Post Hypoxic Demyelination

[magoo]

Thanks for all of the good info Cheer. I hate to see you go, but I completely understand. Please keep bumping up the research, maybe it will change the tone of this site back to the way it used to be? (Oh, I'm going to get jumped on by that remark )

I'm really frustrated with this site...no more discussion of research, and more interest with male-dominated bickering and arguing. No research cited, just opinion. Me thinks a vacation is in order. I'm over at Facebook and thru the Alliance.

Amen. Ugh.

[1eye]

Not sure where I am going, but I ain't lost...

Has anybody heard of epidemiological studies relating 'MS' incidence to altitude (remember many populations live at both predominantly high and predominantly low alltitudes)? Airplanes have not been around that long: maybe what the army brought to the Faroes in WW2 was flight?

[Cece]

let's create a CCSVI subforum, where only research posts are on topic and opinion posts get modded off?

I can contribute if wanted but I am not 100% yet on the research, I forget and have to relearn the same things, ugh.

[Johnson]

Thanks for all of the good info Cheer. I hate to see you go, but I completely understand. Please keep bumping up the research, maybe it will change the tone of this site back to the way it used to be? (Oh, I'm going to get jumped on by that remark 8O )

I'm really frustrated with this site...no more discussion of research, and more interest with male-dominated bickering and arguing. No research cited, just opinion. Me thinks a vacation is in order. I'm over at Facebook and thru the Alliance.

Amen. Ugh.

Word...

[David1949]

Maybe I'm missing something or maybe I've just grown a thick skin, but I don't see all the bickering going on. Compared to some sites I've seen this one seems quite tame. There are rarely any personal attacks or name calling. Could someone post a link to a comment that was offensive?

[Shayk]

David

Personally I think it's best that people pm you with links to offensive remarks. There's no shortage IMO.

Now, back to the thread discussion. I remain interested in research and thought this abstract probably belonged here as well.


Immunological consequences of ischemic stroke: Immunosuppression and autoimmunity

Here we summarize current knowledge on the immunological consequences of ischemic stroke and will discuss implications of these findings for our understanding of the immunopathogenesis of Multiple Sclerosis.

I've never been into the immune gig with MS but one basic understanding of the article I have is that the authors are posing the question: Why does the autoimmune response stop in stroke and persist in MS?

The mechanisms which perpetuate this autoimmune process to result in chronic autoimmunity (MS) or curtail the local autoimmune response (stroke) are not completely understood.

At any rate, it seems like they do identify similarities in the immune response in stroke with that in MS.

An open access article by some of the same authors Functional status of peripheral blood T-cells in ischemic stroke patients

And, another abstract, while it's on stroke, these authors also do MS research.
CD4(+)FoxP3(+) regulatory T-cells in cerebral ischemic stroke

Experimental cerebral ischemic stroke is exacerbated by inflammatory T-cells and is accompanied by systemic increases in CD4(+)CD25(+)Foxp3(+) regulatory T-cells (Treg). To determine their effect on ischemic brain injury, Treg were depleted in Foxp3(DTR) mice prior to stroke induction. In contrast to a recent Nature Medicine report, our results demonstrate unequivocally that Treg depletion did not affect stroke infarct volume, thus failing to implicate this regulatory pathway in limiting stroke damage

Looks like the immune response in stroke is starting to be a "hot topic".

Joan--thanks for all your research and hard work. Please do keep posting here. There's a few of us still interested in research.

Oops, I nearly forgot this, the most recent FDA approved drug for MS also shows some promise in stroke. Fingolimod provides long-term protection in rodent models of cerebral ischemia

Take care all

Sharon

[Rokkit]

Thank you Sharon! This is the way this forum used to be. Maybe we can get back to more of it.

[cheerleader]

Looks like the immune response in stroke is starting to be a "hot topic".

Thanks for the terrific research, Sharon. Great links.
Here's a whole thread I started on the autoimmune reaction of the body in stroke, cerebrovascular disease, carbon monoxide poisoning, and spinal cord injury.
http://www.thisisms.com/ftopict-14856.html

The body develops antigens to myelin based protein in the CSF----just like MS. But in all these other instances this "autoimmune reaction" is secondary to ischemic injury. Ischemia is the primary initiator of antigenic response to MBP. Why isn't this autoimmune reaction considered secondary in MS as well?
And as far as the continuing, chronic nature of the autoimmune reaction in MS in RRMS...it does wax and wane throughout the early disease--(due to hypoxic events or refluxive events leading to localized ischemia?) but eventually burns out once MS becomes progressive. Like lots of little TIAs.

I put it in the general thread, because I believe this new hot topic of studying the immune reaction to stroke needs to be connected to MS studies (not just CCSVI)
thanks again,
cheer

[Johnson]

Thank you Sharon! This is the way this forum used to be. Maybe we can get back to more of it.

I concur.

[silverbirch]

Bump ....



A good demo from top gear

[Shannon]

I remember seeing a study done awhile back on post mortem individuals who had suffered from schizophrenia, and they reported that what they found looked similar to what is found in MS, ie. oligoclonal bands in spinal fluid and something else having to with glial cells in the brain. I wonder if anyone remembers that study, or if I could find it somewhere again? The relationships with other disorders to MS is always interesting to me. My paternal grandfather happened to be schizophrenic, so of course, I was intrigued by the study at the time.

[Shannon]

Okay, I see that I have strayed off-topic (triggered by the discussion about spinal fluid, etc.) BUT, I encourage anyone interested in viral pathogenesis and more importantly, viral evolution within the human genome to read this article in it's entirety. It does deal mostly with schizophrenia, but you will see that MS is also discussed and a clinical trial is even proposed for the end of this year for HERV-W in MS:

http://discovermagazine.com/2010/jun/03 ... :int=0&-C=

I wonder how many of us were born in winter or early spring, when many virus' such as influenza are more prevalent? How it all relates to CCSVI, I don't have a clue, but there has to be some connection to this information and why some are born with deranged veins?

[cheerleader]

New research on hypoxia, high altitude and inflammation from the University of Colorado at Denver, in the New England Journal of Medicine
Hypoxic injury incurred by high altitude/low O2 exposure increases proinflammatory cytokines.
Hypoxia can create inflammation in the brain, and activate the immune system.
http://www.nejm.org/doi/full/10.1056/NEJMra0910283
http://www.ucdenver.edu/academics/colle ... ia2011.pdf

In persons with mountain sickness, for example, levels of circulating proinflammatory cytokines increase, and leakage of fluid ("vascular leakage") causes pulmonary or cerebral edema. Increased serum levels of interleukin-6, the interleukin-6 receptor, and c-reactive protein--all markers of inflammation--were increased in healthy volunteers who spent 3 nights at an elevation higher than 3400 m.
The development of inflammation in response to hypoxia is clinically relevant.

And new research compilation on hypoxic-ischemic brain injury-
How hypoperfusion affects the brain-

This state is characterized by cellular energy failure, membrane depolarization, brain edema, excess neurotransmitter release (particularly the excitatory amino acid neurotransmitters) and uptake inhibition, increases in intracellular calcium, production of oxygen-free radicals, lipid peroxidation, and disturbances in autoregulation of cerebral blood flow at the micro- and macroscopic levels (Calvert and Zhang 2005; Busl and Greer 2010). Hypoxic and hypoxic-ischemic states at least transiently disrupt brain function and, if sufficiently severe and/or prolonged, may lead to neuronal death and irreversible brain injury.

http://www.internationalbrain.org/?q=node/131
cheer