We appreciate the comments by Kumar et al. on our article.1 The referenced Kremer study2 was a retrospective case series and included patients with positive MRI findings only. It is unclear whether the patients with the diagnosis of “encephalitis” met diagnostic or causal criteria outlined by the International Encephalitis Consortium3 and others.4 Indeed, CSF SARS-CoV-2 RT-PCR was negative in 20 patients. In 2 of 3 with CSF pleocytosis (>5 cell/mm3), imaging was performed >2 weeks from symptom onset, possibly representing postinfectious autoimmune encephalitis and not infectious encephalitis. Many of the MRI findings described are nonspecific and can be seen in hypoxic/ischemic brain injury, metabolic encephalopathy, or postseizure. Notably, 100% of “encephalitis” patients required oxygen and 75% had ARDS, suggesting that a proportion of the MRI changes may represent hypoxic/ischemic injury (defined as a global insult due to hypoxemia, hypotension, or cardiac arrest). Although we detected elevated CSF protein in some patients,1 this is nonspecific and can be found in stroke, hemorrhage (or traumatic tap), hypoxic/ischemic injury, diabetes, uremia, tumor, neuropathy, and many other conditions. Because the implications of SARS-CoV-2 neurotropism are far reaching, we believe that it is critical to follow the most rigorous standards and criteria when ascribing encephalitis/meningitis/myelitis to SARS-CoV-2 infection.