CIRCULATING TUMOR-NECROSIS-FACTOR-ALPHA CORRELATES WITH ELECTRODIAGNOSTIC ABNORMALITIES IN GUILLAIN-BARRE-SYNDROME

Autoimmune damage to peripheral nerves, mediated by activated T lympho cytes and macrophages, underlies the pathogenesis of inflammatory demy elination in Guillain-Barre syndrome. Both T lymphocytes and Nacrophag es secrete tumor necrosis factor-alpha, a cytokine that exerts toxic e ffects on myelin, Schwann cells, and endothelial cells. The reportedly high serum levels of this cytokine in patients with Guillain-Barre sy ndrome may reflect the degree of immune activation rather than a direc t pathogenic effect. We compared serum levels of tumor necrosis factor -alpha, interleukin-1 beta, and soluble interleukin-2 receptor with we ll-established electrodiagnostic criteria for primary demyelination in 23 patients with Guillain-Barre syndrome, to assess the relationship between these cytokines and peripheral myelin damage. High serum level s of tumor necrosis factor-alpha mere associated with prolonged distal motor latencies and slowed motor conduction velocities, prolonged or absent F-wave responses, and reduced amplitude of distal compound musc le action potentials, No significant correlation was observed between electrodiagnostic criteria for primary demyelination and serum levels of interleukin-1 beta or soluble interleukin-2 receptor. These finding s suggest a putative role of tumor necrosis factor-cy in the pathogene sis of peripheral nerve demyelination in Guillain-Barre syndrome.