Aa
It's not the amount of lesions...
Hey all,
I went to the Neurologist (a new Neuro and an absolutely great one. One that was compassionate and caring and dern it....listened) yesterday and this is what I was told, that I did NOT know. It is not about how many lesions they see on MRI. It is about the amount of brain atrophy. She said that long before lesions appear, the medical community feels that the axions (axons) in the brain are transversed. Cut in half. Myelin damage long before any lesions are detectable on MRI.
She said this is when the damage from MS starts to occur. She said that what they worry about is the skrinking of the brain tissue. (atrophy) She said this is why it is so vitally important to get one on of the injectable or IV medications very early on, in the disease process.
I am going to do some research on this today and will post what I find out, for those who would like to know.
She was very upset that I have now been so many years without any treatment for the MS, but only for the symptoms. I discussed with her the people on this forum who absolutely feel that they have MS, some have lesions, some don't...she was appalled. She said that if a person already has lesions and they have had all other testing to rule out other disorders, that the patient should push to find another doctor, who will treat them and SOON; if the one they presently have, will not diagnose them with something. She said that the criteria for MS is clear. If a patient meets that criteria, then they should be on preventive therapy as soon as possible. Waiting, is allowing any brain atrophy to progress. She said that this is irreversible.
She said that it can progress to the point where one day, you may wake up blind in one eye or unable to walk without assistance. Just to name a couple of things. It's not worth the risk.
She also told me that person that presents with spinal lesions and very little "sensory symptoms" do not have a good prognosis for the future. Spinal lesions tend to affect the body in debilitating ways. If you present with mostly sensory symptoms and remain that way, this bodes for a more positive outlook for the long term. She said that damage is being done to our myelin whether we are in an attack or not. The axons or axions in the brain are being damaged. As I said, I have to do some more research.
I was crying so hard during my appointment, that I didn't hear everything and take in everything. It's only because I took the love of my life with me, that I remember anything about the appointment.
As some of you may remember, I had a Neuro that took away my MS diagnosis for almost 3 years. That man prevented me from getting the vital treatment for MS that I should have been on. Now the Neuro's from the Medical Center where I went for 8 years, allowed me to be without treatment for 5 of those 8 years. Knowing of the damage that was being done in my brain, for everyday that I was not treated.
I guess the whole point of my post, is not for sympathy, but to stress with every breath left in my body, to FIGHT for answers, if you are not getting them. Fight with everything that is within you, so that if you DO have MS, that you are treated appropriately and NOW...before any further damage occurs in your brain. Once our brains start to atrophy, this is brain tissue that is gone forever.
Heather
I went to the Neurologist (a new Neuro and an absolutely great one. One that was compassionate and caring and dern it....listened) yesterday and this is what I was told, that I did NOT know. It is not about how many lesions they see on MRI. It is about the amount of brain atrophy. She said that long before lesions appear, the medical community feels that the axions (axons) in the brain are transversed. Cut in half. Myelin damage long before any lesions are detectable on MRI.
She said this is when the damage from MS starts to occur. She said that what they worry about is the skrinking of the brain tissue. (atrophy) She said this is why it is so vitally important to get one on of the injectable or IV medications very early on, in the disease process.
I am going to do some research on this today and will post what I find out, for those who would like to know.
She was very upset that I have now been so many years without any treatment for the MS, but only for the symptoms. I discussed with her the people on this forum who absolutely feel that they have MS, some have lesions, some don't...she was appalled. She said that if a person already has lesions and they have had all other testing to rule out other disorders, that the patient should push to find another doctor, who will treat them and SOON; if the one they presently have, will not diagnose them with something. She said that the criteria for MS is clear. If a patient meets that criteria, then they should be on preventive therapy as soon as possible. Waiting, is allowing any brain atrophy to progress. She said that this is irreversible.
She said that it can progress to the point where one day, you may wake up blind in one eye or unable to walk without assistance. Just to name a couple of things. It's not worth the risk.
She also told me that person that presents with spinal lesions and very little "sensory symptoms" do not have a good prognosis for the future. Spinal lesions tend to affect the body in debilitating ways. If you present with mostly sensory symptoms and remain that way, this bodes for a more positive outlook for the long term. She said that damage is being done to our myelin whether we are in an attack or not. The axons or axions in the brain are being damaged. As I said, I have to do some more research.
I was crying so hard during my appointment, that I didn't hear everything and take in everything. It's only because I took the love of my life with me, that I remember anything about the appointment.
As some of you may remember, I had a Neuro that took away my MS diagnosis for almost 3 years. That man prevented me from getting the vital treatment for MS that I should have been on. Now the Neuro's from the Medical Center where I went for 8 years, allowed me to be without treatment for 5 of those 8 years. Knowing of the damage that was being done in my brain, for everyday that I was not treated.
I guess the whole point of my post, is not for sympathy, but to stress with every breath left in my body, to FIGHT for answers, if you are not getting them. Fight with everything that is within you, so that if you DO have MS, that you are treated appropriately and NOW...before any further damage occurs in your brain. Once our brains start to atrophy, this is brain tissue that is gone forever.
Heather
Heather so glad you have found a gem of a neuro. Gives us all hope to keep searching.... THanks for your pep talk to all of us.
Hang in there sweetie, and maybe with treatment at least things will become stable for you.
Sally
Hang in there sweetie, and maybe with treatment at least things will become stable for you.
Sally
Heather, thank you for the interesting post. Did your new doctor specify what is the best medications to be on in order to reduce "atrophy"
This is an interesting question. It wasn't really answered and don't think it can really be answered fully. All I understand, is that our brain suffers each and every time we have an attack...of course; but MS is active whether we are having symptoms or not. So being on one of the MS therapy's, Avonex, Copaxone, Rebif, Tysarbi, etc., is our only chance to reduce the unseen damage going on in our brains everyday. All of the drug company's that make these drugs, "claim" that their drug reduces the brain atrophy. And all of these drugs require an injection or are administered by IV.
My Neuro did tell me that very shortly, maybe next year, there are two drugs that will become available, that we will be able to take by mouth. This will be of great benefit to those of us that have to inject. Great benefit.
I worked very hard in my life in the past two years to lose over 100 pounds and finally come off of daily injections of insulin. Now here we go again...they now want me to take Copaxone, which I will again, have to inject everyday. Life seems unfair sometimes. I will do what I have to do though.
The important thing to remember, is this atrophy that the Neuro talked about, starts very early in the disease process...so it's vitally important to find a Neuro that will listen and take action. If that Neuro even suspects MS, I think he can do no harm to his patient by starting them on one of the MS drug therapys. Anything to help stop the damage being done in the brain and for matter the whole central nervous system.
I always thought it was important before, to push and push, to find a Neuro that will listen to you...now I know that our very quality of life, DEPENDS on it.
Heather
My Neuro did tell me that very shortly, maybe next year, there are two drugs that will become available, that we will be able to take by mouth. This will be of great benefit to those of us that have to inject. Great benefit.
I worked very hard in my life in the past two years to lose over 100 pounds and finally come off of daily injections of insulin. Now here we go again...they now want me to take Copaxone, which I will again, have to inject everyday. Life seems unfair sometimes. I will do what I have to do though.
The important thing to remember, is this atrophy that the Neuro talked about, starts very early in the disease process...so it's vitally important to find a Neuro that will listen and take action. If that Neuro even suspects MS, I think he can do no harm to his patient by starting them on one of the MS drug therapys. Anything to help stop the damage being done in the brain and for matter the whole central nervous system.
I always thought it was important before, to push and push, to find a Neuro that will listen to you...now I know that our very quality of life, DEPENDS on it.
Heather
Thanks so much for this report. I agree it's scary, but vital all the same.
I'm not sure how brain atrophy is recognized or diagnosed. Can it be seen on MRIs? Or is it an absence of matter so that the brain looks smaller? Or something else?
Let us know how you do regarding the new injections. I'm hoping your side effects will be few or none.
ess
I'm not sure how brain atrophy is recognized or diagnosed. Can it be seen on MRIs? Or is it an absence of matter so that the brain looks smaller? Or something else?
Let us know how you do regarding the new injections. I'm hoping your side effects will be few or none.
ess
Quix's famous thread on MRIs, Lesions and Symptoms has a very descriptive paragraph about this. Tried to cut and paste here, but couldn't, because MedHelp insists on putting in all those ridiculous definitions instead (ones that are totally out of context and SO annoying). Anyway, that's a good place to start, so I bumped the whole thread.
ess
ess
Amen ! That you found a doctor who looks on the preventing side and is willing to try something. I sure know how frustrating it is with doctors. I tried to convince my doc.. to just try some of the ms meds. when I had an attack and if it didn't work then maybe we're on the wrong track. They are all afraid to try things for this. I don't know why. God Bless You Eh !!!!!
Heather, I am so thankful that you have found a good neuro. I have a question. Is your neuro saying that brain atrophy is not normal? I have posted this before, but I have brain atrophy and little leg function left, and four neuros told me that brain atrophy and "parenchymal brain volume loss" are normal for a man of 50 yrs old, which I am. So is your neuro saying no to that? If so, then God led you to this person for sure!!
Thanks,
Craig
Thanks,
Craig
Craig, please see
http://radiology.rsnajnls.org/cgi/content/abstract/220/3/606
This pertains to patients with RRMS only. It seems that brain atrophy is to be expected for those patients, more so than in healthy persons. Other info I saw implied that a certain amount of atrophy is normal as we age, so I think the question is not whether atrophy is found, but to what extent.
ess
http://radiology.rsnajnls.org/cgi/content/abstract/220/3/606
This pertains to patients with RRMS only. It seems that brain atrophy is to be expected for those patients, more so than in healthy persons. Other info I saw implied that a certain amount of atrophy is normal as we age, so I think the question is not whether atrophy is found, but to what extent.
ess
Craig,
Ess is 100% on the money with her advice.
And to answer your question Craig, she (my Neuro) is not saying that brain atrophy is not normal. It happens to all of us as we age, to some degree. She was talking strictly about the atrophy seen in MS patients. Atrophy cause by repeated insults to the Central Nervous System due to MS/demyelination.
But again; ess is right... Way to go Ess....glad that you are on the ball...my brain has been "out to lunch" lately, so glad yours is working...LOL
Happy Thanksgiving to all of you, Heather
Ess is 100% on the money with her advice.
And to answer your question Craig, she (my Neuro) is not saying that brain atrophy is not normal. It happens to all of us as we age, to some degree. She was talking strictly about the atrophy seen in MS patients. Atrophy cause by repeated insults to the Central Nervous System due to MS/demyelination.
But again; ess is right... Way to go Ess....glad that you are on the ball...my brain has been "out to lunch" lately, so glad yours is working...LOL
Happy Thanksgiving to all of you, Heather
Thanks so much for sharing this info with all of us!! I am so sorry for what you have discovered about your delay in treatment but am ecstatic that you have found a "Super neuro" to get you straightened out and taken care of.
I hope that she is able to get you some pain relief also! I will be praying for you!
Happy turkey day!
Kristin
I hope that she is able to get you some pain relief also! I will be praying for you!
Happy turkey day!
Kristin
I am glad you have finally found a great neuro, even though it would have been appreciated years earlier, at least she can take great care of you now and stop any further damage.
I really appreciate you forwarding your info to this site, you always have great posts. It is very scary, but MS is scary.
Hope you are having a pain free day! I'm having a brain free day....ha....ha....ha, but I just had to thank you for this info.
Happy Thanksgiving
I really appreciate you forwarding your info to this site, you always have great posts. It is very scary, but MS is scary.
Hope you are having a pain free day! I'm having a brain free day....ha....ha....ha, but I just had to thank you for this info.
Happy Thanksgiving
The subject of MS and brain atrophy appears to be reported widely and there's lots on the web. Science Daily has a particulary interesting article which I'm pasting below. It describes a study that concludes that brain damage is done to what had apparently been thought to be unaffected brain tissue. So here it is:
ScienceDaily (Aug. 30, 2006) — "The effects of multiple sclerosis (MS) extend beyond visibly affected areas into large portions of the brain that outwardly appear normal, according to a study appearing in the September issue of Radiology.
"This disease process in the normal-appearing brain tissue affects the brain globally and has substantial clinical impact," said the study's lead author, Hugo Vrenken, Ph.D., from the Multiple Sclerosis Center at VU University Medical Center in Amsterdam, The Netherlands.
MS is a chronic, autoimmune disease characterized by the destruction of myelin, the protective layers that surround nerve cells. It can affect numerous body functions, and symptoms may include visual and speech impairment, memory loss, depression, muscle weakness, loss of coordination, numbness or pain, bowel and bladder problems and sexual dysfunction.
MS affects approximately 400,000 people in the United States and as many as 2.5 million worldwide, mostly women between the ages of 20 and 50, according to the National Multiple Sclerosis Society.
"The areas of demyelination, or lesions, in patients with MS can be visualized with magnetic resonance imaging (MRI). However, the volume of lesions visible at MRI only correlates moderately with clinical disability measurements," Dr. Vrenken said. "This may be due to disease activity outside the visible lesions."
To gain a better understanding of the effects of MS on the whole brain, Dr. Vrenken and colleagues studied T1 changes in normal-appearing white and gray brain matter in patients with MS.
T1 is a measurement of proton relaxation after exposure to a magnetic field and a radiofrequency (RF) pulse. Due to this RF pulse, protons in the body first reach an excited state and then relax back to a state of equilibrium by funneling the excess energy to the surrounding tissues. T1 refers to the time required for protons to relax to the equilibrium state in this particular manner.
The researchers investigated T1 changes in 67 patients with MS and 24 healthy control volunteers. T1 graphs of normal appearing white and gray matter were significantly different for patients with MS than for controls. Moreover, these graphs differed among patients with MS based on the type of disease: secondary progressive (SP), relapsing-remitting (RR) or primary progressive (PP). The results were most pronounced in patients with SP disease, where at least 31 percent of normal-appearing white matter and 20 percent of cortical normal-appearing gray matter were affected. In RR disease, 16 percent of normal-appearing white matter and 9 percent of cortical normal-appearing gray matter were affected. In PP disease, the normal-appearing white and gray matter affected were 11 percent and 8 percent, respectively. These changes were found throughout the brain, including areas remote from localized lesions that are typically associated with MS.
"These findings demonstrate that in MS, disease processes outside MR-visible lesions are not limited to a few sites but act throughout the brain and affect large fractions of normal-appearing white and gray matter," Dr. Vrenken said.
The researchers also explored correlations between the areas of the brain being analyzed in the patients with MS and the level of atrophy or clinical disability present.
"The results suggest that the damage to normal-appearing brain tissue plays a larger role in the progression of atrophy and clinical disability than do the visible lesions," Dr. Vrenken said."
Adapted from materials provided by Radiological Society of North America.
from http://www.sciencedaily.com /releases/2006/08/060829080502.htm
ess
ScienceDaily (Aug. 30, 2006) — "The effects of multiple sclerosis (MS) extend beyond visibly affected areas into large portions of the brain that outwardly appear normal, according to a study appearing in the September issue of Radiology.
"This disease process in the normal-appearing brain tissue affects the brain globally and has substantial clinical impact," said the study's lead author, Hugo Vrenken, Ph.D., from the Multiple Sclerosis Center at VU University Medical Center in Amsterdam, The Netherlands.
MS is a chronic, autoimmune disease characterized by the destruction of myelin, the protective layers that surround nerve cells. It can affect numerous body functions, and symptoms may include visual and speech impairment, memory loss, depression, muscle weakness, loss of coordination, numbness or pain, bowel and bladder problems and sexual dysfunction.
MS affects approximately 400,000 people in the United States and as many as 2.5 million worldwide, mostly women between the ages of 20 and 50, according to the National Multiple Sclerosis Society.
"The areas of demyelination, or lesions, in patients with MS can be visualized with magnetic resonance imaging (MRI). However, the volume of lesions visible at MRI only correlates moderately with clinical disability measurements," Dr. Vrenken said. "This may be due to disease activity outside the visible lesions."
To gain a better understanding of the effects of MS on the whole brain, Dr. Vrenken and colleagues studied T1 changes in normal-appearing white and gray brain matter in patients with MS.
T1 is a measurement of proton relaxation after exposure to a magnetic field and a radiofrequency (RF) pulse. Due to this RF pulse, protons in the body first reach an excited state and then relax back to a state of equilibrium by funneling the excess energy to the surrounding tissues. T1 refers to the time required for protons to relax to the equilibrium state in this particular manner.
The researchers investigated T1 changes in 67 patients with MS and 24 healthy control volunteers. T1 graphs of normal appearing white and gray matter were significantly different for patients with MS than for controls. Moreover, these graphs differed among patients with MS based on the type of disease: secondary progressive (SP), relapsing-remitting (RR) or primary progressive (PP). The results were most pronounced in patients with SP disease, where at least 31 percent of normal-appearing white matter and 20 percent of cortical normal-appearing gray matter were affected. In RR disease, 16 percent of normal-appearing white matter and 9 percent of cortical normal-appearing gray matter were affected. In PP disease, the normal-appearing white and gray matter affected were 11 percent and 8 percent, respectively. These changes were found throughout the brain, including areas remote from localized lesions that are typically associated with MS.
"These findings demonstrate that in MS, disease processes outside MR-visible lesions are not limited to a few sites but act throughout the brain and affect large fractions of normal-appearing white and gray matter," Dr. Vrenken said.
The researchers also explored correlations between the areas of the brain being analyzed in the patients with MS and the level of atrophy or clinical disability present.
"The results suggest that the damage to normal-appearing brain tissue plays a larger role in the progression of atrophy and clinical disability than do the visible lesions," Dr. Vrenken said."
Adapted from materials provided by Radiological Society of North America.
from http://www.sciencedaily.com /releases/2006/08/060829080502.htm
ess
Thanks for posting this. I haven't been here in a while, but I always find the information and support here to be invaluable.
This post certainly is timely for me. I recently received the notes from my visit with my new neuro in them she states that, for my age, I have a decrease in brain parenchymal volume. So, I take that to mean that I have more than the expected atrophy for my age (I am 45).
Among other sx I have severe cognitive issues. I have read where they are linked more to atrophy than the number of lesions (I believe I have four lesions).
I see the neuro next week, and get a new MRI also. It just might be D day (diagnosis day) for me.
Thanks for all of the info everyone.
This post certainly is timely for me. I recently received the notes from my visit with my new neuro in them she states that, for my age, I have a decrease in brain parenchymal volume. So, I take that to mean that I have more than the expected atrophy for my age (I am 45).
Among other sx I have severe cognitive issues. I have read where they are linked more to atrophy than the number of lesions (I believe I have four lesions).
I see the neuro next week, and get a new MRI also. It just might be D day (diagnosis day) for me.
Thanks for all of the info everyone.
Thank God you have found a good neuro and im sorry for the time other neuros have taken away from you in regards to getting treatment and knowing what is wrong.
This knowledge is frightening and there seems to be so much information and studies going on that shows they still dont know enough about this disease and are stabbing in the dark at times, it seems some patients tick all the boxes and get treatment straight away and others dont and have to wait years for answers.
I pray you will now get proper treatment and knowing what you have you can face forward.
Lots of hugs
samantha
This knowledge is frightening and there seems to be so much information and studies going on that shows they still dont know enough about this disease and are stabbing in the dark at times, it seems some patients tick all the boxes and get treatment straight away and others dont and have to wait years for answers.
I pray you will now get proper treatment and knowing what you have you can face forward.
Lots of hugs
samantha
You are such a supportive group....thank you for your words of hope, help and love....
Heather
Heather
That was great actually!!!
Looks really good on the screen, your computer gone CRAZY!!!!!!!!!!!!!!!
How are you doing?
Samantha
Looks really good on the screen, your computer gone CRAZY!!!!!!!!!!!!!!!
How are you doing?
Samantha
As you can see, my MS "finger" went crazy over the 'post comment' button. I was laughing my rear off, at how stupid this made me look. But it's good to be able to laugh at yourself.
Have a great day, Sam.
Heather
Have a great day, Sam.
Heather
I AM SO GLAD YOU FOUND A GOOD NEURO AND WILL FINALLY BE ABLE TO TAKE BETTER CARE OF YOURSELF!
The brain atrophy statements above also explains upholds the facts that 5% of MS patients never show lesions. But, the autopsy shows this axonal degradation. Fortunately for us, there are many areas of the brain that are not solely eloquent for a particular function and our brain can, therefore, compensate with other areas of our brain. Much of our brain goes unused like the memory in our computers. As the virtual memory of our computer gets limited, the unused/underused areas can be programmed for virtual memory operations. Our brains are similar in a compensatory analogy.
I would also think that it would, therefore, correlate that there are more people with MS than formerly thought as many are having axonal atrophy without lesions and will later develop them.
There are other MRIs (I believe functional and/or spect) that allows quantification of brain atrophy over time. The functionality/blood flow of various areas of the brain can also be monitored, as well, I believe. Also, as the brain atrophies and then shrinks a person gets a larger space around the brain and in the folds and in the periventricular(?) space on the MRIs. I am not a doctor, but this is what the research that I have read seems to indicate.
Atrophy can occur with age and can sometimes be correlated with dementia and alzheimers.
And yes, what you said about the spinal lesions at this point in time seems to hold relatively true according to what I have read. There are many forms of MS, also. Devic's is considered one of the more progressive and usually involves lesions in the spinal cord and NMO (with more sparing in the brain of visual lesions). Interestingly, this form of MS generally does not show the oligoclonal patterns and other typical IgG patterns seen in RRMS. So, for a physician to say that a person cannot have MS without a positive LP is false, if what I have read is correct. In fact, for certain forms of MS, a normal or different CSF result pattern is what the neurologist is looking for rather than the usual oligoclonal banding, etc. typically seen in RRMS. Thus, the CSF results can be an important factor in determining the type and possibly, therefore, the prognosis of some of the other forms of MS outside relapsing-remitting.
Again, I am not a doctor, but I have done a lot of reading and hopefully what I have read is correct and that I have summated it correctly for everyone.
Hope this helps in some way. Thank you for your support on this forum. Hope you and everyone had a fun Thanksgiving!!!
The brain atrophy statements above also explains upholds the facts that 5% of MS patients never show lesions. But, the autopsy shows this axonal degradation. Fortunately for us, there are many areas of the brain that are not solely eloquent for a particular function and our brain can, therefore, compensate with other areas of our brain. Much of our brain goes unused like the memory in our computers. As the virtual memory of our computer gets limited, the unused/underused areas can be programmed for virtual memory operations. Our brains are similar in a compensatory analogy.
I would also think that it would, therefore, correlate that there are more people with MS than formerly thought as many are having axonal atrophy without lesions and will later develop them.
There are other MRIs (I believe functional and/or spect) that allows quantification of brain atrophy over time. The functionality/blood flow of various areas of the brain can also be monitored, as well, I believe. Also, as the brain atrophies and then shrinks a person gets a larger space around the brain and in the folds and in the periventricular(?) space on the MRIs. I am not a doctor, but this is what the research that I have read seems to indicate.
Atrophy can occur with age and can sometimes be correlated with dementia and alzheimers.
And yes, what you said about the spinal lesions at this point in time seems to hold relatively true according to what I have read. There are many forms of MS, also. Devic's is considered one of the more progressive and usually involves lesions in the spinal cord and NMO (with more sparing in the brain of visual lesions). Interestingly, this form of MS generally does not show the oligoclonal patterns and other typical IgG patterns seen in RRMS. So, for a physician to say that a person cannot have MS without a positive LP is false, if what I have read is correct. In fact, for certain forms of MS, a normal or different CSF result pattern is what the neurologist is looking for rather than the usual oligoclonal banding, etc. typically seen in RRMS. Thus, the CSF results can be an important factor in determining the type and possibly, therefore, the prognosis of some of the other forms of MS outside relapsing-remitting.
Again, I am not a doctor, but I have done a lot of reading and hopefully what I have read is correct and that I have summated it correctly for everyone.
Hope this helps in some way. Thank you for your support on this forum. Hope you and everyone had a fun Thanksgiving!!!
Just a bump for those of us who haven't read this post yet. Lots of good info in this thread.
Wow!! This thread occurred during the month I took off and I missed it completely! This is a very, VERY important topic. It is the topic that will be taking center stage as soon as the techniques for quantifying brain volume become available to the general practitioner.
Yes, absolutely axonal degeneration is probably more responsible for our accumulating disability than our T2 inflammatory demyelinating lesions are.
99% of discussion about MS is centered around the visible lesions on the MRI, and around our symptoms and relapses. The appearance of enhancing lesions on the T2 images do correlate with appearance of new symptoms. That is the inflammatory part of MS. And most of the therapies are aimed at reducing this inflammatory process. Our doctors gage disease activity by how many new lesions we get and how many disappear. Some neurologists actually presume to tell us that the MRI picture is 1000% of the truth about our disease. No lesions=no MS. No new lesions=no progression of disease or no disease activity. Some even deny that our symptoms=disease activity if the MRI doesn't show it. We need to RUN from these doctors.
It does appear that the inflammatory demyelinating plaque is most directly related to our relapses and remissions. But, we have always talked about the progressive disability we begin to accrue at some point in our disease. For some this accrual is early. These are the people that complain that some of their symptoms have appeared and steadily worsened since the beginning. This is true for me. For others, they may have little direct axonal loss early in the disease and most of their relapses seem to heal almost completely. Only after many years do they begin to collect disability.
Nothing could be farther from the truth. While there is a lot of research going on with the inflammatory demyelination process, the real bulk of scientific research is focused on the topic above. We KNOW that even before any lesions form, there is some sort of direct attack on the nerve fibers themselves, causing them to die and "drop out." This is called "direct axonal degeneration." They do not demyelinate first. This is happening in the part of the white matter that looks "normal" on the MRIs. What causes this or triggers this is not known, but they are searching for the answers.
Along with this, it is also known that severe, inflammatory demyelinating lesions can also result in death of the neuron and axonal death. But, this is not the cause of most of the loss of central nervous system tissue which results in the appearance called atrophy.
People with MS have an ongoing brain and spinal cord "atrophy" (shrinkage) that is much faster than that which occurs normally as we age. The majority of this is from direct axonal degeneration and death and NOT from inflammatory demyelination. Yet all we hear about is inflammatory T2 lesions.
Researchers are developing elegant ways of measuring brain atrophy on the MRIs. It is done by counting the digital pixels of the amount of CSF in the images. When brain tissue drops out, the new space must be filled with CSF. So as the CSF spaces enlarge, they take up more pixels on the MRI and can be calculated. But, these calculations do not seem to be available to our doctors. I can only think that if our doctors (the ones who are willing to think) had this available, they could look at someone who has classic MS relapses and makes the first Criterion of the McDonald Critieria. (That is, two clinical attacks and two separate clinical lesions) If the MRI showed no inflammatory lesions, then they could look for atrophy. In the presence of atrophy, that could be a new "Positive MRI finding" and the diagnosis could be made without waiting for lesions to show up. T-Lynn (where is she !!) would have been diagnosed earlier.
I think many people, especially those with Primary Progressive Disease, would be able to be diagnosed earlier. PPMS is characterized by much more destruction by direct axonal degeneration than by inflammatory lesions, though some have large amounts of both. Many times people with PPMS have many smaller brain lesions and show early spinal cord atrophy. Because they often do not have the strong inflammatory T2 lesions, they are more likely to have negative LP results. In fact only 60% to 70% of PPMS patients have oligoclonal banding. But, they have early and marked brain and spinal cord atrophy.
Some of the latest studies I have read have discussed that spinal cord atrophy is the most accurate predictor of real disability. I'm watching all of this with great interest.
Well, this was just a jumble of the thoughts I have been wanting to write on this topic and to make into a Health Page. The lesson to take away from this is that there is a whole HUGE amount of disease occurring in our brains that our neurologists can't see as T2 lesions. And only after a huge amount of the axons have died and dropped out will they be able to see the atrophy. Does this explain some of those people with classic MS symptoms (in whom the mimics have been ruled out) who have "normal" MRIs? I think it does.
I like the quote that ess found: "The results suggest that the damage to normal-appearing brain tissue plays a larger role in the progression of atrophy and clinical disability than do the visible lesions," Dr. Vrenken said
We know it's happening. We just have to find our way to neurologists who think and see this process and forget counting MRI lesions.
Comments? I recommend that everyone read this entire thread. These are important concepts and they will be new to many people. I applaud Heather's neuro for being so enlightened.
Quix
Yes, absolutely axonal degeneration is probably more responsible for our accumulating disability than our T2 inflammatory demyelinating lesions are.
99% of discussion about MS is centered around the visible lesions on the MRI, and around our symptoms and relapses. The appearance of enhancing lesions on the T2 images do correlate with appearance of new symptoms. That is the inflammatory part of MS. And most of the therapies are aimed at reducing this inflammatory process. Our doctors gage disease activity by how many new lesions we get and how many disappear. Some neurologists actually presume to tell us that the MRI picture is 1000% of the truth about our disease. No lesions=no MS. No new lesions=no progression of disease or no disease activity. Some even deny that our symptoms=disease activity if the MRI doesn't show it. We need to RUN from these doctors.
It does appear that the inflammatory demyelinating plaque is most directly related to our relapses and remissions. But, we have always talked about the progressive disability we begin to accrue at some point in our disease. For some this accrual is early. These are the people that complain that some of their symptoms have appeared and steadily worsened since the beginning. This is true for me. For others, they may have little direct axonal loss early in the disease and most of their relapses seem to heal almost completely. Only after many years do they begin to collect disability.
Nothing could be farther from the truth. While there is a lot of research going on with the inflammatory demyelination process, the real bulk of scientific research is focused on the topic above. We KNOW that even before any lesions form, there is some sort of direct attack on the nerve fibers themselves, causing them to die and "drop out." This is called "direct axonal degeneration." They do not demyelinate first. This is happening in the part of the white matter that looks "normal" on the MRIs. What causes this or triggers this is not known, but they are searching for the answers.
Along with this, it is also known that severe, inflammatory demyelinating lesions can also result in death of the neuron and axonal death. But, this is not the cause of most of the loss of central nervous system tissue which results in the appearance called atrophy.
People with MS have an ongoing brain and spinal cord "atrophy" (shrinkage) that is much faster than that which occurs normally as we age. The majority of this is from direct axonal degeneration and death and NOT from inflammatory demyelination. Yet all we hear about is inflammatory T2 lesions.
Researchers are developing elegant ways of measuring brain atrophy on the MRIs. It is done by counting the digital pixels of the amount of CSF in the images. When brain tissue drops out, the new space must be filled with CSF. So as the CSF spaces enlarge, they take up more pixels on the MRI and can be calculated. But, these calculations do not seem to be available to our doctors. I can only think that if our doctors (the ones who are willing to think) had this available, they could look at someone who has classic MS relapses and makes the first Criterion of the McDonald Critieria. (That is, two clinical attacks and two separate clinical lesions) If the MRI showed no inflammatory lesions, then they could look for atrophy. In the presence of atrophy, that could be a new "Positive MRI finding" and the diagnosis could be made without waiting for lesions to show up. T-Lynn (where is she !!) would have been diagnosed earlier.
I think many people, especially those with Primary Progressive Disease, would be able to be diagnosed earlier. PPMS is characterized by much more destruction by direct axonal degeneration than by inflammatory lesions, though some have large amounts of both. Many times people with PPMS have many smaller brain lesions and show early spinal cord atrophy. Because they often do not have the strong inflammatory T2 lesions, they are more likely to have negative LP results. In fact only 60% to 70% of PPMS patients have oligoclonal banding. But, they have early and marked brain and spinal cord atrophy.
Some of the latest studies I have read have discussed that spinal cord atrophy is the most accurate predictor of real disability. I'm watching all of this with great interest.
Well, this was just a jumble of the thoughts I have been wanting to write on this topic and to make into a Health Page. The lesson to take away from this is that there is a whole HUGE amount of disease occurring in our brains that our neurologists can't see as T2 lesions. And only after a huge amount of the axons have died and dropped out will they be able to see the atrophy. Does this explain some of those people with classic MS symptoms (in whom the mimics have been ruled out) who have "normal" MRIs? I think it does.
I like the quote that ess found: "The results suggest that the damage to normal-appearing brain tissue plays a larger role in the progression of atrophy and clinical disability than do the visible lesions," Dr. Vrenken said
We know it's happening. We just have to find our way to neurologists who think and see this process and forget counting MRI lesions.
Comments? I recommend that everyone read this entire thread. These are important concepts and they will be new to many people. I applaud Heather's neuro for being so enlightened.
Quix
> I applaud Heather's neuro for being so enlightened.
I do too - this was one of the first threads I found, upon visiting this forum, and I thought it was very important. I'm still looking for a neuro like Heather's - somebody who will look at the symptoms, and not discount them just because there isn't a mark on the MRI.
I do too - this was one of the first threads I found, upon visiting this forum, and I thought it was very important. I'm still looking for a neuro like Heather's - somebody who will look at the symptoms, and not discount them just because there isn't a mark on the MRI.
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