Neuroimmune, small-fiber and sensory–autonomic patterns

What records in this area tend to contain

These are descriptions of records, not diagnostic criteria. Recognising several of them does not mean you have a condition, and none of them is being asserted about you.

• Burning, tingling, or allodynic symptoms in a non-length-dependent or patchy distribution
• Sweating, temperature, or vasomotor changes alongside sensory symptoms
• Skin biopsy, QSART, or autonomic reflex testing with borderline or conflicting results
• Autoantibody or channel-antibody findings of uncertain clinical weight
• Onset after infection, or alongside autonomic and reactivity symptoms
• Immunotherapy raised as a possibility without a clear mechanistic case for it

The analytical work on a case like this

• Symptom distribution and chronology mapped against infectious and immune events
• Every neurological and immunological result, with an explicit statement of what each supports
• Metabolic contributors — glucose handling, B12, thyroid — that are common and correctable
• Post-infectious neuroimmune hypotheses, graded rather than assumed
• Mitochondrial and microvascular contributors where the record supports them
• Overlap with autonomic and mast-cell findings elsewhere in the case

What the work is trying to answer

These are the questions the reconstruction is built around. They are questions, not promises — some records answer them clearly and some do not, and the written synthesis says which.

• How much of the picture is explained by findings already in the record?
• Which equivocal results are genuinely equivocal, and which were collected suboptimally?
• Is there a correctable metabolic contributor that the immune framing has overshadowed?
• What would a neurologist most usefully be asked next, and why?

What would argue against the leading reading

Every synthesis states the alternatives it could not exclude. For this area, the most important ones are:

• Metabolic neuropathy from glucose handling, B12, or thyroid status
• Compressive, structural, or central causes requiring imaging rather than mechanism
• Central sensitisation, where the peripheral nerve is not the origin
• A systemic autoimmune disease not yet formally assessed
• Medication-induced neuropathy, including from agents used for other symptoms

Related reading on this site

• The hEDS–POTS–MCAS triad
• Long COVID and post-viral illness
• Mitochondrial dysfunction

• POTS, dysautonomia and autonomic–GI overlap

  For cases where standing, eating and digesting have become the same problem, and the autonomic label has not explained why it began.

• Long COVID and post-infectious syndromes

  For illness that began with an infection and did not end with it, where the honest position is several competing hypotheses rather than one story.

• hEDS, hypermobility and autonomic–GI overlap

  For hypermobility with dysautonomia, dysmotility and reactivity, where three labels exist and no explanation connects them.

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