The relation between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and demyelinating Guillain-Barre syndrome (GBS) has been defined. We aim to report the clinical features of a child with axonal GBS associated with SARS-CoV-2. A 6-year-old male presented with symmetric ascending paralysis progressed over a 4-day course and 2 days of fever. He had bilateral lower and upper limb flaccid weakness of 1/5 with absent deep tendon reflexes. He had severe respiratory muscle weakness requiring invasive mechanical ventilation. On admission, SARS-CoV-2 returned as positive by real-time polymerase chain reaction on a nasopharyngeal swab. Cerebrospinal fluid analysis showed elevated protein without

Background: The coronavirus disease 2019 pandemic was caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the predominant clinical presentation is a respiratory disease, neurologic manifestations are being recognized increasingly. Case Report: We report 2 children 9 years of age who developed acute disseminated encephalomyelitis-like disease associated with SARS-CoV-2. Seizures and encephalopathy were the main central nervous system symptoms. The cerebrospinal fluid analysis performed within the first week of disease onset showed elevated protein in both children with normal cell count and no evidence of infection including negative SARS-CoV-2 by antibody and polymerase chain reaction. Brain magnetic resonance imaging revealed T2A, fluid-attenuated inversion recovery cortical and subcortical hyperintensity without restricted diffusion consistent with acute disseminated encephalomyelitis–like disease. They received methylprednisolone followed by therapeutic plasma exchange. One of them showed complete clinical improvement and resolution in magnetic resonance imaging findings. The other developed laminar necrosis in brain magnetic resonance imaging and showed significant clinical improvement after therapeutic plasma exchange. He was positive for positive SARS-CoV-2 antibody in cerebrospinal fluid on day 55 of admission. They were both positive for SARS-CoV-2 antibodies in serum after 2 weeks. Conclusions: Our two cases highlight the occurrence of acute disseminated encephalomyelitis–like disease as a postinfectious/immune-mediated complication of SARS-CoV-2 infection.

Background: Coronavirus disease-2019 (COVID-19) is characterized predominantly by respiratory symptoms and has affected a small subset of children. Multisystem inflammatory syndrome in children (MIS-C) has been reported in children following COVID-19. There is increasing report that COVID-19 may also lead to neurologic manifestations. Cerebellar lesions may be observed in viral infections. Case report: We report a child with MIS-C related to severe acute respiratory syndrome coronavirus 2, who developed cerebellar lesion during the disease course. Encephalopathy was the first central nervous system symptom. His consciousness improved but he developed clinical signs of cerebellar dysfunction including ataxia, dysarthria and nystagmus. Brain magnetic resonance imaging (MRI) revealed symmetrical pathological signal changes in both cerebellar hemispheres. Conclusion: We demonstrated the first child with MIS-C to develop cerebellar lesion on brain MRI, suggestive of cerebellitis.

Prevalence and risk factors of neurologic manifestations in hospitalized children diagnosed with acute SARS-CoV-2 or MIS-C.