MS Dinner and Panel Q & A

Tonight I went with my sister and two friends to an MS dinner, which featured an expert panel willing to answer questions. These were the notes I took:

Expert 1
-T-cell vaccine studies have not been positive so far.
-One question is why eye problems exist when the eye has no myelin.
-T-cells can react against myelin, but the question is whether it is myelin basic protein only or another myelin protein.
-So what causes the T-cells to damage the eyes? Are they targeting the nerve cells themselves?
-Stem cells from bone marrow can help repair myelin in the brain.
-Treatment response (DMDs) depends on "what perfect storm created your MS."
-Autoimmune diseases are commonly triggered by antigens--proteins in blood.
-Few people have been able to replicate Zamboni's CCSVI work.
-Please do not have surgical procedures until we see data that the CCSVI theory is true. The risks are too great for these surgeries. A few people have died. [My rebuttal would be that people have died from the MS drugs as well.]
-Autoimmune thyroid disease is more common in people with MS.

Expert 2
-Relapsing-remitting MS is all about inflammation. Primary progressive MS obviously has no relapses, and inflammation is minimal--different than RRMS. PPMS usually starts with lower limb stiffness, difficulty walking. Gilenya is being tested for people with PPMS at Johns Hopkins. Tysabri is being trialed for people with SPMS at UMD.
-Zamboni's study found that 100% of people with MS had CCSVI. Really? Every single person?
-Encourage you not to pursue it--dangerous.

Expert 3
-Epstein-Barr virus increases the risk of having MS.
-The VA is looking at military personnel, especially those on ships, for the effects of lack of sunlight exposure.
-Nortriptyline is a medication that modulates pain the CNS. It changes the ability of the brain to receive pain.
-The National MS Society has funded CCSVI research. There is no standardized approach to the research, so it has been hard to replicate the CCSVI results.
-The Buffalo CCSVI study was done by a Zamboni trainee.
-The is not a single antigen responsible for MS. Need to see it as a global response (something about antigen spread) and modulate that.

And today's data....
Sensory:

-Pins and needles: 1

-Tingles: 1, left thumb

-Paresthesias (burning): 3, feet

-Paresthesias (other): 2, prickles in left sciatic nerve

-Numbness: 2, the usual

-Vision: 2, more floaters today I think

-Nerve pain: 2--but it always gets much worse in the evening when I'm going to bed

Motor:

-Gait: 4, it was not terrible in the morning but bad by the evening

-Sore muscles: 4, calves, quads

-Fine motor: 2

-Weak muscles: 4

-Spasticity: 3, both calves and quads

Cognitive:

-Language processing: 2, got annoyed with certain speakers

-Memory: 3

-Attention: 0

-Confusion: 3

General:

-Fatigue: 3 most of the day but 6 in evening

-Balance: 4

-Sleep: 6, I got six hours of sleep AGAIN. This time because back pain from my period woke me up. I hate when I starts in the middle of the night, because I can't get ahead of the pain with ibuprofen. Anyway, I ended up not being able to sleep from pain and then just not being able to sleep. Now I can't wait to go to bed!

-Bladder: 2

MS Center Research

Clinicoradiological paradox:
MS is more than counting lesions. The lesions on the brain don't always correlate with what is happening to the patient. Sometimes there are NO lesions related to a severe symptom.

Optical coherence tomography (OCT):
This is a way to assess retinal damage. It turns out that MS causes not only optic neuritis (inflammation of the optic nerve, which kills nerve cells--I have this on the left side) but retinal thinning. And retinal thinning is related not only to vision changes but to brain atrophy.

I learned on another website that brain atrophy in MS happens when a bunch of dead areas occur in the brain, and then the brain sort of collapses down on them. Sometimes there is no evidence of brain damage (no lesions) for years, and then suddenly brain atrophy shows up on an MRI. At this clinic, they are using OCT to predict who will have brain atrophy... and prevent it.

Project RESTORE:
REcover, STop, and REgenerate. Recover function, from acute attacks, and from illness. Stop progression of disease and progression of disability. Regenerate nerve cells and myelin. This all sounds great--hopefully they can do at least some of what they aspire. I saw that my doctor is involved with this project.

Clinical trials:
They are trialing three new drugs. One is combining oral estrogen with a common injected disease-modifying drug (DMD). Pregnancy puts MS into remission, so this one sounds promising.

Another trial is to make a common DMD last longer, so that it doesn't have to be injected as often. This is great, but I suspect the main reason they're researching this slightly modified drug is because the patent on that DMD will expire in a few years.

The third trial is of a completely new DMD--one for primary progressive MS. The rest of the DMDs are for relapsing-remitting MS.

Imaging:
They are experimenting with 7 Tesla MRI. Current "high" strength MRI is 3 Tesla, and most are 1.5 or less. I think my brain images were on a 1.0 Tesla machine. It is known that 25% more lesions show up using 3T compared with 1.5T. I wonder how many more would show up using 7T.

They are also experimenting with some imaging techniques I am not familiar with: diffusion tensor imaging, magnetization transfer imaging, and magnetic resonance spectroscopy.

Psychiatric and neurological:
One doctor is interested in the immune-mediated mechanisms of depression and cognitive impairment in MS and several other autoimmune neurological disorders. He is a psychiatrist.

Sensory neuropathy:
One doctor developed a technique to use superficial nerves to study sensory neuropathies associated with immune-mediated neurological disorders: MS and a bunch of others.

Inflammation:
They are researching how to protect nerves from damage due to inflammation. Also trying to understand how new neurons are produced.


This is all going on at the MS Center where I'll see a neurologist on November 23. My guy is mostly focused on treatment--he's still an assistant professor and probably is still establishing his own lines of research.

I'm on the cancellation list, of course, and I certainly hope I can get in sooner!