Journal of the Neurological Sciences
Volume 208, Issue 1 , Pages 39-42, 15 April 2003

HIV-associated Guillain–Barré syndrome

  • Thomas H Brannagan III

      Affiliations

    • Corresponding Author InformationCorresponding author. Tel.: +1-212-888-8516; fax: +1-212-888-9206.
    • Department of Neurology, Weill Medical College of Cornell University, Peripheral Neuropathy Center, 635 Madison Avenue, Suite 400 New York, NY 10022, USA
  • ,
  • Yili Zhou

      Affiliations

    • University of Miami, Miami, FL, USA

Received 12 August 2002; accepted 23 October 2002.

Abstract 

Human immunodeficiency virus-associated Guillain–Barré syndrome (HIV-GBS) has been reported since 1985. Based on previous reports, this neuropathy typically occurs early in HIV infection, even at seroconversion, prior to developing acquired immunodeficiency syndrome (AIDS). Patients with GBS and CD4 counts of <50 have been proposed to have cytomegalovirus (CMV) infection and empiric gancyclovir is recommended. We reviewed medical records of 10 patients with HIV-GBS at five hospitals from 1986 to 1999. The mean CD4 count was 367/mm3 (range 55–800). GBS was the first symptom of HIV infection in three patients. Four patients had AIDS with CD4 counts ranging from 55 to 190. CSF white blood cell (WBC) was 0 wbc/mm3 in four patients, 2–10 wbc/mm3 in three and 11–17 wbc/mm3 in two. Three had recurrent weakness from 9 weeks to 4 years after the onset of symptoms, which persisted. HIV-GBS occurs in early and late stages of HIV infection, and may follow the onset of AIDS. No patients were seen with severe immunosuppression (CD4<50). A mild cerebrospinal fluid (CSF) pleocytosis in GBS suggests HIV infection, but is frequently absent. Compared to HIV-negative people, HIV-GBS may be associated with more frequent recurrent episodes or the development of CIDP.

Keywords:  Guillain–Barré syndrome, HIV, Chronic inflammatory demyelinating polyneuropathy, Cerebrospinal fluid, CD4 count, AIDS

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 Presented in part in abstract form at the 47th annual meeting of the American Association of Electrodiagnostic Medicine, Philadelphia, PA, September 13–16, 2000.

PII: S0022-510X(02)00418-5

doi:10.1016/S0022-510X(02)00418-5

Journal of the Neurological Sciences
Volume 208, Issue 1 , Pages 39-42, 15 April 2003