Anatomical, physiological, psychological and hormonal alterations affect sleep during pregnancy. Sleep appears tobe commonly impaired only after the first trimester. Albeit objective data regarding the reduction of sleep durationand efficiency are not univocal, poor sleep is reported by over half of pregnant women. The reasons underlyingthese complaints are multiple, including lower back pain, gastroesophageal reflux disorder (GERD), increasedmicturition and repositioning difficulties at night. Specific primary sleep disorders whose prevalence drasticallyincreases during pregnancy include obstructive sleep apnea (OSA) and restless legs syndrome (RLS), both relatedto gestational hypertension and gestational diabetes mellitus (GDM). Pre-eclampsia and labor complicationsleading to an increased number of cesarean sections and preterm births correlate with insomnia and OSA inparticular. Post-partum depression (PPD) and impairment of the mother-infant relationship may also be consideredas secondary effects deriving from poor sleep during pregnancy. Recognition and treatment of sleep disordersshould be encouraged in order to protect maternal and fetal health and prevent dire consequences at birth.

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Recent evidence has been accumulating that the sleep of individuals with attention deficit hyperactivity disorder (ADHD) is not only disrupted in a nonspecific way but that ADHD has an increased association with simple sleep related movement disorders such as restless legs syndrome/periodic limb movements in sleep (RLS/PLMS), rhythmic movement disorder (body rocking and head banging), and parasomnias, such as disorders of partial arousal (sleep walking, sleep terrors, and confusional arousals). In addition increased associations have been reported between ADHD and hypersomnias such as narcolepsy and sleep apnea as well as circadian rhythm disorders, such as delayed sleep phase syndrome. These relationships are reviewed and the implications for such associations are explored. Patients with sleep disorders should be queried about the symptoms of ADHD and vice versa.

The objective of this study was to determine whether the macrostructure and microstructure of sleep were altered in non-dipper essential hypertensive patients. Patients included 9 non-dipper essential hypertensive patients and 10 dippers. We measured blood pressure beat-to-beat by Finapres and all stages of sleep by polysomnografically recording simultaneously during spontaneous nocturnal sleep. We analysed blood pressure pattern for 4-min long random periods while the patients were awake and during all stages of sleep; sleep-efficiency (SE), sleep-latency (SL), delta sleep-latency (delta-SL), REM sleep-latency (REM-SL), St. 1, St.2, St.3, St.4 and REM duration and percentage (%) values, and microstructural aspects of sleep (arousal and microarousal temporisation and features). Dipper patients showed a fall in blood pressure (BP) greater than 10% in all stages of NREM sleep; in the non-dipper patients BP fell by less than 10% of waking values in all NREM stages. REM sleep as well as HR were similar in both groups during all stages of sleep. Non-dippers showed the same number of arousals but more microarousals than dippers (p < 0.001). During and after microarousals BP and HR increased in non-dippers, but showed light variation in dippers. Microarousals induced several stage shifts towards lighter sleep. For this reason non-dippers spent less time in stage 4 than dippers (p < 0.001). In conclusion, non-dipper essential hypertensive patients are a subset of patients with central sympathetic hyperactivity responsible for quantitative and qualitative alteration of sleep.