Dengue virus (DENV) is a Flavivirus transmitted to humans by the bite of Aedes aegypti and Aedes albopictus mosquitoes. Over the last 4 decades, there has been a 30-fold increase in worldwide DENV infections, which now total 390 million per year.1 In the Americas, data from the Pan American Health Organization (PAHO)/WHO shows cases increased from 1.5 million between 1980 and 1989, to 16.2 million cases recorded between 2010 and 2020.2 The virus circulates in Southeast Asia, the South Pacific, the Caribbean region, Mexico, Central and South America. In the Americas, recent epidemics indicate that DENV infection has replaced Yellow Fever as the major urban epidemic flavivirus of importance,1 and is the second most common cause of acute febrile syndrome in travelers.3 DENV, once considered an infection of tropical and subtropical regions, is now also found in countries with temperate climates.4,5 For instance, in the United States DENV was previously considered an introduced disease, and now is locally transmitted. This phenomenon is attributed to the adaptability of the Aedes mosquito,6,7 which has migrated, assisted by the mobility and increased travel of the modern population. Additionally, the climate change related rise in global temperatures has positively influenced mosquito hatching rate, survival rate, longevity and lengthened the reproductive season.8,9

It has been demonstrated that in certain countries the 4 serotypes of DENV circulate simultaneously, increasing the risk of epidemics and severe forms of the disease.10 Complications of DENV infection are more frequent in the pediatric population,11 and neurologic manifestations, once considered rare,12 are increasingly recognized, and reported in up to 20 % of patients.13 However, research efforts investigating pediatric neurologic manifestations of DENV infection are scarce, and the case reports lack clinical standardization.