TITLE:
The Impacts of Prenatal and Childhood Heat Stress on Neurocognitive Development: Structural, Endocrine and Functional Alterations
AUTHORS:
Tesfaye Tolessa Dugul
KEYWORDS:
Heat Stress, Neurocognitive Development
JOURNAL NAME:
World Journal of Neuroscience,
Vol.16 No.4,
September
29,
2026
ABSTRACT: Prenatal exposure to maternal heat stress alters fetal neurocognitive courses through both direct physiological disruptions and indirect maternal stress pathways. Maternal hyperthermia elevates core body temperature, triggering systemic inflammation, placental insufficiency, and altered uterine blood flow, which can limit the delivery of oxygen and vital nutrients to the developing fetal brain. At the structural level, heat stress during critical gestational windows can disrupt embryonic neural cell migration, alter synaptic integration, and impair structural growth in key brain regions like the hypothalamus, thalamus and cerebral white matter. Concurrently, maternal hyperthermia triggers elevated cortisol production and systemic stress responses that can alter hypothalamic-pituitary-adrenal axis (HPA) regulation in the fetus. These structural and endocrine disruptions increase the risk of congenital neurodevelopmental defects and establish early vulnerabilities for altered behavioral phenotypes, reduced cognitive capacity, and delayed psychomotor processing later in childhood. During infancy and early childhood, heat stress continues to impair neurocognitive development because of young children’s immature thermoregulatory capacity and higher vulnerability of their brain to thermal strain. Prolonged environmental heat exposure disrupts sleep patterns and elevates physiological stress responses, impeding the rapid synaptic pruning and myelination necessary for optimal central nervous system maturation. Cognitively, these physiological burdens manifest as reduced attentional allocation, impaired working memory capacity, and diminished performance on executive function tasks. Furthermore, persistent thermal exposure during early childhood is associated with slower white matter tract maturation, which impairs neural connectivity and contributes to long-term decrements in learning ability, problem-solving, emotional regulation and academic performance.