Multiple Sclerosis

Multiple Sclerosis

LifeOnTheIce's Story: Cpn & MS

Submitted by lifeontheice on Sat, 2005-10-15 22:26
My first encounter with MS happened in December, 1987 following an enormous “flu”. The right side of my head went numb, as was my mouth and tongue. There was a questionable tingling on the left side of my body, barely discernible, that even I had doubts. That event coincided with my new job and I ignored it telling myself that it was a Bell’s palsy. The trouble was it looked much more like the fifth cranial nerve palsy and even that seemed to be more extensive than expected. I decided to ignore the whole thing. It resolved in several weeks leaving me with hyperparesthesias of my scalp for the next year or so, and permanent, almost unnoticeable minimal right upper lip atrophy.

      In April 1993, I had a sudden problem with the right eye. Vision became blurry, pinkish, there was aching in the back of the orbit. I could not ignore it this time and paid a visit to my friend the ophthalmologist. She could not see what was wrong and delegated me to a retinologist, who after the myriad of the tests was also at loss. In meantime, my mother, my husband and I, all three physicians, decided that I should take high doses of steroids which I did. We went for vacation to Arizona. I had wonderful adventures there getting swollen like a balloon from the water retention, then going into acute, prerenal failure, to be followed by a very funny diuretic phase. When I came back I had a brain MRI, which showed two lesions, related to both events. The differential diagnosis was: infarcts, migraine, and MS. My eye problem was already going away, I chose to believe it was a migraine, even though I had never had headaches, and I kept working and paying more attention to enjoying my life. Somehow, I felt it might not be long till another disaster strikes.

"Notdoneyet's" treatment of MS for Cpn story

Submitted by Jim K on Mon, 2005-09-12 07:23
I was diagnosed with 95% probable MS at age 26, in 1984, following my first full blown attack, which included double vision, ringing in my ears, loss of balance, tingling all over my body as well as numbness and rigidity in my limbs. I had been burning the candle at both ends, which probably set the stage for the full declaration of MS. I recovered in a month or so and was playing slow pitch, softball quite proficiently that summer. When an MRI was introduced to the Foothills Hospital in Calgary around 1986, I was positively diagnosed.

For the next ten years or so, I pretty much ignored the disease and lived a fully active life, trying to do everything. At age 36, I hit a wall. I had moved to Nelson, BC with a new, stressful job and a much warmer, summer climate. I had played slow pitch the previous year, but never ran in Nelson, partly I think, because I quit trying to. It was hard. Walking soon became difficult.

Pilot study to examine effect of antibiotic therapy on MRI outcomes in RRMS

Submitted by mrhodes40 on Mon, 2005-09-05 13:38

Journal of Neurological Science 2005 Jul 15;234(1-2):87-91
"Pilot study to examine the effect of antibiotic therapy on MRI outcomes in RRMS"

The rights to this paper are owned by Elsevier. the whole citation can be purchased
here

Abstract:

Sriram S, Yao SY, Stratton C, Moses H, Narayana PA, Wolinsky JS.

Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37212, USA. subramaniam.sriram@vanderbilt.edu

This trial examined the safety and possible MRI and clinical effects of anti-chlamydial antibiotic therapy in relapsing-remitting MS (RRMS). Newly diagnosed MS patients were selected to participate if they showed Chlamydia pneumoniae gene in their CSF and had one or more enhancing lesions on brain magnetic resonance imaging (MRI). After a 4-month run in phase of monthly MRI, patients were randomized to receive rifampin (300 mg twice daily) and azithromycin (500 mg every other day) for 6 months or placebo (PBO). Patients then had monthly MRI on therapy and two additional scans on months 12 and 14. Lumbar punctures were repeated between months 7 and 8 and within 2 weeks of termination of the study. Data on 4 patients on treatment and 4 on PBO were available for analysis. The primary outcome measure of showing a beneficial effect on enhancing lesions was not met. However, there was a significant difference in brain parenchymal fraction loss favoring those patient receiving antibiotics compared with PBO (p< or =0.02). Three of the four patients on antibiotic therapy cleared the organism from the CSF by month 12; in the PBO group one patient cleared the organism. The reduction in atrophy in patients receiving antibiotics must be viewed with caution, due to the small number of patients studied.

David Wheldon comments on Relapses and Pseudo-relapses In Treating Cpn in Multiple Sclerosis (MS)

Submitted by Jim K on Sat, 2005-08-27 19:08

(Comment from David Wheldon's site http://www.davidwheldon.co.uk/relapse_pseudo.html)

The relapse in early relapsing-remitting MS has a typical pathology irrespective of its location. The first visible event is the orderly, local, mass death of oligodendrocyctes, the cells which support myelin. The myelin associated with these cells then degenerates. Degenerating myelin activates an inflammatory process. When this is over, young oligodendrocytes mature and make new myelin. The clinical counterpart to this pathology (unless it occurs in a silent area) is a loss of function which worsens over several hours to two days. The loss of function remains in place until the inflammation is over and remyelination begins. It will thus be seen that the relapse has a definite pattern and timescale.

Some people experience strange new sensations on beginning antibiotics and are often afraid that these are relapses. While relapses can occur during the first few months of antibiotics, probably initiated by virus infections, these sensations do not fulfil the timescale criteria of true relapses and tend to change their form within a week. Sometimes, in fact, they herald a return of function. What causes these 'pseudo-relapses' I do not know, but I suspect it is rebudding of neurones which make trial-and-error connections. Synaesthesia (crossover of the senses) can sometimes result; as an example, the seeing of flashes of light when hearing a loud noise. They can be quite troubling even when improvement is taking place. Repair takes place at a cellular level; function has to be re-learned at a much higher level.