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Table of Contents    
LETTER TO EDITOR
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1698-1699

Severe Acute Respiratory Syndrome Coronavirus Two (SARS-CoV-2) Associated Guillain-Barre Syndrome


1 Department of Neurology, Yashoda Superspecialty Hospital, Malakpet, Hyderabad, Telangana, India
2 Department of General Medicine, Yashoda Superspecialty Hospital, Malakpet, Hyderabad, Telangana, India
3 Department of Pulmonology, Yashoda Superspecialty Hospital, Malakpet, Hyderabad, Telangana, India
4 Department of Radiology, Yashoda Superspecialty Hospital, Malakpet, Hyderabad, Telangana, India

Date of Submission19-Oct-2020
Date of Decision24-Jan-2021
Date of Acceptance01-Feb-2021
Date of Web Publication30-Aug-2022

Correspondence Address:
Kiran Kumar Ramineni
Department of Neurology, Yashoda superspeciality Hospital, Malakpet, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.355104

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How to cite this article:
Ramineni KK, Mohan Reddy G K, Chakrahari UB, Marupaka SK. Severe Acute Respiratory Syndrome Coronavirus Two (SARS-CoV-2) Associated Guillain-Barre Syndrome. Neurol India 2022;70:1698-9

How to cite this URL:
Ramineni KK, Mohan Reddy G K, Chakrahari UB, Marupaka SK. Severe Acute Respiratory Syndrome Coronavirus Two (SARS-CoV-2) Associated Guillain-Barre Syndrome. Neurol India [serial online] 2022 [cited 2022 Oct 7];70:1698-9. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1698/355104




Sir,

The novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS- CoV-2) infection resulted in one of the largest pandemics ever that has challenged health care systems across the world. Although it has predilection for respiratory system involvement, various other internal organs can be affected simultaneously or sequentially. Neurological complications involving central and peripheral nervous systems in association with this pandemic were reported from various parts of the world.[1]

A 45-year-old man was brought to the emergency department with a history of fever, dry cough, and malaise since 3 days. Vitals included axillary temperature of 99 F, pulse rate of 104/min, blood pressure of 110/70 mm hg, respiratory rate of 20/min, and Spo2 95 percent at room air. He was admitted to isolation ward and computed tomography chest revealed bilateral ground-glass opacities in lungs [Figure 1]. Laboratory investigations were normal except for mild lymphocytopenia, elevated C reactive protein, and interleukin 6 levels. Nasopharyngeal swab tested positive for SARS -CoV-2 by reverse transcription-polymerase chain reaction. He was started on intravenous remdesivir, solumedrol, subcutaneous enoxaparin, symptomatic medication, and supportive care. By day three of admission he was symptomatically better, afebrile, and ambulant without any discomfort. No history of any recent gastroenteritis or vaccination. However on day 7, he developed tingling sensation in both feet and difficulty in walking. Over next 1 day developed weakness of both upper limbs and difficulty in closing eyes. No bowel bladder dysfunction noticed.
Figure 1: High resolution CT scan of the chest through the upper (a) and lower (b) zones reveals bilateral multifocal predominantly peripheral ground glass opacities (white arrows) with solid areas and thin linear opacity on left side. Findings compatible with pulmonary involvement of COVID-19 (CORADS 5)

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He was conscious alert, had bifacial weakness and flaccid quadriparesis with medical research council grade 2 power in lower limbs and grade 3 in upper limbs. No objective sensory loss noted. Serum creatinine phosphokinase level was normal, antinuclear antibody and Human Immunodeficiency Virus 1 and 2 serology negative. Nerve conduction studies revealed prolonged distal latencies, F latencies, reduced compound muscle action potentials and conduction velocities. Sensory conductions revealed typical absent median and normal sural snaps pattern. Cerebrospinal fluid analysis showed mild elevation of protein with normal cell count. Final diagnosis of SARS- CoV-2 associated Guillain-Barre syndrome was made. As the manifestations of Guillain-Barre syndrome occurred during active respiratory infection and CSF cell count being normal, the most likely pathogenesis is parainfectious and immune mediated. Intravenous immunoglobulin 0.4 gr/kg/day was given for five days along with physiotherapy and supportive care. Over next 1 week he improved well and was ambulant with minimal assistance and was discharged in a stable hemodynamic status. At two weeks follow up he maintained overall improvement and was independent for all activities of daily living. His serum anti-SARS- CoV-2 antibodies were positive.

Various neurological manifestations of SARS-CoV-2 infection include headache, anosmia, stroke, seizures, meningoencephalitis, acute disseminated encephalomyelitis, cranial neuropathies, myalgias, Guillain-Barre syndrome, etc.[2] Proposed pathogenic mechanisms include direct viral invasion of blood–brain barrier, coagulopathy, cytokine storm, autoimmunity by molecular mimicry. Guillain-Barre syndrome is a relatively uncommon complication of SARS-CoV-2 infection. Onset can vary between 7 days before the respiratory manifestations to 4 weeks after, supporting both para-infectious and post-infectious pathogenic mechanisms.[3]

Various subtypes of GB syndrome including demyelinating radiculo neuropathy, axonopathy, Miller Fischer variant, facial diplegia have been reported in association with SARS-CoV-2 infection.[2],[4] As these patients will be in isolation areas, upon clinical suspicion early nerve conduction studies and lumbar puncture under personal protective precautions will help in timely diagnosis. In view of the confounding factors like the presence of myalgias, fatigue, medication-induced side effects, and respiratory distress which might be easily attributed to lung involvement, missing early diagnosis of GB syndrome is quite possible. As the timely initiation of specific therapeutic options like intravenous immunoglobulins and plasmapheresis are known to reduce the morbidity, early neurology consultations should be taken for accurate diagnosis.[4] Larger prospective studies may better elucidate the exact pathogenesis and correlation between the occurrence of neurological complications like GB syndrome and final outcome in SARS-CoV-2 infection.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ellul MA, Benjamin L, Singh B, Lant S, Michael BD, Easton A, et al. Neurological associations of COVID-19. Lancet Neurol 2020;19:767-83.  Back to cited text no. 1
    
2.
Garg RK. Spectrum of neurological manifestations in Covid-19: A review. Neurol India 2020;68:560-72.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Zhao H, Shen D, Zhou H, Liu J, Chen S. GuillainBarré syndrome associated with SARSCoV2 infection: Causality or coincidence? Lancet Neurol 2020;19:383-4.  Back to cited text no. 3
    
4.
Webb S, Wallace VC, Martin-Lopez D, Yogarajah M. Guillain-Barré syndrome following COVID-19: A newly emerging post-infectious complication. BMJ Case Rep 2020;13:e236182.  Back to cited text no. 4
    


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