Sorry I got a bit of poo brain and I'm not following you here. You're saying that it is autoimmune. But you're saying anti-ganglioside AB aren't necessarily causing it? Just coincidental? So whats the primary mechanism and target antigen?
Sorry, I probably should have been more clear. There are many Lyme patients who have both SFN and the anti-ganglioside AB at the same time (I've met lots of people on FB)....which is lucky (and unlucky) because the ganglioside panel gets IVIG and the SFN doesn't get IVIG because insurance companies suck. But both conditions improve with IVIG because you are in an antibody situation. They are both an immune-mediated process. Not everyone necessarily has both.
Antibodies for SFN have not really been identified yet (but presumed) and research neurologists are working on trying to figure this out.....therefore we do not have antibody tests for it as of today.
As far as my case I didn't really catch it as I didn't do anything for it aside from change diet months after the fact. Even now if I take antibacterials it improves substantially even though it's been two and a half years. I thought dorsal root damage was implied in SFN but I'm not terribly familiar with this area. My personal opinion on this one was always that the damage was rather reversible if the inflammation was halted
I'm so happy you halted the damage. Your story is not typical. If you join any of the FB SFN groups you will see the amount of suffering and that most people do not get better. Did you ever lose the hair on your legs? This is very common. I don't have to shave my legs anymore because they stopped growing hair.
Dorsal root damage is not necessarily implied in SFN. Most people with SFN do not have dorsal root damage. The most common presentation of this type of neuropathy is that it starts in the hands or feet. Then either stays there and moves up the limb. This implies that there could be a vascular problem caused by something like T2DM.
I also find it interesting the distinguishment between full body and length dependent. My understanding was that it was always full body and the distortion per length only reflected the extent of damage. When mine first came on it was all over my body. As I improved it retreated to my legs. If I take a strong antibacterial I will herx that symptom anywhere on my body however. In other words my acute symptoms are all over and my chronic are distal
The non-length dependent just means that you have face and trunk burning instead of just limb burning. Or that your punch biopsy at your thigh has fewer sweat glands and density than the biopsy on your foot. Either way, the neuromuscular neurologist will assume an immune-mediated process is at work and the dorsal roots are being attacked. If you go to pub med you can read up on this. Use keywords like "non-length dependent small fiber neuropathy", "immune-mediated small fiber neuropathy", "ganglionopathy", "dorsal root ganglia" etc.
There is an experimental MRI that runs a DRG protocol (at Hopkins) that can actually look at your dorsal roots and can see the damage. I only know a handful of people who have had this done but it's the only diagnostic test that can confirm this damage.
Thanks for your response. You seem like you know a lot about this topic and it's been helpful. I sort of saw the connect to GBS and felt it was good enough to move forward but now that the topic is brought up I am interested in understanding it better
I wish I knew nothing about
this topic. My condition came on so hard with full body burning and POTS symptoms that I ended up with a neurological consult in the ER. After that, I was seen by the teaching hospital, was told that I need to get a pain management doc, and the rest is history.
Post Edited (madisongrrl) : 5/7/2017 12:03:04 PM (GMT-6)