Journal of Clinical and Diagnostic Research. 2022 Apr, Vol-16(4): OR04-OR07 4 4 DOI: 10.7860/JCDR/2022/56035.16281 Case Series Internal Medicine Section COVID-19 Associated Guillain-Barré Syndrome- A Case Series PANKAJ KUMAR SAINI 1 , RAHUL GUPTA 2 , GAURAV KUMAR GUPTA 3 Keywords: Acute inflammatory, Coronavirus Disease-2019, Demyelinating, Pandemic, Polyradiculoneuropathy ABSTRACT The outbreak of Coronavirus Disease-2019 (COVID-19) infection with associated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused modified and compromised immune system that gave rise to various immune mediated disease. Various studies on both central and peripheral nervous system involvement has been reported. The common syndromes reported are meningoencephalitis, myelitis and Guillain-Barré syndrome (GBS) etc. This case series reports four cases (45 years old male, 35 years old female, 50 years old male and 65 years old male patients) presenting with the duration from onset of viral illness to neurologic manifestations ranging from 4 days to 60 days. One patient had a typical course of viral symptoms preceding GBS findings and two patient presented with GBS later. A patient was found to be IgG seropositive for SARS-CoV-2 and presented 2 months later of recovery from infection while one case had onset of weakness while having respiratory symptoms. These cases had Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) who presented with acute flaccid paralysis two to three weeks following COVID-19 infection. All the patients received Intravenous Immunoglobulin (IVIG) as treatment and showed significant improvement. It can be concluded that COVID-19 viral infection is probably related as a causal factor for immune mediated illness like GBS and early identification and treatment has good recovery. INTRODUCTION Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), the causative agent for COVID-19 has manifested from asymptomatic to acute respiratory distress syndrome and severe inflammatory response leading to multiple organ dysfunction and death. According to the currently available resources, SARS-CoV-2 can affect every organ in the body, leading to acute organ damage and long-term effects, the latter effects recently being observed [1]. The upper and lower respiratory tracts are the main sites of involvement of SARS- CoV-2 infection. Pneumonia, with typical ground glass opacities in High Resolution Computed Tomography (HRCT) thorax, has been noticed as the typical presentation. Recently increasing reports have shown that SARS-CoV-2 infection is associated with involvement of the central nervous system (CNS) and the peripheral nervous system (PNS) [2-5]. It is either due to direct invasion from virus or indirectly from modified immune response [2]. In this case series, the Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR) proven SARS-COV2 cases were diagnosed with GBS based on clinical findings, Cerebrospinal Fluid (CSF) and electrophysiological findings according to the case definitions described by World Health Organisation (WHO) [3]. CASE SERIES Case 1 A 41-year-old male patient, without co-morbidity, presented with complaints of fever, cough, and mild breathlessness on exertion for three days. His RT-PCR [reverse transcriptase-polymerase chain reaction] from nasopharyngeal swab for SARS-COV2 was positive. High Resolution Computed Tomography (HRCT) severity score was 7/25. The patient was isolated and symptomatic treatment was started. These symptoms recovered in 7 days. After next 10 days, he noticed paresthesia in both feet and both hands. The symptoms progressed, and he found difficulty in getting up from squatting position, climbing upstairs and noticed slippage of footwear. In the next 3-4 days, he noticed difficulty in doing overhead activities, buttoning, unbuttoning, and facial weakness and was hospitalized in non-ambulatory state. On examination, his vitals were normal and oxygen saturation was 95% by pulse oximetry. His single breath count was 30. Cranial nerve examination showed bilateral lower motor neuron facial palsy. The tone was reduced in all four limbs. The Medical Research Council scale (MRC scale) power grading system showed grade 4/5 power in both upper limbs at all joints and reduced handgrip. In both lower limbs, powergrade was 4/5 at hip and knee joints and 3/5 at both ankle joints. All deep tendon reflexes were absent. The plantar response was flexor bilaterally. On sensory examination, joint position sense was impaired upto both ankles in lower limbs and upto both wrists in upper limbs; rest sensations were normal. In the setting of rapidly progressive ascending weakness, generalized areflexia and preceding viral illness, provisional diagnosis of GBS was kept. On further investigations, complete blood count, sugar, renal function test and serum electrolytes were normal. Serum bilirubin was 1.4 mg%, Aspartate Aminotransferase (AST) (57 U/L), Alanine Transaminase (ALT) 104 (U/L), triglyceride (337 mg %) and C-reactive Protein (CRP) (12 mg/L). CSF showed 5 cells/ mm 3 (100%lymphocytes), protein 300 mg/dL (reference range 15-45 mg/dL), sugar 70 mg/dL (blood sugar 96 mg/dL). The serological tests for Human Immunodeficiency Virus (HIV), syphilis, cytomegalovirus (CMV), Epstein-Barr virus (EBV) were negative. The nerve conduction study showed reduced or absent compound muscle action potentials and sensory nerve action potentials in the lower limbs and upper limbs, absent F wave response in the lower limbs, and prolonged F wave response in the upper limbs. This was suggestive of sensory-motordemyelinating polyradiculoneuropathy (AIDP). MRI Lumbosacral spine was normal. He was treated with Intravenous Immunoglobulin (IVIG) with a total dose of 2 g/kg in divided doses for 5 days along with physiotherapy. On fifth day his power improved more than 4/5 in all four limbs and he started walking with minimal support of a person. He was discharged on seventh day with symptomatic treatment and over a month he had near complete recovery except having some paresthesia in both feet.