This Is MS Multiple Sclerosis Knowledge & Support Community

I have to give it to you guys, your faaaaaar braver than me. I have never had an LP, and could not, as it is not a "treatment", and just sounds so invasive; I mean "puncture", who thought that was a good name?

Remind me, do PP & SP MS show bands?

Well they used to call it Spinal Tap, and still do in England! That sounds worse!

I have had 3.....they are really not as bad as everyone makes out (as long as you get a good dr to do it) perhaps I have been lucky.

I've probably had at least a dozen, including the intrathecal methotrexate shots I had. It's not bad at all - a slight bee sting prick of novacaine and then you feel nothing. I get mine hunched over sitting on the doc's table in his office, it takes 10 minutes. I had one last week and for the first time ever I went by myself and had no problems. I lay low the day of and the day after.

An abstract that mentions that myelin basci protein is targeted after stroke, so not only is oligoclonal bands a non specific finding, MBP antibodies are too:

Immune mechanisms contribute to cerebral ischemic injury. Therapeutic immunosuppressive options are limited due to systemic side effects. We attempted to achieve immunosuppression in the brain through oral tolerance to myelin basic protein (MBP). Lewis rats were fed low-dose bovine MBP or ovalbumin (1 mg, five times) before 3 h of middle cerebral artery occlusion (MCAO). A third group of animals was sensitized to MBP but did not survive the post-stroke period. Infarct size at 24 and 96 h after ischemia was significantly less in tolerized animals. Tolerance to MBP was confirmed in vivo by a decrease in delayed-type hypersensitivity to MBP. Systemic immune responses, characterized in vitro by spleen cell proliferation to Con A, lipopolysaccharide, and MBP, again confirmed antigen-specific immunologic tolerance. Immunohistochemistry revealed transforming growth factor β1 production by T cells in the brains of tolerized but not control animals. Systemic transforming growth factor β1 levels were equivalent in both groups. Corticosterone levels 24 h after surgery were elevated in all sham-operated animals and ischemic control animals but not in ischemic tolerized animals. These results demonstrate that antigen-specific modulation of the immune response decreases infarct size after focal cerebral ischemia and that sensitization to the same antigen may actually worsen outcome.

FOUND HERE
ANOTHER ONE HERE

So this paper is discussing how a stroke's size (infarct size) is reduced by treating ahead of time to make sure the animal tolerates myelin basic protein rather than having the immune system attack it.

This would be your tovaxin type approach: make it so the body does not attack myelin=better stroke outcomes.

It is also known that if you give steroids or even the kind of immune suppressive drugs we give MS after stroke it improves outcomes. Again it is seen that the overactive immune system causes damage of its own by simply being there and responding to the stroke.

Of course it goes without saying that autoimmunity does not cause stroke.

If Dr Zamboni had not done his studies yet but the theory was out there as a hypothetical idea, it would still be a compelling theory just based on this other material.

In other words: this "story" about what causes MS is at least equal to the autoimmune "story" that they have been treating us with. Add to that the strong evidence in these large well blinded and controlled studies that it is actually there and it becomes very compelling.

It is a little specious to claim that this CCSVI is "unproven" when autoimmunity has NEVER been proven in MS either. As this thread highlights, a lot of the so called proof of autoimmunity is actually this kind of non specific material that does not actually mean "autoimmunity" at all even though they have been pretending that it does and using it to support the argument that they are justified to give immune suppressives so strong that we can actually get immune deficiency diseases.

There is no scientific moral high ground in the autoimmune model. The emperor has no clothes there.

And that's why I'm not getting involved in the 'debate'.

I've gone beyond personal reasonable doubt, we've acted and time will prove us right or wrong.

This MS business has never been an intellectual game for me, I'm a practical chap.

I've gone beyond personal reasonable doubt

well put me too.

http://www.neurology.org/cgi/content/abstract/65/4/513


Transient Ischemic Stroke lesions.

Background: In a general population of patients with stroke, the rate of new MRI lesions at 1 week was much higher than expected. With patients with minor stroke and TIA having a higher risk of recurrent clinical events, the authors examined whether patients with minor stroke and TIA also had a high rate of asymptomatic lesions on repeat MRI scanning.

Methods: Patients with minor stroke and TIA presenting within 12 hours of symptom onset with a NIH Stroke Scale score less than six, who had a baseline MRI and a 1-month follow-up, were enrolled in this study. The follow-up study was examined for new diffusion-weighted imaging lesions as compared to the baseline study. Clinical or MRI factors predicting recurrent lesions were examined.

Results: A total of 143 patients were enrolled and 14 patients (9.8%; 95% CI 5.4, 15.9) had MR evidence of new lesions at 30 days. Six of these new lesions were clinically asymptomatic (42.9%; 95% CI 17.7, 71.1). A trend to increased likelihood of new lesions at 30 days was seen with progressing baseline scan lesion number (none [2.2%], solitary [12.9%], multiple [19.8%]: p = 0.046). Patients whose mechanism of stroke was large artery or cardioembolic were the most likely to have new lesions on follow-up MRI.

Conclusion: Minor stroke and TIA are associated with a 10% risk of new lesions on MRI and half of these new lesions are asymptomatic. This risk is lower than seen in more severely affected patients with stroke. Patients with multiple lesions at baseline are at an increased risk for new ischemic lesions.




Lesions that don't necessarily correlate with symptoms/severity?

Cool ref Jamie!
I think the bottom line is a lot of stuff can happen in the brain and it can be covered by plasticity, but what is interesting about THAT is these are ischemic lesions from an arterial block-

-in other words the brain blood flow on the way IN got blocked and caused a traditional lack of oxygen incident that we associate with stroke, but we all know that MS can have lesions that are asymptomatic so how interesting that a traditional ischemia can cause ASYMTPOMATIC lesions.

Continuing my research into how CCSVI/stroke is involved with myelin based protein we find in CSF of MS patients. New research:

Background: Ischemic injury to the central nervous system causes cellular activation and disintegration, leading to release of cell-type–specific proteins into the cerebrospinal fluid (CSF). We investigated CSF concentrations of myelin basic protein (MBP), glial fibrillary astrocytic protein (GFAP), the calcium-binding protein S100B, and neuron-specific enolase (NSE) in acute ischemic stroke patients and their relation to initial stroke severity, stroke location, and long-term stroke outcome.

Methods: CSF concentrations of MBP, GFAP, S100B, and NSE were assessed in 89 stroke patients on admission (mean 8.7 h after stroke onset) and in 35 controls. We evaluated the relation between CSF concentrations and (a) stroke severity (NIH Stroke Scale [NIHSS] score on admission, infarct volume), (b) stroke location, and (c) stroke outcome (modified Rankin Scale [mRS] score at month 3).

Results: MBP concentration was significantly higher in subcortical than in cortical infarcts (median MBP, 1.18 vs 0.66 µg/L, P < 0.001). GFAP and S100B concentrations correlated with the NIHSS score on admission (GFAP, R = 0.35, P = 0.001; S100B, R = 0.29, P = 0.006), infarct volume (GFAP, R = 0.34, P = 0.001; S100B, R = 0.28, P = 0.008), and mRS score at month 3 (R = 0.42, P < 0.001 and R = 0.28, P = 0.007). Concentrations of NSE did not correlate with stroke characteristics.

Conclusions: MBP, GFAP, S100B, and NSE display relevant differences in cellular and subcellular origins, which are reflected in their relation to stroke characteristics. MBP is a marker for infarct location. GFAP and S100B correlate with stroke severity and outcome.

http://www.clinchem.org/cgi/content/abstract/56/3/451

Myelin based protein found in the CSF is a marker for stroke infarct and ischemic injury location--MBP is higher in subcortical, rather than cortical infarcts. Just an FYI---the area which is showing the most gray matter deposition of iron in CCSVI in Dr. Haacke's and Dr. Zivadinov's SWI-MRI is the subcortical part of the brain--the thalamus.
And I just want to say, a year later...I really, really miss these kind of posts and these kind posters....(sigh.)
cheer

Thanks Cheer for the info on the O-bands...last time we had a visit with a neuro, it was very unsatisfying. You get the usual "lesion there, O-band here, yes it's MS." I just want to yell, "You know nothing!!" It's even more frustrating, when they also say, "no, it isn't MS, so although your paper describing a patient with vascular abnormalities is very interesting, we can not accept it."
Anyhow, I had not heard you were leaving, so I am hoping you have changed your mind and stay. I haven't the mind nor the time to research papers... I'm more the arts than the sciences, you know? And I need things explained s l o w l y.
Why

Hi Why--started this thread a year ago, and took a break. I've taken some breaks over the past year, but pop back in for periods of time. I try to stay off a thread once it devolves into name calling (which is often, lately).

The fact that O bands are not exclusive to MS and are indicative of vascular disease is very important. New research is showing myelin based proteins in very specific types and locations of infarctions (which is tissue death due to obstructed blood flow.) Much study has been done on arterial infarcts, and hopefully with further CCSVI study, we are entering the era of understanding venous infarction as it relates to blockage of extracranial veins.

Hope you and your husband are hanging in there---
cheer

cheerleader wrote: And I just want to say, a year later...I really, really miss these kind of posts and these kind posters....(sigh.)
cheer

me 2.... i mainly just glance at who posted....

Hmmm, I thought I had seen that before! Now I'll remember it!
Well, we are puttering along....self-cathing seems to result in endless UTIs, which means weakness. Going to try a chiro this week to see if they can make any magic...

These are the kinds of posts I really appreciate. These are the kinds of posts which enabled me to make the decision to go forward 9 months ago. I miss the old posters and their amazing ability to discuss the science in an intelligent manner.
I say re-post ALL of the informative threads from the old days. This board will benefit!!!!!!!!!!!!!!!!!!!!!!!!!!