I have never heard of Difen Flex; this sounds like a supplement of some type. I would recommend asking your doctor if this is safe for you for you to take. We (meaning doctors) rarely know supplements by their commercial or brand name, so it is always useful to find out the exact ingredients before discussing this supplement with your doctor. - Dr. Kinkel

The rollator (seated walker w/ hand brakes) is a wonderful product which has become increasingly popular as an ambulatory device for many people with MS.  However, a rollator is NOT a wheelchair so please keep reading.

Safety and fall risk management is always critical.  Therefore, before using a rollator one should consult their primary physician and physical or occupational therapist.

Rollators are great…for appropriate clients.  Rollators allow people with MS to walk greater distances and when they fatigue, it's a rolling seat and even has a basket to carry items from room to room or store to store.

Many rollators are now lightweight and quite portable.  There are also heavier ones for our bariatric clients or clients that require a more stable base. However in recent years since their increase in popularity I have seen one glaring misuse.  A rollator is not a wheelchair.

At my son's football games, swap meets, and graduations I have seen people pushing their loves ones in a rollator as if it was a wheelchair or transport wheelchair. There is great danger in this, as a rollator's frame does not lock and a rollator folds differently than a wheelchair.  If you use a rollator in this fashion any transition in terrain is a fall risk.

What is the solution?  There are rollators that are especially designed for this usage.  It is a "hybrid" rollator/transport wheelchair. Contact your local medical supply provider or therapist for details.

Keep Fighting On, Big Love!
Tom Mellor, ATP

A Bit About Tom:  Tom Mellor is an Assistive Technology Professional (ATP) with over 20 years of experience analyzing the needs of people with disabilities, assisting in the selection of appropriate assistive technology for the person's needs, and providing training in the use of the selected devices.

Q:  Could we come up with an EBV vaccine? And vaccinate at least the kids of people with MS?

Good question but an EBV vaccine will not work since the virus is very good at evading the immune system.

--Dr. Kinkel

Question:  This is a difficult one, but let's give it a try. I am trying to decide whether or not I should have my own child, since I am terribly afraid of passing the disease to my child. Sometimes I try to encourage myself by thinking that medical research have done a great work lately for MS, and that very soon we might find a cure. In your opinion, how far are we from that moment, where having MS will be not more cumbersome than perhaps a need for taking a lifelong medication?

Answer:  As recently as 10 years ago, I would shy away from directly answering questions like yours, since we did not have the technology or platforms to make rapid advances in MS or other diseases; all of this has changed, largely as a result of networks of physicians and patients beginning to work together to find more rapid solutions to health care problems. This is the crowd sharing revolution that has finally come to medical research. We (meaning the accelerated cure project) just received a large grant from the Patient Centered Outcomes Research Institute (PCORI) to set up a network of 20,000 MS patients for the purpose of large scale research studies. We are also forming a network of sites around the United States for a study called Opt-Up, for optimizing treatment and understanding progressive MS. This will provide many of the tools requires for large scale clinical studies. So I think we already have good solutions for MS patients and will have far better solutions in the next 15 to 20 years.

That being said, it is often difficult to decide on having children even if you do not have MS. So much depends on your prior attitudes towards becoming a parent (is it having children that is important or having your own children?), your age (increased risk of Down’s Syndrome and other chromosomal abnormalities with age), your goals in life, your supports, your finances and your own health. Plus having children is usually a decision between two people, which adds an extra layer of complexity. The risk of MS in your children is almost a minor consideration compared to these issues. The facts are well known; any of your children will have approximately a 9% risk of MS.  So I recommend, all other things being equal, make your decision about having children independent of your concerns that some day they may too develop MS. Hope this helps.

 -- Dr. Kinkel

PLEASE NOTE:  The medical information on this site is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. This information does 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.

Epstein Barr Virus (EBV), also called Human Herpes Virus 4, is ubiquitous, meaning almost every (> 90%) one of us has been exposed to the virus by adulthood. The virus exists in a latent form in B lymphocytes and usually causes no problems. Being exposed and infected with EBV does not by itself increase your risk of MS.  If it did there would be a whole lot of people with MS. It is hypothesized (this means there is not enough evidence to prove this point yet) that the increased risk of MS  occurs only in individuals  with an abnormally regulated host (meaning you) response to EBV; this abnormal host response to EBV may also be linked to vitamin D deficiency.  Now you can see why we encourage people with MS to take Vitamin D.

Q:  I am 18 years old. A few years ago my vision started getting bad and I started to get a lot of floaters in both eyes. I went to a retina specialists and he said it was probably caused by some type of auto immune disease because I had a lot of inflammation in my eye, so we did a bunch of tests for stuff like Lyme disease and a few others. They all came back negative and he said that it could possibly be MS but I didn't have other symptoms so we just kind of figured there is really nothing we could do. In the past few months I've experienced a lot of weird symptoms. A big change was bladder problems. I had to pee way too much and especially at night. And I had a feeling of it not being completely empty and also a hesitancy to urinate. Another symptom was one of my legs felt very weak and just felt really strange,and this lasted about 3-4 weeks. I also have found that my speech has changed, I tend to have trouble saying stuff or articulating my words, sometimes even slurring them. I am planning on getting an MRI when I go home for spring break from college but my question is do you believe that these symptoms are an indication that I could possibly have MS?

Answer:  Those are great questions. I can certainly understand why you would be concerned about MS. In fact there are many things that could be causing your symptoms. An MRI scan of the head and spinal cord as well as a trip to see a neurologist are definitely the first steps and should be done during your Spring Break. Keep us posted. We’d be happy to see you if you are anywhere near San Diego

--Dr Kinkel

PLEASE NOTE:  The medical information on this site is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. This information does 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.

Q:  Somebody on one of the FB MS groups I belong to has mentioned that they are on something called low-dose naltrexone (LDN)? Any recommendations?

Naltrexone is an opiate receptor antagonist used in high doses (50 mg or more) on a daily basis for alcohol or narcotic dependence. Smaller doses (usually 3-5 mg) at bedtime, called low dose naltrexone (LDN), have been advocated by different groups for years to treat a number of conditions including HIV, fibromyalgia, cancer, inflammatory bowel disease and MS, to name just a few. The general hypothesis, for which there is little direct clinical evidence, is that a low bedtime dose of naltrexone helps modulate the immune system in beneficial ways. What is known is that low doses of naltrexone at bedtime paradoxically increase your own endogenous opiate levels; these are substances called endorphins and enkephalins. This makes everything feel a little better. Studies in MS are virtually non existent; a small study by Bruce Cree and colleagues at UCSF suggested that low dose naltrexone may improve well being and pain and daytime fatigue over the short term but there is no evidence that LDN effects the course of the disease. We also do not know if it is safe in long term use. I find that patients often feel better on LDN, particularly those with sleep disorders and discomfort at night; so I will use it for this purpose with attempts at weaning the medication over time. As of now, there is no evidence of any abuse or additive potential to this drug. The drug is not available in this dose formulation so it must be obtained through a compounding pharmacy.

PLEASE NOTE:  The medical information on this site is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. This information does 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.

Q:  Have there been any studies on the impact of oral contraceptives on the course of MS? I was just wondering, since pregnancy is protective, whether taking hormones that prevent ovulation and to some extent mimic pregnancy can help too?

The verdict on oral contraceptives and their effect on MS is still out. Several case control studies, including a recent analysis of the Swedish Multiple Sclerosis registry, suggest that combined oral contraceptives (progestin and estrogen) use is associated with a later age of onset of MS. One study even suggested less severe disease in patients with longer combined oral contraceptive use. Unfortunately, case control studies are not able to prove causation and there are other possible explanations for these results. There is a randomized control study underway to determine if a pregnancy related estrogen (estriol) is effective at decreasing MS disease activity. Although this will help answer many questions, it will not tell us if oral contraceptives are helpful as these contain different hormones. Stay tuned for more information in the future.

--Dr. Kinkel

Q:  Is MS associated with Sjogren's disease?

There is no good evidence that MS is associated with Sjogren’s disease although I do have patients with both conditions.  Sjogren’s disease and many other rheumatologic conditions are difficult to diagnose and frequently associated with many non-specific symptoms that can overlap conditions like MS; symptoms like fatigue, pins and needles sensations, forgetfulness and depressed mood. Rheumatologists and other doctors often draw a panel of autoantibody tests to look for evidence of these conditions. Unfortunately, these tests, while sensitive, are not very specific. This means that if you have something like Sjogren’s disease the test will almost always be positive (i.e. the test confirms the clinical diagnosis) but if the test is drawn on a large population of people with non-specific symptoms a positive result rarely means the person has Sjogren’s disease. To make matters worse, patients with MS more often have positive autoantibody results on these tests that cause diagnostic confusion because there is no clinical evidence of a rheumatologic condition. Many of us have argued for years that these tests should not be routinely obtained as part of the diagnostic work-up for MS but many doctors continue to obtain them. I hope this helps.

--Dr. Kinkel

Q: Some neurologists classify symptoms as either gain of function (for example paresthesia), and loss of function ones (like trouble walking, numbness, etc). In your opinion, where does pain belong in this classification? Is it also a sign of healing? Thanks!

Answer: I am not sure I like the term, “gain of function”, since there is nothing really gained by the acquisition of pain. I would say that neuropathic pain, which is usually described as sharp, jabbing, stabbing, electric or burning, is caused by the generation of abnormal electrical signals in areas of the nervous system responding to injury. Chronic pain is more complex and likely involves a maladaptive response to injury. Please see my most recent blog (http://www.healthcarejourney.com/10/post/2014/02/what-causes-abnormal-sensations-and-pain-in-multiple-sclerosis.html) for a more thorough explanation of abnormal sensations in people with MS.

Q.  What is the connection between a high sodium diet and MS?

A.  There is some very preliminary evidence from animal experiences and cell cultures that a high sodium diet may drive your immune system in the direction of a stronger inflammatory response that theoretically could result in increased damage in MS patients. While this data is not ready for prime time, so to speak, there are other health reasons to beware of using too much salt in your diet. The bottom line for now is to moderate your salt intake for overall health reasons.

--Dr. Kinkel

Question from an MS Patient: 
Is Rituxan an effective treatment for SPMS? What are the benefits or disadvantages? i.e. pros & cons etc. Are there any life-threatening side effects? Would you consider this is a good drug to treat SPMS long term? Do you feel the drug can cause complications-manifest other diseases or illnesses? Are there any results from clinical trials conducted using Rituxan published?

Rituxan (Rituximab) is a chimeric monoclonal antibody that is currently approved for the treatment of two forms of cancer (CD20 positive Non Hodgkin’s Lymphoma (NHL) and chronic lymphocytic leukemia (CLL)) and two immune medicated disorders (moderate to severe rheumatoid arthritis and Wegener’s granulomatosis). It was first approved in 1997 and has been widely used off label to treat a number of rare immune medicated conditions, including neuromyelitis optics (NMO), often with dramatic success. In fact is it currently considered the first line treatment for NMO in many centers around the world. It binds to a protein expressed on the surface of B Cells called CD20 and causes complement mediated lysis of these cells lasting for variable periods of time depending on the dose administered. The mechanism of action in MS is unclear; B cells clearly play a role in the inflammatory response in MS and their elimination seems to benefit many patients. What is unknown is the exact role played by the B cell; for instance some believe the B cell only becomes a problem in MS when co-infected with Epstein Barr Virus.  

Studies of Rituximab in the treatment of relapsing or progressive forms of MS have been few, yet it remains a key treatment option by many MS specialists for certain situations; namely, as an induction therapy for patients with an aggressive onset to their condition, as ongoing treatment in relapsing patients not responsive to other therapies including tysabri or in patients rapidly transitioning to secondary progressive MS despite other available treatment options.  

Why would a drug not even approved by the FDA be considered such an important treatment option by MS specialists? First, those studies that have been done in relapsing forms of MS demonstrate rather dramatic benefits that persist for 6 to 12 months after treatment. MS specialists using the drug in practice report similar benefits in their patients. Studies in progressive forms of MS have reported mixed results which can be expected given the challenges of treating MS at this stage of the disease.  The large phase III study by Genentech in primary progressive MS was a negative study when the entire study population was considered in the analysis. When considering only those patients under the age of 51, those patients with gadolinium enhancing lesions at the beginning of the study or patients with both features, rituximab given every 6 months for 4 courses of treatment significant reduced the rate of sustained disability progression.  A small retrospective analysis of 25 secondary progressive MS patients treated with rituximab every 6 months at the University of Massachusetts in Worcester reported that 84% of patients stabilized or improved while on treatment.

Rituximab is generally safe in most MS patients. The most common side effects are caused by infusion reactions which decrease over time and can be further decreased by administering corticosteroids prior to the infusion. There is also a slight increase in serious infections, though these are treatable. Progressive Multifocal Leukoencephalopathy (PML) has been reported but does not appear as frequently as in Tysabri treated patients. What is unknown are the long term consequences of treatment with Rituximab and the most appropriate dose and dosing interval. Most current dosing regimens are based on the very high doses used to treat cancers, yet we were able to achieve a very good response in relapsing patients given 1/20th of this dose (100 mg) every 6 months for over 3 years of continuous treatment.

Further studies of rituximab are not likely to occur since there is no further patent protection. There are several other monoclonal antibodies in MS clinical trials that target CD20 and delete B cells including ocrelizumab and ofatumumab. Whether these newer treatments offer improvements in safety or efficacy in comparison to rituximab is unclear at this time.

--Dr. Kinkel

PLEASE NOTE:  The medical information on this site is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. This information does 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.

• What is pseudobulbar affect? How is it screened for and determined to be the cause of bursts of crying or laughing?

Pseudobulbar affect (PBA) is a disorder of emotional regulation that occurs in about 10% of people with MS.

The behavior itself is quite striking and easily recognized by those who know what they are looking for; The key feature is the abrupt onset of involuntary laughter or crying that is either out of proportion to the mood state (e.g. something mildly sad that may normally cause a person to sigh may cause an individual with PBA to burst out in near hysterical crying) or totally incongruous with the mood state (person uncontrollably laughs at something others find sad). It is this loss of congruence with the mood state, plus the abrupt onset followed by cessation of the laughter or crying within seconds or minutes, that distinguishes PBA from depression or grief. Unless significant cognitive problems are present, the person is usually aware that the laughing and crying is inappropriate and is embarrassed by their behavior. In early or milder cases the response is more blunted, such as an inappropriate chuckle or a smirk on the face that seems inappropriate.

Although it can be observed at all stages of MS it is far more common in patients with more advanced disease. PBA actually occurs more often in several other neurological diseases, particularly Amyotropic Lateral Sclerosis (ALS), and is therefore not at all specific for MS. It has gone by many different names over the more than 125 years since initially described in the medical literature, including pathological laughing and crying and emotional dyscontrol syndrome, but most theories continue to suggest it is caused by  damage to the neural circuits in the central nervous system responsible for normal  inhibitory control of emotions. Once inhibition is lost, emotions are unleashed in this unpredictable manner.

There is a survey  people can take to determine if PBA is a possible cause of emotional outbursts. This is called the Center for Neurological Study-liability Scale for Pseudobulbar affect. This is provided at the end of this blog. Scores greater than 13 indicate that PBA may be cause of your behavior.

Treatments are available if necessary and partially effective. These include older drugs such as amitriptyline and fluoxetine and a newer drug called Nuedexta (made by Avanir) that is a combination of dextromethorphan (a cough suppressant in most cold remedies) and quinidine (an older drug used in higher doses to control irregular heart rhythms). This is the type of problem that neurologists are trained to recognize and treat as needed.

Don't forget to click on the file below to download the CNS questionnaire to determine if PBA is a possible cause of emotional outbursts.

Rip Kinkel