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.
Listeria species may cause life-threatening events including meningitis and invasive infection in newborns, pregnant women, older and immunodeficient people. The most common Listeria species that causes infection is L. monocytogenes. It is known that Listeria innocua has no pathogenicity. A 9-month-old baby had ventriculoperitoneal shunt and was treated with adrenocorticotropic hormone because of infantile spasms. He was brought to hospital with fever and vomiting. Upon physical examination, the patient seemed uncomfortable and had a temperature of 38.6°C. Laboratory results were as follows: hemoglobin, 6.7 g/dL; leukocyte count, 5420/mm(3) ; platelet count, 169,000/mm(3) ; and C-reactive protein, 100 mg/L (normal <5 mg/L). On analysis of cerebrospinal fluid (CSF), leukocyte count was 480/mm(3) , protein was 46 mg/dL and CSF glucose was 35 mg/dL. L. innocua was isolated in CSF culture. We describe this unusual case of ventriculoperitoneal shunt infection with L. innocua.
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