Quote:
Originally Posted by glenntaj
--in possible symptomatolgy in the vascultic/connective tissue anti-nuclear antibody variant autoimmune conditions (just one of the reasons they are hard to diagnose, and why sometimes people are put in that catchall "unspecified connective tissue disease" category). And, of course, within a given condition, different organ systems/tissues may be targeted to greater/lesser extent.
All of them, however, can have neuropathy as a secondaryeffect, and these are usually through ischemic mechanisms or compressive effects from swelling/inflammation (rather than through autoimmune cross-reactivity, though that is a possibility).
See:
http://www.hopkinsmedicine.org/neuro...europathy.html
http://neuromuscular.wustl.edu/antib...tml#vasculitis |
Thanks - I'm so glad I asked this question here now because these links are invaluable. However - in non scientist layman's terms can you tell me whether this means that the types of secondary neuropathies which often go with vascular and connective tissue diseases are less likely to progress over time? Presumably when the neuropathy is triggered by the inflammatory process then dampening down the immune system might work? - although my rheumatologist warned that in the context of medicine sense/ logic doesn't always prevail.
I feel mine is progressing in that it seems the length dependency is growing but the severity or level of numbness/ intensity of pain has not really altered much in two years that I've suffered it. Some days are worse than others but my main observation is that it seems to be spreading rather than intensifying. Presumably if it was a primary immune mediated neuropathy such as Guillaine Barrre or CIDP then it would be likely to cause demynalation whereas vasculitic neuropathy shouldn't - in theory anyway?