Circulating tumor necrosis factor‐α correlates with electrodiagnostic abnormalities in Guillain‐Barré syndrome

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Abstract
Autoimmune damage to peripheral nerves, mediated by activated T lymphocytes and macrophages, underlies the pathogenesis of inflammatory demyelination in Guillain‐Barré syndrome. Both T lymphocytes and macrophages secrete tumor necrosis factor‐α, a cytokine that exerts toxic effects on myelin, Schwann cells, and endothelial cells. The reportedly high serum levels of this cytokine in patients with Guillain‐Barré syndrome may reflect the degree of immune activation rather than a direct pathogenic effect. We compared serum levels of tumor necrosis factor‐α, interleukin‐1β, and soluble interleukin‐2 receptor with well‐established electrodiagnostic criteria for primary demyelination in 23 patients with Guillain‐Barré syndrome, to assess the relationship between these cytokines and peripheral myelin damage. High serum levels of tumor necrosis factor‐α were associated with prolonged distal motor latencies and slowed motor conduction velocities, prolonged or absent F‐wave responses, and reduced amplitude of distal compound muscle action potentials. No significant correlation was observed between electrodiagnostic criteria for primary demyelination and serum levels of interleukin‐1β or soluble interleukin‐2 receptor. These findings suggest a putative role of tumor necrosis factor‐α in the pathogenesis of peripheral nerve demyelination in Guillain‐Barré syndrome.