Guillain-Barre syndrome presenting with sensory disturbance following a herpes virus infection: a case report.

Introduction: We present a case of an unusual clinical manifestation of Guillain-Barre syndrome following a pre-existing herpes virus infection. Although there have been several reports describing the co-existence of herpes virus infection and Guillain-Barre syndrome, we undertook a more in-depth study of the cross-reactivity between herpes viruses and recommend a follow-up study based on serology tests.

Case Presentation: A 39-year-old healthy Caucasian man with Guillain-Barre syndrome presented to our facility initially with sensory disturbance, followed by an atypical descending pattern of clinical progression. On physical examination, our patient showed hot and cold temperature sensory disturbance under the T4 vertebrae level, symmetrically diminished muscle power mainly to his lower limbs, blurred vision, a loss of taste and paresis and diminished reflexes of his lower limbs. Serology test results for common viruses on hospital admission were positive for cytomegalovirus immunoglobulin M, cytomegalovirus immunoglobulin G, herpes simplex virus immunoglobulin M, herpes simplex virus immunoglobulin G, Epstein-Barr virus immunoglobulin M, and varicella zoster virus immunoglobulin G, borderline for Epstein-Barr virus immunoglobulin G and negative for varicella zoster virus immunoglobulin M. At one month after hospital admission his test results were positive for cytomegalovirus immunoglobulin M, cytomegalovirus immunoglobulin G, herpes simplex virus immunoglobulin G, Epstein-Barr virus immunoglobulin G, varicella zoster virus immunoglobulin G, borderline for herpes simplex virus immunoglobulin M and negative for Epstein-Barr virus immunoglobulin M and varicella zoster virus immunoglobulin M. At his six month follow-up, tests were positive for cytomegalovirus immunoglobulin G, herpes simplex virus immunoglobulin M, herpes simplex virus immunoglobulin G, Epstein-Barr virus immunoglobulin G and varicella zoster virus immunoglobulin G and negative for cytomegalovirus immunoglobulin M, Epstein-Barr virus immunoglobulin M and varicella zoster virus immunoglobulin M.

Conclusions: The clinical manifestation of Guillain-Barre syndrome in our patient followed a combined herpes virus infection. The cross-reactivity between these human herpes viruses may have a pathogenic as well as evolutionary significance. Our patient showed seroconversion at an early stage of Epstein-Barr virus immunoglobulin M to immunoglobulin G antibodies, suggesting that Epstein-Barr virus might have been the cause of this syndrome. Even if this case is not the first of its kind to be reported, it may contribute to a better understanding of the disease and the cross-reaction mechanisms of herpes virus infections. This case report may have a broader clinical impact across more than one area of medicine, suggesting that cooperation between different specialties is always in the patient's best interest.