Author response: Encephalopathy and bilateral thalamic lesions in a child with MIS-C associated with COVID-19
Dori N.Abel, Pediatric Resident Physician, Columbia University Irving Medical Center, Department of Pediatrics; NewYork-Presbyterian Hospital
Submitted November 04, 2020
I thank Calixto Machado for his comments on my publication.1 They provide great insight into the possible etiology of our patient's imaging findings and reversible encephalopathy. We agree with him that our patient's presentation may represent acute hemorrhagic necrotizing encephalopathy with MRI findings, possibly suggestive of cytotoxic edema.2
Whether it was indeed the hyper-inflammatory state that led to abandonment of mitochondrial oxidative phosphorylation,3 with inflammation-targeted treatment our patient fortunately recovered this metabolic pathway and clinically improved.
Further studies are warranted to test these hypotheses. We also suggest that phenotypic heterogeneity may be seen with other premorbid conditions. Our patient had no underlying medical conditions and , therefore, a positive outcome; it is possible, however, that other premorbidities could have worsened outcomes.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Abel D, Ye Shen M, Abid Z, et al. Encephalopathy and bilateral thalamic lesions in a child with MIS-C associated with COVID-19. Neurology 2020;95:745–748.
Harada M, Hisaoka S, Mori K, et al. Differences in water diffusion and lactate production in two different types of postinfectious encephalopathy. J Magn Reson Imaging 2000;11:559–563.
Reiter RJ, Sharma R, Ma Q, et al. Melatonin Inhibits COVID-19-induced Cytokine Storm by Reversing Aerobic Glycolysis in Immune Cells: A Mechanistic Analysis. Med Drug Discov Epub 2020 May 11.
I thank Calixto Machado for his comments on my publication.1 They provide great insight into the possible etiology of our patient's imaging findings and reversible encephalopathy. We agree with him that our patient's presentation may represent acute hemorrhagic necrotizing encephalopathy with MRI findings, possibly suggestive of cytotoxic edema.2
Whether it was indeed the hyper-inflammatory state that led to abandonment of mitochondrial oxidative phosphorylation,3 with inflammation-targeted treatment our patient fortunately recovered this metabolic pathway and clinically improved.
Further studies are warranted to test these hypotheses. We also suggest that phenotypic heterogeneity may be seen with other premorbid conditions. Our patient had no underlying medical conditions and , therefore, a positive outcome; it is possible, however, that other premorbidities could have worsened outcomes.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References