To the Editor: We would like to respond to Josef Finsterer’s comments [1] on our article. We would like to specify that the overall observation of our patient did not exceed 12 h, and that made the exploration limited [2]. The infant presented with seizure with generalized tonic spasm lasting a few seconds, and he had hemodynamic instability and hypothermia at 33.5 degrees. As a consequence, he required emergent intubation. Antibiotic and antiviral therapies were started empirically as well as analgosedation with morphine and midazolam. His laboratory tests showed negative C-reactive protein, metabolic acidosis, and functional acute kidney failure, which prevented the use of contrast in the CCT. As pointed out by Finsterer, the interpretation of multifocal hypodensities may represent embolic cerebral infarction [2], but acute infarcts may also be an expression of cerebral invasion of SARS-CoV-2. Multiple strategies (immunohistochemistry, in situ hybridization, targeted quantitative reverse transcriptase–PCR, and transmission electron microscopy) were employed to assess the presence of Coronavirus in the brain tissue, but the results were almost negative with all the techniques [3]. An immune-mediated process generally spares the brainstem. We completely agree that this diagnosis is not exclusively based on these radiological findings, but the postmortem lumbar puncture was consistent with it. There was no pleocytosis, and the RBC count was 400/mm3. Normal glucorachia and hyperproteinorachia were in favor of encephalitis too. The CSF culture was negative. Investigation for cytokines and chemokines were not available in the laboratory at that time. The infant remained unconscious, with fixed and dilated pupils and a lack of bulbar reflexes. The hemodynamic state was worsening, requiring high doses of epinephrine. Since the infant’s condition deteriorated further, it was not possible to complete the MRI or use steroids. The infant’s parents refused the autopsy.
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References
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