Here is My Question:
My daughter is newly diagnosed. Her only symptom was eye sight. Since her brain MRI showed many lesions (some large) one doctor said she should take Tysabri or Copaxone with steroids. A second opinion said Tysabri and no to Copaxone. She is JC negative. I have been reading about rebound coming off Tysabri so that scares me. Her spinal MRI was clear but had bands in CSF. How do we make this decision for the long term outlook? Right now she has no symptoms so this is hard to understand. Tysabri is a very safe medication to be on if you are JC antibody negative and remain JC antibody negative while on therapy.

Answer:
The risk of rebound is only a problem if you are not switched to another medication in a timely fashion after discontinuing the Tysabri.

Most rebound symptoms occur around 3 months after the last infusion. Hopefully your daughter will not have a need to discontinue the Tysabri.  However, if she does need to stop it, there are many treatment options that can be started within 1 month of discontinuing the Tysabri to avoid the risk of rebound.
 
Benjamin Osborne, MD
Associate Professor of Neurology and Ophthalmology
Director, Neuromyelitis Optica (NMO) Clinic
Director, Neuro-Ophthalmology Clinic
Associate Director of the NIH/Georgetown Neurology Residency Program
Medstar Georgetown University Hospital
3800 Reservoir Road, NW 7PHC
Washington, DC 20007

Here is My Question:
My son was diagnosed with MS 3 years back. He did not take any medication and had no problems. Three weeks ago he got an electric shock while starting a generator. This triggered symptoms like numbness in his leg and arm. He just got out of the hospital after a 5 day course of steroids. His hand is still short weak. His MRI showed 2 new active lesions. He is 20 years now. Is it wise to start injections?

Answer:
In general if someone has MS and is having ongoing relapses (regardless of cause) then we do recommend going on some form on disease modifying therapy. Which one is up to the individual patient in consultation with their treating clinician.
 
Benjamin M. Greenberg, MD, MHS
Vice Chair of Translational Research and Ambulatory Care
Department of Neurology and Neurotherapeutics
Director, Transverse Myelitis, Neuromyelitis Optica Programs
Co-Director, Pediatric CONQUER Program
UT Southwestern Medical Center
Childrens Health

Question:
Can Rebif cause PMI in people with MS?

Answer:
There is no evidence that any of the interferons or glatiramer acetate are associated with the development of PML.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Question:
My neurologist wants me to change from Tysabri to Ocrevus. I have been on Tysabri approximately 4 years with a short period off to try Tecfidera which dropped my white blood count too low to continue. I had a severe case of hives about 20 years ago from Benadryl and was told to never take it again.

I had a severe reaction to a prednisone treatment causing moon face, pseudo cushings, weight gain of >50lbs causing my natural ACTH to rise 3xs over the high end of the scale and, this endocrine nightmare lasted for two years. I exercised. I ate salad, but the endocrinologist said cortisol wins.

With this history of severe reactions to these two medications given with the infusion of rituxan and ocrevus, how am I to take the Ocrevus if I can't take the precursor IV drugs? are these required? With Tysabri I just get the medication and a sodium drip.

Answer:
You need to talk to an allergist about going through a Drug Desensitization protocol in order to receive Ocrelizumab. This would need to be done each time you received the drug.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Question:
Thank you for the detailed answer to my question about MSC legitimacy. Your answer is one I expected and respect. MS sufferers are still wondering why more research isn't done in this area in the USA. Is it a financial issue or is there much being done but we just don't hear about it? Loaded question, do you see a solution in the near future? Thanks again. 

Answer:
There are 3 main limitations to Mesenchymal Stem Cell research for MS in the United States:

1. Scientific investigation in academic centers requires investigators to apply for and receive an investigational new drug (IND) and Biologic License Application (BLA) from the Food and Drug administration. Some investigators have gone through this process but not many. 
2. Funding for such studies is limited until there is preliminary evidence of benefit.
3. The intellectual property issues need to be clarified.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Here is My Question:
Does low blood pressure have anything to do with MS? Thanks!

Answer:
Blood pressure can be quite complicated and the kidneys have a much larger role in this than other organs.  MS does not directly affect the blood pressure.

A. Scott Nielsen MD MMSc
Neurologist and MS Specialist at Kaiser Permanente
KP Fontana and Riverside Medical Centers

Here is My Question:
I've been on Copaxone for 1 year recently diagnosis with MS. I had an MRI and found 2 more lesions with no symptoms...how bad is finding 2 more within a year? I have changed my meds to Tecfidera.

Answer:
This is a hard question to answer as care definitely has to be individualized, but one key is to ensure that the MRI data is correctly interpreted relative to starting the copaxone. For, example, copaxone takes 4-6 months to “kick in” so, if a MRI was done before copaxone, then the medication was started and then one year later a new MRI was obtained that showed new INACTIVE lesions, there would be know way to know if the lesions formed before or after copaxone had ‘kicked in’. Thus, it might not represent copaxone failure.

​If, however, MRIs were obtained after starting copaxone and then again a year later and despite the copaxone there were new lesions, it would suggest that someone was a suboptimal responder to copaxone and changing medication would make sense.
 
Benjamin M. Greenberg, MD, MHS
Vice Chair of Translational Research and Ambulatory Care
Department of Neurology and Neurotherapeutics
Director, Transverse Myelitis, Neuromyelitis Optica Programs
Co-Director, Pediatric CONQUER Program
UT Southwestern Medical Center
Childrens Health
Dallas, Texas

Here is My Question:
I have just been told my vitamin D level is very low. Are there any underlying health conditions that could cause this? 

Answer:
Good question! We don't think so! Most people have developed vitamin D deficiency over the last 20-30 years based on changes in our diet and our environment. It is probably a reflection of a world and not a malabsorption issue.

If there are other concerns that would raise a question of malabsorption we always recommend talking to your physician, but isolated low vitamin D is now (unfortunately) very common.
 
Benjamin M. Greenberg, MD, MHS
Vice Chair of Translational Research and Ambulatory Care
Department of Neurology and Neurotherapeutics
Director, Transverse Myelitis, Neuromyelitis Optica Programs
Co-Director, Pediatric CONQUER Program
UT Southwestern Medical Center
Childrens Health
Dallas, Texas

Here is My Question:
Does Lemtrada work on spinal lesions as well as it does brain lesions? Thank you.

Answer:
Lemtrada, similar to the other DMTs, target the immune system at different points to reduce the likelihood of new lesions or inflammatory events throughout the nervous system (including the spinal cord). Lemtrada (and the other DMTs) have never demonstrated the ability to repair old lesions (which the nervous system does in a limited way).

A. Scott Nielsen MD MMSc
Neurologist and MS Specialist at Kaiser Permanente

Here is My Question:
I posed the question about legitimacy of MSC Study in Panama City to which I received an answer that "We have no Information about this." Are you telling me the NMSS doesn't know Dr. Neil Riordan, doing the study, degreed from Univeristy of Nebraska Medical Center? Please inform all ss MS sufferers that you acknowledge this man?

Thanks

Answer:
First of all, this web site is not affiliated with or part of the National MS Society.

Second, there are many people studying different types of stem cells for the treatment of various diseases. We do not understand what you mean by, “not acknowledging this man” (meaning Neil Riordan). He is just one of many people around the world studying adult stem cells.

Third, it is premature to advocate treatment of people with MS using mesenchymal stem cell therapy outside of clinical trials. 

All therapies for MS require some evidence of benefit and lack of harm before we adopt them into clinical practice. I have no problem with researchers treating patients in the context of well designed and controlled clinical trials with informed consent and adequate follow-up to assess the risk and benefits of the treatment being studied.

Revere (Rip) Kinkel MN
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Here is My Question:
I was diagnosed with RRMS in 2005. I have been on Rebif, Copaxone, Rebif again, Aubagio, and another one (can't remember the name but was an oral pill). I continued to get worse and I was sick the entire time. I also have Chron's disease (small bowel). Since 9/2015 I went thru relapse after relapse, progression in both the brain and spine to the point that my entire spine is one long plaque.

My mobility went to being on my walker full time. I could not even walk a short distance without falling. Sometimes, I could not even get up on my own because my legs would not work. I went on Tysbri and within a few weeks I could put my walker aside. I can only walk fore about 2 hrs before the legs give out but hey, it's two hours! :)

I just got my JCV level back and it is a 3. but the day that they took the blood I had already had 1 dose and they gave me the 2nd dose the day they took the blood. Now, my neurologist is leaving her practice (I've been with her the entire time) and I am having trouble getting into another neurologist and the treatment has been put on hold. I have multiple questions:

1) with a level 3, what are my odds of PMI? 
2) since I received another dose of meds can the level go up?
3) since I only had 2 doses, are my risks of the relapse coming back stronger than what was happening at the time of the first dose?

PS: this med was the ONLY one that did not cause my Chron's to flare. I have had changes in my mood since the meds started but thought it was just the normal course of side effects. Now I am worried because if there is a small chance, my body is usually one that goes thru it..

Sorry for the typing errors, but my fingers have been numb for years now lol

Answer:
If I understand you correctly, you have now received 2 or 3 Tysabri infusions and your JCV antibody index is 3.0. It also sounds as though you have never received any chemotherapy or immunosuppressants in the past.

Remember that the risk of developing PML increases with duration of treatment. Given the information provided your over risk of PML at different time intervals is as follows:

First 2 years of treatment 1 in 1,000 (actually very rare with less than 18 months of treatment) or 0.1 percent. The risk of PML is higher in the first 2 years (about 1 in 500 or 0.5 percent) if you’ve received immunosuppressants in the past. 

After more than 2 years of treatment with tysabri and your risk of PML increases to about 1 in a 100 or 1 percent. So the risks are fairly small for the benefits you are reporting to us.

There is also the option of switching to Ocrelizumab or another highly active therapy after 6-12 months of stability on tysabri infusions. I suspect if you stopped the tysabri now you would lose the benefits rapidly.

Talk it over with your doctors and good luck.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Here is My Question:
I have been diagnosed with fibro, which I reluctantly concur that I have but I have recurrent weakness in the legs (primarily thighs), a slow walking pattern and pain in my legs. I am 54 making this atypical but have never been tested dor MS. I really dislike diagnosing myself by using the web but for the last 5-7 years it's seems every time I look up symptoms it comes with a preliminary diagnosis of MS. Docs have never suggested this. Should I suggest it to them or find different docs?


Answer:
Since the inflammatory event of MS can occur anywhere within the brain, spinal cord, and optic nerves, the resultant symptom can be almost anything.  This is why MS typically comes up as a "need to investigate" possibility for patients experiencing a wide variety of symptoms.

If you wish to have this investigated, you should see a neurologist, preferably a fellowship trained MS specialist who will apply the diagnostic criteria and consider alternatives as well.  Sometimes all that is needed to answer your question is a consultation with a specialist and nothing more.  Sometimes additional evaluation is needed with imaging, blood testing, etc.

A. Scott Nielsen MD MMSc
Neurologist and MS Specialist at Kaiser Permanente

Here is My Question:
I have been taking Aubagio for 3 years. Currently experiencing a flare and recent MRI shows new lesions and old lesions now active. Should I conclude my therapy is not working. Prior to this I was on Avonex for 11 years.

Answer:
The answer to your question depends on the circumstances. Let me provide several examples to illustrate my point:

Example 1: You were placed on Avonex at the onset of your disease 14 years ago with virtually no significant disease activity over 11 years and little loss of function. You became sick of injections and switched to aubagio with no relapses or MRI activity until this recent attack,  your first in many years. In this case I would be looking for something that precipitated or caused the recent attack, such as an upper respiratory tract infection, influenza or a chronic urinary tract infection. You may continue to do well on aubagio if the infection is treated, perhaps with the addition of a course of steroids to clear up the current inflammatory activity in your brain.  In this situation I would get rid of the Aubagio if it is felt that the use of this drug is increasing the number of infections you’ve experienced over the past few years or making you at higher risk of infections. If not, you may be able to continue on Aubagio

Example 2: You were on Avonex for 11 years despite getting  worse over time with or without relapses and probably with MRI activity if this was analyzed correctly. You switched to Aubagio because you were worried about side effects or risks with other DMT choices. You are continuing to experience active disease after 3 years of treatment and continue to lose function over time but are still able to walk with assistance.  This is just the first time you’ve experienced a relapse with MRI activity in several years. You are now under 55 years of age. If this is the case you may be a candidate for highly active treatment such as Alemtuzumab (Lemtrada), Ocrelizumab or Natalizumab (Tysabri). You may still be a candidate for highly active treatment if the details of your case are different than presented in this example, but I would need to obtain more information.

Example 3: Your situation lies somewhere in between these two extreme examples. The choice here would be highly dependent on the details.

Generally, I would only recommend staying on Aubagio if example 1 is more consistent with your case. Your neurologist is in a better position to know the details of your case and advise you further.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

​Here is My Question:
I am working through these thoughts and would appreciate any expert opinion/explanation that might be shared. The questions is based on the premise that 80% of people with MS experience some form of bladder/bowel dysfunction. Thanks for any insight you can share.

As 80% of people with MS have these Bowel and Bladder issues it would be expected that the same effected area could be identified on a MRI scan on whatever machine is used and for all the 80% of people scanned.

Do 80% of MSer’s have lesions on the spine at the same position? Does any research identify the reason why an attack on that nerve in the spine for 80% of people with MS, occurs? 

If the bladder and bowel are controlled in the frontal lobe of the brain, it appears unlikely that MSer’s would have lesion activity in that particular location. I believe lesions are generally not found in the lower section of the thoracic and lumbar spine where you would expect activity would affect bowel and bladder function.

The spinal cord at C3, C4, C5 has 31 pairs of nerves. What are the chances that lesions in 80% of people with MS affects the bowel and bladder function?

What is the commonality among people with MS that causes so many to have this problem?


​Answer:
​These are excellent questions on bladder control and relatively easy to answer.

It helps to understand that the control of urine and fecal storage and elimination (i.e. bladder and bowel control) is an essential function involving large areas of the central and peripheral nervous system stretching from the most anterior part of your frontal lobes to the very end of your spinal cord and the plexus of nerves that supply the organs of elimination. This provides a very large territory for any potential neurological disease to cause problems with elimination. This is one of the reasons why almost any multifocal neurological disease can, and often dose, cause problems with elimination control at some point in the illness. This is particular true of diseases like MS that create demyelination and axon loss in white matter tracts involved in the control of bladder function. In fact there is a fairly good correlation between involvement of the spinal cord or brainstem pathologically by MS and symptoms of bladder dysfunction;  both occurring, as you mentioned, in about 80 % of patients.

However, many of the neural pathways that control urination are in regions of the brainstem and spinal cord that are difficult to see on standard imaging techniques; this is due to the location of these pathways in or near the gray matter of the cord or cerebral aqueduct and fourth ventricle of the brainstem or the lower parts of the spinal cord, all areas more difficult to image on MRI. We also know that very small lesions, below the resolution of imaging, can create bladder symptoms because some of the important pathways are small and condensed. Lastly is far more common for bladder problems to occur with bilateral involvement of the spinal cord or brainstem but this bilateral involvement does not need to occur at the same level or location.

There is no single or common location for lesions to cause bladder symptoms and the urination symptoms created are the same (usually urinary urgency and hesitancy with variable amount of incontinence) regardless of the location of lesion anywhere between the brainstem and the sacral spinal cord.

I hope this helps.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego

Here is My Question:
Hello! Back when I was diagnosed with MS I sent Dr. Nielsen a list of supplements (EPA, DHA, d3, b-12 and a b complex) I started taking in an attempt to boost nerve health. He told me that long-term exposure of b6 as pyridoxine can cause peripheral nerve damage that is irreversible and quite painful. My wife, just recently, purchased a plexus dietary supplement that contains b6 as pyridoxine hydrochloride (2.5 mg and suggests 1 to 4 tablets daily). 

Is this the same vitamin? Is the chance of causing nerve damage the same for someone who does not have MS?

Thank you to Dr. Nielsen and the rest of the specialists that maintain this site. It's a wonderful resource.

Answer:
Yes, this is the same and can cause problems with a part of the nervous system called the dorsal root ganglion (which resides next to the spinal cord and relays sensory information).  Toxicity with pyridoxine (b6) tends to accumulate over a year or so. 

A. Scott Nielsen MD MMSc
Neurologist and MS Specialist at Kaiser Permanente

Here is My Question:
Hello. I have been diagnosed with MS and I am taking the treatment for it. My question is can I drink naturally extracted pure cane juice? Will it negatively affect my health?

Answer:
“naturally extracted pure cane juice” is just another name for sugar. There are few if any additional nutrients. Sugar is wonderful in controlled amounts.

Revere (Rip) Kinkel MD
Director of the Multiple Sclerosis Program
Clinical Neurosciences Director
Professor of Clinical Neurosciences
University of California San Diego