Summary: Sleep patterns in reading disabled (n = 24) and normal control (n = 15) 8-10-year-old boys were compared to examine suggested relationships among sleep, maturational and cognitive processes. Sleep was recorded in the laboratory for four consecutive nights (two adaptation, two baseline) using standard polysomnography. Analyses revealed variations across nights for both groups reflecting adaptation to the sleep laboratory, but such effects were attenuated in reading disabled subjects. Group comparisons on baseline sleep measures (nights 3 and 4 collapsed) revealed that reading disabled children showed significantly more stage 4 sleep, less rapid eye movement (REM) sleep, a longer REM onset latency and, related to this, an extended initial non-REM (NREM) cycle. Chronic sleep deprivation and maturational delay are prominent among factors that could result in such variations in sleep architecture, and these factors, alone or in combination, could impair information processing and contribute to cognitive deficits noted in reading disabled children. Key Words: Reading disabled children-Sleep-REM latencyAdaptation-Maturational delay.Developmental reading disabilities constitute possibly the most debilitating of learning disorders both in terms of prevalence (estimates of 5-15% of the school-age population) and negative personal, social and behavioral consequences (1,2). Despite the increased attention given this disorder over the past 30 years by both clinicians and researchers (3-6), there remain significant uncertainty, contradiction and controversy surrounding definition and diagnosis (4,7). Frequently suggested etiological factors include a maturational delay in the establishment ofleft hemispheric dominance for linguistic processing (8-11) or in the development of cerebral regions considered necessary for reading (2,12,13), possibly resulting in neurodevelopmental abnormalities such as disruptions of pathways associated with the functional system for reading (4,12) and reversed cerebral asymmetries (14,15 evoked potentials (18,19), dichotic listening (20-23) and visual half-field procedures (24-27), However, these approaches have yielded inconsistent results and offer limited evidence for neurologic deficits in this population (13). Nevertheless, recent reviews suggest an underlying central nervous system (eNS) dysfunction for this disorder (4,13,28). The most direct evidence for a neurological basis for reading disabilities has come from postmortem cytoarchitectonic (29-33) and imaging (34) studies of brains of dyslexic individuals, which have demonstrated cortical abnormalities and variations in structural symmetry. The anomalies observed, although present in a small number of often poorly documented clinical studies, are thought to be consistent with reading failure (2,13).Research into the behavioral and etiological features associated with these disorders has focused on variations during wakefulness where the negative effects impact most noticeably. However, studies of sleep could prove useful because...