Please forgive my lack of moderation, dear Waleed Kassar. 40 years of experience with MS patients showed me indeed there are patients who are helped by the one or the other remedy. What all these experiences amounted to, however, is the urgency of individually tailored cures, and that these might only be achievable by what my booklet on "Multiple Sclerosis & CCSVI" suggests.

I haven't looked into it, but I suppose that a cytokine storm could be a cause for any immune related condition or syndrome. I think the focus relating to covid19 and CNS is mainly on epilepsy and cognitive deficits, still possible MS symptoms

This hypothesis would predict that immunosuppression would lessen the impact of Covid-19 (like in MS). The immune system wouldn't be as efficient in killing the cells as it used to, in this case.

Interesting theory.

Immunomodulation (but not immunosuppression in general) could potentially lessen the impact of (severe) Covid-19-complications. Tocilizumab (or other IL-6 inhibitors) possibly have a positive effect on (severe) Covid-19-complications.

Article Interleukin-6 Causes Endothelial Barrier Dysfunction via the...

Preprint Interleukin-6 in COVID-19: A Systematic Review and Meta-Analysis

Article Tocilizumab, an anti-IL-6 receptor antibody, to treat COVID-...

Article Tocilizumab treatment in COVID-19: A single center experience

https://www.biorxiv.org/content/10.1101/2020.04.08.029769v1

http://www.chinaxiv.org/abs/202003.00026

A potential problem with immunosuppression in general: rheumatoid arthritis patients, for instance, often get Methotrexate (mtx). Mtx is an immune suppressor that could potentially raise IL-6 (Olsen, 2014).

Article Methotrexate induces production of IL-1 and IL-6 in the mono...

Thank you very much. I agree with you many clinical studies prove a mild positive effect of immunomodulatory drugs (for instance I am under Rituximab and follow it closely even if it has a limited effect). It fits with the hypothesis as the immune system would be "weaken" in his attacks against the glial cells. Another interesting observation supporting the viral hypothesis is the current phase IIb trial of the Temelimab.

Studies from Carmen Guaza's group using a model of MS based on viral infection (with Theiler's virus) support the viral contribution to the pathogenesis in this disease

Please, Dr. Cazé, allow my reminding you of an abysmal gap separating the long-celebrated anatomical pathological MS-specifications (Carswell's lithograph of 1838, Charcot's lithograph in Ordenstein's thesis of 1867) and the clinical MS "forms" deprived of any specific morphological evidence.

The latter admits of endless etiopathogenic interpretations. The former not.

Azithromycin promising medicine for COVID 19 in early stage by effecting on mTOR and immune system

What I'm even more eager to learn about, Waleed Kassar, is how COVID 19 manifests in the CNS of patients with and without multiple sclerosis, the latter with and without immunomodulating treatments - especially in the lesion progression evident on serial MRIs.

Hasn't this been mainly as a complication of immunomodulatory treatments, Nasir Mustafa?

Hasn't the picture of primary varicella-zoster infections been well illustrated on MRIs ... and been shown to be radically different from what MS originally showed at post mortem? What is shown in my attachment (on double-clicks on the downward arrow in the middle of its menu line) has also been summarized in 2002: http://www.ms-info.net/evo/msmanu/984

Thank you Nasir Mustafa I'll look into the paper

I'm still wondering. Can a retrovirus infect oligodendrocytes and direct the healthy immune system against these cells to go out of them - causing MS?

Franz Schelling I don't understand your first remark, sorry I am not a virologist nor MD.

Why not wonder why clinical MS research hasn't produced a single piece of evidence that allows us to directly recognize the disease, Romain Daniel Cazé? In simply reiterating dogmatized conjectures, clinical neurology opened the "Porte de l'enfer" of endless speculations about neither properly identifiable nor curable a disease.

A closer look at the history of multiple sclerosis shows how clinicians knowing nothing about the conditions proper identification struggled at best to

> Forge Dawson's fingers from randomly sown encephalitis spots; > Stealthily replace Carswell's 'Peculiar Diseased State' by Rindfleisch's tabetic speckles; > In forgetting besides anything about Rucker's periphlebitis retinae, any prelesional "MS sans myelin" finding.

In not addressing these points will just go on to talk past each other.

Searching for the cause of a disease seems to be a good way to cure it, no? Franz Schelling

In my point of view

It is an immunity disturbance due excessive production of antibodies that unlike what happens in COVID 19 so MS patients are lower ability to develop serious symptoms if they will have infected . Further research are required

Romain Daniel Cazé, is there a clinical or immunological property that would allow identifying MS? How to search for, or even find a cure for a disease having no perceptible identity?

Waleed Kassar, which piece of evidence allows us to assume COVID 19 and multiple sclerosis shared some property that enabled our curing them in comparable ways?

In my point of view

The first evidence female comparing to male, in MS female double than male, while, in COVID 19 male double than female.

But the medicine of MS Should be reducing if the patients get infected or probability to get infection that for sure is refer to physician

Further research are required

Somewhat circumstantial, this piece of evidence, Waleed Kassar, isn't it?

Why not compare COVID 19 and MS directly, in doing our best to focus on their perceptible identifying features?

Dr. Franz

l wish I can help, that might help

MS highly antibodies, no proliferation, more in female and children ,anabolic dependent ,m TOR suppressive action

COVID 19 lower antibodies , proliferation, lower in female and children, catabolic dependent , m TOR excessive action

best regards

waleed

Is adding ever new non-specific MS lab and gender data making good for their lack of specificity, Waleed Kassar?

COVID 19 viruses, by way of contrast, have specific properties, specific antibodies, by which they are to be indubitably recognized.

I wish you could find out what I have put together as unmistakable anatomical pathological and lesion-spread features for identifying MS beyond any shadow of a doubt.

There has actually not been but a single objection to what has been compiled at

http://www.ms-info.net/evo/msmanu/984 (in 2002 :))

Otherwise, let's simply agree to disagree - offering my critique of the pandemonium of mainstream MS research would take too much of your time and researchgate space.

Dr.Franz it in my pleasure to have this discussion with you.

Identifying spot of light about MS it might help such as ( stimulating catabolic action that might bettering patients )

considering that I'm not neurologist

best regards

waleed

I have not yet seen anything in writing on the this, but I writing for Brazilian Immunology Society, say that this is possible. However, the multiple sclerosis is an multicausal disease and its is very dificult causal correlation, so far, knowing that MS is, also an autoimmune disease and, that many virus trigger immunological responses with potential for neuroinflammation and subsequent attacks against myelin. So, its possible, once that Coronavirus, as multisystem virus, the multiple sclerosis be promoted.

All depends on how multiple sclerosis (MS) is understood:

Understood as a process of neurological incapacitations having no distinctive physical property of its that is, besides, bound to remain unexplained, MS invites endless speculations about any cause or combination of MS causes, including virus(es) ... which yet must not be demonstrated as, otherwise, MS was no longer unexplained - and would show the characteristics of such injurious processes.

In relying on Carswell's and Charcot's original pictorial MS definitions and the later observations of the same findings, it becomes necessary to find some physical cause(s) for the given lesion spread.

Here, any attempt to improve on the published explanations of these MS-specific cerebral and/or spinal lesion developments has the potential to speed up the corresponding conditions' cures.

Franz Schelling

sir I think that prostaglandin stimulant and warm natural bath as well as energetic food, will be helpful why ?

because the problem is increasing differentiation pathway of the cell, will produce more lymphocytes leading to increasing antibodies, the balance might help patients. I trying to do me best with this issue

best regards

Please forgive my lack of moderation, dear Waleed Kassar. 40 years of experience with MS patients showed me indeed there are patients who are helped by the one or the other remedy. What all these experiences amounted to, however, is the urgency of individually tailored cures, and that these might only be achievable by what my booklet on "Multiple Sclerosis & CCSVI" suggests.

As for the, at times beneficial, "... warm natural bath as well as energetic food" effects it might yet be argued that both can prove individually detrimental a well:

All too much has here already been written under the heading of "Uhthoff's phenomenon".

The patient whose microscopical cervical cord findings led, in 1867, both Carl Frommann and Jean-Martin Charcot to speaking of the condition as a primary form of tissue hardening (sclerosis) had, in fact, died from not feeling his last warm bath was getting too hot - just to show that many MS remedies had their problematic sides as well.

Franz Schelling

we should take in our consideration the defect is due to metabolic reaction associated with genetic expression on one direction only which is anabolic reaction. That lead to reduction in myelnin production and repositioning on brain. For that I think the best advice in medications, should have role in regulate the metabolic reaction and daily behavior as well as neuro medicins, depending on nutritionists associated with neurologists

Article Myelination and mTOR

best regards

Ever heard of a metabolic reaction associated with a genetic expression that was diagnostic of MS, or even allowed the original identification of the condition, Waleed Kassar?

Nobody who read my "Multiple Sclerosis & CCSVI" booklet yet questioned that anatomical pathology achieved both of the latter goals.

Sorry, it takes time to verify what has been written and, above all, shown here ... and, apparently even greater efforts to falsify it.

May be infectious mononucleosis ?

With an MS declared to be not explainable symptoms, what might not be - always never committally - advanced for explaining it, Dr. Al Khalidi?

Hi Dr. Hasanain A. Al-Khalidi , thank you for providing a plausible answer. Franz Schelling could you avoid not answering the question and only posting your theory relative to MS (out of focus here) or I'll be obliged to report your posts.

Hasanain A. Al-Khalidi they are multiple candidates for viral triggers in MS and I agree with you mononucleosis is one of them, one good candidate is also the herpes virus. But does any of them directly attack oligodendrocytes?

Sorry for worrying about parallels that seem hard to see, Dr. Romain Daniel Cazé.

It's a pity I always seem to rely on background knowledge most aren't able to access.

All neurodegenerative diseases has as in common microenvironment the neuroinflammation. The multiple sclerosis, also. The SARS-CoV-2 promotes pyroptosis and presented tropism from CNS. We know that murine models, as with Theiler's encephalomyelitis virus, elicit SM. Moreover, the SM is a multifocal and multifaceted disease with much triggers undetermined, as others neurodegenarative disease. I think that would is determinant for study of COVID-19 as an possible SM promoters role. In addition, as trigger for others neurodegerative disease, as AD and PD. Others juvenile diseases as Diabetes mellutus 1, can also be elicited. In addition, genetic people with predispose can response with others autoimmune diseases with poor or null correlation with innumerable viral disease. Thus, this is moment for rastreable studies.