Is Small Fiber Neuropathy Causing Your Dysautonomia?

Small fiber neuropathy has become one of the most frequently discussed diagnoses in the dysautonomia community. And for good reason -- it shows up in a significant percentage of POTS patients, and it can explain a wide range of autonomic symptoms that otherwise seem disconnected.

But there's a problem with how most patients understand SFN, and it starts with the word "neuropathy" itself.

Neuropathy Does Not Mean Your Nerves Are Dead

This is the single biggest misconception we encounter. When patients hear "neuropathy," they hear "nerve damage" -- and they interpret that as permanent, irreversible destruction. It sounds terminal. It sounds like those nerves are gone.

That is not what neuropathy means.

Neuropathy means something is wrong with the nerve. The nerve is not functioning correctly. It could be inflamed. It could be compressed. It could be under metabolic stress. But "not working right" is very different from "dead."

Nerves can heal. They do heal. If you identify what is causing the dysfunction and address it, nerve function can improve -- sometimes dramatically. We've seen patients whose nerve function measurably improved within days once the underlying driver was addressed. Not months. Days.

That doesn't happen if the nerve is dead. It happens because the nerve was impaired, not destroyed.

Immune-Based SFN Is Not the Same as Blood Sugar SFN

This is a big one, and it gets missed all the time.

Classic small fiber neuropathy -- the kind associated with diabetes, prediabetes, and metabolic syndrome -- follows a predictable pattern. It starts in the feet and works upward. Toes first, then the foot, then the ankle, then the calf. This is the "stocking-glove" distribution you may have read about. It's length-dependent: the longest nerves get hit first because they're the most metabolically vulnerable.

But immune-based small fiber neuropathy -- the kind we see after viral illness, with autoimmune conditions, or in many post-COVID and dysautonomia patients -- does not follow that pattern at all.

Immune-based SFN is patchy.

Instead of a neat bottom-to-top progression, you get scattered hotspots. Maybe the left thigh is affected but the right thigh is fine. Maybe there's a patch on the torso. Maybe the hands are involved but the feet are relatively spared. The immune system doesn't attack nerves in an orderly fashion -- it creates an uneven, seemingly random distribution of dysfunction.

So when we look at testing, a test designed to catch stocking-glove neuropathy can completely miss patchy immune-based disease. And that's where a lot of people get stuck.

Why Punch Biopsies Can Miss It

Punch biopsies can be really great because we can see all the little fiber densities and we see a lot of real high detail. But if we zoom out, sometimes that causes us to miss them.

For the classic length-dependent neuropathy, biopsies work well. If the disease is progressing from the feet upward, a biopsy at the ankle will catch it reliably.

But for patchy, immune-based SFN, the biopsy is only as good as where you put it. If you biopsy a spot that happens to be unaffected, you get a normal result -- even though the patient has significant nerve dysfunction nearby.

• A normal biopsy does not rule out immune-based SFN -- it may just mean the biopsy missed the affected area
• Side-to-side differences matter -- if the left leg tests differently from the right, that's a clue the distribution is patchy, not length-dependent
• Positional differences matter -- if nerve function changes when the patient is upright versus lying down, we may be looking at something more complex than peripheral nerve disease

The punch biopsy gives you a highly detailed, zoomed-in view of one specific spot. That's valuable. But you also need to zoom out and look at the bigger picture -- the pattern, the distribution, and the context.

How SFN Drives Dysautonomia Symptoms

If you're worried about whether or not small fiber neuropathy could be causing your dysautonomia symptoms — it could be the tachycardia of POTS, could be the gastroparesis of dysmotility, could be the impaired sweating of thermal regulation. It will likely be kind of confined to one of those areas, or if it's a widespread immune problem, it might be more patchy in its distribution.

But here's the nuance: in immune-based SFN, these autonomic symptoms may be confined to certain areas or appear in a patchy distribution, just like the sensory findings. One region of the body might be significantly affected while another region functions normally.

The Key Test: Do Your Symptoms Change with Position?

This is something we pay very close attention to, and it's rarely evaluated in standard neuropathy workups.

If a patient has reduced cold sensation in their feet, and that finding is consistent regardless of whether they're lying down, sitting, or standing -- that's more likely a true peripheral nerve issue. The nerve fiber density is reduced, and position doesn't change it.

But if that same loss of cold sensation improves when the patient lies down and worsens when they stand up, something else is going on. Peripheral nerve damage doesn't care about gravity. Nerves don't regenerate when you lie flat and degenerate when you stand up.

What does change with position is blood flow and brain output.

If autonomic function in the extremities is position-dependent, we want to look up the chain a little bit more and look more centrally. We actually want to see if we have a central problem that's causing a distribution error. It may look like small fiber neuropathy, but it may actually be that we're changing the output from the brain to those nerves. So we might check cerebral blood flow with transcranial Doppler to see what's happening upstream.

This is not a rare finding. We see it regularly. And it changes the entire treatment approach, because you can't fix a brain output problem by treating peripheral nerves.

Nerves Can Improve -- This Is Not Necessarily Permanent

If there's one thing we want every SFN patient to understand, it's this: small fiber neuropathy is not automatically a life sentence.

Yes, in some cases -- particularly advanced diabetic neuropathy with years of uncontrolled blood sugar -- nerve damage can be permanent. But in immune-mediated, inflammatory, or post-infectious SFN, the nerves are often impaired rather than destroyed.

If you are able to heal the underlying problem, nerves can heal. Nerves can improve function. We can reduce inflammatory load and we can see them start to operate well — and sometimes that can be like within days.

What we actually observe is that in many people, if you address what's driving the dysfunction, nerve function improves. We have seen autonomic symptoms resolve as the underlying driver was addressed.

So if that's a diagnosis that you've had and it's got you kind of bummed out, I just want to give you a little bit of hope. This may just be a stepping stone along the way. It's beat up right now. The question is: how do we figure out what's driving it and get it back on track?

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