Recieved my MRI imaging back..your thoughts?

[MrChris]

So i went for a baseline MRI on April 22 before i started my treatment of Copaxone. This would be the first MRI since October
and only the 3rd since the onset of symptoms in Aug 2014. I have another appointment to see my neurologist on May 25 to
review the images. The one lesions measuring 25.2mmx27mm has me rather worried. Your thoughts?

[MrChris]

I also must mention that these pictures were captured before they had administered contrast. Once the contrast was injected, no lesions were showing on the imaging.

[cheerleader]

I'm going to give you the good news. No enhancing lesions is a good thing...it means your blood brain barrier is intact.
Also, you've had a bunch of lesions come and go in 6 months, which I also see as a good thing. Your brain is actively healing areas of damage--even some pretty large lesions.

I am by no means an MRI tech---but it's also nice to see you do not have much brain atrophy (brain tissue loss), and your third ventricle size is good. Atrophy areas show up as black on MRI, where the cerebrospinal fluid fills in. This is becoming a useful measurement for MS disease severity. http://bmjopen.bmj.com/content/3/9/e003582.full You might want to ask your neuro how your thalamus and brain stem look.

Make sure to rule out nutritional deficiences (vitamin B12, vitamin D), blood clotting issues (antiphospholipid), take great care of yourself, eat well, don't smoke, get daily exercise, and let us know how it goes. hang in there!!
cheer

[MrChris]

Hi Cheerleader,

Thank you for the words of encouragement.

Vitamin D Blod levels are 96n/mol
Cant remember my b12 levels, however i know that they are ok.
Antiphospholipid. It's the first a hear about that. I do know that the neurlogist that diagnosed me ran so meny blood tests that it made the lab techs head spin..lol I'll have to look into it.

Also, They found oligiclonal bands in my CSF and i am registering 120ms for visual evoked.

[cheerleader]

Sure--I know it's scary.
My husband's now past 8 years since dx with no progression-- on copaxone, new diet, lifestyle, exercise, had his veins repaired, too. He's still really active, working, jogging, so there's hope! Glad the neuro ordered lots of blood tests. It's important to rule out other stuff, especially before beginning an MS med.
Antiphospholid antibodies (or Hughes Disease) is another MS differential.
http://www.hughes-syndrome.org/about-hu ... /brain.php

Having oligoclonal bands can happen in other situations, like stroke or ischemia, Lyme disease or herpes. It's not specific to just MS.
http://onlinelibrary.wiley.com/doi/10.1 ... 0/abstract

I've been looking at the vascular connection to MS for awhile now--and I view MS as a slow, ongoing situation of low oxygen and blood flow to the brain which creates ischemic injury. Here's my blog, if you ever get interested in learning more.
http://ccsviinms.blogspot.com

all best,
cheer

[MrChris]

Would you happen to know if o bands are associated with Hughes?

[cheerleader]

yes, bands can be associated with antiphospholipid antibodies.
http://www.neurology.org/cgi/content/me ... ts/P02.152

[MrChris]

So i presume the only way to decipher between the two diseases is to actually administer the blood tests for Hughes?

My first symptoms that led me to the hospital were stroke like. Losing all strength and fine motor control in my right arm and hand and some facial paralysis that also affected my speech. I had a relapse in Dec '14 this time with dysarthria and bowel dysfunction.

Ever since the onset last year (Aug '14) ive also been getting headaches almost on a daily basis and I have a constant ear pressure and have been plagued with sinus problems. I also can no longer walk heel to tow with my eyes closed with out having severe balance issues.

In hind sight. For the previous 5 years i would get pins and needles in my hands and finger..but only when they were elevated IE hands on steering wheel for extended periods of time, riding my dirt bike, or even lying in bed with my tablet. For a year prior, from time to time, i would also get a severe case of vertigo when i would awaken from a deep sleep. I also found this past winter my extremities would get severely cold if they were not covered up and would take an abnormal amount of time (for me) to warm back up.

I pass all sensory testing with flying colors that my neurologist performs.

So this is why to this day i question my diagnosis of MS.

[centenarian100]

Out of curiosity cheer, if you are so skeptical of the medical establishment, why does your husband take copaxone which is likely one of the least effective disease modifying therapies.

First, I'll start off by mentioning the evidence in favor of copaxone:

Copaxone has been shown to be effective in relapsing remitting multiple sclerosis in MRI and relapse outcomes in multiple high quality clinical trials. This includes the two pivotal trials and the CONFIRM trial (one of the pivotal trials for tecfidera where copaxone outperformed the placebo arm). In the CombiRx trial, GA was superior to avonex in MRI outcomes and both protocol derived and non-protocol derived relapses. In the BEYOND trial and REGARD trials, copaxone was equal to betaseron and rebif respectively. Copaxone also delayed progression to CDMS from CIS in the PreCISe trial.

Now, onto the evidence against copaxone:

There is no good evidence to suggest that copaxone has any benefit on disability, either short term or long term. In three large well known clinical trials, copaxone failed to meet the sustained disability endpoint (CONFIRM and the two pivotal trials).

A Cochrane review was published in 5/2010 of a review of 16 randomized controlled trials between 1987 and 2007. Their conclusion: “The data showed no beneficial effects on disease progression in both MS forms, a slight beneficial effect in the reduction of risk of relapses in RRMS patients and no benefits in PMS patients.”

Copaxone is not FDA approved for reducing the progression of disability, and this does not appear on the package insert or product monograph.

Now, a 15 year open label follow up in GA treated RRMS patients did show a modest EDSS benefit and lower risk of SPMS in patients who stayed on the drug vs those who dropped out. However, this was unrandomized and unblinded, and it is well known that patients doing poorly on a treatment are likely to have a higher dropout rate. There was also a large difference in the average disease duration between the two groups (13 yrs for the copaxone group versus 22 years for the dropout group).

So why such loyalty to copaxone if multiple sclerosis is not an autoimmune disease? Copaxone does not enter the blood stream generally speaking, so it certainly does not repair nerve tissue or improve blood flow to the brain. It is only known to work through immunological mechanisms, and it is literally the only multiple sclerosis disease modifying therapy to never clearly demonstrate any effect whatsoever on disability in a clinical trial

[centenarian100]

Also, you've had a bunch of lesions come and go in 6 months, which I also see as a good thing. Your brain is actively healing areas of damage--even some pretty large lesions.

Active multiple sclerosis lesions generally shrink spontaneously. This is part of the natural history of multiple sclerosis.

[MrChris]

I finally got my paws on the radiologists report.

"There has been significant interval enlargement of the vertically oriented T2 hyperintense demyelinating lesion extending fom the left thalamus superiorly into the white matter of the left centrum simiovale. The lesions previously measures 0.8x0.9cm in axial plane and now measures 2.7x2.5cm in axial plans. Conversly, a lesions in the right centrum semiovale has decreased in size from 1.7x1.8cm on the previous study to 0.6x1.0cm in axial plane. Multiple other lesions remain present and are not significantly changed in the interval. These lesions are located in the juxtacortical and periventricular white matter of the supratentorial brain.

There is no evidence of lesions involving the infratentorial brain.


there is no abnormal restricted diffusion. There is no T1 black holes, nor do any of the demyelinating lesions demonstrate evidence of significant enhancement."