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Burning pain: axonal dysfunction in erythromelalgia.

Michelle A Farrar1, Ming-Jen Lee2, James Howells3

  • 1Department of Neurology, Sydney Children's Hospital and School of Women's and Children's Health, University of New South Wales, Sydney, Australia.

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Summary
This summary is machine-generated.

Erythromelalgia (EM) patients exhibit altered peripheral nerve function, with abnormal responses to heat potentially linked to neurovascular issues. Treatment with mexiletine showed promising results in some patients.

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Area of Science:

  • Neuroscience
  • Clinical Neurology
  • Peripheral Nerve Disorders

Background:

  • Erythromelalgia (EM) is a rare neurovascular disorder causing severe burning pain, erythema, and warmth, often triggered by heat.
  • The underlying pathophysiology of EM, particularly peripheral axonal dysfunction, remains incompletely understood.

Purpose of the Study:

  • To investigate peripheral axonal excitability in patients with Erythromelalgia.
  • To explore how temperature changes and therapeutic interventions affect axonal function in EM.

Main Methods:

  • Utilized threshold tracking techniques to assess peripheral axonal excitability in 23 genetically characterized EM patients (EMSCN9A+ and EMSCN9A-).
  • Measured stimulus-response curves, strength-duration time constant (SDTC), threshold electrotonus, and recovery cycles in median motor and sensory axons.
  • Examined changes in axonal excitability with controlled heating and response to mexiletine treatment.

Main Results:

  • EM patients displayed higher resting thresholds and rheobase compared to controls.
  • Sensory axons in EM patients showed significantly greater changes in threshold electrotonus with depolarizing and hyperpolarizing preconditioning.
  • Heating induced axonal depolarization and increased SDTC in EMSCN9A+ patients, unlike healthy subjects.
  • Mexiletine treatment improved symptoms in 4/9 EMSCN9A+ patients, correlating with reduced SDTC.

Conclusions:

  • This study provides the first evidence of peripheral axonal membrane dysfunction in primary EM using threshold tracking.
  • Observed changes suggest systemic neurovascular abnormalities, possibly involving Na/K pump overactivity and chronic post-ischaemic hyperpolarization.
  • Axonal depolarization during heating may represent acute ischemic events triggering EM symptoms.