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Studies in hypertensive populations to date suggest that nondipping during the night, heightened blood pressure variability during the night, and nocturnal hypertension all predict future risk for cardiovascular morbidity and mortality, and are better prognostic factors than daytime hypertension. This chapter discusses the effects of sleep apnea treatment on hypertension. Although the prevalence of obstructive sleep apnea (OSA) increases with age, younger patients with OSA may be more prone to having cardiovascular consequences, including hypertension. Several studies suggest that the association between OSA and hypertension is more robust in the non-elderly. Different screening questionnaires have been developed and tested in attempts to identify patients at high risk for OSA. More studies are necessary to further elucidate pathogenetic mechanisms by which OSA causes hypertension and to determine the magnitude of the effect of OSA and its treatments on blood pressure.
Interest in the effects of total sleep deprivation dates back over one hundred years. After the discovery of rapid eye movement (REM) sleep in the 1950s, selective REM-deprivation studies have been performed in animals and humans. All studies have shown progressively higher pressure for REM sleep as REM deprivation increases. Studies also show that significant REM rebound occurs after selective REM deprivation and total sleep deprivation. Over the past few decades, newer methods have been developed to reduce confounding factors in REM- or paradoxical sleep-deprivation (PSD) studies of animals but, unfortunately, many findings cannot be generalized to humans. Most current PSD studies employ either the gentle handling or forced locomotion technique, and are most often carried out in rats. Forced locomotion techniques like the disk-over-water method have allowed the study of fairly prolonged PSD in rats. Total sleep deprivation (TSD) in rats leads to a host of sleep deprivation effects (SDEs), including eventual death. Development of SDEs seems to correlate with degree of PSD. Paradoxical sleep-deprivation studies in rats show almost identical results, but only occurring over a longer period of time. REM sleep appears to play a vital role in thermoregulation in rats, leading to considerable hypothermia. The heat-loss theory explains the inverse relationship between energy expenditure (EE) and temperature, which eventually is observed in TSD and PSD studies in animals. No human REM sleep-deprivation studies have indicated such profound changes, though no comparable studies have been conducted. From early on, REM sleep-deprivation studies in humans have focused on the cognitive effects of deprivation. Several studies suggest deficits in short-term memory consolidation with REM-sleep deprivation in both humans and animals, though the issue remains controversial. Recent studies suggest that sensitivity to pain increases with selective REM-sleep deprivation in animals, but no convincing evidence is found in human studies.
Kleine-Levin syndrome (KLS) is a rare neurological disorder primarily affecting young subjects. The first episode usually begins within a few hours, with patients becoming extremely tired, generally after an identifiable triggering event, such as a banal infection in most cases, alcohol intake, or a head trauma. The symptomatic periods involve hypersomnia, and cognitive, behavioral and psychological problems, and last from two days to several weeks. The most difficult differential diagnoses are psychiatric disorders (psychosis and depression), hence many patients are sent to the psychiatric department before the diagnosis of KLS is made. Recent methods of investigation such as SPECT indicate that the brain dysfunction could be larger than expected, and would encompass both cortical and subcortical (and especially thalamus and hypothalamus) areas. This general picture and the fluctuating symptoms in KLS are consistent with the possibility of an autoimmune mediation of the disorder.