Neuroscience and biomarkers of sleep in preterm and term infants: From state organization to clinical translation.

Infant sleep, viewed across the preterm-to-term continuum, is best understood not as a behavioral backdrop but as a developing neurobiological control system whose state organization offers a clinically accessible window onto central nervous system maturation. In this chapter we synthesize evidence on sleep across three contexts - the NICU, the post-discharge period, and community samples - and across three nested levels of organization: macro-architectural cycling between active, quiet, and indeterminate sleep; microstructural EEG features such as spindles, slow oscillations, and graphoelements; and the gradual emergence of circadian timing. We argue that infant sleep functions simultaneously as a mediator of brain development, a moderator of early vulnerability, and a marker of neurodevelopmental risk - a triple role that justifies treating sleep assessment as a core component of neonatal care rather than a supplementary concern. Yet the path from biomarker to bedside is far from frictionless. We examine the strengths and inferential limits of polysomnography, conventional and amplitude-integrated EEG, behavioral state coding, actigraphy, and autonomic-cardiorespiratory metrics, and we develop a reliability-validity-specificity framework for evaluating candidate biomarkers against the moving baselines of maturation, medication, illness, and environment. Throughout, we flag where current evidence supports causal mechanism, where it is merely correlational, and where the direction of effect may be bidirectional. The chapter closes with a three-step clinician-researcher bridge - assess, contextualize, decide - designed to translate multimodal sleep data into age-corrected, context-aware clinical decisions. Sleep, properly read, is not a research curiosity. It is a routine instrument of neurodevelopmental care.