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From the Department of Neurology (Drs. Ho, Hsieh, Sheikh, Flanigan, McArthur, Cornblath, and Griffin), Johns Hopkins University School of Medicine, Baltimore, MD; the New York State Department of Health (Dr. Kiehlbauch), Wadsworth Center, Albany NY; the Department of Neurology (Dr. Willison), Southern General Hospital, Institute of Neurological Sciences, University of Glasgow, Glasgow, Scotland; the Zanvyl Krieger Mind-Brain Institute (Dr. McKhann), Johns Hopkins University, Baltimore, MD; and the Department of Pathology and Laboratory Medicine (Dr. Nachamkin), University of Pennsylvania School of Medicine, Philadelphia, PA.
Supported in part by USPHS grants RO1-NS34846 and RO1-NS31528. Dr. Ho was supported by USPHS Special Fellowship NS09286 and Dr. Nachamkin by the Cooperative State Research Service, U.S. Department of Agriculture (#93-37201).
Received June 13, 1996. Accepted in final form August 29, 1996.
Address correspondence and reprint requests to Dr Ho, Department of Neurology, Johns Hopkins Hospital, Pathology Building 509, 600 N. Wolfe St., Baltimore, MD 21287-7609.
Article abstract-We investigated the possible mechanisms of paralysis and recovery in a patient with the acute motor axonal neuropathy (AMAN) pattern of the Guillain-Barre syndrome. The AMAN pattern of GBS is characterized clinically by acute paralysis without sensory involvement and electrodiagnostically by low compound motor action potential amplitudes, suggesting axonal damage, without evidence of demyelination. Many AMAN patients have serologic or culture evidence of recent Campylobacter jejuni infection. Pathologically, the most severe cases are characterized by wallerian-like degeneration of motor axons affecting the ventral roots as well as peripheral nerves, but some fatal cases have only minor changes in the roots and peripheral nerves, and some paralyzed patients with the characteristic electrodiagnostic findings of AMAN recover rapidly. The mechanism of paralysis and recovery in such cases has been uncertain. A 64-year-old woman with culture-proven Campylobacter upsaliensis diarrhea developed typical features of AMAN. She improved quickly following plasmapheresis. Her serum contained IgG anti-GM1 antibodies. The lipopolysaccharide of the organism bound peanut agglutinin. This binding was blocked by cholera toxin, suggesting that the organism contained the Gal(beta 1-3)GalNAc epitope of GM1 in its lipopolysaccharide. Motor-point biopsy showed denervated neuromuscular junctions and reduced fiber numbers in intramuscular nerves. In contrast, the sural nerve biopsy was normal and skin biopsy showed normal dermal and epidermal innervation. In AMAN the paralysis may reflect degeneration of motor nerve terminals and intramuscular axons. In addition, the anti-GM1 antibodies, which can bind at nodes of Ranvier, might produce failure of conduction. These processes are potentially reversible and likely to underlie the capacity for rapid recovery that characterizes some cases of AMAN.
NEUROLOGY 1997;48: 717-724
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