredog]

Here is the link to that missing report:

http://www.ncbi.nlm.nih.gov/sites/entre ... t=Abstract

http://ajrccm.atsjournals.org/cgi/conte ... 71/12/1325

I have the complete report somewhere on one of my computers, just threw out a printout of that the other day, it was a good read.

http://www.med.umich.edu/opm/newspage/2 ... sorder.htm

My understanding is neuro pathways may remap themselves to other healthy parts of the brain but with ischemia, cells don't grow back, I would assume that would be the same in other types of brain injury including the effects from loss of oxygen.

http://physrev.physiology.org/cgi/conte ... /79/4/1431

From the above article:

J. Hypoxia/Ischemia

Unilateral carotid occlusion is combined with hypoxia. In adults, the oxygen is lowered to ~3% and leads to eventual infarction in the MCA territory. It is essentially a focal insult that is now used infrequently (895) because adult animals do not survive the prolonged hypoxia reliably enough (948). However, the technique has been very successfully adapted to neonates that can reliably survive for days after insults of up to 3.5 h, and it is considered a very good model for major forms of neonatal metabolic brain damage (1164). Oxygen is generally lowered to 8% (for review, see Refs. 948, 959, 1141). This is almost a pure hypoxic insult, because the hypoxic vasodilation brings blood flow up to near control levels on the ligated side (982), although lateral cortex and caudoputamen still show blood flow reductions (368).

Fifteen to thirty minutes of hypoxemia (3%) causes early ischemic cell change and delayed neuronal death in CA1-CA3, striatum, and layer 5 of cortex in adults, much like global ischemia (980). In young rats, exposures of 60 min or longer to 8% hypoxia cause delayed development of infarct providing ATP levels fall to between 50 and 70% of control values (1213), much like their values in focal ischemia.

[rested gal]

Equally depressing... (Hey, we gotta laugh, or.. )

Neural consequences of sleep disordered breathing: the role of intermittent hypoxia.

So. All this makes me more convinced (not that I needed convincing) of the importance of using "cpap" EVERY sleeping moment. Even for naps.

We might not be able to undo all the previous damage, but we can sure prevent more damage from happening.

Janelle, a cpaptalk member from a couple of years ago, used to say in her sig line:

"That's your life hanging on the bedpost. Wear it!"

[Goofproof]

It pays to keep the cells from dieing off or being stressed unnecessarily. Everything we do that's harmful to our bodies should be stopped, A mind is a terrible thing to waste. Jim

[TXKajun]

Dang, ya mean I'm gonna be this stoopid the rest of my life???

Kajun

[DreamStalker]

So this would be a brain on hypoxia? ...



... and this would be a brain on xPAP? ...

[Babette]

Absolutely! My REALLY BIG BRAIN is just that size!

I personally have killed off lots of brain cells committing numerous felonies in several states. Good bless our state university system! But I digress...

I don't believe cells are regenerated. Brain or otherwise. I'm currently watching my stepfather retrain himself to be a functional human being after a mysterious breach of the blood/brain barrier 4 years ago. He's got alot of function and cognition back, but there are some missing things: His vision. His hearing. Certain memories. He remembers his high school pranks very well. He does not remember the time I broke my foot in the mid-1980's and had to move back in with him so he could care for me. That's really frightening to me that he can't remember something that significant in both our lives.

I think people with way more education than I can debate this, but I agree with the earlier post - far better to prevent brain cell death than try to "repair" the little suckers.

As Nancy Reagan said - Don't do drugs!

LOL,
B.

[Patrick A]

Okay




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[Rabid1]

Scary stuff RG. I wonder if there's any correlation between OSA and Alzheimer's.

Then there was that recent study that showed if you lose too much gray matter you become a.............. Congressman!

[Goofproof]

Scary stuff RG. I wonder if there's any correlation between OSA and Alzheimer's.

Then there was that recent study that showed if you lose too much gray matter you become a.............. Congressman!

Loss of brain mass won't make you a congress person, or even president, for that you require gene damage. Jim

[socknitster]

Scary stuff RG. I wonder if there's any correlation between OSA and Alzheimer's.

Rabid, it wouldn't surprise me if a link to that isn't eventually found. Late stage Alzheimer patients apparently sleep a lot. My grandmother went to bed one night at 11pm and didn't get up again until 6 pm the next day.

My dad is caring for her and his father. He is like: how do I make sure she takes her medicine, should I wake her up? As violent as she gets (and confused) it is tempting to just let her sleep all the time.

I'm not saying that is why I think there could be a link, just an observation about how an Alt patient sleeps a lot.

Jen

[Rabid1]

Jen,

I agree. One thing is for certain. OSA can't help Alzheimer's victims.

[JimW]

I've worked with at least one individual whose dementia was directly attributable to OSA. A relative had observed that individual to sometimes go four to five minutes without breathing while sleeping. Five minutes seems to ring a bell in terms of the time it takes without breathing for brain damage to set in, if I remember my CPR training correctly. Breathing is good!

[Rabid1]

I've worked with at least one individual whose dementia was directly attributable to OSA. A relative had observed that individual to sometimes go four to five minutes without breathing while sleeping. Five minutes seems to ring a bell in terms of the time it takes without breathing for brain damage to set in, if I remember my CPR training correctly. Breathing is good!

That's correct, but are there people with OSA that actually go that long without taking a breath?

And who would stand by for 4-5 minutes watching a relative suffocate?