AXONAL FORM OF GUILLAIN-BARRE-SYNDROME - EVIDENCE FOR MACROPHAGE-ASSOCIATED DEMYELINATION

We report on the clinical, electrophysiological, and pathological find ings in a patient with pure motor and axonal Guillain-Barre syndrome, who died 29 days after onset. There was marked reduction of compound m otor action potential amplitudes and denervation potentials in the tib ialis anterior muscle. Motor and sensory conduction velocities of medi an nerve were normal. Peroneal nerve was inexcitable at the ankle but its latency from knee to tibialis anterior was normal. F waves were ab sent or delayed. The major burden of pathological changes fell on vent ral spinal roots. Fundamental lesions included segmental demyelination , axonal degeneration, widespread endoneurial lipid-laden macrophage i nfiltrates, remyelination, and clusters of small regenerating fibers. These findings suggest that axonal damage in the axonal form of Guilla in-Barre syndrome is secondary to demyelination.