I believe many patients here experience that stocking pattern neuropathy, in the form of "burning feet", or problems with cold hands. Part of this may be a consequence of reduced peripheral blood flow while upright due to autonomic dysfunction. Damage to the autonomic nervous system commonly causes a shift toward increased activation of the sympathetic nervous system, which has all kinds of consequences, particularly impaired sleep and orthostatic intolerance.
While many characteristics suggest autoimmune disease, I want to caution people that current management of such illnesses is far from satisfactory. The alternative of chronic infection by pathogens we don't recognize as particularly harmful -- unless they appear in a special context -- continues to interest me. Just how obvious a pathogen can be, and still be overlooked, shows up in my recent posts on
borrelia miyamotoi and
babesia microti.
While b. miyamotoi is a microscopic spirochete bacterium, b. microti is an actual multicelled parasite. At the same scale we can be infected by a wide range of yeasts and fungi, some of which produce powerful toxins against competitor species. At a smaller scale we are essentially all infected with multiple herpes or papilloma viruses which only rarely cause cancer or a fatal encephalitis. Even within the cell nucleus we carry many copies of HERVs which infected our ancestors. A few of these show disturbing evidence of recent activity. In a variety of disease states we find expression of HERVs, but most of the time these do not produce replication-competent virions. If their genes are passed through the germ line, they don't need to be highly infective. No law of nature requires them to put all their genes in a single convenient package for us to find. Our cell nuclei are convenient enough for viruses.
Yes, we may very well be experiencing problems due to misdirected immune response. We may also have infectious agents which need treatment. If immune response has been (naturally) throttled back to limit damage from autoimmunity we may also have recognizable overgrowth of other microbes. It may be my own idée fixe, but this is the pattern I see in a number of recognized autoimmune disorders.
Diagnosis of autoimmune disorders takes us into another mind-warping tour of the history of medical practice. At one time, (after the initial strong rejection of the concept) it was hard to find any autoantibodies, and there were efforts to increase sensitivity of tests. Later, it was decided that too many people were being diagnosed with autoimmune diseases. The result was that the push for sensitive tests ended, and thresholds for levels characteristic of autoimmune disease were raised to match clinical signs like the visible rash in SLE. Laboratory evidence was chosen and interpreted in a way that supported previous clinical judgment. By-and-large patients with MS, RA and SLE remained sick. Each new clinical entity became a battleground of opposing medical opinions. Objective evidence had less effect on practice than commonly believed.
