Miller Fisher syndrome secondary to Epstein-Baar virus mononucleosis Emily Tainara Miranda Alves1 , L

Miller Fisher syndrome is a rare variant of Guillain-Barre syndrome and usually presents with at least two of the following features: ataxia, areflexia, and ophthalmoplegia. Male patient, 16 years old, without comorbidities. Odynophagia began, followed by diarrhea and asthenia. Prescribed antibiotic therapy for tonsillitis. After one week hospital admission with neurological examination with mild dysarthria, global grade 5 strength, bilateral naso-index dysmetria, walking gait, positive romberg and areflexia. Tomography and magnetic resonance imaging of normal. Liquor with protein cytological dissociation. Electroneuromyography with absence of H reflex bilaterally, suggestive of demyelinating neuropathy. Abdominal ultrasound with homogeneous splenomegaly. Cervical ultrasonography with prominent reactive looking lymphnodes. Epstein Barr virus Reactive IgM and non-reactive IGG. A diagnostic hypothesis of Miller Fischer syndrome secondary to mononucleosis was raised, despite a negative anti-GQ1B antibody. Immunoglobulin at a dose of 0.4 kg/kg/day was requested. Patient followed immunoglobulin infusion in intensive care unit bed. He was discharged from the hospital, maintaining only mild gait ataxia. Miller Fisher syndrome within the spectrum of Guillain-Barré syndrome occurs due to an aberrant acute autoimmune response to a previous infection, such as the Epstein-Barr virus. Approximately two-thirds of cases are preceded by symptoms of an upper respiratory tract infection or diarrhea. Miller Fisher syndrome is mainly associated with dysfunction of the cranial nerves, but as exemplified in our case, it can occur in its absence. Several studies have suggested that antibodies against gangliosides, anti-GQ1b, are a specific feature, but the absence of antibodies does not exclude the disease. Cerebrospinal fluid shows proteincytological dissociation. Electroneuromyography may show reduced or absent sensory responses. Imaging may be normal or show thickening and enhancement of the spinal nerve roots. Treatment is aimed at supportive care and the therapy of choice is IV immunoglobulin or plasmaphere. Assertive diagnosis associated with early treatment contributes to a favorable clinical response.