News|Videos|July 6, 2026

Diagnosing Immune-Mediated Small Fiber Neuropathy in Clinical Practice: Matthew Evans, BM, BCh, DPhil

Matthew Evans, BM, BCh, DPhil, consultant neurologist at the University of Oxford, discusses the diagnostic approach to small fiber neuropathy and the challenges of confirming immune-mediated disease. [WATCH TIME: 3 minutes]

WATCH TIME: 3 minutes

“The biggest challenge isn't usually recognizing the phenotype. It's obtaining objective evidence that the small nerve fibers are damaged while making sure you've carefully ruled out the common and treatable causes before pursuing a more extensive inflammatory workup.”

Diagnosing small fiber neuropathy (SFN) remains one of the more challenging aspects of peripheral neurology. Although many patients present with characteristic symptoms, including burning pain and altered temperature sensation, confirming the diagnosis often requires specialized testing while simultaneously excluding large fiber neuropathies and identifying potentially treatable underlying causes. As interest grows in immune-mediated forms of SFN, establishing a rigorous diagnostic framework has become increasingly important before considering disease-specific therapies.

At the 2026 Peripheral Nerve Society (PNS) Annual Meeting in Maastricht, Netherlands, Matthew Evans, BM, BCh, DPhil, presented a session titled Immune-Mediated Small Fiber Neuropathy: Is it for Real? The presentation reviewed the current diagnostic approach to SFN, explored the evidence supporting autoimmune involvement in select patients, and discussed the strengths and limitations of existing structural and functional diagnostic tools used to confirm disease.

In a conversation with NeurologyLive®, Evans discusses the practical diagnostic pathway for evaluating patients with suspected SFN, emphasizing the importance of recognizing characteristic clinical features, excluding large fiber involvement, and obtaining objective confirmation through skin biopsy or quantitative sensory testing. He also explains why identifying secondary causes, including diabetes and hereditary transthyretin amyloidosis, remains a critical component of the diagnostic workup before pursuing broader inflammatory investigations.

Click here for more PNS 2026 coverage.


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