The latest from Neurology on MS.
Takin’ It to the Streets- by the Doobie Brothers/Michael McDonald
You don’t know me but I'm your brother (even though you're not an MD)
I was raised here in this living hell (Planet Lunatic)
You don’t know my kind in your world (most MDs don't have MS)
Fairly soon the time will tell (even MD's will get sick)
You, telling me the things you're gonna do for me (you already do-
helping patients nourishes the psyches of MDs)
I ain’t blind and I don’t like what I think I see (got to improve vision in MS patients)
Takin’ it to the streets (no, not Wall Street)
Takin’ it to the streets (all those Main Streets)
I've always had this fantasy to take the neurological literature to "the people". You know, "Take down the wall, Mr. Gorbachev", the wall of "secret expertise" that shields the medical profession from the public by way of "special scientific articles only doctors can understand".
So I'm reading the hot off the presses October 7th edition of the journal Neurology this month and I see a couple of articles on MS and I say: "Take it to the streets, Kenneth. Let the millions (or is that like eleven of you) who read your blog know about the latest in MS research.”
A.D. Goodman of the University of Rochester et al did a "Dose comparison trial of sustained release fampridine in MS". Lower extremity strength and self-assessed ambulation was significantly better in those who received this oral medication under study.
This is exciting though more research is required. This drug also known as 4-aminopyridine is a blocker of voltage-dependent potassium channels. Rather than working on the immunology of MS, the drug would appear to work on a restoration of electrical physiology in the demyelinated nerve. Goodman notes that other studies suggest that fampridine may be associated with improvements in visual function, strength, ambulation, fatigue and endurance.
While these other studies did not clarify dose of fampridine, this new research indicated that 10 and 15 mg. of fampridine worked best in improving strength and gait in the MS patients studied.
I look forward to reporting more on related exciting work on this medication. As I have noted elsewhere, a "concerted effort" is required. That can come about by way of a "medical research revolution" as opposed to critical next steps lingering on the vine because there's no "central governor" of medical investigations.
In the same issue, Wang from Harvard et al followed up on the ever intriguing association of Epstein Barr Virus and MS. His group first made the point that antibodies to a myelin oligodendrocyte glycoprotein (MOG) can cause demyelination (a key process in MS) in experimental animals. They then found that individuals with these antibodies have an increased risk of developing MS. In other words, a single neurological event that suggests a type of MS attack (a CIS), when associated with the presence of these anti-MOG antibodies, contributedto predict a second neurological event- i.e., conversion to clinicallydefinite MS.
Very provocative is the Wang finding that there would appear to be cross reactivity between MOG antibodies and antibodies to Epstein Barr nuclear antigen (EBNA). Translation? MOG antibodies may kick in after a patient contracts infectious mononucleosis and/or Epstein Barr infection. It is known that the presence of EBNA antibodies is a strong risk factor for the development of MS. Is the MS triggered because there is "confusion" in the immune system? Since MOG may be chemically similar to EBNA, the body could be producing antibodies not only to the EBNA but also to MOG, which in turn causes demyelination followed by clinical MS.
It should also be noted that the antibodies found against MOG were IgG class which is the type most associated with autoimmune disease (which includes an illness such as MS). Clearly, more work needs to be performed to clarify what Wang has uncovered.
Mazurek from New York notes a recent article by Shi in Neurology that indicated that APOE e4 gene is associated with cognitive decline in patients with MS. This is interesting since same gene also increases one's chance of getting Alzheimer's. Mazurek also cites an Enzinger article that showed that using proton magnetic resonance spectroscopy (available in some centers), a brain chemical called NAA (N-acetyl aspartate) was lower in MS patients with impaired thinking who also had the APOE e4 gene. A suggestion to clarify these associations through future studies was made by Mazurek. Such gene and brain chemical analysis may be important in identifying and then preventing dementia in MS patients in the future.
There you go: late breaking MS news- it’s not just for neurologists anymore……..
Published On: October 31, 2008