In Reply: We would like to thank Hickey and DiFazio for their interest in our manuscript.1 While we were aware of the numerous studies and case reports describing rotavirus-related central nervous system complications, we chose to limit the review to cases where rotavirus was identified in the cerebrospinal fluid (CSF). In this regard, we add 3 additional publications of children with rotavirus gastroenteritis and identification of rotavirus from the CSF by reverse transcriptase-polymerase chain reaction (RT-PCR). The first was reported from researchers in Australia2 describing 2 children 13 and 32 months of age with rotavirus gastroenteritis and neurologic complications of encephalopathy and encephalitis, respectively. The second from South Africa described 2 neonates with rotavirus infection; one child had apnea, but the other had no neurologic symptoms.3 The third report described a 9-year-old child with rotavirus gastroenteritis and generalized weakness that progressed to flaccid paralysis.4 A more complete discussion of central nervous system issues and rotavirus infection follows. The objectives of these studies fall into 3 major categories: (1) determining the proportion of children with central nervous system issues who have rotavirus infection,5–10 (2) determining the proportion of children with gastroenteritis and seizures who have rotavirus infection,11–13 and (3) determining the proportion of rotavirus infected children with CNS manifestations.14–22 In the studies examining the role of rotavirus in CNS disorders, 8.6% of children with non–polio acute flaccid paralysis,5 1.9% to 23.5% with hemorrhagic shock encephalopathy,6,7 1.1% to 2.1% of children with encephalitis,8,9 and 1.3% of children with febrile seizures10 had rotavirus detected in their stool. In the studies of children with gastroenteritis and afebrile seizures, 46% to 63.7% were found to have rotavirus infection.11–13 In the studies examining the proportion of children with rotavirus disease who develop CNS manisfestations the prevalence of any type of seizure was 2.0% to 20.3%;14–17,19–22 afebrile seizures developed in 2.1% to 12.3%,16,18,20,21 febrile seizures in 3.7% to 8.0%,16,20,21 and 1.7% developed encephalitis.19 To provide a more complete review of case reports of children with rotavirus gastroenteritis and CNS complications without evidence of rotavirus in the CNS, we have provided a Table (Supplemental Digital Content 1, https://links.lww.com/INF/A195) that summarizes these cases.23–41 Of the 34 cases identified with sufficient information for evaluation, all 34 had seizures and 9 had encephalitis or encephalopathy. The outcomes were described in 76% of children. Four children died, 2 were reported to have a slow recovery, 3 had significant neurologic issues, and 17 were reported to be normal at follow-up. Children with seizures alone were more likely to have a normal outcome compared with children with seizures and other neurologic diagnoses (100% vs. 31%). Ten of the 34 children had evaluations done to determine the presence of rotavirus in the CNS and the results were all negative. We agree that performing lumbar punctures in children with CNS presentations such seizures is not routinely indicated or necessary. However, in children with more serious disease, examining the CSF for the presence of rotavirus could provide useful information and prevent further unnecessary evaluations. Therefore, just as testing is done to identify the etiologic agent for other serious CNS infections even when no specific therapy is available, we continue to advocate for rotavirus testing. Our understanding of rotavirus-associated CNS manifestations is limited. Some cases may be a result of electrolyte imbalances, hemodynamic issues resulting in shock, inappropriate hydration, or precipitation of seizure activity in children with underlying diseases. Other cases may be due to toxin-like activity or direct CNS invasion of rotavirus. We agree that further study is warranted to better understand the pathophysiology, prevalence, spectrum, and outcome of rotavirus-associated CNS disease. Mary Allen Staat, MD, MPH Michelle Dickey, MS, APRN David I. Bernstein, MD, MA Cincinnati Children's Hospital Medical Center University of Cincinnati College of Medicine Department of Pediatrics Division of Infectious Diseases Cincinnati, OH