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Concurrent Longitudinally Extensive Transverse Myelitis and Guillain-Barré Syndrome in a Child Secondary to COVID-19 Infection

A Severe Neuroimmunologic Complication of COVID-19

Khera, Daisy MBBS, MD*; Didel, Siyaram MBBS, MD*; Panda, Samhita MD, DM; Tiwari, Sarbesh MD, DM; Singh, Kuldeep MD, DM*

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The Pediatric Infectious Disease Journal: June 2021 - Volume 40 - Issue 6 - p e236-e239
doi: 10.1097/INF.0000000000003124
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Common manifestations of coronavirus disease 2019 (COVID-19) infection are related to respiratory tract involvement. COVID-19 infection also can present with many atypical neurologic manifestations like febrile encephalopathy, meningoencephalitis like illness, Guillain-Barré syndrome (GBS) and acute cerebrovascular disease.1 However, no literature is available regarding concomitant GBS and longitudinally extensive transverse myelitis (LETM) in a child with COVID-19 infection.


An 11-year-old previously healthy girl presented to outside hospital with acute onset severe flaccid paralysis. She also had associated history of fever without any other viral prodrome. The weakness gradually worsened with ascending pattern of weakness for next 2 days and she developed respiratory failure on the third day of illness, requiring artificial respiratory support. She also developed bowel and bladder incontinence on day 3 of illness. There was no history of cough, cold, vomiting, loose stool, neck pain, ear discharge, sore throat, pain abdomen or any rash; no history of any unknown bite, trauma, altered sensorium, any bleeding manifestation, recent vaccination or any other injection and no history of speech abnormality, abnormal movements, headache, anosmia and parasomnia. Her past and family history was noncontributory. She was treated in another hospital in an intensive care unit with immunoglobulins and steroid along with ventilatory support for 3 days. In view of no improvement, child was referred to our center for further management with clinical diagnosis of transverse myelitis (TM).

At presentation to our center, she was on manual respiratory support with bag and tube. Her pulse rate was 110/min, blood pressure was 110/80 mm Hg, oxygen saturation was 99% on bag and tube ventilation. She was conscious and following verbal commands. Anthropometry was normal for her age and pupils were bilaterally equal and reactive to light. On neurologic examination, she had normal cranial nerve examination and hypotonia in all four limbs, bilateral upper limb power was 4/5 and bilateral lower limb power was 0/5 along with no bowel and bladder sensation. Her reflexes were elicitable in biceps (2+), triceps (2+), supinator (1+) and absent in ankle, knee and other superficial reflexes and plantar was mute. Meningeal signs were absent, and other systemic examination was within normal limits. Our initial clinical diagnosis of acute flaccid paralysis secondary to TM, acute demyelinating encephalomyelitis and GBS was considered, and child was shifted to pediatric intensive care unit for further management. In view of history of fever and COVID-19 pandemic, her COVID-19 reverse-transcription polymerase chain reaction was sent, which was reported negative twice, but her serology for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) antibodies (total IgG and IgM) was positive (Table 1). Magnetic resonance imaging brain revealed focal subcortical fluid-attenuated inversion recovery hyperintense lesions at right parietal subcortical white matter with diffusion restriction. Imaging of spine showed long segment intramedullary T2 hyperintense signal in the lower dorsal cord extending from D7 to D10 vertebra level without enhancement. Contrast study demonstrated thickening and smooth enhancement of cauda equina nerve roots (Fig. 1). The imaging features suggestive of acute lesion in brain along with cauda equina nerve roots enhancement without clinical encephalopathy raised a possibility of GBS along with LETM. Her work up for other neuropathic viruses, serum antiaquaporin-4 antibody also called neuromyelitis optica antibodies and serum myelin oligodendrocyte glycoprotein were negative. Her nerve conduction study was reported as motor axonal polyradiculopathy involving predominantly peroneal more than tibial nerve. She partially responded to intravenous pulse methylprednisolone and intravenous immunoglobulin treatment in the form of mild improvement in the power of all four limbs, but we were unable to take her off respiratory support; hence, she was treated with five sessions of plasma-exchange therapy. She gradually improved after 2 weeks of hospitalization and was successfully extubated. Her follow-up imaging after 6 weeks of onset of illness showed significant resolution of magnetic resonance imaging signal changes in brain and spine and complete disappearance of cauda equina nerve root enhancement (Fig. 2). Her motor power improved and she is able to walk independently with good bowel and bladder control and no neurologic deficit.

TABLE 1. - Investigations
Investigation Day 1 of Admission D9 D12
Hb (11.5–14 gm/dL) 10.3 8.6 11.5
TLC (4000–1,1000/mm3) 8800 10,510 14,440
DLC—N/L (22–55/15–45%) 68/25.9 82.7/15/1 72/21.5
Platelet (1.5–4.5 lakhs) 533,000 94,000 399,000
PT (s)/INR 12.5/0.95
Procalcitonin (<0.05 ng/mL) 0.06
hsCRP (< 1 mg/dL) 3.5 2.6
Calcium (9–11 mg/dL) 7.7 9.1
SGOT (9–24 U/L) 20
SGPT (13–45 U/L) 24
ALP (150–420 U/L) 40
Serum total protein/serum albumin 8.9/3.5
Urea (5–18 mg/dL) 35
Creatinine (0.2–0.6 mg/dL) 0.58
Sodium (130–145 mEq/L) 120 130 137
Potassium (3.5–5 mEq/L) 5.1 4.38 4.28
CSF Sugar—70 (gm/dL), WBC-6, RBC-6 Protein—380 (gm/dL) C/S, G/S—negative
Antinuclear antigen (< 1.5) Negative
Multiple sclerosis panel – IgG serum/IgG CSF 2310/112 mg/dL
Oligoclonal bands Not seen in CSF or serum
COVID-19 serology (IgG + IgM) 2.2 (< 1.0) positive
Adenovirus (qualitative PCR) Not detected
Enteroviruses (qualitative PCR) Not detected
Epstein-Barr virus (qualitative PCR) Not detected
HHV7 (qualitative PCR) Not detected
HHV6 (qualitative PCR) Not detected
Human parechovirus (qualitative PCR) Not detected
Parvovirus B19 (qualitative PCR) Not detected
VZV (qualitative PCR) Not detected
CMV (qualitative PCR) Not detected
HSV-1 (qualitative PCR) Not detected
HSV-2 (qualitative PCR) Not detected
ALP indicates alkaline phosphatase; CMV, cytomegalovirus; C/S, culture sensitivity; CSF, cerebrospinal fluid; DLC, differential leukocyte count; G/S, Gram stain; Hb, hemoglobin; HHV, human herpes virus; hsCRP, high-sensitivity C-reactive protein; HSV, human herpes simplex virus; N/L, neutrophil/lymphocyte count; PT/INR, prothrombin time/international normalized ratio; RBC, red blood cell; RT-PCR, reverse-transcription polymerase chain reaction; SGOT, serum glutamic oxaloacetic transaminase; SGPT, serum glutamic pyruvic transaminase; TLC, total leucocyte count; VZV, varicella zoster virus; WBC, white blood cell.

The sagittal T2 image (A) shows abnormal hyperintense signal of the lower dorsal cord extending from D7 to D10 vertebra levels without any cord expansion. The postcontrast T1FS sagittal (B) and axial (F) images of the dorsal spine show enhancement of the cauda equina nerve roots without enhancement of the lower dorsal cord. The MRI of the brain with axial FLAIR (C) and diffusion images (D) shows focal subcortical hyperintense lesions with restricted diffusion at right parietal white matter without any perilesional edema. No abnormal postcontrast enhancement was demonstrated (E). FLAIR indicates fluid-attenuated inversion recovery; MRI, magnetic resonance imaging; T1FS, T1-weighted fat saturation.
Follow-up imaging done after 6 weeks of initial presentation. The sagittal T2 image (A) shows significant reduction in the cord hyperintense signal with residual hyperintensity at only D10 vertebra level. The postcontrast T1FS sagittal (B) and axial (E) images of the dorsal spine show complete resolution of the enhancement of cauda equina nerve roots. The MRI of the brain with axial FLAIR (C) and diffusion images (D) shows significant resolution of the right parietal white matter lesions. FLAIR indicates fluid-attenuated inversion recovery; MRI, magnetic resonance imaging; T1FS, T1-weighted fat saturation.


The clinical spectrum of COVID-19 in children is still evolving. As per evidence available until now, it mostly remains asymptomatic, but at times can lead to critical illness, leading to morbidity and mortality in children. Many specific manifestations in children were reported as part of overwhelming activation of proinflammatory systems with cytokine storm such as Kawasaki like illness or cutaneous manifestations similar to hand-foot-mouth disease. More severe hyperinflammatory manifestations associated with COVID-19 infection in children include Pediatric Multisystem Inflammatory Syndrome, a close mimicker of Kawasaki disease leading to multiorgan failure.2 This cytokine storm leads to excessive coagulability, multiorgan failure and death in children.3 Many respiratory viruses have neuroinvasive properties and activate the immune response in the brain. They can be directly cytotoxic or cytopathic and can lead to neurologic manifestations. The immunologic event following viral invasion of central nervous system (CNS) may act as neuroprotective mechanism or can lead to acute life-threatening conditions like acute demyelinating encephalopathy, acute TM and GBS-like illness along with other long-term neurodegenerative sequelae.4 A literature review of 765 COVID-19 cases by Yachou et al4 showed that various neurologic manifestations and complications associated with COVID-19 infection were present in 18% cases. These included most common symptoms related to olfactory system affection like anosmia, either partial or complete along with uncommon severe complications like GBS, TM, cerebrovascular accidents, encephalitis, acute myelitis and LETM.4–8 Koyuncu et al9 elaborated various factors pertaining to virus (mutation increasing virulence) or host (immunocompromised or associated comorbidity) responsible for CNS involvement by various viruses. Although many adult cases are reported with various neurologic manifestations of COVID-19 including GBS and/or LETM, pediatric cases reported with GBS or LETM are scarce.6–8,10,11 A recent multicenter collaborative study on neuroimaging manifestations in children with SARS-CoV-2 infection showed cauda equina nerve root enhancement in 21% of cases and most of these patients presented with GBS-like neurologic features.12,13

This is the first pediatric case that reports the concurrent occurrence of GBS with LETM secondary to COVID-19 infection. This case report will increase awareness in pediatric fraternity regarding CNS manifestation of SARS-CoV2 infection.


SARS-CoV-2 needs to be considered in the differential diagnosis of every febrile case with CNS manifestations in the current era of COVID-19 pandemic for timely appropriate treatment and optimal outcome.


1. Ellul MA, Benjamin L, Singh B, et al. Neurological associations of COVID-19. Lancet Neurol. 2020;19:767–783.
2. Ahmed M, Advani S, Moreira A, et al. Multisystem inflammatory syndrome in children: a systematic review. EClinicalMedicine. 2020;26:100527.
3. Jose RJ, Manuel A. COVID-19 cytokine storm: the interplay between inflammation and coagulation. Lancet Respir Med. 2020;8:e46–e47.
4. Yachou Y, El Idrissi A, Belapasov V, et al. Neuroinvasion, neurotropic, and neuroinflammatory events of SARS-CoV-2: understanding the neurological manifestations in COVID-19 patients. Neurol Sci. 2020;41:2657–2669.
5. Koh JS, De Silva DA, Quek AML, et al. Neurology of COVID-19 in Singapore. J Neurol Sci. 2020;418:117118.
6. Baghbanian SM, Namazi F. Post COVID-19 longitudinally extensive transverse myelitis (LETM)-a case report [published online ahead of print September 18, 2020]. Acta Neurol Belg. 2020:1–2.doi:10.1007/s13760-020-01497-x.
7. Fumery T, Baudar C, Ossemann M, et al. Longitudinally extensive transverse myelitis following acute COVID-19 infection. Mult Scler Relat Disord. 2020;48:102723.
8. Krupp LB, Tardieu M, Amato MP, et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler. 2013;19:1261–1267.
9. Koyuncu OO, Hogue IB, Enquist LW. Virus infections in the nervous system. Cell Host Microbe. 2013;13:379–393.
10. Sedaghat Z, Karimi N. Guillain Barre syndrome associated with COVID-19 infection: a case report. J Clin Neurosci. 2020;76:233–235.
11. Katal S, Balakrishnan S, Ghola A. Neuroimaging and neurologic findings in COVID-19 and other coronavirus infections: a systematic review in 116 patients. J Neuroradiol. 2021;48:43–50.
12. Lindan CE, Mankad K, Ram D, et al. Neuroimaging manifestations in children with SARS-CoV-2 infection: a multinational, multicentre collaborative study. Lancet Child Adolesc Health. 2021;5:167–177.
13. Abdi S, Ghorbani A, Fatehi F. The association of SARS-CoV-2 infection and acute disseminated encephalomyelitis without prominent clinical pulmonary symptoms. J Neurol Sci. 2020;416:117001.

COVID-19; children; Guillain-Barré syndrome; longitudinally extensive transverse myelitis

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