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Axonal form of Guillain–Barré syndrome: Evidence for macrophage‐associated demyelination
Author(s) -
Berciano José,
Coria Francisco,
Montón Fernando,
Calleja Jesús,
Figols Javier,
Lafarga Miguel
Publication year - 1993
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880160709
Subject(s) - remyelination , medicine , axonal degeneration , guillain barre syndrome , denervation , pathological , acute motor axonal neuropathy , nerve conduction velocity , tibialis anterior muscle , compound muscle action potential , pathology , neuroscience , anatomy , electrophysiology , myelin , biology , central nervous system , skeletal muscle , immunology
We report on the clinical, electrophysiological, and pathological findings in a patient with pure motor and axonal Guillain–Barré syndrome, who died 29 days after onset. There was marked reduction of compound motor action potential amplitudes and denervation potentials in the tibialis anterior muscle. Motor and sensory conduction velocities of median nerve were normal. Peroneal nerve was inexcitable at the ankle but its latency from knee to tibialis anterior was normal. F waves were absent or delayed. The major burden of pathological changes fell on ventral spinal roots. Fundamental lesions included segmental demyelination, axonal degeneration, widespread endoneurial lipid‐laden macrophage infiltrates, remyelination, and clusters of small regenerating fibers. These findings suggest that axonal damage in the axonal form of Guillain–Barré syndrome is secondary to demyelination.