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Does Campylobacter jejuni infection elicit "demyelinating" Guillain–Barré syndrome?

From the Department of Neurology (Drs. Kuwabara, Ogawara, Misawa, Mori, Hiraga, Kanesaka, and Hattori), Chiba University School of Medicine, Japan; and Department of Neurology (Drs. Koga and Yuki), Dokkyo University School of Medicine, Tochigi, Japan.

Address correspondence and reprint requests to Dr. Satoshi Kuwabara, Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan; e-mail: kuwabara-s{at}faculty.chiba-u.jp

Background: Campylobacter 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.

Objective: To investigate whether C. jejuni infection elicits AIDP.

Methods: In 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.

Results: There 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.

Conclusion: Patients 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.

Received January 20, 2004. Accepted in final form March 26, 2004.

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