GUILLAIN BARRÉ SYNDROME POST SARS-COV-2 INFECTION: A CASE REPORT

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Guillain Barre Syndrome (GBS) is a syndrome usually consisting of paralyzing illness following an infectious process. SARS-COV-2 virus has well documented complications including pneumonia, ARDS, nephropathy, and thrombosis. Neurologic sequelae of GBS, as described in our case are much less common (1). CASE PRESENTATION: An 85-year-old African American male with recent COVID-19 infection, who presented to the emergency department with bilateral lower extremity weakness and bilateral upper extremity tingling for 24 hours. Vital signs were stable on admission. Physical exam revealed quadriparesis and sensory loss, areflexia of L4 and S1 and no saddle anesthesia. MRI brain and cervical spine revealed no signs of myelitis. Due to concern for COVID-19 post viral syndrome in the setting of new, rapidly progressing neurological symptoms, IVIG therapy was initiated. An EMG study was performed and was consistent with length dependent sensory and motor polyneuropathy, with mixed demyelinating and axonal features. Furthermore, there was minimal to absent recruitment of most muscles, consistent with high severity of disease. Patient's condition continued to worsen. He was intubated and placed on mechanical ventilatory support. While on mechanical ventilation, plasma exchange (PLEX) was initiated with subsequent improvement of his symptoms. Eventually, he was transferred to acute inpatient rehab to continue recovery. DISCUSSION: The most common peripheral nervous system manifestations of COVID-19 usually involve anosmia and chemosensory dysfunction (2). Case reports have shown an association between COVID-19 and GBS. It remains unclear whether humoral molecular mimicry, as seen in C. Jejuni, is also the driving mechanism behind the pathogenesis of GBS in SARS-CoV-2 (3). Reports have highlighted that no known SARS-CoV-2 epitopes have been found to be homologically similar to human peripheral nerve tissue and therefore unable to support immune driven, previously widely described molecular mechanisms of GBS (4). However, this lack of clear genetic similarity does not exclude immune mediated response as it's possible that immunogenic proteins could be modified post-translationally or have non-linear antibody epitopes driving such response (5). In addition, although there has been no evidence of SARS-CoV-2 detection in CSF (6), a small sample size of CSF studies from COVID 19 patients likely points towards overall inflammation caused by virus leading to immune cascade and possible infiltration of immune cells locally leading to CNS injury (7). CONCLUSIONS: Clinicians treating COVID-19 viral syndromes should be aware of the association between COVID-19 and GBS, especially when caring for patients with rapidly progressing neurologic disease. Further work needs to be done to broaden the understanding of pathogenesis of GBS in such cases. REFERENCE #1: Montalvan V, Lee J, Bueso T et al. Neurological manifestations of COVID-19 and other coronavirus infections: A systematic review. Clinical Neurology and Neurosurgery 194. REFERENCE #2: Lechner M, Chandrasekharan D, Jumani K, Liu et al. Anosmia as a presenting symptom of SARS-CoV-2 infection in healthcare workers - A systematic review of the literature, case series, and recommendations for clinical assessment and management. Rhinology. 2020 Aug 1;58(4):394-399. REFERENCE #3: Loshaj-Shala A, Regazzoni L, Daci A, Orioli M, Brezovska K, Panovska AP, et al. Guillain Barre syndrome (GBS): new insights in the molecular mimicry between C. Jejuni and human peripheral nerve (HPN) proteins. J Neuroimmunology 2015;289: 168–76. DISCLOSURES: No relevant relationships by Mateusz Gorecki, source=Web Response no disclosure on file for Dean Kalam;No relevant relationships by Ahamed Khalyfa, source=Web Response