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.
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
Sriram S, Yao SY, Stratton C, Moses H, Narayana PA, Wolinsky JS.
Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37212, USA. email@example.com
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.
(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.