Multisystem inflammatory syndrome in children is a recently described complication in the late phase of Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infection involving systemic hyperinflammation and multiorgan dysfunction. The extent of its clinical picture is actively evolving and has yet to be fully elucidated. While neurologic manifestations of SARS-CoV-2 are well-described in the adult population, reports of neurologic complications in pediatric patients with SARS-CoV-2 infection are limited. We present a pediatric patient with SARS-CoV-2 infection with development of multisystem inflammatory syndrome and acute encephalopathy causing delirium who was found to have a cytotoxic lesion of the corpus callosum on neuroimaging. Cytotoxic lesions of the corpus callosum are a well-known, typically reversible entity that can occur in a wide range of conditions, including infection, seizure, toxins, nutritional deficiencies, and Kawasaki disease. We hypothesized that the cytotoxic lesion of the corpus callosum, in the index case, was secondary to the systemic inflammation from SARS-CoV-2 infection, resulting in multisystem inflammatory syndrome in children. ABBREVIATIONS: CLOCC ¼ cytotoxic lesion of the corpus callosum; COVID-19 ¼ coronavirus disease 2019; IVIG ¼ intravenous immunoglobulin; MIS-C ¼ multisystem inflammatory syndrome in children; PCR ¼ polymerase chain reaction; SARS-CoV-2 ¼ Severe Acute Respiratory Syndrome coronavirus 2 S evere Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infection in the pediatric population is not wellunderstood and has, until recently, been thought of as a relatively mild disease compared with that in adults. Most reported symptoms in children are fever, respiratory tract infection, or asymptomatic infection. 1 More recent reports in the pediatric population, however, describe a multisystem inflammatory syndrome in children (MIS-C). 2-6 In the adult population, neurologic manifestations of coronavirus disease 2019 (COVID-19) are being reported with increasing frequency, including seizure, Guillain-Barré syndrome, vasculitis, stroke, cranial nerve palsy, and general encephalopathy. 7-11 Cases of neurologic manifestations in pediatric patients have been limited. We report the case of a pediatric patient positive for COVID-19 who presented with fever, vomiting, diarrhea, cough, difficulty walking, and delirium.

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In Plasmodium vivax malaria, mechanisms that trigger transition from uncomplicated to fatal severe infections are obscure. In this multi-disciplinary study we have performed a comprehensive analysis of clinicopathological parameters and serum proteome profiles of vivax malaria patients with different severity levels of infection to investigate pathogenesis of severe malaria and identify surrogate markers of severity. Clinicopathological analysis and proteomics profiling has provided evidences for the modulation of diverse physiological pathways including oxidative stress, cytoskeletal regulation, lipid metabolism and complement cascades in severe malaria. Strikingly, unlike severe falciparum malaria the blood coagulation cascade was not found to be affected adversely in acute P. vivax infection. To the best of our knowledge, this is the first comprehensive proteomics study, which identified some possible cues for severe P. vivax infection. Our results suggest that Superoxide dismutase, Vitronectin, Titin, Apolipoprotein E, Serum amyloid A, and Haptoglobin are potential predictive markers for malaria severity.

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Background: Motor unit number index (MUNIX) is a validated electrophysiological biomarker in amyotrophic lateral sclerosis. MUNIX studies in spinal muscular atrophy (SMA) are limited. Methods: Later-onset SMA children (n = 13; three SMN2 copy number) were evaluated for Hammersmith Motor Function Scale Expanded (HMFSE) and MUNIX of right abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles. Agematched healthy controls (n = 8) were enrolled to obtain normative APB and ADM MUNIX values. Results: Mean APB and ADM MUNIX values in SMA subjects were significantly reduced (P < .001) compared with controls. HMFSE scores strongly correlated with ADM MUNIX (r 0.63). Conclusions: APB and ADM muscle MUNIX studies are feasible in SMA type 2 children. ADM MUNIX correlated with disease severity on motor function testing.

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Objective. Lipodystrophy is a recently recognized complication of juvenile dermatomyositis (juvenile DM). Until now, the diagnosis has been based only on the physical appearance of the patient. We quantified the patterns of fat distribution in a cohort of patients with juvenile DM. Methods. Twenty patients with juvenile DM were enrolled along with a matching number of controls. Both groups underwent standard anthropometric measurements including assessment of skinfold thickness using Harpenden Skinfold Caliper (Holtain, Dyfed, UK). Glucose tolerance test and serum lipid estimates were performed in the study group but not in controls. Results. Patients with juvenile DM had lower mean weight, height, and mid-upper-arm circumference as compared with controls; these differences were statistically significant (P < 0.05). Eight (40%) of 20 patients had lipodystrophy on physical appearance. When assessed by skinfold caliper, there was loss of subcutaneous fat at the mid-axillary site in 65% of patients, at the subscapular in 60%, and at the suprailiac site in 55%. Serum triglyceride levels were increased in 12 of the 18 patients who underwent this test. Oral glucose tolerance test results were normal in all 20 patients. Conclusion. Sixty-five percent of our patients with juvenile DM were found to have loss of subcutaneous fat on quantification compared with 40% on physical appearance alone. Maximum fat loss occurred at the mid-axillary skinfold site. A significant number of patients with juvenile DM (66%) had hypertriglyceridemia. We hypothesize that lipodystrophy and hypertriglyceridemia could well be integral components of what may be an expanded juvenile DM syndrome.