Sarah
Postpolio/ MS similarity
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SarahLonglands
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LOL Brock, Mr. Rhodes is Marie, M. R. Rhodes and she is one of the best friends anyone could have.
Sarah
Sarah
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
Every time I see a post where someone is quoting a neuro as saying that MS "burns itself out", I am just aghast at the neuro. I would like for someone to show me some EVIDENCE that this is the case instead of just saying it.mrhodes40 wrote:
Buying the neurologist's theory that MS burns itself out and SPMS is like PPS, if there is not inflammation and the "MS process" has burned itself out and now you are just stuck with SPMS which is a degeneration of the workaround nerves, then they should last as long as polio survivers nerves do and they should only break down to the extent that the original exacerbations did.
In other words once you reach the SPMS phase in that model it should mean things calm down a lot and you should stay at that functional level for decades, only to maybe lose ground in old age to the level of your worst exacerbation because that is the only area of these workaround nerves .
MS would not be the feared disease it is if that was true and people would look forward to the SPMS phase because it would mean the end to new losses, although you potentially could lose as much as you had in your worst exacerbation.
I kind of think he is wrong about the PPS idea. I bet there is some loss along those lines, but my guess is that it is in addition to the regular degeneration of MS, that it occurs in late years and it is probably invisible by that time in the MSers life.
The positive thing in that is that some of the drugs for RRMS might help SPMS too if they are regenerative and protective as well as antiinflammatory.
THoughts? flaws in my logic?
marie
My own experience is that I have gotten worse every year I have had this disease even though I have been out of the RRMS inflammatory stage for several decades. There has never been a time when I thought that I was stable and not getting worse or that the MS had "burned out".
It is more difficult to know what the daily subtle changes are in my health, but when I look back one year, two years, or five years, it is very clear that the disease is continuing to worsen and that I am continuing to go downhill.
My first three neuros are now dead and two others have retired, so it is not possible to go back to the originals that saw me in some of my worst conditions. But if I could see some of them, I do not believe any would tell me that the disease was burned out.
Is it possible that those of us with SPMS who know that no treatment exists for us simply do not go to the doctor for neurological testing and we are in fact hidden to the medical society and thus are counted as doing well or that it is implied that our disease has been arrested?
The one main difference I have seen when reverting from RRMS to SPMS is that I no longer have bad relapses. Instead, it is a continuing slow physical disablement with few small relapses that usually happen after another illness such as the flu or a cold. But during this time frame when SPMS took over I have gone from being able to walk holding on to my husband's arm to using a walker or wheelchair all of the time. To me that is more telling than some doctor saying that the disease will basically calm down over the years.
My sister-in-law, who I have known for over 40 years, had polio as a child. She has walked with a noticeable limp all of these years due to one leg being shorter and deformed from the polio. She has not changed in any other ways physically during all of these years. Her disease has indeed "burned out". Mine has not and I believe neuros that continue to say such a dumb thing are truly uninformed.
As far as a med that can be used to treat both types of MS, I have no idea when or if that will happen. Like many others on this forum, I believe that no resolution will come for those of us stuck with this disease until the culprit causing it is found. I do hope that those of you just beginning the long years ahead with MS are helped at some point with something that gets to the cause and not the symptoms.
gwa
Had once hypothesized that PPS was similar to Varciella.
At one point Varicella is "Chicken Pox" with one generally self limiting manifestation and later in life Varicella reactivation presents in another manifestation "Shingles".
Previously dormant virus migrates and creates new havoc with different disease presentation. Everyone with "Chicken Pox" as a child isn't predestined to get "shingles" later in life.
Since everyone with polio isn't predestined to PPS, why couldn't the same be true for polio virus? The dormant virus acts in the brain in a new way - PPS?
If we look at other so called "autoimmune" diseases like MS similar disease staging occurs to RRMS, SPMS, PPMS, etc...
Take the disease Rheumatoid Arthritis (RA), like MS, it too comes in several forms. Early aggressive with explosive onset and rapid erosision in joints and then also in varying degrees of severity including a mild and generally self limiting presentation. RA is by many rheumatologists considered to be a disease that for many patients eventually "burns it self out" and patients "smolder" to varying degrees with disease at this point.
Also like MS, patients with RA, can have low tender and swollen joint counts (standard RA measurement), considered to have burned out/smoldering disease and at this point, really start to erode in the joints. Signs and symptoms seem to be down but the most permanently damaging form of the disease - joint erosion - at play behind the scenes.
Also like MS, RA had been found to have causal links to not only certain food proteins but also virus, bacteria, fungal and other pathogenic causes.
Begs the question, if people are infected with something - be it viral, bacteria - etc... or most likely some combination of pathogens, at some point, in some subset of the infected, does the infection change form, change mechanism of damage ?
Just thowing out possible theories...
At one point Varicella is "Chicken Pox" with one generally self limiting manifestation and later in life Varicella reactivation presents in another manifestation "Shingles".
Previously dormant virus migrates and creates new havoc with different disease presentation. Everyone with "Chicken Pox" as a child isn't predestined to get "shingles" later in life.
Since everyone with polio isn't predestined to PPS, why couldn't the same be true for polio virus? The dormant virus acts in the brain in a new way - PPS?
If we look at other so called "autoimmune" diseases like MS similar disease staging occurs to RRMS, SPMS, PPMS, etc...
Take the disease Rheumatoid Arthritis (RA), like MS, it too comes in several forms. Early aggressive with explosive onset and rapid erosision in joints and then also in varying degrees of severity including a mild and generally self limiting presentation. RA is by many rheumatologists considered to be a disease that for many patients eventually "burns it self out" and patients "smolder" to varying degrees with disease at this point.
Also like MS, patients with RA, can have low tender and swollen joint counts (standard RA measurement), considered to have burned out/smoldering disease and at this point, really start to erode in the joints. Signs and symptoms seem to be down but the most permanently damaging form of the disease - joint erosion - at play behind the scenes.
Also like MS, RA had been found to have causal links to not only certain food proteins but also virus, bacteria, fungal and other pathogenic causes.
Begs the question, if people are infected with something - be it viral, bacteria - etc... or most likely some combination of pathogens, at some point, in some subset of the infected, does the infection change form, change mechanism of damage ?
Just thowing out possible theories...
Great point, interesting post Daisy! It seems that some of these diseases do have a two phase nature.Begs the question, if people are infected with something - be it viral, bacteria - etc... or most likely some combination of pathogens, at some point, in some subset of the infected, does the infection change form, change mechanism of damage ?
Picking up on the stage angle, several infective things have stages like syphilis and lyme, both have well defined stages that are different in manifestation. Syphilis even has one type problem in the brain and a special separate one in the cord called tabes dorsalis. If one is treated with antibiotics the spinal functional losses are difficult to resolve.
One of the most watershed moments for me mentally was when I read the story of a Dr Kalokerinos who was responsible for public health and vaccination of aboriginal children. They had a death rate from vaccination of about one in two (He wrote a book, every second child).
He discovered that they had a low level vitamin c deficiency because these children often had a recent respiratoy infection which depleted their resources to the point the vaccination was devastating to the immune system and they became severely, life threateningly ill.
These kids were given a gram of vitamin c, mind you that's an amount that one can buy at the store, and, voila, kids were safe.
If these kinds of subtle undetectable differences in people's nutiritional status make all the difference in a vaccination for some people then why not in infection?
PPS is not thought to be a reactivation, but it sure is similar to MS in that it is a late development of an earlier process.
OTOH, If it is a reactivation, then it would seem that some people who had the "mild" version who noted only a cold like illness would get the later reactivation, whereas with the other theory that it is deterioration of substitute nerve pathways, makes sense if it is only people who had severe polio in the first round. I do not know the answer to that at all, if people with mild polio ever develop PPS, or people are told they have PPS only to be shocked to realaize they ever had polio at all.
Last edited by mrhodes40 on Wed Aug 06, 2008 9:26 am, edited 1 time in total.
SPMS is something different with it's lack of inflammation but here's what I have been thinking this last couple of days:
MS, thought to be autoimmune, is inflammatory in the early stages and we say that eventually causes the permanent damage to the nerves that then deteriorate without ceasing.
Some even speculate that the inflammation got "stuck" behind the BBB and is self sustaining, but since there is little to no inflammation at that point I am not buying that.
If MS is autoimmune then why would it turn off at that point? Why stop being an inflammatory autoimmune process?
ANd if it has turned off, then would not the deterioration be limited and stop some time after that? We know the brain is plastic. Even people who had strokes a long time ago can recover function with effort.
But no, the SPMS phase in non-inflammatory AND it goes on and on as GWA mentions. Getting worse and worse with continually new losses.
If you go with the PPS idea and say well the inflammatory part is over but the nerves are just deteriorating because they are weaker nervepathways being workarounds of earlier damage done during the RRMS phase, then, again I say why would those pathways not last 50 years like they do in PPS patients?
Why would MS patients stop having inflammation (supposedly stopping the autoimmune attack phase) and then have progressive deterioration that starts immediately, and which involves new areas? Doesn't this indicate there is degeneration with no inflammation?
And since we know MS even from the earliest phases is both degenerative as well as inflammatory (the main reason given for using DMARD's the minute diagnosed), and we also know that the SPMS phase is degenerative ONLY, does not that make the common denominator degeneration?
Why create this story about inflammation and decide that is the culprit for everything when degeneration is the constant?
I think the answer is that MS is a degenerative disease and inflammation is just the body's reponse to it. Simple as that. In later phases the inflammation does stop obviously but the degeneration, the real disease process, continues which is why people get new deficits and continue to lose new function not just the functions that were impacted in the inflammatory phase.
The MS process has NOT stopped in the SPMS phase, it is just not inflammatory any longer.
That's the conclusion I have come to.
The interesting question is, what causes the degeneration?
MS, thought to be autoimmune, is inflammatory in the early stages and we say that eventually causes the permanent damage to the nerves that then deteriorate without ceasing.
Some even speculate that the inflammation got "stuck" behind the BBB and is self sustaining, but since there is little to no inflammation at that point I am not buying that.
If MS is autoimmune then why would it turn off at that point? Why stop being an inflammatory autoimmune process?
ANd if it has turned off, then would not the deterioration be limited and stop some time after that? We know the brain is plastic. Even people who had strokes a long time ago can recover function with effort.
But no, the SPMS phase in non-inflammatory AND it goes on and on as GWA mentions. Getting worse and worse with continually new losses.
If you go with the PPS idea and say well the inflammatory part is over but the nerves are just deteriorating because they are weaker nervepathways being workarounds of earlier damage done during the RRMS phase, then, again I say why would those pathways not last 50 years like they do in PPS patients?
Why would MS patients stop having inflammation (supposedly stopping the autoimmune attack phase) and then have progressive deterioration that starts immediately, and which involves new areas? Doesn't this indicate there is degeneration with no inflammation?
And since we know MS even from the earliest phases is both degenerative as well as inflammatory (the main reason given for using DMARD's the minute diagnosed), and we also know that the SPMS phase is degenerative ONLY, does not that make the common denominator degeneration?
Why create this story about inflammation and decide that is the culprit for everything when degeneration is the constant?
I think the answer is that MS is a degenerative disease and inflammation is just the body's reponse to it. Simple as that. In later phases the inflammation does stop obviously but the degeneration, the real disease process, continues which is why people get new deficits and continue to lose new function not just the functions that were impacted in the inflammatory phase.
The MS process has NOT stopped in the SPMS phase, it is just not inflammatory any longer.
That's the conclusion I have come to.
The interesting question is, what causes the degeneration?
When research focuses more on these aspects that you have brought up, we will be closer to some meds that help. All of the focus on lesions is a waste of time, in my opinion. That was stuck even further in my mind, after I went through an MRI last year which showed no lesions.mrhodes40 wrote:SPMS is something different with it's lack of inflammation but here's what I have been thinking this last couple of days:
Why create this story about inflammation and decide that is the culprit for everything when degeneration is the constant?
I think the answer is that MS is a degenerative disease and inflammation is just the body's reponse to it. Simple as that. In later phases the inflammation does stop obviously but the degeneration, the real disease process, continues which is why people get new deficits and continue to lose new function not just the functions that were impacted in the inflammatory phase.
The MS process has NOT stopped in the SPMS phase, it is just not inflammatory any longer.
That's the conclusion I have come to.
The interesting question is, what causes the degeneration?
That would sound wonderful if I had been on any drug for all of these years and could give the drug credit.
The truth is that I have not been on anything for over 20 years and before that I was only on steroids for periods of bad relapses. I am really concerned that all of this focus on number of lesions is very unhelpful to all of us.
What needs to be happening is research that targets the neuro degeneration of the brain and CNS in general. At that point, science will be on the right tract.
All of the attention to lesions and autoimmunity has gotten us nowhere for decades and is keeping our treatment in the Dark Ages.
Did I mention that I agree with your conclusions, mrhodes?
gwa
Hi GWA
You know, we are in an interesting an unenviable position. Unlike some others whose feet are on this path in the last 10 years, we have been promised and have seen things not work out time and again.
What happens to us? We get critical and stop buying into the status quo because our own lives are proof of the opposite.
In spite of this I am now an EDSS 6 (self assessed; cane use all the time) and SPMS! That is what all the stopping of inflammation was supposed to prevent!
It took 6 years after going on cop to begin to see that I was slipping in spite of the great MRI's and the lack of inflammation. I kept blaming it on lack of exercise or an off day but eventually I recognized there was real loss there and I was limping all the time. Now at 11 years we see the results in undeniable clarity; SPMS.
My biggest fear is that 10 years from now there will be a plethora of reports that gee, all the newer immune suppressant therapies have surprisingly still allowed SPMS to happen! Rapidly follwed by a collective head scratching and bemusement and puzzlement among the neurological community as they regroup and finally recognize that the degenerative component was far more important than the inflammatory and that they need to figure out what is causing it and address it. They'll be back at first base.
What I really want is for the recognition to come now and for them to get going this month, this week!
I have kids and grandbabies, none of whom seem at this point in time to have MS but I really want this thing cleared up. For all of us.
that's how I feel this week.
You know, we are in an interesting an unenviable position. Unlike some others whose feet are on this path in the last 10 years, we have been promised and have seen things not work out time and again.
What happens to us? We get critical and stop buying into the status quo because our own lives are proof of the opposite.
Ihear you! I got copaxone the month it came out and have had no inflammation all since that time on any MRI. I could jog--JOG-- three times a week at that time. I did have some very slight increase in lesion size in an MRI in '05 that was considered to be inconsequentially small, no enhancement at the MRI time.That would sound wonderful if I had been on any drug for all of these years and could give the drug credit.
In spite of this I am now an EDSS 6 (self assessed; cane use all the time) and SPMS! That is what all the stopping of inflammation was supposed to prevent!
It took 6 years after going on cop to begin to see that I was slipping in spite of the great MRI's and the lack of inflammation. I kept blaming it on lack of exercise or an off day but eventually I recognized there was real loss there and I was limping all the time. Now at 11 years we see the results in undeniable clarity; SPMS.
My biggest fear is that 10 years from now there will be a plethora of reports that gee, all the newer immune suppressant therapies have surprisingly still allowed SPMS to happen! Rapidly follwed by a collective head scratching and bemusement and puzzlement among the neurological community as they regroup and finally recognize that the degenerative component was far more important than the inflammatory and that they need to figure out what is causing it and address it. They'll be back at first base.
What I really want is for the recognition to come now and for them to get going this month, this week!
I have kids and grandbabies, none of whom seem at this point in time to have MS but I really want this thing cleared up. For all of us.
that's how I feel this week.-
cheerleader
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Marie and gwa,
Thanks to both of you for speaking plainly about your situations. You are right, current medicine focuses on stopping inflammation, because lesions are something that can be quantified. Docs and big pharma can't point to a picture of neurodegeneration, it cannot be seen on current MRIs. My husband has loads of lesions and little disability. I don't think copaxone alone has slowed his disease (for now) It may have calmed the inflammation, but what about neurodegeneration?
I'm excited about the research being done in protein aggregation and mitochondrial disfunction, and how this affects neurodegeneration. Most of the research is in Alzheimers....but I hope it might carry over into MS. For all our kids.
AC
Thanks to both of you for speaking plainly about your situations. You are right, current medicine focuses on stopping inflammation, because lesions are something that can be quantified. Docs and big pharma can't point to a picture of neurodegeneration, it cannot be seen on current MRIs. My husband has loads of lesions and little disability. I don't think copaxone alone has slowed his disease (for now) It may have calmed the inflammation, but what about neurodegeneration?
I'm excited about the research being done in protein aggregation and mitochondrial disfunction, and how this affects neurodegeneration. Most of the research is in Alzheimers....but I hope it might carry over into MS. For all our kids.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
I agree there is exciting work in other fields, thanks for reminding me, Cheer! I forgot in my fog of mental adjustment to the new diagnosisI'm excited about the research being done in protein aggregation and mitochondrial disfunction, and how this affects neurodegeneration. Most of the research is in Alzheimers....but I hope it might carry over into MS. For all our kids.
AC
I will not deny it is possible, but I lean the other way towards the idea that the MS process is some type of degenerative process that inflammation is trying to correct/heal.situation of degeneration in the "SEEMING" absence of inflammation?
Again the pathology that Prineas and Barnett photographed and documented where in the nerves were dead with no immune system there at all supports the idea that the degeneration comes first.
My personal experience seems to support it. That's all I'm saying.
If we could get MRI's that can look at microglia and see if they are activated or not (probably impossible) in areas where we have altered N-Acetyl aspartate changes or other functional changes indicative of degeneration we might get somewhere.
At any rate, degeneration is an important component to address, for everyone no matter what you believe is the cause of MS.
My personal favorite theory is an infective cause that has been overlooked and grossly misunderstood.
thanks everyone for participating in this debate about the idea that SPMS might be the same mechanism at PPS
We generally seem to conclude that:
1 although some people have thought PPS might be similar to SPMS, no one elses doctor seems to be offering that explanation to them
2 PPS degeneration is limited to areas formerly impacted and SPMS is not
3 there are a number of illnesses that have well defined stages that are known to be infective (polio syphilis vericella). Though this proves nothing, is supports my favorite idea for the MS cause which is that it is infective because it shows that infective illnesses may present in such a staged manner.
4 In spite of my shock and general need to adjust to my new diagnosis, you guys have been kind to participate in this thread. Thanks.
