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 pleocytosis. He was diagnosed with GBS associated with SARS‐CoV‐2 infection. The nerve conduction study was suggestive of acute motor axonal neuropathy. Ten consecutive therapeutic plasma exchange sessions with 5% albumin replacement followed by four sessions on alternate days were performed. On Day 12, methylprednisolone (30 mg/kg/day for 5 days) was given. On Day 18, intravenous immunoglobulin (2 g/kg/day) was given and repeated 14 days after due to severe motor weakness. On Day 60, he was discharged from the hospital with weakness of neck flexor and extensor muscles of 3/5 and the upper limbs and the lower limbs of 2/5 on home‐ventilation. Our patient is considered to be the youngest patient presenting with a possible para‐infectious association between axonal GBS and SARS‐CoV‐2 infection. The disease course was severe with a rapid progression, an earlier peak, and prolonged duration in weakness as expected in axonal GBS.

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.

Background: Coronavirus disease 2019 may have neurological manifestations including meningitis, encephalitis, post-infectious brainstem encephalitis and Guillain-Barre syndrome. Neuroinflammation has been claimed as a possible cause. Here, we present a child with multisystem inflammatory syndrome in children (MIS-C) who developed pseudotumor cerebri syndrome (PTCS) during the disease course. Case: A 11-year-old girl presented with 5 days of fever, headache and developed disturbance of consciousness, respiratory distress, conjunctivitis and diffuse rash on her trunk. Immunoglobulin M and G antibodies against severe acute respiratory syndrome coronavirus 2 were positive in her serum. She was diagnosed with MIS-C. On day 10, she developed headache and diplopia. Left abducens paralysis and bilateral grade 3 papilledema were observed. Brain magnetic resonance imaging revealed optic nerve head protrusion, globe flattening. She was diagnosed with secondary PTCS. Papilledema and abducens paralysis improved under acetazolamide and topiramate. Neurological examination became normal after 2 months. Conclusion: PTCS may emerge related to MIS-C.