Prominent Distal demyelination is a feature of Zika-Associated Guillain Barré Syndrome (P4.136)

Objective: To describe the electrodiagnostic fndings in a group of patients with Zika virus-associated Guillain Barre Syndrome (GBS) and identify specific characteristics that identifies this condition. Background: In countries affected by recent outbreaks of Zika virus infection there has been an increase in the incidence of GBS. Although electrodiagnostic studies have been performed in some recently published studies, detailed descriptions of the electrodiagnostic findings in patients with this Zika-associated complication are not available. Design/Methods: A prospective surveillance study for cases of Guillain Barre Syndrome has been implemented in Puerto Rico since February 2016. All patients fulfilling Brighton Collaborative Criteria levels 1 through 3 for GBS, underwent RT-PCR and IgM ELISA tests for Zika, Dengue and Chikungunya virus in serum, and in some cases CSF and urine. In addition, electrodiagnostic studies of the upper and lower limbs were performed in all patients consulted to the neuromuscular medicine service with a diagnosis of GBS, and who tested positive for active or recent Zika virus infection. Results: Electrodiagnostic studies were performed in 10 patients with proven Zika-Associated GBS. The distal motor latencies for the median, ulnar, fibular (peroneal) and tibial nerve ranged from 3.6 to 29 msec (median, 9.5 msec) and were more prolonged for the median nerve (range 5.3 to 29 msec; median 12.95 msec) and the tibial nerve (range 6.4 to 18 msec; median 11.0 msec). In comparison the motor conduction velocities ranged from 19 to 64 m/s (median, 40 m/s) and were slowest in the tibial nerve (range 33.6 to 52 m/s; median 39 m/s) and the fibular nerve (range 29 to 60m/s; median 39.25 m/s). Conclusions: In Zika-Associated GBS, the electrodiagnostic studies show more pronounced demyelination in the distal segments of the motor nerves. This finding could represent a marker of the specific pathophysiologic mechanism of demyelination in this condition. Study Supported by: The study has been supported by the Puerto Rico Department of Health, The Centers for Disease Control and Prevention and by NIH award number U54MD007587 Disclosure: Dr. Betances has nothing to disclose. Dr. Luciano has received personal compensation for activities with Sanofi-Genzyme Corporation as a speaker. Dr. Carlo has received personal compensation for activities with Sanofi-Genzyme as a speaker. Dr. Deliz-Roldan has nothing to disclose. Dr. Alfonso has nothing to disclose.