Céline Communal1, Anne Filleron2, Sandrine Baron-Joly1, Randa Salet1, Tu-Anh Tran3. 1. Department of Paediatrics, Nîmes University Hospital, Nîmes, France. 2. Department of Paediatrics, Nîmes University Hospital, Nîmes, France; INSERM U 1183, Montpellier-Nîmes University, Nîmes, France. Electronic address: anne.filleron@chu-nimes.fr. 3. Department of Paediatrics, Nîmes University Hospital, Nîmes, France; INSERM U 1183, Montpellier-Nîmes University, Nîmes, France.
Abstract
BACKGROUND: Miller Fisher syndrome, a variant of Guillain-Barré syndrome, is an acute inflammatory demyelinating polyradiculoneuropathy that may occur weeks after a bacterial or viral infection. Campylobacter jejuni and Haemophilus influenzae are frequently reported etiological agents. PATIENT DESCRIPTION: We describe a boy with Miller Fisher syndrome following Epstein-002DBarr virus primary infectious mononucleosis. He presented with bilateral dysfunction of several cranial nerves and hyporeflexia of the limbs but without ataxia. Miller Fisher syndrome was confirmed by the presence of anti-GQ1b antibodies in a blood sample. Epstein-Barr virus was identified by polymerase chain reaction and serology. CONCLUSION: Epstein-Barr virus should be considered as a Miller Fisher syndrome's causative agent. The physiopathology of this condition may involve cross-reactive T-cells against Epstein-Barr virus antigens and gangliosides.
BACKGROUND:Miller Fisher syndrome, a variant of Guillain-Barré syndrome, is an acute inflammatory demyelinating polyradiculoneuropathy that may occur weeks after a bacterial or viral infection. Campylobacter jejuni and Haemophilus influenzae are frequently reported etiological agents. PATIENT DESCRIPTION: We describe a boy with Miller Fisher syndrome following Epstein-002DBarr virus primary infectious mononucleosis. He presented with bilateral dysfunction of several cranial nerves and hyporeflexia of the limbs but without ataxia. Miller Fisher syndrome was confirmed by the presence of anti-GQ1b antibodies in a blood sample. Epstein-Barr virus was identified by polymerase chain reaction and serology. CONCLUSION:Epstein-Barr virus should be considered as a Miller Fisher syndrome's causative agent. The physiopathology of this condition may involve cross-reactive T-cells against Epstein-Barr virus antigens and gangliosides.