Behavior sleep disruption

A final limitation of stimulant treatment alone has to do with its applicability to home behavior problems. Many pharmacotherapists limit the use of stimulants to school hours during the 9 months of the academic year, to avoid growth and appetite suppression, sleep disruption, and other undesirable side effects. This leaves parents to their own devices to manage impulsive, oppositional, and disruptive behavior in the afternoons and evenings, weekends, and summers. When no other treatment is provided, parents frequently resort to coercive, hostile, and overly punitive interactions with their children, which may exacerbate rather than improve the child s behavioral problems. This is a par-... 

Benzodiazepines (such as clonazepam) are used widely to induce sleep, but they disrupt the normal sleep architecture. Children also have a tendency to become more irritable and hyperactive with hypnotics. In severe cases, benzodiazepines could be given for 3-5 days to facilitate a behavioral treatment program. Trazodone, though not specifically studied in children, may be a safer alternative for more chronic sleep problems if over-the-counter (OTC) diphenhydramine does not work. 

Another approach considers the effects of various ligands on their receptors located in the diencephalic and mesiotemporal areas. Cell clusters in the hypothalamus coordinate the normal regulation of the vegetative functions of sleep, appetite, and sexual drive, which are typically disrupted in severe depression. In addition, the limbic area modulates many aspects of behavior and mood that are characteristically disturbed in affective disorders. 

Although severe disruption in the sleep-wake cycle is a common feature of dementia, the use of BZDs in such cases may also produce significant behavioral toxicity. Alternative drug approaches include bedtime use of olanzapine in nondepressed patients or trazodone in depressed patients. 

Other studies indicate that sucrose does not cause hyperactivity. Carbohydrate ingestion increases levels of serotonin (5-hydroxytryptamine), a brain neurotransmitter that promotes relaxation and sleep. Dietary sucrose should theoretically have a calming effect and reduce activity, manifestations which have been observed in case studies (63). To date, clinical investigations have failed to show a significant connection between sucrose consumption and aggressive or disruptive behavior (66). 

That adverse consequences would arise—were it not for the active inhibition of movement—is made dramatically clear by patients who lose their innate ability to block other motor outputs and hence enact their sometimes self-injurious dream scenarios. We will come back to this story when we discuss the tendency of some legally prescribed, consciousness altering drugs to mimic those CNS degenerative diseases that cause this so-called REM sleep behavior disorder. The one motor system whose REM sleep activation results in real, not fictive movement is, of course, the one that moves the eyes rapidly, giving REM its name. There is no need to inhibit this system, because its motor output creates no behavioral disruption of sleep or other adverse consequences for the dreamer. 

Further disruption of REM sleep is related to the presence of hallucinations and REM sleep behavior disorder in Parkinson s patients. A decrease in REM sleep has been associated with nocturnal hallucinations (125), and REM intrusion during daytime hallucinations has been reported (126). More than one third of Parkinson s patients also suffer from REM sleep behavior disorder (RBD) (127,128) or REM sleep without atonia (128). In these patients, there is also a significant reduction in total sleep time. In many cases RBD is diagnosed several years prior to the onset of Parkinson s disease (129), although a link between disease severity and duration and the presence of RBD has also been reported (128). RBD is most often treated with the administration of clonazepam (104,129). Patients with comorbid dementia and depression also experience a high level of sleep disturbance, associated with nocturnal vocalizations and hallucinations (130). One side effect of many antidepressant medications, however, is insomnia and sleep disturbance (131). 

Clearly, more experimental research is needed to tease apart the developmental influences of sleep restriction and/or disruption on a range of daytime functioning behaviors and cognitive skills. Additionally, studies are needed that restrict sleep for extended periods of time to identify deficits that may be associated with the typical sleep patterns of children and adolescents. 

Population-based surveys typically have found that a substantial percentage of people report that they do not get sufficient sleep (1). While the exact prevalence may be disputed, it is an accepted fact that many people get insufficient sleep. In addition to those recognizing their insufficient sleep are other individuals who show objective evidence of excessive sleepiness, deny difficulty with sleepiness, and yet show normalization of their alertness with extended time in bed (TIB) (2). Consciously or subconsciously, people employ various stratagems to counteract the disruptive effects of their sleep loss. While the functionally disruptive effects and health risks associated with sleep loss and its consequent daytime sleepiness are generally recognized, questions remain regarding what behavioral and environment factors act as countermeasures to sleep loss and daytime sleepiness, as well as to their effectiveness and duration of effect. 

This chapter will review all of the behavioral and environmental interventions that may act as countermeasures to the disruptive effects of sleep loss on waking function. The literature addressing this question is very limited, not well organized, and quite diverse. Many questions remain unanswered. Before reviewing the evidence regarding countermeasures, we will provide a conceptual analysis of the issues surrounding them. 

This information suggests that early pharmacological REM sleep suppression or other types of state disorganization may disrupt brain and behavioral development. Behavior in adulthood may still be changed as a consequence of the abnormal development, but also as a result of the aberrant adult sleep pattern. Therefore, chronic early REM sleep-like state suppression or other types of state disorganization may be important neurobehavioral teratogenic mechanisms (see also refs. 77, 118, 129). 

Slater et al., from the Eli Lilly Research Labs, published an article in 1978 concerning the inhibition of REM sleep in cats. Disruption of REM sleep can cause emotional disturbances. The Eli Lilly researchers reported that they were at a loss to explain why cats receiving fluoxetine for several days began to hiss and growl or why this behavior decreased with continued treatment. ... 

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