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BackgroundCaregivers of children with autism spectrum disorders (ASD) and developmental disabilities (DD) implement myriad strategies to support their children during daily activities and routines, which are laden with sensory stimuli. Children’s sensory features are often characterized by three patterns of response (i.e., hyperresponsiveness, hyporesponsiveness, sensory seeking), and little is known about how caregivers’ strategies differ among these patterns. Therefore, we used a mixed methods analysis to examine the complex interplay between children’s sensory response patterns, child characteristics (diagnosis, chronological age, mental age), and caregiver strategies. Specifically, we examined how children’s sensory response pattern scores were associated with caregiver strategies within sensory response pattern and at the item level. Lastly, we described the differential strategies implemented by caregivers of children with ASD and DD by sensory response pattern.Materials and MethodsParticipants included children with ASD (n = 77) and DD (n = 40) aged 2–10 years. Caregivers completed the Sensory Experiences Questionnaire-2.1. A convergent parallel mixed methods approach was used to analyze data.ResultsChildren’s sensory response pattern scores were significantly, positively associated with caregiver strategies within each sensory pattern (hyperresponsiveness, hyporesponsiveness, seeking); however, child mental age, and chronological age were not significantly related to the rate of caregiver strategies across patterns. While caregivers of children with ASD reported using more strategies, child diagnosis did not moderate the association between child sensory response pattern scores and the rate of caregiver strategies used. Item analysis demonstrated specific child behaviors in response to sensory stimuli that elicited high rates of strategies among caregivers. Qualitative analysis revealed distinct themes characterized caregiver strategies within each sensory pattern for children with ASD and DD.ConclusionOur findings demonstrated specificity of caregiver strategies to children’s sensory response patterns in the context of families’ everyday lives, which were not contingent on child diagnosis, mental age, or chronological age, thereby highlighting universal qualities of caregiving for young children who experience varying levels of sensory challenges. Targeted intervention approaches may differentially incorporate types of strategies based on sensory response patterns to more optimally facilitate children’s activity participation.

Infants exposed to Zika virus (ZIKV) prenatally may develop birth defects, developmental deficits, or remain asymptomatic. It is unclear why some infants are more affected than others, although enhancement of maternal ZIKV infection via immunity to an antigenically similar virus, dengue virus (DENV), may play a role. We hypothesized that DENV immunity may worsen prenatal ZIKV infection and developmental deficits in offspring. We utilized a translational macaque model to examine how maternal DENV immunity influences ZIKV-exposed infant macaque neurodevelopment in the first month of life. We inoculated eight macaques with prior DENV infection with ZIKV, five macaques with ZIKV, and four macaques with saline. DENV/ZIKV-exposed infants had significantly worse visual orientation skills than ZIKV-exposed infants whose mothers were DENV-naive, with no differences in motor, sensory or state control development. ZIKV infection characteristics and pregnancy outcomes did not individually differ between dams with and without DENV immunity, but when multiple factors were combined in a multivariate model, maternal DENV immunity combined with ZIKV infection characteristics and pregnancy parameters predicted select developmental outcomes. We demonstrate that maternal DENV immunity exacerbates visual orientation and tracking deficits in ZIKV-exposed infant macaques, suggesting that human studies should evaluate how maternal DENV immunity impacts long-term neurodevelopment.

Congenital Zika virus (ZIKV) exposure results in a spectrum of disease ranging from severe birth defects to delayed onset neurodevelopmental deficits. ZIKV-related neuropathogenesis, predictors of birth defects, and neurodevelopmental deficits are not well defined in people. Here we assess the methodological and statistical feasibility of a congenital ZIKV exposure macaque model for identifying infant neurobehavior and brain abnormalities that may underlie neurodevelopmental deficits. We inoculated five pregnant macaques with ZIKV and mock-inoculated one macaque in the first trimester. Following birth, growth, ocular structure/function, brain structure, hearing, histopathology, and neurobehavior were quantitatively assessed during the first week of life. We identified the typical pregnancy outcomes of congenital ZIKV infection, with fetal demise and placental abnormalities. We estimated sample sizes needed to define differences between groups and demonstrated that future studies quantifying brain region volumes, retinal structure, hearing, and visual pathway function require a sample size of 14 animals per group (14 ZIKV, 14 control) to detect statistically significant differences in at least half of the infant exam parameters. Establishing the parameters for future studies of neurodevelopmental outcomes following congenital ZIKV exposure in macaques is essential for robust and rigorous experimental design.