RichGotsPots

What clinical data are you suggesting is collected during battery of tests listed on #1?

Re:#2: this sounds like the Thermoregulatory Sweat test offered ay Mayo and Cleveland Clinic. But Rich, I know you know about that test so you must be thinking about something different.

I haven't looked into all of Mayo's and Clevelends testing in awhile. i remember seeing a video where one of the clinics put people in a clear box/room and heated it up. I don't recall them using thermography but like I said it was a long time ago that I looked. As far as I know the thermo sweat test is with the powder that changes color..

But if they are using Thermography in the hot box, I don't understamd why they would need to heat it up. Normal conditions should be perfectly fine. There is also a technique called Kirlian photography that might apply

Actually its strange. i had back to back glucose tests. I fasted for the first one and it came up very high and then I fasted for the 2nd one 5 days later and it was the 2 hour test and it was all normal. So strange

That's why I prefer to try IVIG first. It actually boosts your immune system while stalling for your nerve fibers to regenerate. But it wont give you a super immune system of anything it just restores it to a good/normal level, so you can still catch thing but not as much are with (TNF-alpha).

I posted it not as a cure all but as an example that is find out we have sfn and then treat the cause we can beat this!

Just a warning for anti-tumour necrosis factor-alpha (TNF-alpha) they can leave you open to infections of every type, fungus, parasites, virus and bacterial. So make sure to report even a tiny cold to your treating dr.

In the meantime, Cinnamon may be worth a try. It's been used as medicine for centuries. It may also counter the neurotoxic factors released by activated glial cells in the brain. These toxins kill the myelin-producing oligodendrocyte cells.

A neurological scientist at Rush University was granted $750,000 from the NIH to see if cinnamon can stop the destructive inflammatory process of MS. Prior research by the Rush team showed sodium benzoate, a component of cinnamon, inhibited inflammatory molecules and blocked MS disease progression in mice.

I purchased organic bulk cinnamon from a local food coop and will start my own trial. Unfortunately, I am not eating sugar or grains or I would enjoy this self trial with cinnamon rolls!

http://www.rush.edu/webapps/MEDREL/servlet/NewsRelease?id=1503'>http://www.rush.edu/webapps/MEDREL/servlet/NewsRelease?id=1503

http://link.springer.com/article/10.1007%2Fs11481-013-9447-7'>http://link.springer.com/article/10.1007%2Fs11481-013-9447-7

Keep in mind for the most part we are not concerned with myelin only somewhat in the group b fibers which are lightly myelinated. But the main focus first is the unmyelinated fibers. So if cinnamon helps myelin it wont help us. Unless it some how repairs what I theorizes are dysmyelination of the group B fibers but thats theory. The facts are that for sure most of use have Group C small fiber unmyelinated neuropathy.

I meant fasting glucose test. And it should I don't have Diabetes. I was actually on the low side of the normal range..

Sounds like a huge plus to me. My resting HR is between 70-100 on average it's 90

Hey Everyone,

#1. I don't know if they do this anywhere, except maybe at a neuro or regular biofeedback lab. But why don't they test us with noise or while watching an action movie or while we sing or try different foods or smell things? I don't what it will prove but it's definitely not being explored enough and it's a huge reason for our symptoms so why not?

#2. A thermographic camera or infrared camera- in medicine its called thermography. I've been wondering is they can use ultrasenative thermals to be able to spot thermal regulation problems.

What you guys think?

The thing to keep in mind is that autonomic neuropathy has been healed in many patients by treating the underlying causes. Atomic specialist are rarely involved in the treatment of underlying causes except with a few exception. One example of major cause of Autonomic neuropathy is Diabetes. I posted the other day that Autonomic neuropathy actually got worse with an abrupt control of glucose but down the line/longterm autonomic neuropathy was healed in most of the patients with type 1 and a lot with type 2 that controlled their Glucose. The point I'm trying to make has nothing to do with glucose but rather that abrupt hormonal changes negatively affect neuropathy and that controlling a cause of neuropathy long enough to let the body heal itself seems to be key.

Most autonomic treatments are symptomatic, masking the real problem and not providing any real relief from the cause. So I hold that the key is protecting the fibers and creating a healing environment. That will be different for all of use because of the 100 of causes that we don't have in common.. Someone can be nauseous from a car ride and another could be nauseous from Chemotherapy but yet one medicine or ginger can help both causes. So these symptomatic meds are helping tons of people and they have a great purpose indeed, but more focus needs to be on neuro protection and regeneration.

So I was doing some reading and found an interesting study in patients with "idiopathic" sfn:

Gain of Function Na 1.7 Mutations in Idiopathic Small Fiber Neuropathy; Faber et al http://lib.bioinfo.pl/pmid/journal/Ann%20Neurol'>Ann Neurol. 2011 May 20;

Anyway the gist of this study was out of 28 patients, 8 (almost 30%) had cSNPs (coding mutations) in a sodium channel that is present in small fiber nerves. These mutations caused a hyper-excitability of neurons and they are hypothesizing that increased activity (i.e. more sodium coming through) may be causing some degeneration in the fibers. Apparently lots of sodium can be taxing on the neurons. 7 of 8 of the patients with these mutations had autonomic dysfunction and most had a younger than normal age of onset for the sfn and no other cause could be identified.

This is really interesting to me...I think I may do some experimenting on myself. A huge part of my job is analyzing human genomic DNA for mutations in the protein that our lab studies in relation to glaucoma. Well I have a ton of my own DNA in our lab's freezer because we all participated as "controls" in our current study. My boss has already told me he'd be fine with me sequencing proteins of interest to see if I can get to the bottom of some of my problems. I think I may check out to see if I could find anything out. We also do electrophysiological studies of proteins similar to those in this paper. I may even be able to do some functional testing of any potential mutations found to see if there are changes.

Nice find! Let me know how the DNA pans out.

Were do you live?

Issie

Rich, I think your spot on. Issie, so are you! The below link is a MUST READ, it's long, but SO worth the read.

http://physrev.physiology.org/content/82/4/981.long'>http://physrev.physiology.org/content/82/4/981.long

While I appreciated the link btwn both, I think the paper isn't anything new in that it's well known that autoimmune disease, diabetes (which is believed to be autoimmune in nature) and sarcoidosis (which is somewhat autoimmune) all can cause neuropathies. So no one would ever dispute that. I don't think the paper pointed to any insight as to why.

It was shocking that it stated,"Indeed, sympathectomy does not just relieve pathological pain in the body region ipsilateral to the CRPS-initiating event; rather, it also relieves pain arising from anatomically impossible mirror-image sites, that is, the identical body region contralateral to the initiating event." Sympathectomy is a rather unnerving procedure, excuse the pun hehe. Many people who have that surgery end up with autonomic neuropathy and dysfunction. I guess just bothered me that they focused only on sensory neuropathy rather than autonomic neuropathy..

62 votes so far, any newbies feel free to vote

Just did my first fasting glucose test. Was not fun. The 1st 30 minutes I felt slighlty symptomatic but after that I was fine. i don't like fasting or not being allowed to drimk water the 2 hours for the test.. But hey it's about time I got tested lol

As notted on Dinet's "what helps" section "Erythropoietin (EPO)reportedly works in 80% of patients (Grubb, 2002)"

That's really an amazing % and I've polled on here many times to try to get some info about EPO but not too many of us have apparently tried it because of its expensive and monitoring.

Well imagine my surprise when I went researching for Neuropathy treatments for us and I stumbled upon ARA290 named that way because it's only in clinical trials right now.

One of the biggest problems with EPO is it's dramatic hemodynamic affect cause patients tohave to discontinue it. But when patients can tolerate its affects it can be a huge help in symptom relief.

ARA290, a Peptide Derived from the Tertiary Structure of Erythropoietin, that Produces Long-term Relief of Neuropathic Pain. Here comes the best part, "Exogenous erythropoietin inhibits develop- ment of allodynia in experimental painful neuropathy be- cause of its antiinflammatory and neuroprotective properties at spinal, supraspinal, and possibly peripheral sites. The au- thors assess the effect of a nonhematopoietic erythropoietin analog, ARA290, on tactile and cold allodynia in a model of neuropathic pain (spared nerve injury) in rats and mice lack- ing the ?-common receptor (?cR?/? mice), a component of the receptor complex mediating tissue protection."

The key words being "antiinflammatory and neuroprotective properties" and "mediating tissue protection"

This may be how EPO helps the most and the best part about ARA290 is that there are virtually no adverse hemodynamic affect compared to EPO.

Let's all keep an eye out for this medicine

Here is the link to the manufactorer with some inital trials http://araim.org/publications/

glutathione is one of the bodies most powerful healers our bodies has, bar none. And it has been clinically shown that Whey protein can help build it up in the system. It's an big antioxident too and can not be absorbed but taking glutathione supplements.

I've been reading up on CIDP which is a serious polyneuropathy and they do test that with spinal fluids..

1. You mention this is "theory #3,". What were theories # 1 and 2? Or were they infantile versions of this same theory?

2. So help me clarify your theory. This is my interpretation of what you've said. Please fill in any gaps or correct any wrongs:

-------

Dysautonomia may have many different causes (autoimmune, mast cell, viral, etc) but in a majority of the cases, where the real problem is an ANS issue and not simply mimicking autonomic dysfunction, the common mechanism behind Dysautonomia is a dysmyelination of the Group B fibers and/or a dysfunction of the group C fibers.

Furthermore this means that for most of us Dysautonomia is degenerative (unless we find a way to

regenerate the myelin sheath of our preganglionic fibers that have been damaged or a way to correct the non-myelinated post ganglionic fibers that are improperly functioning.)

3. I think I understand what you mean about dysmyelination of group B fibers but I am unclear on what you suspect is happening with the unmyelinated post ganglionic fibers.

4. In your theory do some of us have problems with group B fibers only, group C fibers only and/or a

combination of group B and C fibers? (you alluded to this but I was unclear)

5. Since there are exceptions to the mostly myelinated preganglionic fibers (in group such as the

preganglionic fibers that connect to the adrenal medulla where the preganglionic fibers are not

myelinated how does this theory apply? Or not apply?

6. What is the source of your stated percentages of efficacy of nerve conduction studies, QSART testing and SFN biopsies? And to clarify is 88% efficacy of SNF biopsies the higher level skin biopsy testing Group C or more traditional SFN biopsy testing group B? (interestingly while at Vanderbilt in January Dr.

Biaggioni said that approx 30% of the POTS patients they see test positive on QSART for SFN. Although anedotal in nature this is different than your stateed 50%.) At that time I was surprised it was so low. But furthermore, I was surprised during all three nerve tests I've had done (an EMG done locally, and two QSARTS - Cleveland Clinic and Vanderbilt) that they all came back normal. I've wondered, "How can that be when I have such difficulty with parasthesias, Allodynia, and frequent loss of feeling/ blood flow in my arms and legs?". This theory might begin to explain it.

7. Is the primary role of the CNS in this theory that of releasing various chemical mediators that effect

the PNS? Or do you suspect there significant dysmyelination and dysfunction occurring in the brain stem and spinal cord as well?

8. How do you suspect this dysmyelination affects something symptomatic like erratic hemodynamics? Or is that for studies on down the line?

Cheers! KSBG

1. I have previous posts with theory 1 and theory 2 on here somewhere. 1st was about regional BP, the second was about damaged Endothelial tissue affecting regional BP (Vandy is actually testing for endothelium dysfuction now as I understand)

2. Correct but I believe its Dysmyelination of group B (which I think messes up function that relate more to CNS but not directly and it causes disturbances they are more mental (for lack of a better term) like intolerance to noise or visual, feeling anxious, etc..) and the other part is that Group C fibers aren't just dysfunctional but they are totally damaged (neuropathy) which causes dysfunction.

Not exactly degenerative in both fibers only group C. The body constantly has a process to regenerate fibers its slightly different depending on whether myelin or unmyelinated fibers are involved. But I'm saying for dysmyelination group B they regenerated incorrectly so there isn't technically a neuropathy just malformed myelin sheath bouncing the messages around. In Group C there is degeneration and most likely the causes are preventing the regeneration, thats why when an autoimmune person get IVIG and the cause it cleared out temporarily the Group C fibers get a chance to regenerate themselves without disturbance.

3. I think answer 2 addresses this.

4. The only way we will really know is if we all get tested. i have polled on here and other forums and not even 1/10 have been tested. Also Mayo for example doesn't believe in the skin Biopsy, probably because they developed the QSART, which is the biopsy's competition. No one has looked into my Group B theory so don't know about that yet but even Mayo acknowledges that at least 50% have group C sfn. I figure its higher because the lack of sensitivity to both tests. So it remains to be seen yet..

5. group B fibers are very serious especially since they connect to the CNS. I think the only ones of us that would have this group of neuropathies are very very seriously degenerative illnesses like ALS or Parkinson's where the disturbances will be highly "mental" in nature. These illnesses have polyneuropathies and I think go a little deeper than a typical dysautonomia. Possibly a pure autonomic failure has some group b neuropathy. Again its hard to say unless we really start looking closer at this group b.

6. http://brain.oxfordjournals.org/content/131/7/1912.abstract?ijkey=57f7432bb3b0b7aa5145cd6f3e9d48a9c41cda1b&keytype2=tf_ipsecsha

7. Its not clear yet, but that will hopefully come in an update down the road. But my hunch is CNS has to do more with group B, but group C I feel definately plays a rold.

8. Its down the line it could be either group or both groups or just Group C neuropathy only. For example group C controls thermal regulations and sweat and maybe just that little dysfunction can throw off hymodynamics completely, an internal gloabal warming

Here is an example of how nerves regenerated incorrectly:

Gustatory sweating, It is thought that ANS fibres to salivary glands have become connected in error with the sweat glands after nerve regeneration...

This is after an operation where they purposely try to cause small fiber neuropathy to reduce sweating in the chest, but it goes wrong..

Hey Joe, curious if you started taking it again?

Lemon- you're welcome

Jangle- back when I had my first Pots theory it related to various regional perfusion issues. I suggested that they use a very simple TTT brain SPECT test that could easily these issues. I know Cleveland now uses some nuclear testing for perfusion but Idk if it has lead to any real treatments. When BP issues are isolated to lungs for example, systemic BP can be totally different. I believe that has also been seen with Kidney BP as well. Systemic BP meds affect the region areas just not profoundly enough and then they can alter the systemic BP too much in the wrong direction..

I have found links between NOS and small fiber neuropathy. Loose connective tissue surrounds surround blood vessels and nerves. It also attaches epithelial tissue to organs. Epithelial tissue is responsible to NO regulation and some how the damaged nerves messing with epithelial's regulation. Its like a reffered short circuit or dysfunction..

Rama- thanks for the study, good to see some international work like this.

Issie did you say that your BP is actually low on LDN?

Rich, have you ever heard of shingles? Random activation of herpes zoster, lives in the nerves.

Yes but again there are really over 40 known causes of small fiber neuropathy including infectious diseases. Would take me all day to list them and the relationship. What it comes down to is how to protect against damage or fix the damage..

It would be great if as a group we tried to zero in on all the researchers specifically focused on this. The typical Peripheral Neuropathy specialist hardly has anything to do with the autonomic part of it, they focus on the motor and sensory issues. I would like to get some more top notch college labs interested in this.