Annals of Indian Academy of Neurology
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Table of Contents
Year : 2021  |  Volume : 24  |  Issue : 4  |  Page : 622-623

Post Covid-19 guillain barre syndrome

1 Department of Neurology, Aster Medcity, Kochi, Kerala, India
2 Department of Physiatry, Aster Medcity, Kochi, Kerala, India

Date of Submission07-Aug-2020
Date of Acceptance11-Sep-2020
Date of Web Publication16-Apr-2021

Correspondence Address:
Dr. Boby Varkey Maramattom
Department of Neurology, Aster Medcity, Kochi, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_853_20

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How to cite this article:
Maramattom BV, Zachariah AN, Meleth HA, Zachariah ZT, Mathew K M. Post Covid-19 guillain barre syndrome. Ann Indian Acad Neurol 2021;24:622-3

How to cite this URL:
Maramattom BV, Zachariah AN, Meleth HA, Zachariah ZT, Mathew K M. Post Covid-19 guillain barre syndrome. Ann Indian Acad Neurol [serial online] 2021 [cited 2021 Oct 25];24:622-3. Available from:

Dear Editor,

The neurological complications of the present COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 are well documented.[1] As of the 10th September 2020, the global SARS-CoV2 infections have crossed 27 million with over 4.3 million cases and 73,000 death from India. There are a few reports of neurological complications of COVID-19 from India; however, post-COVID-19 Guillian–Barre Syndrome (GBS) as an immune-mediated phenomenon has not been reported.[2],[3],[4]

A 60-year-old man with a history of diabetes and hypertension on treatment was evaluated for cough 2.5 months earlier. Nasal swab RT-PCR was positive for SARS-CoV2. Repeat nasal swab tests were negative on day 16. Nine weeks after his last negative test, he developed left leg weakness and buckling at the knees. Over the next 3 days, he developed an asymmetrical lower limb weakness [Left > right], unsteadiness, and paresthesias of all limbs. On examination, he had grade 4/5 MRC scale power in his upper limbs, 1/5 power in the proximal lower limbs, upper limb ataxia, bifacial weakness, and global areflexia without any sensory signs. CSF study showed an albumin-cytologic dissociation [5 WBC's with elevated protein- 187.3 mg/dL]. CSF RT-PCR for SARS-CoV2 was not performed as it was 10-11 weeks after his acute illness. Nerve conduction studies showed absent F waves, prolonged distal latencies, and slowed conduction velocities. His routine blood tests were normal, LDH- 311 U/L (125–220, ferritin 88 ng/ml (18.7–323), and serology was non-reactive for HIV, Hepatitis B and C viruses. He was diagnosed to have postinfectious GBS and treated with IVIg at 2 gm/Kg over 5 days along with intensive physiotherapy. Over the next 10 days, he worsened to MRC grade 2/5 power in all limbs with limb ataxia and areflexia. He also developed neck and truncal weakness. By day 19, he started improving [grade 3/5 power]. An MRI whole-body STIR muscle imaging was normal. Serum CPK levels were normal. An EMG on day 19 was essentially normal. On day 22, his serum ganglioside antibody panel testing by indirect ELISA were positive for IgG-Gd1b antibodies. His Anti-SARS-CoV2 antibodies [Roche™ Anti-SARS-CoV-2 assay using the double antigen sandwich (DAGS) format] were also highly reactive (60.3) {Biological reference interval > 1.0}, suggesting a post-COVID convalescent phase. This assay detects high-affinity IgM, IgA, and IgG antibodies which appear in the 2nd week of illness. It uses an electrochemiluminescence immunoassay analyzer (ECLIA) and is comparable to an EDI™ ELISA test.[5] By day 27, he was able to sit without support.

The incidence of neurological complications in COVID-19 approaches ~ 36% in large series [Figure 1].[6] Both cranial and peripheral neuropathies [including GBS and Miller Fisher syndrome] have been documented in the acute phase of COVID-19 illness.[7],[8] The neuromuscular complications are linked to direct neural invasion of the coronavirus, infective leptomeningitis or to para or postinfectious immune-mediated phenomena. Most reports of GBS in COVID-19 is documented with acute SARS-CoV2 infection. Most patients have presented in the acute phase of the illness with a mean period of ~ 11 days from the onset of acute viral illness.[9] In some patients, GBS alone without any other symptoms has been the presenting manifestation of COVID-19. COVID-GBS cases were similar to non-COVID-19 GBS, showing a demyelinating pattern on electrophysiological studies, albumino-cytologic dissociation in the CSF and negative for SARS-CoV-2 RT-PCR on CSF.[10] Tested sera were negative for serum anti-ganglioside antibodies in most patients. Like our patient, a few cases showed serum anti-GD1b ganglioside antibodies with Miller–Fisher syndrome.
Figure 1: Shows the clinical picture of COVID-19 infection and the course of our patient correlated with the week of illness

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Most reports have shown a consistent response to intravenous immunoglobulin or plasma exchange with improvement within 8 weeks in the majority. The vast majority of reports of GBS with COVID-19 have been para-infectious and post-infectious GBS is rare.[11],[12] As experts have predicted an uptick in post-infectious immune-mediated neurological complications after the peak of the pandemic, our report is noteworthy in its documentation of a post-COVID-19 GBS. To the best of our knowledge, this is the first report of a post-COVID-19 immune-mediated neurological disorder from India.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Maramattom BV, Bhattacharjee S. Neurological complications of Covid-19. A contemporaneous review. Ann Indian Acad Neurol 2020;23:468-76.  Back to cited text no. 1
  [Full text]  
Handa R, Nanda S, Prasad A, Anand R, Zutshi D, Dass SK, et al. Covid-19-associated acute haemorrhagic leukoencephalomyelitis. Neurol Sci. Neurol Sci 2020:1-4. doi: 10.1007/s10072-020-04703-z [Epub ahead of print]  Back to cited text no. 2
Ghosh R, Dubey S, Finsterer J, Chatterjee S, Ray BK. SARS-CoV-2-associated Acute hemorrhagic, necrotizing encephalitis (AHNE) presenting with cognitive impairment in a 44-year-old woman without comorbidities: A case report. Am J Case Rep 2020;21:e925641.  Back to cited text no. 3
Padroni M, Mastrangelo V, Asioli GM, Pavolucci L, Abu-Rumeileh S, Piscaglia MG, et al. Guillain-Barré syndrome following COVID-19: New infection, old complication? J Neurol 2020;267:1877-9.  Back to cited text no. 4
Egger M, Bundschuh C, Wiesinger K, Gabriel C, Clodi M, Mueller T, et al. Comparison of the Elecsys® Anti-SARS-CoV-2 immunoassay with the EDI™ enzyme linked immunosorbent assays for the detection of SARS-CoV-2 antibodies in human plasma. Clin Chim Acta. 2020;509:18-21.  Back to cited text no. 5
Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, et al. Neurologic manifestations of hospitalized patients with Coronavirus disease 2019 in Wuhan, China. JAMA Neurol 2020;77:1-9.  Back to cited text no. 6
Zhao H, Shen D, Zhou H, Liu J, Chen S. Guillain-Barré syndrome associated with SARS-CoV-2 infection: Causality or coincidence? Lancet Neurol 2020;19:383-4.  Back to cited text no. 7
Chan JL, Ebadi H, Sarna JR. Guillain-Barré syndrome with facial diplegia related to SARS-CoV-2 infection. Can J Neurol Sci 2020;29:1-3.  Back to cited text no. 8
Caress JB, Castoro RJ, Simmons Z, Scelsa SN, Lewis RA, Ahlawat A, et al. COVID-19-Associated Guillain-Barre syndrome: The early pandemic experience. Muscle Nerve 2020; 10.1002/mus 2020;62:485-491.  Back to cited text no. 9
Alberti P, Beretta S, Piatti M, Karantzoulis A, Piatti ML, Santoro P, et al. Guillain-Barré syndrome related to COVID-19 infection. Neurol Neuroimmunol Neuroinflamm 2020;7:e741.  Back to cited text no. 10
Toscano G, Palmerini F, Ravaglia S, Ruiz L, Invernizzi P, Cuzzoni MG, et al. Guillain–Barré syndrome associated with SARS-CoV-2. N Engl J Med 2020;382:2574-6.  Back to cited text no. 11
Virani A, Rabold E, Hanson T, Haag A, Elrufay R, Cheema T, et al. Guillain-Barré syndrome associated with SARS-CoV-2 infection. IDCases 2020;18;20:e00771.  Back to cited text no. 12


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