Normal Sleep

An interesting question comes up in connection with psychotic patients suffering from dementia praecox catatonia. The psychosis is due unquestionably to an over-dispersed state, and we must therefore conclude either that the sleep of such patients is theoretically quite different from ordinary sleep or that the centers of consciousness may be over-agglomerated while some centers of thinking are over-dispersed. So far as I can learn, these patients do sleep normally as a rule. Consequently one portion of the brain must be over-agglomerated at times, even though another portion of the brain is over-dispersed. 

Sleep architecture in narcolepsy is distinctly abnormal. Recall that sleep normally begins in a NREM phase and that the first phase of REM does not occur until about 90 minutes after falling asleep. The patient with narcolepsy, in sharp contrast, experiences REM onset within 15 minutes of falling asleep. 

If patients have predominant symptoms of insomnia or psychomotor agitation, a more sedating drug (e.g., trazodone or mirtazapine) may benefit initially but could be problematic later in therapy (i.e., cause excessive sedation once sleep normalizes). 

The duration of the problem determines whether transient or chronic insomnia underlies sleep loss. Transient insomnia refers to no more than a few nights of poor sleep, which generally results from challenges such as (a) acute illness, (b) stress, (c) suboptimal circadian time for sleep, or (d) a disruptive sleep environment. In the absence of these challenges the individuals typically sleep normally. That is, they judge their sleep to be satisfactory. It is reasonable to conclude, therefore, that the impact of transient insomnia on waking function can be extrapolated from partial sleep deprivation research conducted in normal sleepers. Such studies limit the amount of sleep obtained, on one or more nights, just as in the case of transient insomnia. 

Now, you might say that we have come a long way from dreaming and even from brain activation in sleep, but I don t think so and I hope that a moment s reflection will show you why. To explain why sleep normally defends us from such fates, we must assume that it is the change in brain state, with all its chemical and electrical transformations, that keeps us healthy. A second reason, admittedly theoretical, is that our drive to sleep is so intense, so demanding, and so enduring that it must have important survival functions. 

A 29-year-old woman took citalopram (40 mg/day) while breast feeding her 5-week-old daughter. The maternal citalopram concentrations were 99 ng/ml in the serum and 205 ng/ml in the breast milk. The serum concentration in the infant was 13 ng/ml, and the child s sleep was fitful and disturbed. The dosage of citalopram was reduced to 20 mg/day and the two feeds after each daily dose were replaced by artificial nutrition. One week later the infant was sleeping normally, and the serum citalopram concentrations in mother and infant had fallen to 35 ng/ml and 2 ng/ml, respectively. 

A good night s sleep may do much more than refresh the psyche. Melatonin is a hormone that acts as an antioxidant that combats the free radicals (see Section 3.6.6) that can cause genetic damage. Cortisol is another hormone that helps regulate the immune systan. The disruption of normal sleep cycles results in less melatonin production and lower cortisol activity. Perhaps that may be one reason that shift workers have higher rates of breast cancer than women who sleep normal hours. Regular sleep may help to battle cancer. 

Process operators are expected to be exercising normal surveillance of the process. Therefore, alarms are not appropriate for situations known to the operator either through previous alarms or through normal process sui veillance. The sleeping operator problem can Be addressed by far more effective means than tne alarm system. 

In conditions of acute sleep deprivation, "microsleeps" will occur more and more often. These very short sleeps do not have the recuperative value of normal sleep, and the sleep-deprived person still feels sleepy and performance still degrades even though there may be a large number of microsleep periods. 

The synchronised oscillatory activity between the intrinsically linked thalamus and cortex. Under normal circumstances there is a level of activity which changes during the sleep-wake cycle increasing during periods of slow wave sleep. Excess synchrony occurs in conditions such as epilepsy. Thiazolidinedione... 

Respiratory drive and rhythm are depressed by barbiturates. Coughing, sneezing, hiccupping, and laryngospasm may occur during anesthesia with barbiturates. Sedative ot hypnotic doses of barbiturates teduce heatt tate and blood pressure to levels found in normal sleep. Anesthetic doses produce more pronounced effects. Barbiturates cross the placenta when used in labor, they can cause respiratoty depression in neonates. Anesthetic doses dectease force and frequency of uterine contractions among pregnant women. 

These rhythms seem to be innately programmed although they can be adjusted. For instance, in a normal environment, the sleep-waking cycle of humans is obviously synchronised ( entrained ) with the (24-h) dark-light cycle whereas it assumes a period of around 25-27 h in a (time-free) environment where there are no diurnal cues. Interestingly, when humans are in a time-free environment, the change in the rhythm of... 

The first serious attempts to identify and characterise an endogenous somnogenic agent was carried out by Pappenheimer and colleagues (see Pappenheimer 1983) who found that transferring samples of CSF from sleep-deprived goats into normal rabbits... 

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