Small Fibre Neuropathy in Hypermobility & ADHD

Some sensations are difficult to explain, even to yourself.

A burning in the feet at night. A sudden electric flicker across the skin. A sense that your body is reacting too strongly, too quickly, or long after something has happened.

Many people with hypermobility or neurodivergence recognize this pattern. It often gets folded into broader explanations like anxiety, chronic pain, or “just part of your condition.”

But for some, there is a different layer to consider.

Small fibre neuropathy.

Not as a label to limit you, but as a framework that can bring coherence to experiences that have felt scattered or dismissed.

This blog is for educational purposes and does not replace medical advice. It is intended to help you ask better questions and make more informed decisions with your healthcare team.

What is small fibre neuropathy?

Small fibre neuropathy, often called SFN, affects the smallest nerve fibres in the body, known as A-delta and C fibres.

These fibres are responsible for:

• Pain and temperature sensation

• Autonomic functions like heart rate, blood pressure, digestion, and sweating

• Interoception, the sense of what is happening inside your body

This is why SFN is not just about pain. It can show up as:

• Burning, stinging, or electric sensations, often in the feet or hands

• Tingling or pins and needles

• Skin sensitivity to touch or temperature

• Patches of numbness

• Dizziness or heart rate changes when standing

• Digestive changes without a clear cause

For many, what stands out is not just the symptoms, but how they fluctuate. Symptoms can feel delayed, disproportionate, or difficult to predict.

Why does small fibre neuropathy happen?

Small fibre neuropathy is often described as a nerve problem, but in many cases it is better understood as a system problem that shows up in the nerves first.

These small nerve fibres are highly sensitive. They sit close to the surface of the skin and around blood vessels and organs. Their job is to constantly monitor change, like temperature, pressure, and internal signals from the body.

Because of that role, they are also more vulnerable when the system around them is unstable.

In most cases, several mechanisms combine.

1. The nerves are under stress, so they change how they signal

Small nerve fibres become more reactive when they are stressed or not functioning optimally.

This can happen due to:

• Reduced energy supply Nerves need constant energy to maintain stable signalling. If oxygen delivery is inconsistent or nutrients like B12 or glucose are low, the nerve cannot regulate its activity properly.

• Structural strain In hypermobility, connective tissue provides less support. This can affect both the nerve itself and the small blood vessels around it, increasing vulnerability to irritation.

• Repair or damage processes If fibres are damaged or regenerating, they can become “irritable” and fire more easily or unpredictably.

The result is not random. It is a nerve that has lost some of its ability to regulate when to fire and when to stay quiet.

2. Blood flow and autonomic regulation are less stable

Small fibres depend on very small blood vessels. In hypermobility and dysautonomia:

• blood vessel tone can fluctuate

• circulation may be uneven

• blood pressure and heart rate changes affect delivery of oxygen and nutrients

Even small changes in supply can affect nerve function, because these fibres have high energy demands and low reserve.

This contributes to symptoms that:

• fluctuate

• worsen with standing, heat, or fatigue

• improve with rest or position changes

3. Inflammation lowers the threshold for nerve activation

Inflammation is one of the clearest drivers of nerve sensitivity.

Inflammatory signals can:

• directly irritate nerve endings

• change ion channel activity, making nerves fire more easily

• lower the threshold so normal input is perceived as pain

This means the nerve is not just damaged. It is chemically pushed into a more reactive state.

4. The internal environment affects how well nerves can function

Nerves rely on specific nutrients and hormones to maintain structure and stable signalling.

For example:

• Vitamin B12 supports the integrity of nerve fibres

• Iron supports oxygen delivery, which is required for energy production

• Thyroid hormones regulate how quickly nerve cells produce and use energy

• Glucose provides the main fuel for nerve activity

When these are insufficient or unstable:

• energy production becomes inefficient

• signal transmission becomes inconsistent

• nerves fatigue more easily and become more sensitive

This is why symptoms like burning or tingling can appear during iron deficiency, B12 deficiency, or thyroid dysfunction.

In these cases, the nerve is reacting to metabolic stress, not necessarily permanent structural damage.

5. The brain amplifies and struggles to filter incoming signals

All nerve signals are processed by the brain. In neurodivergent individuals:

• more sensory input may be registered

• signals may take longer to settle

• filtering of non-threatening input may be less efficient

When peripheral nerve input increases, this can lead to:

• sensations that spread or linger

• difficulty switching off pain

• a build-up of sensory overload

So the experience depends on both signal generation and signal processing.

Bringing it together

Small fibre neuropathy usually develops when multiple stressors overlap:

• metabolic or nutritional strain

• unstable blood flow and autonomic regulation

• inflammation

• structural vulnerability

• increased sensory processing load

This combination makes nerve fibres more reactive, not because they “decide” to be, but because their environment no longer supports stable function.

How common is it in hypermobility?

Research over the past decade has established a clear connection between hypermobility syndromes and small fibre neuropathy.

The first direct evidence came from Cazzato et al. (2016) , who investigated 24 adults with Ehlers-Danlos syndrome (20 with hypermobility type, 3 with vascular type, 1 with classic type). Every single patient showed reduced small nerve fibre density on skin biopsy, regardless of EDS subtype. Sural nerve conduction studies were normal in all patients, confirming that the problem was specifically in the small fibres. Pain intensity was moderate to severe in 19 of 24 patients .

A larger study by Fernandez et al. (2022) examined 79 patients with hypermobile EDS or hypermobility spectrum disorder referred to a pain centre. Using both structural testing (skin biopsy) and functional testing (quantitative sensory testing), the researchers found:

• 78% showed reduced intraepidermal nerve fibre density on biopsy

• 70% showed abnormal thermal detection on quantitative sensory testing

• 58% had definite small fibre neuropathy (abnormal on both measures)

• Only 9% had completely normal findings

These findings were confirmed by Igharo et al. (2023) , who prospectively studied 31 patients with hypermobile EDS and 31 healthy controls. They found that 61% of hEDS patients met diagnostic criteria for small fibre neuropathy based on skin biopsy. Notably, the nerve fibre loss was generalized, present in both proximal (thigh) and distal (lower leg) sites, rather than following the typical "length-dependent" pattern seen in many other neuropathies .

More recently, a 2025 study by Kersebaum et al. explored sensory and autonomic function in hEDS, finding that all participants exhibited loss of A-delta fibre function, with those experiencing dysautonomia showing additional C-fibre impairment. The study also identified vascular hyperelasticity as a contributing factor, suggesting a connection between connective tissue differences and small fibre dysfunction .

Taken together, these studies show that the overlap between hypermobility and small fibre neuropathy is substantial:

This does not mean everyone with hypermobility has SFN, but the evidence indicates the overlap is significant, often under-recognized, and likely contributes to the chronic pain and autonomic symptoms that many people experience.

What about neurodivergence?

Here, the science is still evolving, but the overlap is becoming harder to ignore.

What is already well established is that ADHD and autism involve differences in:

• Sensory processing

• Interoception

• Autonomic regulation

Many people experience the body as louder, less predictable, or harder to interpret.

What is now being explored is how these systems intersect.

Hypermobility, neurodivergence, and small fibre neuropathy appear to share overlapping mechanisms, including:

• Connective tissue differences

• Autonomic nervous system variability

• Immune and inflammatory influences

When sensory input is already amplified, changes in small nerve fibre function can compound the experience.

It is not simply pain. It can feel like a build-up of signals that are harder to filter, regulate, or recover from.

Common contributors and overlapping causes

Burning, tingling, or altered sensation does not always come from primary small fibre damage.

In many cases, the nervous system is reacting to something that is missing, dysregulated, or placing it under stress.

Some of the most common contributors include:

• Iron deficiency Can affect oxygen delivery to nerves and is often linked to burning or restless sensations, especially in the feet

• Vitamin B12 deficiency A well-established cause of nerve dysfunction and altered sensation

• Vitamin B1 or B6 imbalance Both deficiency and excess can disrupt nerve signalling

• Thyroid dysfunction Can increase nerve sensitivity, pain, and overall nervous system reactivity

• Blood sugar dysregulation Even early changes can affect small nerve fibres and their ability to function consistently

• Autoimmune processes In some cases, the immune system directly targets small nerve fibres

• Inflammatory states Ongoing inflammation can increase nerve sensitivity and amplify symptoms

How is small fibre neuropathy diagnosed?

Diagnosis can be complex and is not always linear.

The most specific test is a skin biopsy, which measures small nerve fibre density. Reduced density supports a diagnosis of SFN.

Autonomic testing can also assess how the nervous system regulates functions such as heart rate, blood pressure, and sweating.

It is important to note that in hypermobility and immune-related cases, SFN is often non-length dependent. This means symptoms may appear in the face, torso, or upper limbs, not only in the classic feet and hands pattern.

In practice, diagnosis often combines:

• Symptom patterns

• Clinical history

• Exclusion of other causes

Not everyone will access formal testing. Pattern recognition still plays a central role.

What to track and describe to your doctor

Clear descriptions can change the direction of a consultation.

It can help to track:

• Type of sensation Burning, tingling, stabbing, numb, electric

• Location Feet, hands, widespread, shifting, symmetrical or not

• Timing Worse at night, after activity, during stress, delayed by hours or days

• Triggers Heat, cold, standing, food, hormonal shifts, illness

• Associated symptoms Dizziness, heart rate changes, digestive issues, sweating differences, fatigue

• What helps or worsens it Rest, movement, compression, hydration, nutrition

• Relevant history Hypermobility, ADHD, autism, thyroid issues, nutrient deficiencies, autoimmune conditions

This turns a vague experience into usable information.

An integrated approach to support

Small fibre neuropathy does not sit in one system, so support cannot either.

At Paramotion, the focus is on building a body that is more responsive, not just less symptomatic.

Nervous system regulation as a foundation

Gentle, consistent input helps reduce baseline reactivity. Breath work, pacing, and predictable routines are more effective than intensity.

Movement that respects variability

The response to movement is often delayed. What happens the next day matters more than what happens in the moment. Low-load, controlled strength work builds capacity without triggering flares.

Nutrition and internal environment

Nerve health depends on what is available to the body. Iron, B12, thyroid function, and blood sugar regulation are foundational, not optional. Adequate protein and omega 3 intake support repair and resilience.

Circulation and positioning

Connective tissue differences can affect blood flow. Compression, posture adjustments, and gentle rhythmic movement can reduce symptom intensity.

Sensory pacing

Sensory input accumulates. Reducing unnecessary load, whether texture, temperature, or environment, creates space for recovery.

Medical support when needed For some, medication is part of the picture. Options that are sometimes used for SFN include:

• Low‑dose naltrexone (LDN): reduces neuroinflammation and may improve pain and autonomic symptoms

• Gabapentinoids (gabapentin, pregabalin): commonly prescribed for nerve pain, though tolerance and side effects vary

• Sodium channel blockers (e.g., mexiletine, lamotrigine): sometimes used for specific types of neuropathic pain

• Intravenous immunoglobulin (IVIG) or other immunomodulators: considered when SFN has an autoimmune driver

These are not first‑line for everyone, and they come with risks and benefits that should be discussed with a specialist. For others, addressing underlying nutritional, metabolic, or immune contributors leads to meaningful improvement without medication. The right path depends on the individual presentation.

Final thoughts

Small fibre neuropathy exists in the spaces between systems.

Between neurology and connective tissue. Between sensory processing and physiology. Between what can be measured and what is felt.

For many hypermobile and neurodivergent individuals, it offers a way to connect experiences that previously felt unrelated.

Not every symptom will fit. Not every path will look the same.

But when the pattern is recognized, it opens the door to more precise, more responsive ways of working with the body.

If this reflects your experience, start by observing your patterns.

Notice not only what you feel in the moment, but what happens hours or days later. That is often where the most useful information lives.

At Paramotion, we support hypermobile and neurodivergent individuals in understanding the difference between nerve sensitivity, tissue response, and nervous system overload.

If you are ready to make sense of your symptoms and build a more responsive approach to your body, this is where that work begins.

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