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 Table of Contents  
Year : 2022  |  Volume : 15  |  Issue : 2  |  Page : 168-172

COVID-19-associated Guillain–Barre syndrome: A case series with review of literature

Department of Medicine, S P Medical College, Bikaner, Rajathan, India

Date of Submission29-Dec-2021
Date of Acceptance22-Jan-2022
Date of Web Publication24-May-2022

Correspondence Address:
Dr Harish Kumar
B-3 Shastri Nagar, Bikaner - 334 001, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/kleuhsj.kleuhsj_407_21

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Globally, millions of people are rapidly infected with COVID-19 and it has spread worldwide from January 2020 to till date. Coronavirus mostly affects the respiratory system; it can also result in several multisystem complications. This is a case series of four patients admitted in the department of medicine with post-COVID-19 Guillain–Barre syndrome (GBS). SARS-CoV-2 mainly affects the respiratory system but multiple organ damage is being reported recently, neurologic damage is one of them. SARS-CoV-2 causes neurologic damage including, by direct attack the nervous system through angiotensin-converting enzyme receptor, secondary to an immune reaction against SARS-CoV-2, retrograde transport, cytokine, and hypoxia-related injury. However, pathogenesis is not fully understood. It is hypothesized that the cause of GBS in covid patients is due to immune-mediated. It is hypothesized that inflammatory cytokines may play a role in an immune-mediated neuropathy. In this era of pandemic, we are concern about the involvement of respiratory and gastrointestinal systems only, involvement of other systems is underestimated. It is very important to be aware of association of GBS with COVID-19. Although neurological involvement in COVID-19 is rare, early diagnosis and treatment can reduce morbidity and mortality. We should always think about COVID-19 infection in a patients presented with GBS after respiratory or gastrointestinal involvement.

Keywords: COVID, Guillain–Barre syndrome, immune, nerve, reflex

How to cite this article:
Kumar H, Kumar S, Mali M. COVID-19-associated Guillain–Barre syndrome: A case series with review of literature. Indian J Health Sci Biomed Res 2022;15:168-72

How to cite this URL:
Kumar H, Kumar S, Mali M. COVID-19-associated Guillain–Barre syndrome: A case series with review of literature. Indian J Health Sci Biomed Res [serial online] 2022 [cited 2022 Jul 2];15:168-72. Available from: https://www.ijournalhs.org/text.asp?2022/15/2/168/345833

  Introduction Top

On the recent research basis or repotted cases on the SARS-CoV-2, it is rapidly seen that the virus not only affect the repertory system (COVID-19) but also damage all the organs as well, particularly the heart, the central nervous system and peripheral nervous system (PNS), the gastrointestinal system, and the renal system.[1],[2],[3] Although it primarily involves the respiratory tract and lung with mild cough to severe ARDS, neurological manifestations associated with SARS-CoV-2 infection ranged from a simple headache, seizure, and dizziness to a more severe presentation such as stroke or encephalitis.[4]

The most common peripheral nervous system disorder is Guillain–Barre syndrome (GBS) included its subtype such as acute inflammatory demyelinating polyradiculoneuropathy.[5] GBS is an acute immune-mediated demyelinating polyneuropathy affect primarily the peripheral nervous system and nerve roots usually after upper repertory tract infection or gastrointestinal infection. It is manifested with the acute progressive ascending polyradiculoneuropathy with diminished or absent deep-tendon reflexes. Patients may be involve cranial nerves, sensory, or autonomic system.[6] Different cases and studies have been reported in the literature worldwide suggested that an association between SARS-CoV-2 infection and the development of GBS.[7],[8],[9] In the present case study, we report the four cases of COVID-19 who were admitted in the department of medicine with features suggestive of GBS.

  Case Series Top

Case 1

A 35-year-old male was vaccinated first dose on May 1, 2021, after 6–7 days of vaccination, he developed fever, sore throat, and generalized weakness for this patient was investigated for COVID-19 reverse transcription–polymerase chain reaction (RT-PCR) on May 8, 2021, which was positive. There was no breathlessness, cough and saturation were normal on room air at the time of COVID-19. The patient was completely recovered from mild COVID-19. After 10 days, on May 18, 2021, the patient was admitted with complain of tingling and numbness in bilateral lower limbs which was progressed to weakness and involve both lower and upper limbs. There was no history suggestive of cranial nerve, bowel, or bladder involvement. Cranial nerve examination was normal. Motor examination revealed generalized hypotonia, Grade 1/5 power in both lower limbs proximally and Grade 1/5 distally, while both upper limbs power was grade 1/5 proximally and grade 1/5 distally as per the Medical Research Council (MRC) grading. Deep-tendon reflexes were universally absent, and the plantar response was mute. Sensory examination was normal. His single-breath count was 8. Saturation was being dropped to 80% after 2 days. The patient was intubated and put him on ventilator support with continuous positive airway pressure mode. The patient was conscious, cooperative and well oriented to time, place, and person. His routine blood investigations including complete blood count, liver, and kidney function tests were normal. Serum Vitamin B12 levels and thyroid function tests were normal, COVID-19 testing was positive by nasopharyngeal swab RTPCR. Inflammatory markers were universally elevated. Chest X-ray was normal. Contrast-enhanced magnetic resonance imaging (MRI) of the spine was done after improving the patient which was normal in study. Nerve conduction study (NCS) of both upper and lower limbs was suggestive of pure motor axonal polyneuropathy.

The patient was provisionally diagnosed with GBS on the basis of history and clinical examination. Albuminocytological differentiation was present in cerebrospinal fluid (CSF). The patient was started on intravenous immunoglobulin (IVIG): 0.4 g/kg body weight per day for 5 days. Saturation was improved after complete dose of IVIG and extubated the patient on May 29, 2021. After extubation, the patient maintains saturation on 2 liters of oxygen for 2 days. There was no further progression of his symptoms after starting IVIG, and the patient was discharged with normal saturation on room air after 22 days of hospital stay with Grade 2/5 power in both lower limbs and Grade 2/5 power in both upper limbs.

Case 2

A 43-year-male patient was admitted June 14, 2021, with a chief complaint of acute onset of weakness in bilateral lower limbs which was progressed to upper limbs and difficulty in swallowing and speech within 3 days. Recent history of vaccination was absent.

He has been diagnosed earlier with COVID-19 after developing cough, fever, and generalized body ache, with positive nasopharyngeal swab RT-PCR for SARS-CoV-2. Chest X-ray was normal. He had no neurological involvement or anosmia at that time. He was received azithromycin 500 mg once daily for 5 days, Vitamin C 1000 mg once daily for 2 weeks, and zinc acetate three times daily for 2 weeks at home isolation. After complete resolution of his symptoms, the patient became negative nasopharyngeal swab RT-PCR.

After 20 days of recovery from COVID-19, patients presented with the difficulty in walking which was progressive in nature and involve upper limbs with difficulty in swallowing and speech. Bladder and bowel were normal. Physical examination showed normal temperature of 37°C, blood pressure 110/80 mmHg, heart rate 78 beats/min, respiratory rate 18/min, and oxygen saturation of 99% on room air with no respiratory symptoms or signs. On neurological examination, the patient was alert, conscious, and oriented with normal higher mental functions. Cranial nerves assessment was normal. Motor examination showed normal tone, muscle power examination revealed weakness in four limbs with a MRC Scale of grade 3/5 in proximal muscles, Grade 3/5 in distal muscles of the upper extremities, Grade 2/5 in proximal muscles, and Grade 2/5 in distal muscles of the both lower extremities. Deep-tendon reflexes were absent, and the plantar response was flexor bilaterally. Sensory assessment showed normal.

Initial laboratory investigations were as follows: white blood cells (WBCs) count of 10.0 cells per microliter (neutrophils = 72.2% and lymphocytes = 20.4%), red blood cells of 3.72 million cells/mcL, and hemoglobin 12.9 g/dL, and platelet count is 420,000 platelets/mcL. Erythrocyte sedimentation rate of 11 mm/h and C-reactive protein was 5 mg/L. His international normalization ratio was 1.34, serum glucose 7.4 mmol/L, BUN 3.8 mmol/L, Cr 88 umol/L, alanine aminotransferase 40 U/L, potassium 4.5 mmol/L, sodium 138 mmol/L, and HbA1c was 6.1%. CSF analysis showed Cerebro- Spinal Fluid (CSF) analysis showed high protein, normal glucose levels, no WBCS, negative culture and sensitivity for bacterial infection. Neurophysiological study was performed and showed decreased velocity, decreased muscle action potential, and findings revealed with acute demyelinating motor and sensory polyneuropathy. MRI of the spine was normal. Our patient received 0.4 g/kg/day of IVIG for a duration of 5 days and he had marked improvement of his symptoms, and he could walk with unilateral support in the 5th day of infusion with no respiratory or autonomic manifestations on discharge. His follow-up after 15 days showed muscle power of Grade 5/5 with marked improvement, and he could walk without support.

Case 3

A 52-year-old female patient 3 weeks before this hospital admission has a history of fever, cough, and dyspnea with normal saturation on room air, for which nasopharyngeal swab was taken for COVID-19 RT-PCR. The test was positive, and the patient was diagnosed as mild COVID-19-positive pneumonitis category. There was ground-glass opacity in high-resolution computed tomography (CT) scan with COVID-19 score 6/25 and was treated with azithromycin, Vitamin C, zinc, and paracetamol for 5 days at home. She then had a new onset of pain, tingling, numbness, pins, and needles sensation in the bilateral lower limbs with mild weakness. These same symptoms then progressed to the upper extremity over the next 24 h with difficulty in walking. This progression triggered the patient for admission in the department of medicine. She had no history of pain in cervical region, headaches, loss of consciousness, changes in mental status, changes in vision and speech, difficulty swallowing, seizure, and symptoms of urine/bowel. Physical examination showed stable vital signs, and motor power was 3/5 in all four extremities, diminished deep-tendon reflexes in both upper and lower extremities, and a negative Babinski sign bilaterally.

Laboratory findings include a white cell count of 11.5 × 109/L, normal erythrocyte sedimentation rate, C-reactive protein, Vitamin B12 level, and thyroid hormone. A MRI scan of brain was normal and cervical spine with screening of rest of spine showed degenerative changes. Lumbar puncture was performed to rule out GBS. CSF revealed findings suggestive of albumin-cytologic disassociation with a white cell count of 4 cu/mm and protein count of 142 mg/dL. NCS show demyelinating feature. As the diagnosis of GBS became, the patient was given 2 mg/kg intravenous immunoglobulins for 5 days and power of the muscle was monitored. After starting of treatment, no signs of respiratory muscle weakness and power of lower limbs were improved with 4/5. After receiving this treatment, the patients symptoms improved significantly and she was discharged refer to physical medicine and rehabilitation department.

Case 4

A 38-year-old female, presented to the outpatient department with chief complaints of loose motion 3 weeks back which lasted for 5 days, followed by history of progressive lower limb weakness and 2-day history of tingling and numbness in bilateral upper limbs without weakness 4 days back before admission. The patient had the history of cough and sore throat without fever. We decide for COVID-19 RT-PCR tests which were negative. Then, we decide to do serology or antibody test of COVID-19 which was positive. Chest X-ray showed evidence of bilateral lower zone haziness, and high-resolution CT showed ground-glass opacity. This further favors the diagnosis of post-COVID-19 infections during symptoms of diarrhea. On examination, vital was stable, temperature 98.8°F with 99% SpO2 on room air. Neurological examination revealed power proximal 4/5, distal 4/5 as per MRC grading in lower limbs. Upper limb power was normal across all joints. The deep-tendon reflexes were absent in lower limbs and normal in upper limbs. Sensory examination was normal. Complete blood count, serum sodium and potassium, liver, and kidney function tests were normal. Serum vitamin B12 levels and thyroid function tests were normal. NCS was suggestive of pure motor demyelinating polyneuropathy in lower limbs. Contrast MRI of whole spine showed mild degenerative changes of the spine. CSF examination showed albumin-cytological dissociation. IVIG was given at 0.4 g/kg body weight/day for 5 days with other supportive treatment. Neurological improvement was observed over the next 5 days, and the patient was discharged after 10 days. At the time of discharge, the patient had 5/5 in lower limbs.

  Discussion Top

SARS-CoV-2 is an envelope, nonsegmented, single-stranded, positive-sense RNA virus which primarily affects the upper respiratory tract and lung. Although its primarily targets the respiratory system, however, nervous system involvements are not uncommon,[10] through direct damage by specific receptors, immune-mediated injury to nerves, cytokine induce damage, hypoxia, and retrograde transport along nerve fibers.[11] Many cases are reported of neurological damage by COVID-19 with manifestation of stroke, seizure but only few cases of GBS associated with it. Literature shows that it is not by direct attack of virus but due to immunological damage of the peripheral nerves. Most cases are preceded by respiratory and gastrointestinal infections. The prognosis is poor as compared to nonCOVID-19-associated GBS.[12]

In the present case series, three patients had a history of respiratory tract infection and one patient presented with gastrointestinal symptoms with the duration of 10 days to 30 days from the symptoms or COVID-19 RT-PCR positivity to diagnosis of GBS. One patient was preceded by gastrointestinal symptoms whose IgG antibody to COVID-19 was positive. Three of them presented with neurological deficits and had no respiratory features secondary to COVID-19, and these were all quite well with treatment. One patient presented with GBS after 10 days of complete recovery from the mild COVID-19 RT-PCR positive and normal X-ray along with neurological deficits continued to deteriorate and need to ventilator support. After starting treatment for GBS with IVIG, patients were improved and discharged on tracheostomy. Two patients were discharged with the full recovery, whereas two patients were with the neurological deficit. There was good response to IVIG, and no mortality was seen. Keddie et al.[12] showed that the number of reports about SC2-GBS (SARS-CoV-2-associated GBS) is increasing and that the outcome is worse compared to non-SC2-GBS. However, in our case series, the prognosis is good as compared to nonCOVID-19-associated GBS. It may be explained by hypothesis that post-COVID GBS could be due to immune-mediated autoantibodies or direct damage of peripheral nervous system.[13] Excellent response to IVIG thus favoring an immune-mediated pathogenesis may not by direct viral damage. The pathogenesis of GBS in secondary bacterial infection is due to cross-reactivity while it may not the reason in postviral GBS.[14] The pathogenesis post-COVID GBS is not completely understood. It may be due to post-COVID in pandemic or any other cause, we could not explained.

Although overall prevalence of GBS has decreased/increased, since the pandemic between March 2020 and till date in North West part of Rajasthan as compared to previous years 2015 to December 2019 is a matter of study. Decrease cases of GBS may be due to use of mask, hand sanitizers, strict lockdowns, or awareness of hygiene which leads to decrease cases of gastrointestinal cases. Those patients who are admitted with outbreak of pandemic bilateral pneumonitis ARDS being focused on survival of these patients so this leads to poor concern on COVID-19-associated GBS and work-up for neuropathy may be incomplete due to mild manifestations or due to occurrence during ICU stay. Keddie et al.[12] found the prevalence of GBS did not increase between March 2020 and May 2020 as compared to the years 2016–2019.

GBS is an acute, inflammatory demyelinating polyradiculopathy which is immune mediated after infection including Campylobacter jejuni, cytomegalovirus, Epstein–Barr, and Zika virus, and also reported with respiratory syndrome caused by coronavirus.[15],[16] In our case study, the patient developed the classical GBS phenotype, with cytological dissociation in CSF after testing positive for SARS-CoV-2.

In this study, we reported the patient showing progressive weakness of the bilateral lower limbs progressed to upper limbs with numbness, tingling 7–10 days after the resolution of fever, cough, or recovery from the mild COVID-19 positivity with normal chest X-ray or bilateral pneumonitis. The clinical features and the electrophysiological findings along with the presence of IgG to SARS-CoV-2 supported the diagnosis of post-COVID-19 GBS. Specifically, the neurophysiologic findings with level 2 diagnostic certainty for GBS according to the Brighton Criteria (consistent clinical features and supporting NCS, but not CSF).[17],[18] Active SARS-CoV-2 infection was excluded by a complete recovery of the typical antecedent symptoms, the absence of the viral genome in the nasopharyngeal swab, and negative chest radiography. Contribute to raise awareness of the possible association between GBS and SARS-CoV-2 infection. The underlying mechanism of injury could be an autoimmune reaction against peripheral nerve antigens.[19]

In the present study, all the patients had increase proinflammatory markers may be due to COVID-19 infection. These inflammatory mediators and cytokines may play a role in triggering an immune-mediated neuropathy.[20]

All our patients developed the features of GBS, after postrecovery of COVID-19 symptoms, which is similar with GBS that occurs after the infections.[21] All the patients had an excellent response to IVIG and were discharged within 10–15 days of starting treatment. Two patients were fully recovered, whereas two patients were discharged with neurological deficit. Mortality was not seen in this case series.

Declaration of patient consent

The authors declare that they have obtained consent from patients. Patients have given their consent for their images and other clinical information to be reported in the journal. Patients understand that their names will not be published and due efforts will be made to conceal their identity but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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