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Just about every day we post something new on HealthCare Journey. Like today we didn't post anything on this page, but we did post on Debbie's Research Blog READ BLOG...the question is, do you always come to this page to seek new information on the site, or do you look on the home page, or the news and events page? Let us know where you seek information on the site. Thank you! Here is My Question:
For how long is it recommend to take taking 325mg aspirin with Tecfidera? Is there another alternative? Answer: An adult aspirin (325mg) is typically used to pre-treat the flushing symptoms associated with Tecfidera. There is not a standard guideline regarding the duration of pre-treatment, but it should be noted that flushing as it relates to Tecfidera tends to improve or resolve within the first month of initiating the medication. If you've been on Tecfidera and are not experiencing the flushing reaction, consider stopping the aspirin as it may no longer be needed. Since aspirin can help treat other serious conditions, you should first consult with your doctor. Another option is to take Tecfidera after a high protein and fat meal (think peanut butter) as this may also limit the flushing side effect. There is no evidence that an aspirin will help the other common side effect of Tecfidera: stomach and GI tract upset. However, taking the Tecfidera after a meal may help mitigate this temporary side effect as well. A. Scott Nielsen MD MMSc Virginia Mason Multiple Sclerosis Center Here is My Question:
I have just been told my JCV titre level is 0.63. What is the cut off level when on Tysabri? Answer: The JC virus antibody index is reported as positive with values about 0.4, but there are no strict cut off values. By this I mean that an individual’s risk of PML depends significantly on their index value. Those with persistent index values below 0.6 have almost no risk of PML, those with persistent index values between 0.6 and 1.5 have an intermediate risk of PML and those with persistent index values > 1.5 have a high risk of PML with long term treatment. Whether or not you chose to remain on Tysabri at any given index value depends on your response to prior treatments, your disease characteristics, your other medical problems and your aversion to risk. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego We have had people ask for suggestions on how to effectively manage their medications, so this blog is in reponse those questions...READ MORE
Here is My Question: After 2 years on Tysabri my neurologist suggested that I start getting infusions each 6 weeks instead of each 4 weeks, even though I am JCV negative. What would be the benefit? What is the evidence about efficacy of 6 week or 8 week dosing regimen? Thanks! Answer: Good question. The main reason such a change in dosing frequency (from every 4 weeks to every 6 or 8 weeks) is considered is based on preliminary evidence that doing so may reduce the risk of progressive multifocal leukoencephalopthy (PML) while maintaining the effectiveness of Tysabri. The rationale behind this is that we know that Tysabri saturates alpha-4-beta-1 integrin receptor by >80% after the infusion, and the saturation remains above 75% when you go back to get your next infusion 4 weeks later. At 6-8 weeks after the infusion, the saturation drops to ~70% and then ~40% two weeks later. The interaction between this receptor on your white blood cells and the blood vessel wall allows the cell to get into the central nervous system and potentially lead to an MS relapse. Tysabri blocks this interaction which is presumably why it works so well in reducing the number of clinical attacks, MRI lesions, and attenuating disability over time. This receptor-Tysabri interaction is a double-edged sword, however. The white blood cells are also needed to survey the central nervous system and eradicate foreign invaders (ie, the JC-virus that causes PML). So, by altering the dosing frequency of tysabri, we are hoping to allow enough saturation of the integrin receptor by tysabri to protect patients from MS but at the same time, allow enough opportunity for the white blood cells to gain access to the nervous system to "keep an eye" on foreign viruses--particularly the one that causes PML. Preliminary data on this topic presented at the American Academy of Neurology meeting in 2014 can be found below: 
This multicenter observational data is preliminary but so far suggests that extending the dosing of Tysabri to every 6 to 8 weeks appears to maintain the drug's effectiveness against MS and at the same time, they have not observed a case of PML. Of course, this is just preliminary, and they are continuing the observational study to confirm these findings.
Hope this helps. A. Scott Nielsen MD MMSc Virginia Mason Multiple Sclerosis Clinic Here is My Question:
What can I do for my fatigue? I am exhausted all the time. I was diagnosed in November. I have lesions on my brain and neck. Spinal tap was completed to confirm. The neurologist I am seeing is not doing much. I am going to see one in Grand Rapids in February. Some days my entire body itches and I get a lot of tingling in my feet and legs. Help!! Any suggestions? Answer: One of the most effective treatments for fatigue is related to life style modifications. In particular exercise, optimal sleep, diet, stress mitigation. There are many resources that you can investigate, including NMSS, Rocky Mountain MS Center, etc. Here are some links: http://www.healthcarejourney.com/fatigue.html http://www.healthcarejourney.com/q--a-for-virtual-ms-center/multiple-sclerosis-and-fatigue-ways-to-fight-it http://www.healthcarejourney.com/patient-blog/tired-of-fatigue-with-multiple-sclerosis http://www.nationalmssociety.org/Symptoms-Diagnosis/MS-Symptoms/Fatigue Augusto Miravalle MD University of Colorado Multiple Sclerosis Center Question:
These are all symptoms I am having or have had over the past 6 years but worse and more chronic the past 3 years...horse voice, difficult breathing, vision problems, arm and hand pain, numbness, carpal tunnel, memory issues, balance problems, hearing loss, legs tighten straight, etc. I have not been diagnosed with Multiple Sclerosis but I think I'm having a flair. The past few weeks with worsening. Could that be MS and can I go to the emergency room to have it diagnosed? I'm extremely worried. Answer: I would require much more information to determine if MS is a possibility in your case. Your symptoms certainly sound like they are a result of some problem in your nervous system. Since the symptoms have been present for some time and do not sound life threatening, I would recommend that you see a neurologist as an outpatient. The emergency room is for acute onset problems or life threatening problems. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Question:
What is your opinion on RRMS treatment that includes minocycline? The studies by Dr. Ian Duncan and others look very promising. Answer: There is evidence that minocycline may beneficially modulate immune responses and decrease microglial activation in various animal models. The effect on microglial activation is thought to be potentially neuroprotective although there is also evidence that minocycline may inhibit remyelination which would not be so good. Studies in MS are mixed. I seem to recall an older combination study with interferons that showed minimal benefit and resulted in an increased incidence in vaginal infections. I don’t think this study was ever published since I can not find it on Pubmed. There was a small Canadian study of minocyline in combination with glatiramer acetate (Copaxone) in MS patients that suggested some potential benefit in MS but the number of patients studied was very small and the authors rightfully warned about the need for further clinical trials before using minocyline in clinical practice, especially when so many good therapies are already available. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
I have had RRMS since I was about 20 years old. I am now 57 years old and have been told I now have SPMS. I have tried all medications as well as Tysabri last year. My MRI has never ever changed. I have had 7 lesions always. I am also JCV positive. I never had any kinds of major symptoms that interrupted my daily living. In October 2013 I fell and broke my foot. I have never walked again on my own and now I am in a wheelchair. My doctor wants to me to try Rituxan. My question is can I develope PML with the first dose? Thank you for your time. Answer: As you will see from previous blogs and answers to questions, no one develops PML after being off Tysabri for more than 6 months and there is no relationship between JCV antibody testing and risk of PML on Rituximab. In fact the risk of PML in Rituximab treated MS patients appears to be low. Therefore, the answer to your question is, it is very very unlikely (< 1/25,000) you would develop PML after one dose of rituximab based on the information you’ve provided. Other risk factors such as lymphopenia or prior chemotherapy treatment could increase this risk. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
I want to start by saying that I know I am very blessed to be dealing with the relatively minor issues that I do. I've done a little research, trying to learn a little about MS so I wouldn't have to ask silly questions, but it seems the more I read the less I felt like I really knew about the topic. I am a 55 year old male and was diagnosed with primary progressive MS about 3 years ago. Symptoms like leg and torso numbness, burning pain in leg and torso, spasticity, fatigue, and pain associated with unrelated back issues as well as some cognitive and bladder issues have been gradually getting worse. The burning in my leg is pretty much constant now and too intense to tolerate at times, and the other symptoms have worsened also making walking much more difficult and range very limited. And sleeping... My understanding is that my treatment options are limited to treating each symptom, and it seems to me at least that to this point that has had limited success. So anyway, the question I guess is really one of expectations. I just need to know...are the gradually worsening symptoms what I should be expecting and something I just need to deal with somehow? Is there any point to whining to my neurologist again? Answer: I'm sorry to hear about your struggles with the progressive nature of your MS. It is telling that you refer to your problems as "relatively minor issues." I applaud you on your ability to take perspective and notice where things are good in respect to your MS and functional status. Some individuals (regardless of whether they have MS) always focus on the negatives, which in my experience as a physician working with patients dealing with a chronic illness, is very disabling by that fact alone. You are correct in that the current state of MS therapeutics is extremely limited for reparative strategies due to the underlying damage to the nervous system caused by MS. There are some interesting experimental therapeutics currently being investigated in phase I and II clinical trials right now (anti-lingo and rhIgM22 antibodies), and we patiently wait on what we learn about these biologics. You are also correct that the progressive phase of MS is primarily dealt with in terms of treating symptoms. Based on the nature of the symptoms, strategies involving symptomatic pharmaceuticals, cognitive rehabilitation, and physical medicine and rehabilitation measures can be used (among others). I would counsel you to always bring up your symptoms and concerns with your neurologist. While it is important to recognize the limitations to medicine and the state of treatment for MS as it currently stands (which it appears you do), it is important to keep in mind that there are symptomatic therapeutic approaches that could be very beneficial to you. As a MS neurologist, I must admit that I can't read my patient's mind, and I find it very difficult to know how to help unless they speak up. We genuinely want to help, and you shouldn't feel that you are whining (your word). Please see this communication from a patient perspective on this topic: http://www.healthcarejourney.com/patient-blog/communication. Many times, the physiatrist (a doctor who focuses of rehabilitation medicine) will play a lead role in the progressive symptomatic treatment of patients with MS in concert with the neurologist. Most comprehensive MS centers have these physician subspecialists that can be integral in your treatment team. Hope this helps, A. Scott Nielsen, MD MMSc Virgina Mason Multiple Sclerosis Clinic Question:
I have been to two neurologists and have gotten 2 MRIs. Both have been abnormal MRIs. They tell me they believe its MS but they are not sure. Everywhere I go they have not confirmed that I have MS. I am a 22 year old student and the symptoms I currently experience are right head and right eye pain and some blurriness at times. I had other symptoms 2 years ago that were all MS symptoms according to my doctor but I stopped thinking about this disease and change my lifestyle, I lost weight and ate healthy and experience no symptoms at all for 2 years! Until now again. I feel tired most of the time and always sleepy. I come from a Latino family and have no family history of this disease. I am scared to start medication because besides these symptoms I feel fine. I have a new appointment with an MS expert in SD in a month and if he confirms MS, I will need to start medication. Will the medication make me feel better or make me worse? Thank you so much for all the support and for answering questions. Answer: Those are all good questions. If you end up seeing me in San Diego, we can address them in more detail. Here are my brief responses: 1. MS is really a clinical diagnosis. MRIs are confirmatory in the correct clinical context only. They are also somewhat useful to prognosticate the severity of the disease. Please read my earlier blog on establishing a diagnosis of MS. READ BLOG 2. It is actually typical for patients to improve and remain stable for a while only to have symptoms return. This is why we refer to the symptoms as relapsing-remitting. 3. There are many good treatments for MS but all are, by and large, preventative. This means it most important to start treatment BEFORE problems develop. 4. Some treatments can restore function and improve symptoms but responses, especially early in the course of the disease. Revere (Rip) Kinkel, MD Director of the UCSD Multiple Sclerosis Center Here is My Question:
I have been on Tysabri for 1 year and my most recent JCV test came back stratified at 1.29. My research indicates that this is still in a low risk range if you have not been on an immunosuppressant drug prior to taking Tysabri. I was on Copaxone for 8 years before starting Tysabri. My question is this...is Copaxone considered an immunosuppressant drug? And if it is, would it be possible for me to change to the 6-8 week regimen to be less at risk of PML but still receive the benefits of Tysabri? Answer: These are excellent questions. Copaxone is not considered an immunosuppressant and there is no evidence that prior treatment with Copaxone increases the risk of PML on Tysabri therapy. Your risk of PML with long term (greater than 2 years) Tysabri treatment is probably between 1 in 500 and 1 in 1000. If you’ve remained stable or even improved on Tysabri, it is very reasonable to increase the interval between infusions to every 8 weeks in an attempt to lower your risk of PML. As I have stated in prior blogs, there is mounting evidence that this strategy may be effective, even though it is not a proven strategy at this time. I usually increase the interval between infusions after 18 months of treatment. Revere (Rip) Kinkel, Director of the UCSD Multiple Sclerosis Center PLEASE NOTE: The information/opinions on this site should be used as an information resource only. This information does not create any patient-HCP relationship, and should not be used as a substitute for professional diagnosis and treatment. Please consult your health care provider before making any healthcare decisions or for guidance about a specific medical condition. Question:
Hi. I am a 29 year old female. I have been experiencing urinary urge incontinence. It began around September 2013 with having to to urinate frequently and some urine coming out if I didn't get right to the bathroom. This continued all year and then between March and May I woke up from sleep mid-urination about three times. For a period of about a week I also had barely any sensation in terms of sexual stimulation. I then went to my physician in May who said I was not diabetic and did not have a urinary infection. He was not worried that I had MS. He sent me to the urologist and I asked her if I could have MS and she said it was highly unlikely. She put me on Vesicare which I only took for about a month but it worked. She also said to see if losing weight might help (I am 5'2 and was about 184 lbs). I was supposed to go for a follow up but did not go. I have lost about 20 pounds. Since May I have not experienced any urge incontinence. It started up again last week and the other morning I woke up and apparently had urinated in my sleep without waking up during it. That night I had taken some Klonapin for anxiety. Not sure if that might have contributed to the situation that night. Anyway, I am very concerned about MS. I went to the eye doctor last year and since then my eyesight has seemed to have gotten worse with regards to distance. I have also had depression for about 4 years which I have been working on with my psychiatrist. Besides that I have not experienced any symptoms. I have made an appointment again with the urologist. Should I be concerned that this is early stages of MS? Thank you so much. Answer: Sudden onset of urge incontinence at the age of 29 is unusual without an underlying cause, and there are many possible causes other than MS. When you see the urologist ask him or her if you have detrusor sphincter dysynergia or DSD. The urologist can do specific testing to determine if you have DSD or another mechanism causing the urge incontinence. If there is evidence of DSD, you should be seen by a neurologist to help determine the underlying cause. Good luck. Revere (Rip) Kinkel MD Director of the UCSD Multiple Sclerosis Center Here is My Question:
My daughter has been on Tecidfera for one year. She just turned 18. She did test positive for JC virus and it was on the high side. She has been on other drugs but they haven't work so don't know what we will do if this one doesn't work out. I'm so worried about PML and so is she. I guess my question is how do you if you have PML? Is the only way to do an MRI ? Also what blood tests should be done? Is there any thing we need to be watching for? Answer: I can certainly understand your concern given the recently publicity but I’m going to ask you to keep this concern in prospective and remember the following: 1. The risk of PML in people with MS taking Tecfidera appears to be very low 2. There is no known link between JC virus antibodies and the risk of PML in people taking Tecfidera 3. The main known risk factor for the development of PML in people on Tecfidera is a prolonged drop in absolute Lymphocyte count. As long as your daughter has her absolute lymphocyte count checked every 3 to 6 months and stops Tecfidera if her counts persistently drop below 500, her risk of PML should remain low. Many of us are looking at ways to further define risk factors for PML in patients on Tecfidera and other common drugs, but monitoring the lymphocyte count is the best way to monitor people currently taking Tecfidera. To do this she only needs an order for a complete blood count (CBC), a test done routinely in every blood lab. Please note that monitoring lymphocyte counts as a means of determining the risk of PML is NOT useful in patients on either Gilenya or Tysabri. Gilenya lowers lymphocyte counts routinely below 500 without apparently increasing the risk of PML and Tysabri raises lymphocyte counts and still has the highest risk of PML among all the MS drugs. Please see my previous blog for more information on this issue READ MORE Good luck and keep being a great mom asking the important questions. Revere (Rip) Kinkel DISCLAIMER: The medical information and opinions on this site are provided as an information resource only, and are not to be used or relied on for any diagnostic or treatment purposes. The information and opinions expressed do not create any patient-physician relationship, and should not be used as a substitute for professional diagnosis and treatment. Please consult your health care provider before making any healthcare decisions or for guidance about a specific medical condition. Here is My Question:
I started Tysabri in Sept 14' and really haven't seen much change. My MS was better when I was on Rebif. Since starting Tysabri I had a severe UTI which thru my MS for a loop. Is the Tysabri not working? I feel leary about the infusions because for the past 4 months I have had problems with Tysabri. My doctor says it's not the Tysabri. Should I seek another neurologist? I'm very confused! Answer: Dear Confused: Your story is one that is familiar to any MS Specialist and a cause of frustration among many people with MS. To help you understand what is happening, let’s break down the phases people go through when they initiate any a disease modifying treatment: Treatment initiation and titration phase (first 3-6 months) This will vary from one treatment to another. For instance, with interferons like Rebif, the dose is usually started low and increased over the first month to allow your body time to accommodate to the flu-like side effects which tend to be maximal at onset and lessen with time. The process of accommodation to these natural interferon related symptoms can take 1-3 months. Most patients will discontinue treatment between 3 and 6 months after starting an interferon if they are not able to find a way to lessen these side effects. For other treatments like Tysabri or Alemtuzamab there is no dose titration phase but your body must still accommodate to the side effects of treatment initiation which lessen over time. Patients on Tysabri, and especially those on Alemtuzamab, may experience significant infusion reactions which represent a hypersensitivity response to the drug. Other common early side effects with Tysabri include headaches and fatigue during or following infusions, both of which tend to improve over time. In fact studies suggest that MS associated fatigue actually decreases over time in Tysabri treated patients. In my experience Tysabri treated patients also experience a slightly increased rate of urinary tract infections after treatment initiation that may or may not lessen over time. If the infections do not lessen after 6 months of treatment or respond to urinary acidification, methenamine hippurate or other preventative measures, then you may need to stop Tysabri, if only to determine if this was the cause of the frequent UTIs. I would try not to stop Tysabri prior to 6 months of treatment, since this will increase your risk of hypersensitivity reactions if Tysabri is ever restarted in the future. For Alemtuzamab, there is a much greater early increased risk of infections (Reactivation of herpetic infections like shingles or bacterial infections) associated with the dramatic decrease in white blood counts. This also lessens after the immune system is reconstituted in the first 6 to 9 months. The disconcerting part of treatment initiation is that many people with MS experience these problems before a treatment has a chance to fully exert its beneficial effects. For instance, the benefits of Tysabri typically begin to kick in after the first 3 months of treatment. Copaxone also has a delayed initiation of action whereas interferons tend to have a more rapid onset of action. It is also during this interval that your body is recovering from the ongoing inflammatory activity present in your nervous system prior to initiation of treatment. The recovery process itself can create unpleasant symptoms such as pins and needles sensations, burning and electrical shocks, which doctors and patients may misinterpret as an inadequate response to treatment. You may also experience an MS relapse during the first few months on treatment, particularly if the treatment was started during an interval of heightened inflammatory activity. These symptoms and relapses must be interpreted within the context of recently initiating a treatment and expected maximal onset of action of that therapy. In most cases relapses in the first 3 months are treated with steroids and the disease modifying therapy is continued to allow more time for the benefits of treatment to accrue. Treatment stabilization phase (begins 3-6 months after starting treatment) This phase usually begins 3-6 months after treatment is started. By this time you should have accommodated to any side effects (or stopped the treatment) and usually obtained a new baseline clinical and MRI evaluation on your given treatment. It is during this phase of treatment that your begin to ask whether the drug is working adequately. This is usually too short an interval after treatment start to determine if the treatment is slowing disease progression. For most patients, the benefits of the drug are judged during this interval by the frequency and severity of relapses and interval assessment of MRI activity. For interferon treated patients, a repeat MRI of the head with and without gadolinium 6 months after starting treatment can assist you and your doctor in determining if you should continue treatment, regardless of how well the interferon is tolerated. Many studies have now determined that continued inflammatory activity 6 months on MR imaging after starting interferons suggest a less than adequate treatment response and a reason for switching therapy. Side effects may still occur during this phase of treatment but should not be significantly affecting quality of life. If side effects are still a problem, you should consider alternative treatments depending on your risk factors and prior treatment trials Long Term Treatment phase (greater than 12 months after starting treatment) It is during this phase of treatment that you and your physician will begin to determine if the treatment is capable of altering the long term course of your disease by halting disease progression. For most patients the process of disease progression is very slow with significant fluctuations in performance from visit to visit. A standard neurological examination is not capable of detecting this progression over time and, in fact, it is unusual to see worsening from visit to visit if the interval between visits is short (every 3-4 months). To assist you and your physician it is best to obtain quantitative measures of your performance at regular visits that can be compared and even grafted. These measures may include a 25 foot walking time, a timed up and go test, a 6 minute walk, a 9 hole peg test, sloan low contrast scores a symbol digit modality test or other timed tests of working memory and information processing speed and certain self report measures. It is important that a person get training in both administering and taking the test to eliminate the learning phase. For most of these tests, a 15 to 20% worsening in the test score indicates a significant change especially if persistent with a continued downward trend. In the near future, you will be able to assess the long term effects of treatment by using a quantitative evaluation of brain volumes on repeat MR imaging. At present this is only done in clinical trials Depending on where you are in the course of the disease your physician will continue to use relapses and MRI activity to determine the benefits of treatment during this phase but it is important to remember that relapses and MRI activity naturally decreases over time especially in individuals over the age of 50 making these assessments less sensitive to the detection of ongoing disease activity despite treatment. It is during the long term treatment phase that we begin to assess patients for the long term side effects of treatment. For Tysabri this means assessing for the development of progressive multifocal leukoencephalopathy (PML) which is most common after 24 months of treatment. For alemtuzamab this is the period when individuals begin to develop autoimmune conditions like Grave’s disease, idiopathic thrombocytopenic purport (ITP) and glomerulonephritis. Most injectibles (interferons and copaxone) have very few long term side effects that are of concern although interferons have been rarely associated with accelerated cardiovascular disease and autoimmune thyroid and liver disease So to answer your question directly, I would suggest monthly urinalysis and urine culture and continuing on Tysabri for at least 6 months. You should be taking vitamin C with every meal to acidify your urine (500 to 1000 mg to get the pH less than 6) and if you catheterize yourself, may sure you use sterile technique and dispose of the catheters after each use. If urinary tract infections continue at a rate greater than twice a year you should see a urologist specializing in female urination issues. Revere (Rip) Kinkel, MD Director of the UCSD Multiple Sclerosis Center Question:
Are Plegridy and Rebif similar? I was told by my neurologist that they are. Answer: The generic name of Rebif is Interferon Beta 1a. This is a recombinant protein identical to human Interferon Beta 1a, Plegridy is the same protein, Interferon Beta 1a, with a polyethylene glycol side chain attached. This alters the pharmacokinetic and pharmacodynamic properties of the protein to allow for a longer sustained duration of effect with fewer injections (every 2 weeks instead of every 2 to 3 days). This process of pegylation does not alter the safety profile or the efficacy the drug . Pegylation actually decreases the immunogenicity or the tendency of your own immune system to create antibodies that block the ability of interferon to bind to the interferon receptor and carry out its intended actions to treat your MS. Revere (Rip) Kinkel Director of the UCSD Multiple Sclerosis Center Question:
At what age do doctors generally start giving the kids pills for MS as opposed to injections? Answer: There are no guidelines on this and all medications used in pediatric MS are used “off label”, meaning none have been approved by the FDA for pediatric MS. Each case is considered individually and many aspects of the child’s history must be taken into account. Thus, there is no specific age at which oral medications are uniquely considered in children. Benjamin M. Greenberg, MD, MHS Director, Transverse Myelitis and Neuromyelitis Optica Program Director, Pediatric Demyelinating Disease Program Department of Neurology and Neurotherapeutics Department of Pediatrics Cain-Denius Scholar of Mobility Disorders University of Texas Southwestern Medical Center |
PLEASE NOTE: This information/opinions on this site should be used as an information source only. This information does not create any patient-HCP relationship, and should not be used as a substitute for professional diagnosis and treatment. Please consult your health care provider before making any healthcare decisions or for guidance about a specific medical condition.
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