Sleep medicine reviews
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Sleep medicine reviews · Jun 2007
ReviewPersistent sleepiness in CPAP treated obstructive sleep apnea patients: evaluation and treatment.
Nasal continuous positive airway pressure (CPAP) is an effective treatment for most patients with obstructive sleep apnea syndrome (OSAS), improving sleepiness, cognitive function and mood. A number of patients, however, complain about persistent sleepiness after CPAP. In these cases another clinical history should be carried out to confirm the diagnosis of OSAS, to check CPAP compliance and to exclude associated conditions such as poor sleep hygiene, depression, narcolepsy or idiopathic hypersomnia. ⋯ This impairment, if present in humans, could be another reason for residual sleepiness after CPAP. Modafinil has been shown to reduce subjective sleepiness after CPAP in OSAS patients. Further studies are warranted to clarify the way in which CPAP modifies sleepiness.
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Unlike other physical ambient factors (i.e. electromagnetic fields or air pollutants), noise is perceived by a specific system (auditory system) in humans. It is therefore a phenomenon that is sensed and evaluated by everybody, and this is why exposure to noise is one of the most, if not the most, frequent complaints of populations living in large cities. In these areas and their surroundings, the sources of noise most frequently cited are traffic, followed by neighbourhood noises and aircraft noises. ⋯ Ambient noise, for example, is external stimuli that are still processed by the sleeper sensory functions, despite a non-conscious perception of their presence. Over the past 30 years, research into environmental noise and sleep has focused on different situations and environments, and therefore the findings are variable. However, it still seems necessary for some fundamental questions to be answered on whether environmental noise has long-term detrimental effects on health and quality of life and, if so, what these effects are for night-time, noise-exposed populations.
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Sleep medicine reviews · Feb 2007
ReviewOpioids, sleep architecture and sleep-disordered breathing.
Opioid use whether acute or chronic, illicit or therapeutic is prevalent in Western societies. Opioid receptors are located in the same nuclei that are active in sleep regulation and opioid peptides are suggested to be involved in the induction and maintenance of the sleep state. mu-Opioids are the most commonly used opioids and are recognized respiratory depressants that cause abnormal awake ventilatory responses to hypercapnia and hypoxia. Abnormal sleep architecture has been reported during the process of opioids induction, maintenance and withdrawal. ⋯ More recently, central sleep apnoea (CSA) has been reported with chronic opioid use and 30% of stable methadone maintenance treatment patients have CSA. Given these facts, it is sobering to note the paucity of human data available regarding the effects of short and long-term opioid use on sleep architecture and respiration during sleep. In this manuscript, we review the current knowledge regarding the effects of mu-opioids on sleep and respiration during sleep and suggest research pathways to advance our knowledge and to explore the possible responsible mechanisms related to these effects.
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Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. ⋯ According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.