An acute motor axonal neuropathy developed within 4 days of the appearance of the varicella rash in a 26-year-old male reported from the University of Geneva, Switzerland. A distal weakness of arms rapidly extended to the legs and was followed in 3 days by a severe bilateral flaccid paralysis. Sensation was normal. DTRs were present and plantar responses were absent. CSF on admission contained 4 cells/mm3 and 0.61 g/l protein; 1 week later, 17 cells and 2 g/1 protein. Serum anti-VZV IgG was 1:800 on admission and 1:1600 after 1 week. EMG showed an acute axonal motor polyneuropathy; 6 weeks later, there were fibrillation potentials and signs of neurogenic atrophy. Nerve conduction velocities showed no conduction block. Slow recovery and signs of reinnervation followed plasmaphareses, but a motor deficit persisted at 15 month follow-up. [1]

COMMENT. Despite the cytoalbuminologic dissociation in the CSF, characteristic of a demyelinating Guillain-Barre syndrome, the EMG showed a primary motor axonal neuropathy without demyelination, and cranial nerves and DTRs were preserved. Campylobacter jejuni is the most frequent infectious agent causing motor axonal neuropathy, but this form of Guillain Barre syndrome may rarely be associated with varicella.