1) cortical gray-matter inflammation,
2) rise of an inflammatory toxin of demyelination Quinolinic Acid
3) a mechanism that explains periventricular inflammation and lesions secondary to BBB breakdown and gray-matter inflammation.
4) A possible reason for heterogeneous plagues prevailing
5) The increased incidence of MS in Lyme endemic areas
6) Intracellular infection in neurons explains lack of positive serology tests and patient relapses after antibiotics.It seems that if spirochetes play a role in forming some plaques similar to MS plaques, then in order to get good data for treatment research we must consider trying to separate the Spirochete Sclerosing componant from the rest of the data.For example an immune modulating drug might help true MS but if the data is mixed with patients from Lyme endemic areas that have not been separated in these trials, then treatment may have brief improvement and then a worsening without knowing which patients have an infectious component.In the hundreds of biopsies used in this study were any also stained with anti-Borrelia antibody fluorescent stains or silver stains? If not we can make no conclusions that spirochetes did not play a role in the gray-matter pathologies.Tom Grier (A survivor a primary progressive MS)
Earlier this year research by Sam Donta here SPECT Brain Imaging in Chronic Lyme DiseaseConclusions: Brain SPECT scans are abnormal in most patients with chronic Lyme disease, and these scans can be used to provide objective evidence in support of the clinical diagnosis. The use of certain antibiotic regimens seems to provide improvement in both clinical status and SPECT scans.
Figure 2FIGURE 2. SPECT scan of the brain before (A) and after (B) antibiotic treatment. These transaxial images are from a 51-year-old man diagnosed with Lyme disease with a recent change in memory. Representative pretreatment images show hypoperfusion within the mid posterior and mid temporoparietal cortex bilaterally. Representative posttreatment images (14 months later) reveal improved perfusion to the posterior temporoparietal cortex bilaterally, correlating with improved symptoms. Perfusion within the remaining cerebral cortex, basal ganglia, thalamus, and cerebellum was normal.