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We all know how those Oligo bands are used to diagnose MS....the bands show signs that IgG has been elevated in the CNS, and myelin is being destroyed. The story MS patients have been told is that this is caused by a rogue immune system, eating up their myelin for no good reason.

BUT....Oligo bands are found in other cerebrovascular diseases...not just MS.

Oligoclonal immunoglobulin (Ig) bands were found in cerebrospinal fluid (CSF) by agarose gel electrophoresis and thin-layer polyacrylamide gel isoelectric focusing in 10 patients with cerebral infarction and 2 patients with transient ischemic attacks. Immunofixation revealed that the oligoclonal Ig was of the G class. One patient also had a band of free lambda light chains. The appearance of oligoclonal IgG during the course disease was observed in one patient, and the disappearance in six patients. Only three patients had elevated CSF IgG levels or abnormal synthesis rate of IgG in the nervous system. The oligoclonal reaction observed in acute cerebrovascular disease may reflect a polyclonal B-cell activation within the central nervous system after brain tissue damage.

http://www.ncbi.nlm.nih.gov/pubmed/6785663

If CCSVI is creating hypoxic brain tissue damage, than those oglio bands are not so surprising. Brain tissue damage activates B cells and the immune system...and stroke is not considered an "auto-immune" disease.
cheer

Oligoclonal bands also show up in the cerebrospinal fluid of patients with dementia..

The prevalence of oligoclonal bands in the CSF of patients with primary neurodegenerative dementia
Abstract.
Background: Recent guidelines from the United States and Europe on the diagnosis and management of dementia include advice that younger patients with dementia should undergo CSF examination, which frequently includes analysis for oligoclonal bands (OCB). The presence of CNS specific OCB has traditionally been considered suggestive of an inflammatory aetiology, although the interpretation of such a finding in the presence of a normal CSF white cell count and protein is more difficult.

http://www.springerlink.com/content/alchay4vglk2cw3f/

And not to put too fine a point on it, but dementia is also not considered an "auto-immune" disease.
cheer

Good points Cheer,

1. Why are there oligoclonal bands in the spinal fluid that point to an autoimmune process?

and

2. How can blocked jugular veins give you a lesion on your spine which is no where near the stenosis?

Those were my neuros 2 main points to argue against CCSVI.
I have got him an invite to the conference so hopefully he will go and his questions can be answered!

LR1234 wrote:Good points Cheer,

1. Why are there oligoclonal bands in the spinal fluid that point to an autoimmune process?

and

2. How can blocked jugular veins give you a lesion on your spine which is no where near the stenosis?

Those were my neuros 2 main points to argue against CCSVI.
I have got him an invite to the conference so hopefully he will go and his questions can be answered!

We can answer your neuro's questions today, but I'm sure he'll be more convinced hearing it from doctors

#1 see above. oligo bands and B cell activation occur in neurovascular disorders/stroke/dementia- and are in response to tissue damage/hypoxia which we see in CCSVI. No autoimmunity is necessary to get those bands.

#2 Dr. Zamboni's new paper on collateral circulation that forms due to CCSVI....it affects venous return throughout the body-
http://www.ncbi.nlm.nih.gov/pubmed/19534716

The significance of collateral circle is still neglected. To the contrary, substitute circles are alternative pathways or vicarious venous shunts, which permit the drainage and prevent intracranial hypertension. In accordance with the pattern of obstruction, even the intracranial and the intrarachidian veins can also become substitute circles; they permit redirection of the deviated flow, piping the blood toward available venous segments outside the central nervous system.

cheer

Cheer, this is what I was getting at in my posts the other month.

I am becoming more and more convinced that MS 'relapses' are the waxing and waning of ischemic events.

Jamie

I am becoming more and more convinced that MS 'relapses' are the waxing and waning of ischemic events.

Not sure what's convincing you but your idea seems to be consistent with this research--

Mild cerebral hypoxia-ischemia produces a sub-acute transient inflammatory response that is less selective and prolonged after a substantial insult

Cerebral ischemia initiates various injurious processes including neuroinflammatory responses such as activation of microglia and increases in cytokine and nitric oxide release

A mild insult produced a transient (1-2 days post) increase in activated microglia/macrophages within subcortical white and not gray matter but transiently increased cytokine or nitrotyrosine expression in cortex and not white matter.

There was also prolonged scattered cell death in cortex and white matter over weeks along with loss of myelin/axons and cortical atrophy at 4 weeks post-insult.

Thus, a transient neuroinflammatory response occurs following a mild insult whereas prolonged scattered cell death occurs for weeks, particularly in white matter.

I've had the thought that MS might be a "slow" stroke--for lack of better words. Here's New York- Presbyterian Hospital's take onCerebral Insufficiency

Cerebrovascular insufficiency may go symptom-free and undetected for years, until the sudden onset of a stroke.

The most common symptoms of a cerebrovascular insufficiency are:

•Weakness or numbness of the face, arm, or leg, especially on one side of the body

•Confusion or difficulty speaking or understanding

•Problems with vision such as dimness or loss of vision in one or both eyes

•Dizziness or problems with balance or coordination

•Problems with movement or walking

•Severe headaches with no other known cause

Looks like a very familiar laundry list to me.

Sharon

Sharon

I posted about this a while ago!



The pattern of ischemic stroke and symptoms are the same as MS but more violent.

There is even such a things as a transient ischemic attack that can cause MS type symptoms that go away.

Now if the ischemia was caused by vascular rather than arterial, thus less violent, methods then that would explain the waxing and waning and longer course of the MS damage.

Even the differences in disease type would correlate with blockage type as outlines in Zambonis paper.

It all fits.

Jamie

Oops--sorry I missed it.

Sharon

123

Sharon-
Thanks for the fantastic research. Yes, the list of symptoms looks alarmingly familiar...and the description of CCSVI in MS as a "slow stroke" is right on. I know we've been round this mulberry bush before, and I remember your thoughts, Jamie. We are like minded, buddy. It sure does seem like the glove is fitting, Chris.

Just found it interesting that the one "proof" of autoimmune attack of MS the neuros point to, those oglio bands, can be found in stroke, ischemia, dementia and other neurovascular disorders. And the fact that immune modulating medicines sort of work for awhile while the disease is inflammatory makes sense. But that does not mean MS is autoimmune. I think the neurological community took a giant leap of faith into the arms of pharmaceutical industry, and it is soon going to come back to haunt them.
cheer

Agreed above and with Sharon's thoughts.

Now, can we do LP pre and two months post surgery?

I'd have that as part of my study.

Shayk wrote:I've had the thought that MS might be a "slow" stroke--for lack of better words.

That's interesting because ever since I started having symptoms of PPMS, I've thought of MS as like having a stroke in slow motion.

Jamie wrote:Now, can we do LP pre and two months post surgery?

I've been wondering if the oligo bands might disappear following CCSVI repair.

Cheer: I admit I was bummed when you said you were leaving TIMS. But if this is how you leave, feel free to leave anytime.

Rokkit

Yes glad to see you still around Cheer:)!!!

I am going to copy and paste your post as a reply to my neuro's questions on e-mail:)

L x

Cheer

Just found it interesting that the one "proof" of autoimmune attack of MS the neuros point to, those oglio bands, can be found in stroke, ischemia, dementia and other neurovascular disorders

That's very interesting indeed--pathological studies (Barnett, Prineas, etc.) indicate the IgG in MS is non-specific.

Immunoglobulins and complement in postmortem multiple sclerosis tissue

INTERPRETATION: IgG and complement immunostaining of

disrupted myelin in MS lesions, frequently cited as an indication of

pathogenic anti-myelin antibodies, is a nonspecific feature that cannot be

interpreted as evidence of a distinct pathogenesis or serve to define

particular variants of the disease

Have a good day everyone.

Sharon

Jamie,

You mentioned you'd be happy to have spinal taps pre and post op. It makes so much sense to me and is something I've discussed off-board.

My neuro does a tap every 6 months. His primary reason for me is to make sure I don't have JC virus antibodies, since I'm on Ty. But he is also a reasearcher and uses the fluid in other analysis. He repeatedly looks at the macrophage, fetuin, and the osteopontin counts. It is a very quantitative view of MS immune activity.

I'd be the first one to line up for pre and post op taps. I'm very analytical and they are proof positive for me. I believe they are the window to activity moreso than an MRI.

If the neurologists ever come together with the interventional radiologists on CCSVI, and start to see the body as one system, then we'll have wholistic treatment and care. I just hope on Sept 8th, a huge shock wave hits the neurologists and they open their eyes to the reality of CCSVI.

Michelle