Could this be an indicator that I have progressiveMS not RR?

[zjac020]

Thank you both.

I have had one relapse in the past, hence im still technicallly CIS, i have a feeling the CCSVI hasnt worked and maybe the blockage is slightly worse in some of the veins now, that would explain a few things. Nothing has majorly changed, so unless MRIs detect new lesions or i have another relapse, then i guess ill continue being CIS.

I agree that I think this disease is either one that takes a dozen different courses or a dozen differnt diseases with a few similarities and hence the labelling (CIS, RR, SP, PP) is very limited.

Scott1 - uric acid was always towards the low end, but still within reason. I read some of the trials on inosine (uric acid precursor, as im sure you already know) and incorporated inosine into my regimen to keep my UA towards the higher end of the range. It seems to have worked.

Thanks all

[Scott1]

Hi,

That's good news about the uric acid.

When I was first diagnosed over 20 years ago there was very little information available. It was superficial and often founded on ignorance. It is a lot better these days.
I am happy to try to answer questions but you are doing the right thing looking under every rock. Sometimes understanding about your own situation comes from reading broadly about things that immediately don't seem to relate. Can I suggest a few books to broaden your knowledge 1) The Sinatra Solution: Metabolic Cardiology by Stephen Sinatra, 2) Healing Lyme disease coinfections by Stephen Harrod Buhner, 3) Essential of Neural Science and Behaviour by Kandel,Schwartz and Jessell and absolutely anything written anywhere by Csaba Szabo on Peroxynitrite (http://www.nature.com/nrd/journal/v6/n8 ... d2222.html ).

Remember there is no magic bullet and you are peeling an onion so go layer by layer. I still don't know what you find when you finish peeling!

Regards

[David1949]

1 eye I'm not sure why you are so insistent that all MS is the same. Many people with RRMS are plagued by relapses. I have PPMS and have never had a relapse or remission after 20 years with the disease. Also, the drugs that are somewhat effective for RRMS cases are not effective at all for PPMS. The age of onset is also different being about 10 years later for PPMS than RRMS. And the distribution between men and women is different. RRMS is 2 to 3 times more common in women than in men , but PPMS effects men as often as women.

[Scott1]

Hi,

I think the distinction to draw is between symptom and cause. The symptoms can vary but the cause has a common path. Otherwise they are different diseases. There seem to be too many overlaps for that to be true. I hear everything you say about the differences but its obviously a multifactorial affliction. Location, infection and coinfection, metabolic disturbances, age, gender, exposures to stress, and so on will all impact. There is no predictive tool that forecasts accurately the time and nature of MS onset. It's a huge jump to then say we don't know what is happening but these symptoms are different forms of the same disease. It's probably the same disease with poor descriptions.
Regards

[vesta]

Thank you both.

I have had one relapse in the past, hence im still technicallly CIS, i have a feeling the CCSVI hasnt worked and maybe the blockage is slightly worse in some of the veins now, that would explain a few things. Nothing has majorly changed, so unless MRIs detect new lesions or i have another relapse, then i guess ill continue being CIS.

I agree that I think this disease is either one that takes a dozen different courses or a dozen differnt diseases with a few similarities and hence the labelling (CIS, RR, SP, PP) is very limited.

Scott1 - uric acid was always towards the low end, but still within reason. I read some of the trials on inosine (uric acid precursor, as im sure you already know) and incorporated inosine into my regimen to keep my UA towards the higher end of the range. It seems to have worked.

Thanks all

I would suggest getting a FONAR cine upright MRI to determine if your cerebrospinal fluid is obstructed. upright doc can answer questions on the subject. I myself think progressive MS is caused by skeletal obstructions of blood/cerebrospinal fluid flow, pressure ON the vein rather than a problem IN the vein which means venoplasty will be of little use. Or pressure directly on the spine, CSF. Regards

[hmacoli]

Hi Scott

Very interesting post about EBV ant their effects on MS. It has clarified some aspects of my MS as a younger suffer of EBV in an aggresive way when I was 5 years all, just after my tonsils were unfortunately removed, because furthermore it wasn't necessary because I didn't suffer in that moment of tonsils infection.

My question is related with arginine because it is no clear to me if arginine intake as a supplement may enhance virus like EBV. The links and the information about this aminoacid tends to avoid it in people with virus like herpes( EBV seems to be a kind of herpes HHV 4). In the other hand Dr Lawrence who followed LDN therapy with other supplements, recommends to try to enhance oxide nitric NO in endothellium through by different ways. He doesn't exactly talk (that I know) about arginine but it is curious that this supplement tends to promote NO interchange. I would like to know your oipnion about this question
Thanking in advance
Hugo

[lyndacarol]

Very interesting post about EBV ant their effects on MS. It has clarified some aspects of my MS as a younger suffer of EBV in an aggresive way when I was 5 years all, just after my tonsils were unfortunately removed, because furthermore it wasn't necessary because I didn't suffer in that moment of tonsils infection.

Hi and welcome to ThisIsMS, Hugo.

I am curious… Do you know if nitrous oxide was involved in the surgery to remove your tonsils? Nitrous oxide is often used with children – nitrous oxide inactivates B12 in the body. If B12 levels were low to begin with, an actual B12 deficiency could have been created.

[Scott1]

Hi Hugo,

Good question.

It's probably best to break it down. I never think about limiting NO . I'd rather focus on the form of Nitric Oxide synthase (NOS) involved. There are two distinct forms; constitutive and inducible. The constitutive form is either neuronal or endothelial. They are fine. The inducible form (iNOS) is the variety the body creates when confronted with injury (eg you cut yourself) or when the constitutive forms are not available. It is structurally different and more stable than the other varieties. iNOS is elevated in studies of people with MS.
If the body is producing assymetricdimethylarginine (ADMA) that will inhibit all isoforms of NOS. This means it's more likely that the iNOS will end up as the predominant form. On it's own that's not an issue unless there is a source of excess superoxide and it combines with the resultant NO to produce peroxynitrite which is bad news.
I use arginine to offset the problem of ADMA. It's a useful vasodilator and you need to do something else to deal with the superoxide. As an EBV infected B cell is a prolific producer of superoxide then you need to directly affect the EBV. My preference is valacyclovir as it puts a stop in the codan of the EBV to stop it replicating. Over time, the viral load will drop.
I set my thinking out here - http://www.thisisms.com/forum/regimens- ... 24019.html

The important thing to remember is you need a multipronged approach. There is no one single thing to do where you can say that's enough.

Regards

[MrChris]

Zjac020,

Id be interested in knowing what your lyme testing came back as and what antobodies tested Indicative or positive?