GBS is yet a unique and rare neurological manifestation of SARS-CoV-2, and still, 42 cases are being reported in the literature [3]. Our case of a young boy, presented with sudden onset symmetrical lower limb weakness followed by an episode of fever is a unique presentation of COVID-19 provoking the GBS-AMSAN variant. GBS, an acute monophasic polyneuropathy affects patients from around the world indifferent of race, age, and gender. This acute paralyzing illness most of the time proceeded by an infectious disease [4]. Apart from COVID-19, various other microbes are found to be a culprit in provoking this life-threatening illness which includes Campylobacter jejuni, Haemophilus influenza, Ebstein Barr virus, Cytomegalovirus, Zika virus, Influenza A virus, Mycoplasma and SARS-CoV-2 akin SARS and MERS [5]. Several different mechanisms are being proposed as the sole cause of GBS formation [6]. Four subtypes of acute peripheral neuropathy are included in GBS. As time propels, we get to know a few mechanisms to understand the pathophysiology behind the formation of GBS. There exists a marked resemblance between acute inflammatory demyelinating polyneuropathy (AIDP) and experimental autoimmune neuritis based on histology. The main culprit behind all the mayhem is the T-cell, which became active against peptides from myelin proteins P0, P2, and PMP22. Although this T-cell mediation is dubious there is substantiation of autoantibodies and compliment. The axonal subtypes of GBS, AMAN, and AMSAN, are antecedent by the formation of antibodies to the axolemmal gangliosides that direct macrophage to attack the axons at the nodes of Ranvier [7].

The pathogenesis of the formation of GBS in patients suffering from COVID-19 is still debatable. SARS-CoV-2 triggers inflammatory cells which leads to the cascade of the production of several different inflammatory cytokines and inflammatory processes [8]. ACE-2-R is the common site to be attacked by both SARS and SARS-CoV-2 [1, 8]. Various organs (lung, kidney, skeletal muscle, nervous system, and liver) inside human beings have these receptors over their cell membrane [2]. The notorious COVID-19 attaches to the cell membrane by its viral spike (S) protein, which later binds to the ACE-2 enzyme and sialic acid residue containing ganglioside, including GaINAC residues of GM1 [9]. Molecular mimicry is the proposed mechanism of autoimmunity for the formation of GBS [10]. COVID-19-causing GBS may sometimes deficit with the autoantibody formation, in such cases a parainfectious phenomenon is proposed, arbitrated by a generalized, hyper-inflammatory response. Talking about an axonal variant of GBS, AMSAN, which is in our case an unusual presentation [11]. However, a similar pattern of progression of the disease, i.e, respiratory symptoms of COVID-19 later progresses to GBS, supports COVID-19 as being the sole reason behind causing this acute paralyzing illness. So, in the pandemic of COVID-19, it’s the keen responsibility of every physician to have this dreadful neurological manifestation somewhere in the back of his mind, while managing patients suffering from the virus and arranging at least one follow-up visit soon after discharge. To prevent dreadful complications of GBS like respiratory paralysis, pulmonary embolism, cardiac arrest, and sepsis, an aggressive management plan including IVIG should be planned earlier. As far as the causative mechanisms whether due to molecular mimicry or direct neurological invasion has yet to be established and need more clinical review and literature studies [11].