Course and outcome of a voltage-gated potassium channel antibody negative Morvan's syndrome

Carlo Rinaldi1, Cinzia Valeria Russo, Alessandro Filla

  • 1Department of Neurological Sciences, Federico II University, Via Pansini, 5, 80131, Naples, Italy. rinaldi.ca@gmail.com

Insights

Morvan's syndrome can occur without voltage-gated potassium channel (VGKC) antibodies. This case study highlights a patient with Morvan's syndrome, myasthenia gravis, and thymoma, showing an autoimmune origin despite undetectable VGKC antibodies.

Area of Science:

  • Neurology
  • Immunology

Background:

  • Morvan's syndrome is a rare autoimmune disorder affecting peripheral nerves, central nervous system, and autonomic systems.
  • It is typically associated with high serum voltage-gated potassium channel (VGKC) antibody titers.
  • Previously, VGKC antibody positivity was considered a hallmark of Morvan's syndrome.

Observation:

  • This report details a patient with Morvan's syndrome, myasthenia gravis, and a history of thymoma.
  • The patient presented with clinical features consistent with Morvan's syndrome.
  • Notably, serum VGKC antibody levels were undetectable in this patient.

Findings:

  • The clinical presentation mimicked VGKC antibody-associated Morvan's syndrome.
  • The patient did not respond to plasma exchange, a standard treatment for VGKC antibody-associated conditions.
  • However, the patient showed a positive response to corticosteroid therapy.

Implications:

  • This case challenges the notion that VGKC antibodies are essential for Morvan's syndrome diagnosis.
  • It suggests alternative autoimmune mechanisms may underlie Morvan's syndrome.
  • The findings support an autoimmune etiology for Morvan's syndrome, even in the absence of VGKC antibodies, and highlight corticosteroids as a potential treatment.

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