• S Kuwabara, K Ogawara, S Misawa, M Koga, M Mori, A Hiraga, T Kanesaka, T Hattori, and N Yuki.
• Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. kuwabara-s@faculty.chiba-u.jp
• Neurology. 2004 Aug 10; 63 (3): 529-33.

BackgroundCampylobacter jejuni enteritis is the most common antecedent infection in Guillain-Barré syndrome (GBS). C. jejuni-related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports described many cases of the demyelinating subtype of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]) after C. jejuni infection.ObjectiveTo investigate whether C. jejuni infection elicits AIDP.MethodsIn 159 consecutive patients with GBS, antibodies against C. jejuni were measured using ELISA. Antecedent C. jejuni infection was determined by the strict criteria of positive C. jejuni serology and a history of a diarrheal illness within the previous 3 weeks. Electrodiagnostic studies were performed weekly for the first 4 weeks, and sequential findings were analyzed.ResultsThere was evidence of recent C. jejuni infection in 22 (14%) patients. By electrodiagnostic criteria, these patients were classified with AMAN (n = 16; 73%) or AIDP (n = 5; 23%) or as unclassified (n = 1) in the first studies. The five C. jejuni-positive patients with the AIDP pattern showed prolonged motor distal latencies in two or more nerves and had their rapid normalization within 2 weeks, eventually all showing the AMAN pattern. In contrast, patients with cytomegalovirus- or Epstein-Barr virus-related AIDP (n = 13) showed progressive increases in distal latencies in the 8 weeks after onset.ConclusionPatients with C. jejuni-related Guillain-Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C. jejuni infection does not appear to elicit acute inflammatory demyelinating polyneuropathy.

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