Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) typically presents with respiratory illness and fever, however some rare neurologic symptoms have been described as presenting complaints. We report a case of an acute motor and sensory polyneuropathy consistent with Miller-Fisher Syndrome (MFS) variant of Guillain Barre Syndrome (GBS) as the initial symptom. Case Report: A 31-year old Spanish speaking male presents with two months of progressive weakness, numbness, and difficult walking. He had multiple cranial nerve abnormalities, dysmetria, ataxia, and absent lower extremity reflexes. An extensive workup including infectious, autoimmune, paraneoplastic, metabolic and neurologic testing was performed. Initially SARS-CoV-2 was not suspected based on a lack of respiratory symptoms. However, workup revealed a positive SARS-CoV-2 polymerase chain reaction test as well as presence of Anti-Ganglioside – GQ1b (Anti-GQ1b) immunoglobulin G antibodies. Discussion: Miller Fisher syndrome (MFS) is a variant of Guillain-Barre syndrome (GBS) characterized by a triad of ophthalmoplegia, ataxia, and areflexia. The patient’s exam and workup including Anti-GQ1b is consistent with MFS. Conclusion: SARS-CoV-2 infection in patients can have atypical presentations similar to this neurologic presentation. Prompt recognition and diagnosis can minimize the risk of transmission to hospital staff and facilitate initiation of treatment.

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Endometriosis is a painful condition characterized by growth of endometrial cysts outside the uterus. Here, we tested the hypothesis that peripheral innervation and prostaglandin levels contribute to endometriosis-associated pain. Female Sprague-Dawley rats (n=16) were surgically instrumented by transplanting uterine tissue onto mesenteric arteries within the pelvic cavity to create a model of endometriosis which forms extra-uterine endometrial cysts and vaginal hyperalgesia. Our results describe a significant positive correlation between endometriosis-induced vaginal hyperalgesia and cyst innervation density (sensory, r =0.70, p =0.003; sympathetic, r =0.55, p = 0.03), vaginal canal sympathetic innervation density (r =0.80, p =0.003), and peritoneal fluid levels of the prostaglandins PGE2 (r =0.65, p =0.01) and PGF2α (r =0.63, p =0.02). These results support the involvement of cyst innervation and prostaglandins in endometriosis-associated pain. We also describe how sympathetic innervation density of the vaginal canal is an important predictor of vaginal hyperalgesia.