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Question:
I have been on 5 medications. Avonex, changed due to silent exacerbations, Rebif for 11 yrs, changed due to efficacy no longer working, Tysabri, stop after 2 yrs due to JC virus, Tecfidera, not efficient enough, and Aubagio, stopped due to skin peeling reactions and high blood pressure. Even though my MRI's may show no new lesions, I am losing my balance, and my vision is deteriorating from constant optic neuritis. I want to try the new medication Lemtrada, because I did the absolute best on Tysabri and I seem to do better on IV medications. However, my neurologist says that I am not sick enough and refuses and says other neurologists will refuse also. Now, I am currently on no medication because the one the neurologist backs (Copaxone) takes 9 months to get into the system and I want a medication that slows down all symptoms not just the lesions on the brain. Is this true about no neurologist prescribing Lemtrada? How can I get this new medication prescribed to me? Answer: First of all it sounds like you have secondary progressive MS, since you describe progressive worsening problems with balance and vision in the absence of relapses or new lesions on MRI. You may be in the early stages of SPMS, but I can not determine this from your description. There is no evidence that Copaxone is beneficial at this stage of disease and this option would not be appropriate. Tysabri was not beneficial in a recent secondary progressive trial, although people in the early stages often benefit from Tysabri. Lemtrada (alemtuzumba) was not helpful to people with secondary progressive MS but similar to Tysabri may be beneficial in early SPMS patients who continue to experience inflammatory activity (relapses or new MRI lesions in the past year or two at most). Based on the information provided, the best choice right now would be Rituximab (especially if you are under age 55), but this is often not authorized by insurance as a treatment for MS patients. The second best choice is to restart Tysabri, since you know you responded and tolerated this treatment in the past, and switch to Ocrelizumab when this is approved by the FDA, hopefully by the end of 2016. The risk of PML is only significant after 24 months of re-treatment with Tysabri even in patients who are JC virus positive and you would be switching to Ocrelizumab before that amount of time on treatment. Your risk of PML is particularly low if your JCV antibody index in less than 1.5. To determine if Lemtrada is a reasonable option would require me to gather a lot more information about your condition. As mentioned above Lemtrada was not beneficial in prior secondary progressive clinical trials and there are short and long term risks associated with this treatment. Discuss these options with your MS specialist. Good Luck Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego 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.
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Question:
Hi! My MS has progressed into Secondary-Progressive from RRMS. I have difficulty walking due to lesions on my spine. I use a walker at home and a scooter for church, shopping, etc. Sometimes I feel like I am yearning for the scooter more and more. I am blessed to be able to still use my legs, albeit it is not easy. I don't want to fall down the rabbit hole of dependence. As hard as it is, I feel I need to tough it out and use my walker for certain outings instead of the scooter. If I "push" myself, is there a benefit for using what little ability I still have in my legs, or am I aggravating my condition and advancing it? Thank you for your time! Answer: You are not going to aggravate your condition if you push yourself to use your legs more. However, safety should always be your number one priority! It sounds like the scooter is the appropriate device for you to be using for your community outings, though I do understand your concern that if you don’t “use it you’ll lose it.” My advice would be to minimize your use of the scooter in your home as much as is possible, as long as you are SAFE. If you feel the need to use your scooter in the home for safety reasons, try to make a point to stand up and walk around your house 1x/hour (or whatever is reasonable for you). If you like to watch TV you can make it a goal to make some time for exercises during commercial breaks. You can do exercise from a sitting or standing level. If you are looking for some exercises the MS society has great resources. You could also seek out the assistance of a local physical therapist who can prescribe exercises specific to your needs! I hope this help! Keep your head up and keep moving; but within safe limits of course!!! Sarah Wargo, PT, DPT, MSCS Mount Sinai Rehab Hospital and Mandell Center for MS Hartford, CT Answer: Maintaining a standing posture and continuing to walk, if safe, are both important in people losing the ability to walk and finding themselves more and more dependent on wheelchairs or scooters. The important thing is to make sure you avoid falls and do not place unnecessary strains on your knee or ankle joints. To continue walking, people no longer able to walk on their own often resort to sling supports from a ceiling mount or even Lokomat devices at rehab centers. In the near future, robotic frames will be available to assist with walking in paraplegics. The benefits of just maintaining a standing posture through the use of a standing frame in people unable to walk are considerable. As noted in a prior blog on our site, standing frames provide the following benefits:
Make sure you meet with a physical therapist who is a neurological clinical specialist several times a year to make your walking is safe with your current devices and to determine if any joints require additional support. Good luck Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Question:
How is PPMS diagnosed? I had a small attack 2 years ago. Numbness, temor, bladder issues. All resolved. MRI negative for a year. Stopped doing MRIs and in the past year, I've had stiffness in muscles and I can't walk up stairs. My feet are on fire. Numbness that goes and comes and I have a hard time with my left foot because it feels heavy to walk on. The more I walk I want to favour it more. I am 48 years old . Could I have PPMS? Answer: PPMS is diagnosed on the basis of slow but steady worsening of neurological function consistent with multifocal demyelination of the central nervous system with MRI abnormalities and CSF abnormalities. You can not have relapses; therefore, you can not have PPMS based on your description. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Hey everyone! We want to let you know about something new. Daryl Kucera (shown in the picture below on the right) was diagnosed with MS in 2001. He is a certified personal trainer and young sports conditioning coach, and is also the founder and owner of the MS Forward fitness gym in Omaha, NE. He has started 'virtual' exercise classes, where you can connect and actually participate in a class virtually OR if you would prefer to just watch a video to exercise, that is available too. Watch the clip below to find out more! If you are interested in learning more about how to participate in these virtual exercise classes, let us know! Here is My Question:
What MRI machine and protocol best detects any changes in lesions or enhancing lesions? I'm feeling physical changes, but the MRI report shows no changes and I want to be informed. Thank you so much for answering my question. Answer: An MRI done to detect a change in disease state is only as good as the last MRI scan your received. Otherwise you are trying to compare apples to oranges. Let me explain. Imagine you obtained the highest resolution MRI scan available with the thinnest possible slices and all your brain tissue is imaged (we call this a volumetric image acquisition). This scan may show 60 discrete lesions with a resolution allowing you to confidently identify lesions as small as 1 mm diameter in the cortex. This will not help you if the prior MRI was obtained on a conventional 1.5 or even a 3.0 Tesla scanner with slice thickness of 3 to 5 mm and a gap between slices. The conventional scan may only identify 20 lesions and any comparison of the scans may suggest, inappropriately, that you suddenly developed 40 new lesions !! Other technical factors can make comparisons difficult even when the scans are obtained on the same scanner. This is why we recommend all our patients obtain a new baseline study on a 3 Tesla MRI scanner using volumetric 3-dimensional imaging with pulse sequences allowing us to perform automated registration and segmentation for comparisons of scans between time points. Unfortunately, few centers have this capability at present. For the time being it is best for you to obtain repeat MRIs on the same scanner used previously using the same imaging protocol and slice orientation for all scans. Even when this is done, changes on MRI do not correlate one to one with changes in symptoms or changes examination. For over three decades, we have referred to this phenomenon as the clinical radiological paradox. In many ways MRI findings and changes on MRIs over short intervals (1-2 years) do a better job of predicting clinically meaningful changes in neurological function that may occur in the future Gadolinium enhancement on an MRI represents new breakdown of the blood brain barrier and is associated with acute inflammation. There is not a one to one relationship between relapses and gadolinium enhancement although enhancement may flare up around periods of relapses. This gadolinium enhancement does not correlate well with future disability in untreated patients but does correlate well with future lack of response to a disease modifying therapies if the enhancement persists on future scans at least 6 months after starting the disease modifying therapy. Highly active disease modifying therapies (such as Tysabri, Alemtuzumab, Rituximab and Ocrelizumab) virtually eliminate gadolinium enhancing lesions and are often not obtained after an individual is stable on a highly active disease modifying therapy for more than a year. The vast majority of enhancing lesions persist as T2 bright spots without gadolinium and will be detected as new interval lesions on a later scan. Hope this helps Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
Can a relative afferent pupillary defect and pallor of the optic disc disappear? I have conflicting reports from neurologist and opthamologist. How frequently or easily are these misdiagnosed and does it make a difference is practioner is using direct eye exam or dilated eye exam? Answer: An afferent pupillary defect can disappear over time depending on what caused the afferent pupillary defect (the vast majority of the time it is due to optic nerve damage, for example, optic neuritis). If the cause of an afferent pupillary defect is a mild case of optic neuritis with excellent recovery it is possible for the afferent pupillary defect to disappear. However most of the time, once an afferent pupillary defect occurs, it is rare for it disappear. However optic nerve pallor does not disappear. Once an optic nerve is damaged and pallor sets in, it is irreversible. Both an afferent pupillary defect and optic nerve pallor may both be misdiagnosed for a variety of reasons (including but not limited to: the experience of the physician doing the exam, presence or absence of cataracts, etc.). An afferent pupillary defect can only be tested prior to dilation (once the eyes are dilated one can no longer test for an afferent pupillary defect). It is usually easier to detect optic nerve pallor on a dilated eye exam but a competent physician can detect it even on a direct, undilated exam. Sincerely, Benjamin Osborne, MD Associate Professor Departments of Neurology and Ophthalmology Georgetown University Hospital Question: How does Lemtrada work? In your opinion is it safe?
Answer: Mechanism of Action: Alemtuzumab (Lemtrada) is a monoclonal antibody directed against CD52, a protein expressed at high levels by both mature circulating B and T lymphocytes and at lower levels on circulating monocytes, macrophages and eosinophils. There is little expression of CD52 on mature natural killer (NK) cells, neutrophils and haematological stem cells. Following treatment there is a rapid and sustained reduction in circulating lymphocytes with a return of the B cell population within 6 months and a more sustained depletion of circulating T cells for more than 12 months. This selective reduction in lymphocytes is presumably the mechanism of action of this treatment in MS. Lymphocytes are the driving force behind all adaptive immune responses and are implicated in the pathogenesis, propagation and maintenance of central nervous system inflammation and tissue injury in multiple sclerosis. Other disease modifying therapies (DMTs) that specifically target lymphocytes include Rituximab, a monoclonal against a protein called CD20 on the surface of only mature B lymphocytes and Natalizumab (Tysabri), a monoclonal antibody that binds to alpha 4 integrin, a protein on the surface of lymphocytes and mononuclear cells required for circulated blood cells to bind to the lining of small blood vessels in the brain and cross the blood brain barrier into the tissue. Following treatment with Alemtuzumab, there is less depletion of lymphocytes residing in lymphoid organs (lymph nodes and spleen) and preservation of neutrophils and bone marrow derived stem cells. The selective reduction in circulating lymphocytes and preserved neutrophils is the reason that few treated patients experience severe infections following treatment. The more rapid return of B lymphocytes compared to T lymphocytes following treatment with Alemtuzumab has been implicated as the reason for the high incidence of system autoimmune disease following treatment. It is speculated that autoimmunity occurs as a result of B cell and plasma cell responses in the absence of normal T cell regulation. Most of the autoimmune diseases following treatment with alemtuzumab involve the thyroid gland. Less commonly autoimmunity can target blood platelets causing a reduction in platelet counts and a high risk of bleeding (called idiopathic thrombocytopenic purpura or ITP for short) orvery rarely an autoimmune disease of the kidneys develops (called Glomerulonephritis). You can also enter "Lemtrada" in the search button on the upper right corner of this page to read more about Lemtrada. http://www.healthcarejourney.com/q--a-for-virtual-ms-center/what-long-term-data-is-there-on-lemtrada Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
How long can a relapse last for...days, weeks, months? Answer: 80% of people reach maximal deficits from a relapse in 2 weeks and 90% within 4 weeks. This is followed by a variable period of stability, usually a few days to 2 weeks, followed by slow improvement to a new baseline state with or without residual problems from the relapse. 80% of people reach maximum recovery within 3 months and 90% within 6 months. The rest can take up to a year to recover, although we now know that recovery can continue beyond a year if the underlying disease is thoroughly controlled. Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
How does foot drop start? My left foot at the ankle feels weak and uncomfortable to walk on. I can walk straight no issues. Answer: A foot drop is an inability to dorsiflex the foot (move upward at the ankle joint). The first symptom noticed is catching the toe or foot on the ground while bringing the leg forward during your normal stride. If more severe, a person with a foot drop walks with a high step gait during the forward swing phase to allow the foot to clear the ground. Others may notice that the foot makes a loud slapping noise when it hits the ground. If a foot drop is caused by a central nervous system problem, there may be a spastic or dystonic turning in of the foot while walking. This may create a sense of instability or discomfort at the ankle joint since the foot can roll over during normal walking. You can read more about foot drop on our symptom page for it...READ MORE Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego Here is My Question:
Hello I have MS And on January 5th this year I had laminectomy surgery on my back. Does MS slow my recovery down? Answer: Here is a past Q&A that you can read to answer your question: http://www.healthcarejourney.com/q--a-for-virtual-ms-center/disease-modifying-therapies-and-outpatient-surgery A. Scott Nielsen MD MMSc Neurologist and MS Specialist at Kaiser Permanente Here is My Question:
I am a 43 year-old female and was recently diagnosed with MS just last month. Late December 2015, I suffered from an attack of optic neuritis and spent three days in the hospital for IV steroid treatment and other diagnostic tests. Other than the IV steroids and a three week taper of oral prednisone, I have never been on any other DMTs or immunosuppresants. The ON has been my only symptom, as well as some minor facial tingling. My MRIs showed approximately 3-4 active lesions and 3-4 inactive lesions. None on C or T spine. I take medication for hypertension and hypothyroidism. My MS specialist neurologist is recommending Rutixan as my first form of treatment for MS. I am JC positive, not sure of exact level. I know there have been no reported cases of PML in MS patients treated with Rituxan, and that the risk is about 1 in 25,000. Is Rituxan normally used as a front line treatment for MS? It seems very aggressive to me, but my neuro said that he wants to treat it aggressively, as I am so young and have so little disability at this point. He wants to keep it that way. Do the benefits of this treatment outweigh the risks of PML? How long could I safely take Rituxan before having to consider switching to another DMT? I've read that patients can only take Rituxan for 2 years max.? I have ruled out Tysabri, Tecfidera, and Gilenya due to PML risk. How small or large is the PML risk in Gilenya as compared to Rituxan? Is Aubagio more effective than the interferon drugs in regards to delaying disease progression, number of relapses, and number of MRI lesions? Not looking for recommendations, just a little guidance. =) Answer: Being JC Ab positive has only been shown to a significant predictor of risk for PML in patients taking natalizumab (Tysabri) and it has not been shown to be a valid predictor of PML in patients on other MS therapies. Because there are only a handful of cases of PML in patients taking Gilenya (five patients) or Tecfidera (three patients), there are no recommendations for screening patients with the JC Ab test to guide therapy choices. No one knows the actual risk of PML with the oral medications but it appears to be significantly lower when compared to natalizumab. While Aubagio has not had any reported cases of PML yet, I would not be surprised if a case or two is eventually reported over the next several years. As you mentioned, the risk of PML with rituximab is also very low. Rituximab is sometimes used as an option for treating relapsing MS patients but it is not commonly used as the first medication. You will need to discuss with your neurologist how much “risk” you are willing to take in being aggressive in the treatment of your MS for the future potential benefits (decreased disability, decreased relapses, decreased MRI lesions). Once you decide how much risk you are willing to take you will be better prepared to choose which medication to start. Please type in "PML" or "JC" in the search box in the upper right hand corner of this page and you will find many questions and answers about these topics. Benjamin J. Osborne, MD Department of Neurology MedStar Georgetown University Hospital 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. Share this blog with others to share the information! http://bit.ly/1KXwyoZ
Here is My Question:
I have a cousin that swears she has MS but has never been tested for it. Can I just look at you and say you have MS even when there has been no testing? She has had MRI's for something else but they don't have any lesions, is it possible she has MS or no? Answer: Please read our page on diagnosis for MS. Only a neurologist (preferably an ms specialist) can render the diagnosis. Another Q&A that would be helpful to read would be this...READ MORE A. Scott Nielsen MD MMSc Neurologist and MS Specialist at Kaiser Permanente Question:
What is the difference between lack of fine motor skills in the hands between arthritis and MS? Answer: Fine motor deficits in arthritis is due to pain and stiffness (restricted motion) in the joints. With MS, the joint isn't affected, but the nerve signal to the muscles in the hand and arm are affected which can lead to clumsiness due to poor coordination of the arm and hand. A. Scott Nielsen MD MMSc Neurologist and MS Specialist at Kaiser Permanente Here is My Question:
My 17-year-old son was diagnosed with Tumefactive MS last year. Over the past month, he has been experiencing pain in his testicles. Specifically, the pain is based in the epididymis and radiates up the vas deferens into the groin. There is no swelling or bruising. Even after 2 ultrasounds and several physical exams, they have no cause for this pain. Can MS cause pain in strange places? Answer: Pain and odd sensations isolated to the genital regions is more common in women with MS but can occur in men as well. Other conditions can cause referred pain, including kidney stones. Benjamin M. Greenberg, MD, MHS Director, Transverse Myelitis, Neuromyelitis Optica Programs Director, Neurosciences Clinical Research Center Co-Director, Pediatric CONQUER Program UT Southwestern Medical Center Childrens Health Dallas, Texas Tel 214-645-0555 Here is My Question: I had been on Tysabri for 7 years and stopped the infusions in November (PML risk is too great). I had been on Copaxone for 7 years prior to Tysabri. Currently, I'm getting monthly steroid infusions until I make a decision for a new DMT. I am 56 years old and am concerned about my future disability. I do not have new lesions on my recent MRI's, but does this mean that my disease swill come back at the same rate it would have prior to starting Tysabri? What are the chances for this occurring and how does one know how the disease will progress after stopping Tysabri? I work part time and my biggest complaint is extreme fatigue. Is there a way to know how this disease will present itself in the future? Answer: You ask a question that many of us have been trying to answer for years; Is there a way to predict future disease activity? Unfortunately the predictors we use are very imprecise. I can however give you some useful information from the details in your question. 1. If you just had an MRI scan 3 months after stopping Tysabri and there are no new or enlarging T2 signal abnormalities (the white spots) you do not have to worry about getting PML 2. You still have a risk of relapsing in the next 3 to 4 months from stopping Tysabri. Monthly steroids are not very effective at preventing the relapses that can occur after stopping tysabri 3. You should probably restart another DMT asap. Options could include Gilenya, Tecfidera, or Rituximab. Of those three only Rituximab has the ability to significantly decrease the risk of relapsing after stopping Tysabri. As you may or may not know, people with MS who stop Tyabri have a 30 % chance of relapsing in the next 6 months. Most of these relapses are minor but about 10 % are severe. The risk of relapsing after you stop tysabri is greater if you had highly active disease before starting Tysabri. Highly active means many enhancing lesions on MRI of several significant relapses in the 2 years prior to starting tysabri. 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 been on Copaxone 20mg for 14 years and I have never had a problem until they switched me to Glatopa 7 months ago and I am now having balance problems and walking problems and for the first time. People are asking if I'm ok as I am now showing MS symptoms I am just wondering if it can be because of switching me to the generic. Answer: The first thing to do is make sure that your balance problems are related to MS, since there are many possible reasons for impaired balance If your MS specialist feels certain that this problem is a result of your MS, then I would think through your problem in the following way: The FDA determined that Glatopa is equivalent to Copaxone. The most reasonable explanation for your worsening symptoms, therefore, is the natural history of MS in an era of partially effective treatments that reduce relapses only. Let me explain: Treated MS patients frequently go through 3 phases of their disease. The first phase consists of relatively frequent relapses (perhaps 2 or more in the first 3 years) before starting on treatment. While people with MS sometimes experience an occasional relapse early after the onset of treatment (first 6-12 months) once an effective treatment is started they often experience very few relapses and may go many years with apparent stability; This is the second phase of your disease. I refer to this stable period as only “apparent”, because we can often detect changes over time using quantitative measures of brain volume on MRI scans. Even if your doctor is obtaining regular MRI scans the radiologist will not detect these changes in brain volume, and usually will report your MRI as stable because no apparent new lesions are developing. The third phase of the disease begins 10 or more years after the onset of treatment and after this second period of apparent stability. This is simply the secondary progressive phase of MS. The real question is what to do about your current problem. I would recommend a repeat MRI of the brain with and without gadolinium to determine if there is any new inflammatory disease activity (new or enlarging T2 lesions or enhancing lesions since a scan within a year). If this is the case I would consider treatment with IV high dose steroids followed by a switch to a more highly active disease modifying therapy (DMT). These highly active treatments include Tysabri, Rituximab and Alemtuzamab. The choice of DMT will depend on many factors including the degree of inflammatory disease activity, your risk factors for disease worsening, your aversion to risk and your co-morbid medical conditions. If there is no significant inflammatory disease activity, go ahead with the high dose IV steroids and determine the amount of improvement and the length of improvement. If your improvement lasts for over 6 weeks, you may consider continuing on regular 3 to 5 days courses of IV high dose steroids (no prednisone taper) every 2 months without the Glatopa. If Rituximab is available to you now (this varies by insurance), this may be a good choice as well. If rituximab is not available, your doctors may consider Ocrelizumab once it is approved by the FDA. If your balance is off you should also talk to your doctor about working with a physical therapist and using a cane or rollator type walker to prevent falls. Good luck Revere (Rip) Kinkel MD Director of the Multiple Sclerosis Program Professor of Clinical Neurosciences University of California San Diego The three lucky winners are: Betty L Catherine H Laura B We will send you an email today to notify the three of you and get your home addresses so Mindy can ship your book to you!  |
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.
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