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Neurology. 2004 Aug 10;63(3):529-33.

Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome?

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  • 1Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. kuwabara-s@faculty.chiba-u.jp

Abstract

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.

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PMID:
15304587
[PubMed - indexed for MEDLINE]
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