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All of the information that the author discovered has been compiled into a downloadable ebook so that purchasers of Outsmart Insomnia can begin putting the methods it teaches to use as soon as possible.

As a whole, this ebook contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

The discovery of REM sleep

In 1953, Eugene Aserinsky, then a graduate student studying physiology at the University of Chicago, wired up his 9-year-old son, Armand, and other children to perform electroencephalogram (EEG) and electro-oculogram (EOG) recordings in his rebellious experiments on attention carried out with the encouragement of the neurophysiologist, Ralph Gerard. As is so often the case, the monumental scientific discovery of REM sleep occurred in part by happenstance. When the child subjects became bored by Aserinsky's protocols, they fell asleep and, because they were young, evinced rapid eye movement (REM) periods shortly after sleep onset during which they dreamt. Aserinsky reported his observations to his supervisor, Nathaniel Kleitman, who suggested that they record the sleep of adults. The rest is history. All of Aserinsky and Kleitman's adult subjects showed EEG activation, REM periods, and when awakened reported long complex dreams, not at sleep onset but at 90-100 minute intervals...

Aserinsky and Kleitman revisited REM sleep and immaturity

The reason that Aserinsky stumbled onto REM sleep in the first place is because he was studying children who were bored and fell asleep and, fortunately, REM sleep occurs closer to sleep onset in the young. Not only does it occur at sleep onset but it occupies a greater proportion of a greater amount of sleep in the younger the child. The newborn human infant spends 50 of its sleep time in REM. Since infants sleep 16 hours per day, they achieve nearly 8 hours of REM sleep per day With prematurity, these numbers increase further, until at 30 weeks of gestation, the human fetus spends 24 hours day in a brain-activated state that is something more like REM sleep than wakefulness or NREM. Thus, I would argue that REM sleep in infancy serves brain development in the specific enhancement of cognition and consciousness. This over-commitment to REM sleep by immature animals has not gone unnoticed. Howard Roffwarg, Joseph Muzio, and William Dement theorized in 1966 that REM favored development...

Delta frequency 14 Hz EEG activity during NREM sleep

The cellular basis of delta waves (0.5-4 Hz) originating in thalamocortical neurons is that a hyperpolar-ized membrane potential in cortically projecting thalamic neurons permits the occurrence of delta waves in thalamocortical circuits. In both the thalamus and cortex, a phasic input to the hyperpolarized membrane causes a calcium-mediated depolarization (low threshold spike, LTS) on which a burst of sodium-mediated spikes occur (low threshold burst). The slow time course of delta waves is determined by the time course of the LTS and the subsequent hyper-polarization to re-enable another LTS. Any factors persistently depolarizing the membrane in either thal-amic or cortical neurons will block delta waves through inactivation of the calcium channels mediating the LTS, and these are the wake-active systems illustrated in Fig. 2.1b. Cholinergic input from BF to the cortex, and from LDT PPT to the thalamus, is thought to be especially important in arresting delta waves. Also, brainstem...

Pontinegeniculooccipital PGO waves preceding and during REM sleep

One of the important advantages of animal work is the ability to record intracranial EEG and neuronal activity. Thus, investigators are able to detect a transitional state that occurs just before the onset of REM sleep, often termed REM-T. The sleep researcher monitoring pontine reticular neuronal activity easily detects the impending onset of REM by the flurry of activity on the oscilloscope or an audio monitor - all of this stigmatic subcortical activity occurring before the change of externally recorded polysomnographic signs of REM. As depicted in Figure 2.3, REM-T is Figure 2.3 Changes in the membrane potential(MP) of a pontine tegmentalneuron over the sleep wake cycle in the cat. These EEG and neuronalrecordings illustrate the paucity of reticular activity during NREM sleep and the frenzy of activity during REM sleep. As well, the premonitory transition period of the approach of REM sleep is not visible in the corticalEEG. The first trace of the top panel(a) is EMG from the deep...

Pontine cholinergic activation during REM sleep

Pharmacological experiments have indicated a particular role of cholinergic transmission in both wake-fulness and REM sleep promotion. The cholinergic neurons of the midbrain tegmentum, particularly of LDT PPT, are crucial for control of both wakefulness and REM sleep. Non-specific lesioning of this region, by means of intracerebral kainic acid injections, attenuates REM sleep, and the amount of cholinergic cell loss correlates with the REM sleep loss 126 . Of particular interest, some neurons of LDT PPT discharge selectively during wakefulness and or REM sleep 26,27 . The LDT PPT neurons that fire preferentially during REM sleep are often termed REM-on neurons. A separate subpopulation of LDT PPT cholinergic neurons is active during both wakefulness and REM sleep and is referred to as wake REM-on neurons. Systemic administration of the acetylcholine-esterase (AChE) inhibitor physo-stigmine during NREM sleep induces REM sleep 127 . Direct injections of the cholinergic agonist...

Physiological changes occurring in sleep stages

During NREM and tonic REM sleep the sympathetic activity (fight or flight) of the ANS decreases 14 , whereas the parasympathetic activity (rest and repose) progressively increases until it peaks in deep sleep (SWS) 15 , where blood pressure and heart and respiratory rates reach their lowest values 16 . Notably, increased sympathetic activation observed in individuals affected by sleep apnea, a condition characterized by chronic SWS deficits, may theoretically increase their risk of developing diabetes 17 . Abnormal peaks of sympathetic activity have also been reported during phasic REM in patients affected by melancholic depression, although their relationship with this psychiatric disorder is not clear 18 . Blood pressure and cardiac output are markedly reduced during NREM sleep relative to wakefulness. During REM sleep these cardiovascular parameters reach their peak values during sleep, although mean values are generally lower than during waking 16 . Episodes of arrhythmia are also...

Functional neuroanatomy of sleep stages

In comparison to NREM sleep, REM sleep is characterized by an increase in neuronal activity, brain metabolism, and rCBF in the pons, midbrain, Figure 3.4 Brain maps showing changes in rCBF from waking to NREM (top), NREM to REM (middle), and REM to waking (bottom), measured with H215O PET. Top panel brain regions with decreased rCBF during NREM sleep compared with presleep wakefulness. The reduction is expressed in Z scores, ranging from 1 (light purple) to 4.5 (deep purple). Significant rCBF reductions were observed in the pons (A, arrowhead), midbrain (B, short arrow), basalganglia (B, long arrow C, medium arrowhead), thalamus (C, short arrow), caudalorbitalcortex (B, smallarrowhead), and cerebellum (A, arrow). Similar rCBF decreases were found in the anterior insula (B, medium arrowhead), anterior cingulate (C and D, smallarrowheads), as wellas in the orbital (B, medium arrow), dorsolateralprefrontal(C, medium arrow D, smallarrow), and inferior parietallobes (D, medium arrow)....

Dreams and sleep disorders

This section will focus on several sleep disorders which have been studied in relation to dreaming insomnia, sleep apnea syndrome, narcolepsy, and restless legs syndrome. For other diagnoses, like idio-pathic hypersomnia, or NREM parasomnias, such as sleepwalking or night terrors, systematic dream content analytic studies are lacking. However, extensive reviews are available for nightmares 72 , REM sleep behavior disorder (see Chapter 10 Parasomnias), and dreaming in post-traumatic stress disorder 19 . Schredl et al. 73 found an elevated dream recall frequency in insomnia patients in contrast to healthy controls a finding which was no longer significant if number of nocturnal awakenings (self-report measure) was statistically controlled. This parallels the correlation between nocturnal awakenings and increased dream recall in healthy persons 22 . Percentage of dream recall after REM awakenings carried out in the laboratory did not differ between insomnia patients and controls 74 ....

Pontine sublaterodorsal nucleus activation during REM sleep

Excitatory cholinergic projections from LDT PPT to regions of the pontine RF may be responsible for some of the characteristic phenomena of REM sleep. One pontine RF region important for muscle atonia, just ventral to LC, was later defined as the perilocus coeruleus alpha in the cat (also termed the subcoer-uleus (SubC) or sublaterodorsal nucleus (SLD) in the rodent). Seminal investigations by Jouvet and colleagues revealed that lesions of the perilocus coeruleus alpha in the cat produced suppression of muscle atonia during REM sleep 129 . Larger lesions of this area, including neighboring pontine regions connected to the superior colliculus and amygdala, caused oneiric (i.e. dream-like) behavior during REM sleep, including locomotion, attack behavior, and head movement 130 . Recent models of REM sleep suggest that these muscle atonia-on neurons are kept silent during wakefulness by means of GABAergic inputs from neighboring RF regions. Figure 2.4 Select LDT PPT, presumptively...

REM sleep and the binding problem

According to protoconsciousness theory, REM sleep serves binding automatically and spontaneously. No supervision is needed. And according to this new theory, all mammals that have REM sleep have proto-consciousness. When they wake up, they have varying degrees of what Gerald Edelman calls primary consciousness 32 . According to the complexity of their brains, they may also achieve some degree of secondary consciousness. But, as far as we know, only humans have directed thought, propositional intent, and awareness-of-awareness. This sophisticated adaptation is presumably dependent on the acquisition of symbolic language.

Neural systems involved in vigilance state regulation REM sleep

Aserinsky and Kleitman in the 1950s first documented the rapid eye movements indicative of REM sleep in humans, and coined the term REM sleep 113,114 . REM sleep mechanisms involve brain regions and systems that differ from those involved with NREM sleep induction and maintenance. Jouvet and colleagues, employing transections, determined that regions of the brain rostral to the midbrain and caudal to the medulla were not necessary for the brainstem activity seen during REM sleep 115,116 . Lesion and transection studies in cats of the dorsolateral pons abolished the REM state. As described previously, this area includes the wakeful-ness-active noradrenergic, serotonergic and wakeful-ness REM-active cholinergic neurons 117,118 . REM sleep is characterized by a return from the high-amplitude, slow-frequency cortical EEG profile evident during deep NREM sleep to fast-frequency, low-voltage EEG activity, such as that seen during wakefulness. Hence, REM sleep is also referred to as...

Insomnia history of the chief complaint

Insomnia is a repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite adequate opportunity for sleep and results in some form of daytime impairment 5 . Stated in another way, an insomnia complaint can involve difficulty in initiating sleep, multiple nocturnal awakenings, a difficulty in reinitiating sleep, early morning awakening, or a combination of these. From the standpoint of diagnosis and treatment, it is important to identify the portions of sleep that are affected. The time of onset and duration of symptoms also should be determined. Insomnias of long duration are thought to have greater impact on daytime functioning. Although such beliefs seem to be clinically supported, they have yet to be confirmed by systematic studies. Additionally, there is considerable variability in the definition of the time course for acute and long-term insomnia, with minimum durations for chronic insomnia ranging from 30 days to as long as 6 months 6 . The...

Insomnia

A HOP pillow is the best known soporific and has been for a long time. The secret of success against insomnia lies in not packing it too tightly, and renewing the dried hops every four to six weeks (Thomson. 1976). The pillow's sedative action was used to combat other conditions, too. Lindley tells us that they were prescribed for mania. George III is said to have slept always on a hop pillow (Genders. 1971). Pillows are stuffed with the dried leaves of CATMINT, too, for the smell is supposed to help the sleepless (Sanford). NETTLE seems an unlikely plant to be associated with cures for insomnia, but it certainly is in both the medical sense and also as a charm. In the Highlands, we are told that nettle leaves chopped very small and mixed with whisked egg-white used to be applied to the temples and forehead. This remedy was mentioned as early as the beginning of the 18th century by Martin, who particularly speaks of fevered patients benefitting from the treatment. In Wales, they used...

Sleep stages

Human sleep occurs in several cycles of NREM-REM sleep across the night, each approximately 90 to 110 minutes long, which can be further classified into different sleep stages 11 . Sleep stages are identified based on three electrophysiological parameters EEG, EOG, and EMG activity, the latter usually recorded from neck or chin muscles. For clinical and research purposes, sleep is usually scored in 30 second epochs. The criteria of sleep stage scoring, established by Rechtschaffen and Kales (R& K) 12 , have been REM sleep twitches can also occur at the transition into sleep. These hypnic jerks, also known as positive myoclo-nus, are sporadic, generally benign, and are more common after sleep deprivation. Brief episodes of Stage N1, usually lasting a few seconds, tend to occur during the daytime in sleepy subjects, either due to sleep disorders or sleep deprivation, and can have dire consequences in situations that require a constant high level of awareness, such as driving. Stage...

Neurobiological progress of sleep medicine

During the same period in which dream laboratory research was flourishing, remarkable progress was being made using the (feline) animal model of sleep that William Dement had also given the field 10 . The prime mover of this initiative was Michel Jouvet, a French neurosurgeon working in Lyon, who had spent a year at the University of California at Los Angeles (UCLA) founded by Horace Magoun, the co-discoverer with Giuseppe Moruzzi of the reticular activating system 11 . Jouvet quickly localized the REM generator system to the pons 12 and suggested that the forebrain was activated, the eyes were caused to move, and spinal reflexes were inhibited 13 during REM sleep all from that central locale. With this discovery, dreaming could thus be redefined as the inevitable subjective experience of a specific physiological pattern of brain activation in sleep. As it turned out, all mammals shared this brain activation process in sleep, casting doubt, albeit Figure 1.1 Rapid eye movement sleep....

The rise of sleep medicine

Figure 1.2 The originalreciprocalinteraction modelof physiological mechanisms determining alterations in activation level. (a) Structuralmodelof reciprocalinteraction. REM on cells of the pontine reticular formation are cholinoceptively excited and or cholinergically excitatory (ACH1) at their synaptic endings. Pontine REM off cells are noradrenergically (NE) or serotonergically (5HT) inhibitory 2 at their synapses. (b) Dynamic model. During waking, the pontine aminergic system is tonically activated and inhibits the pontine cholinergic system. During NREM sleep, aminergic inhibition gradually wanes and cholinergic excitation reciprocally waxes. At REM sleep onset, aminergic inhibition is shut off and cholinergic excitation reaches its high point. (c) Activation level. As a consequence of the interplay of the neuronalsystems shown in (a) and (b), the net activation levelof the brain (A) is at equally high levels in waking and REM sleep and at about half this peak levelin NREM sleep....

Developmental considerations

Although antecedence does not guarantee causality, this temporal sequence means that REM sleep could be a protoconscious state. What is meant by the term protoconsciousness First, it means that a primitive sense of self could be instantiated. To paraphrase Descartes, my brain is activated, therefore I am. When my self (or ego) is activated, I move. My self is therefore an agent. This is point two. According to Rodolfo Llinas, agent-initiated movement is instantiated early in development 31 . Not only does the self-organized autoactive brain instantiate agent-initiated movement but it simulates both the sensory and emotional concomitants of that activity. These are points 3 and 4. REM sleep creates a self that acts, and feels, in a virtual world.

The interaction of dreaming and waking consciousness

Since REM sleep brain activation precedes waking (and may occur before even birth), it follows that while it may instantiate self, self-as-agent, movement, sensation, and emotion, it could not support dreaming as we know it in adults. For adult dreaming to occur, specific content information would need to be gleaned in waking and cognitive capacity would need to evolve, as it clearly does, accounting for the fact that adult dreaming does not occur before ages 6-8 33 . Another empirical example of this principle is the vision-free dreaming of the congeni-tally blind person. Vice versa, in order for a normal person to see, in either waking or dreaming consciousness, the contentless formal frame supplied by REM sleep brain activation is essential. The emerging picture is of a two-way street REM sleep brain activation provides the formal substrate for waking consciousness and waking consciousness provides the perceptual building blocks for dream consciousness.

Neural systems involved in vigilance state regulation wakefulness

During REM sleep, the cortical EEG profile returns to low-voltage high-frequency activity, but is accompanied by an overall lack of movement and postural tone. A more detailed review of the EEG EMG profile of NREM and REM sleep is provided later in this chapter. Baron Constantin Von Economo studied the worldwide flu epidemic in the late 1920s, and observed that in patients who developed encephalitis lethargica, a neuropsychiatric disorder characterized by either severe insomnia or hypersomnia, the anterior hypothalamus was damaged in the post-mortem tissue of patients that had suffered from insomnia whereas damage posterior to the hypothalamus at the junction of the forebrain and brainstem was identified in patients that exhibited excessive sleepiness 7 . Therefore, he concluded that the brain's sleep-inducing regions were located in the anterior hypothalamus, and wakefulness-promoting regions were located in the posterior hypothalamus. As described below in the...

GABAergic preoptic nuclei

Gamma-aminobutyric acid (GABA) is the most prominent inhibitory neurotransmitter in the central nervous system. A variety of anesthetics and hypnotics act on GABA receptors. For example, benzodi-azepines depress wakefulness arousal circuitry by means of modulation of the GABA-A receptor. Although GABA is an important neurotransmitter for sleep induction, some groups of GABA neurons may be involved in wakefulness as well as REM sleep control (see below). The ventrolateral preoptic nucleus (VLPO) receives input from a variety of different nuclei of the arousal circuitry, including serotonergic and nor-adrenergic input 104 . VLPO projections to a variety of the wakefulness-related nuclei use the neurotrans-mitters galanin and GABA 105 . The core of VLPO contains neurons that largely project to TMN, while the extended cluster surrounding region is more connected to other arousal-related regions, such as LC and the raphe nuclei 105 . Specific lesions located in the central cluster of VLPO...

Noradrenergic and serotonergic inhibition of REMactive neurons

Noradrenergic and serotonergic neurons have been described as wake-on REM-off. These neurons decrease activity as REM sleep approaches, and are largely silent during REM sleep. LC noradrenergic and raphe serotonergic neurons counteract the REM-on neuronal activity of LDT PPT neurons, by means of a substantial projection to LDT PPT that acts on inhibitory alpha 2 adrenergic and 5-HT1A receptors, respectively (for review, see 25 ). As depicted in Figure 2.4, Thakkar and colleagues demonstrated that REM-on neurons of LDT PPT, but not wake REM-on neurons, were inhibited by 8-OH-DPAT, a selective 5-HT1A agonist 128 . Sero-tonergic REM-off neurons act on LDT PPT neurons, thus accounting for their REM-selective discharge (with the same effect postulated for LC nor-adrenergic neurons). Therefore, during REM sleep, as serotonergic raphe and noradrenergic LC neurons cease activity, LDT PPT neurons are disinhibited.

Neurophysiology and neuroimaging of human sleep

This chapter reviews the characteristics of human sleep, with particular emphasis on REM NREM sleep stages and their physiological correlates, and describes the electrophysiological assessment of normal sleep and sleep disorders with polysomnography (PSG), as well as the standardized clinical tests utilized to establish the daytime consequences of sleep disorders the multiple sleep latency test (MSLT) and the maintenance of wakefulness test (MWT). The organization of sleep (sleep architecture) in young healthy adults, and the effects of age, psychiatric disorders, and psychoactive medications on sleep architecture are discussed. Finally, several neuroimaging techniques are described, including functional magnetic resonance imaging (f-MRI), positron emission tomography (PET), and high-density

Monitoring normal human sleep

EEG, since it was first utilized by Hans Berger in 1929 to describe brain rhythms (alpha, beta) generated during waking 42 , has been extensively employed to investigate sleep activity. In combination with EMG (which assesses muscle activity) and EOG (which measures eye movement), EEG has played a critical role in characterizing the different stages ofNREM as well as REM sleep. EOG electrodes are placed in pairs (above and below the eye or to the left and right of it) in order to track vertical and horizontal eye movements. EOG electrodes can detect the slow, rolling eye movement associated with NREM sleep stage N1 as well as the rapid eye movements that occur during REM sleep. EMG recordings are performed to monitor changes in tonic and phasic muscle activity during sleep. For example, EMG activity is markedly decreased during REM sleep, when skeletal muscles are virtually paralyzed (atonia). EMG is usually recorded from chin electrodes over the submen-talis muscle. Additional...

Monitoring abnormal sleep polysomnography

The diagnosis of sleep disorders or for clinical research 45 . In addition to EEG, EOG, and EMG activity, the variables monitored during clinical PSG include (a) limb movements via EMG electrodes on arms and or legs (b) electrocardiogram (ECG) using chest leads (c) respiratory effort with thoracic and abdominal piezoelectric belts or respiratory inductive plethysmography (RIP) belts (d) airflow at nose mouth via heat-sensitive devices called thermistors and or nasal pressure transducers and (e) oxygen saturation via pulse oximetry. PSG is commonly indicated for (1) the diagnosis of sleep-related breathing disorders (SRBDs) (2) titrating positive airway pressure (PAP) in patients with SRBDs (3) cases of suspected narcolepsy and (4) monitoring sleep behaviors (parasomnias) that are potentially harmful or are particularly unusual for age of onset, duration, and frequency of occurrence 46 . PSG is also employed in patients with neuromuscular disorders reporting sleep complaints, in...

Clinical tests to establish daytime sleepiness

Sleep-related complaint reported by patients seen in sleep disorder centers 47 . Sleepiness can be caused by sleep deprivation, sleep fragmentating disorders (e.g. sleep apnea) 48 , disorders of central hypersom-nolence (e.g. narcolepsy), or certain types of medications 49 . Decreased productivity, problems in interpersonal relationships, and increased risk for motor vehicle accidents are some of the most common consequences of excessive sleepiness 50 . Daytime sleepiness can be measured with subjective questionnaires, such as the Stanford sleepiness scale (SSS) 51 and the Epworth sleepiness scale (ESS) 52 , or by using objective electrophysiological tests. The SSS ratings reflect the subject's self-reported level of sleepiness at the time of report, while the ESS scores indicate the subject's self-evaluated propensity to fall asleep under various circumstances. Both questionnaires, although inexpensive and easy to administer, can be confounded by factors such as the individuals'...

Applications of neuroimaging techniques in sleep medicine

Over the last two decades, several neuroimaging techniques, including positron emission tomography (PET), anatomical and functional magnetic resonance imaging (MRI and fMRI), magnetic resonance spectroscopy (MRS), single photon emission computed tomography (SPECT), and high-density electroencephalography (hd-EEG), have been increasingly utilized in research and clinical settings (Table 3.5). For example, neuroimaging techniques have been employed in a range of experimental conditions to further our understanding of normal brain activity during wakefulness. Additionally, given their ability to provide valuable information on brain activity changes in different states of vigilance (e.g. sleep-wake cycle) 8 as well as in various pathological conditions (e.g. psychiatric and sleep disorders) 107,108 , these techniques have been used in sleep research to better characterize fundamental aspects of normal sleep and of sleep disruption. Some of these aspects include (a) the functional...

Neuroplasticity and sleep

Neuroimaging studies have begun to reveal the relationship between waking activities such as learning and memory, which induce brain plasticity, and sleep. For example, recent PET studies found that several brain areas, including sensorimotor, premo-tor, and anterior cingulate cortices, which were activated during a serial reaction time task, had higher rCBF and showed a stronger functional connectivity during REM sleep in previously trained, relative to untrained, subjects 134,135 . Furthermore, two fMRI studies that employed either motor-sequence memory 136 or visual texture discrimination 137 tasks reported that the brain areas involved in learning these tasks showed higher activity 12 hours after a training session in subjects who were allowed to sleep relative to the subjects who were kept awake. These findings suggest that neuronal plasticity occurring during waking has an effect on subsequent sleep and that sleep might have a role in modulating these plastic changes.

The problem with evolution

These complex interactions have led to much confusion regarding sleep function. First, not all changes in the brain or the body during sleep may be critically important in a given species. Some may reflect vestigial aspects of sleep that once were adaptive, but during the course of evolution have lost their importance, much like the appendix, or pilo-erection in humans. An example of such a vestigial sleep process may be sleep-related changes in thermoregulation in humans 11 . A reduction in heat production (and associated metabolism) during sleep may have been an adaptive, energy-conservation strategy in our smaller mammalian ancestors (the so-called energy conservation theory of sleep) 23,24 , but the energy savings obtained in humans is minuscule 6 - and likely offset by the increased brain metabolism of REM sleep 25 .

Ontogenetic considerations

Sleep amounts, brain activity, and sleep regulation undergo dramatic transformations during development 31 . The most prominent changes are in the amounts and types of sleep, with overall sleep amounts (and REM sleep in particular) being much higher in early life than at any other point in the lifespan 31 . The regulation of sleep is also quite different in developing mammals. Circadian rhythms in sleep and wake are not observed at birth, even though the states of REM and non-REM (NREM) sleep are present in many species 31 . The classic homeostatic increases in EEG slow-wave activity and REM sleep amounts following sleep deprivation are also absent in neonatal juvenile rats 32,33 and appear quite abruptly coincident with changes in sleep-deprivation-induced neurotrophins 34 . On the other hand, neonatal sleep time is finely regulated 32 , which suggests (see below) that it must serve some purpose for the developing animal. Sleep in developing non-mammalian vertebrates and...

Neural theories of sleep function

A universal feature of sleep across the animal kingdom is that it involves both behavioral and neural withdrawal from the outside world. Behaviorally, this is manifested by an animal constructing and or securing an isolated area that is safe from predators and reduces exogenous sensory input. Neurologically, sleep is associated with the activation of inhibitory mechanisms that reduce sensory transmission through the thalamus, and during REM sleep, inhibit motor output 7,90 . In addition, while the effects of sleep loss on somatic function are variable, and possibly restricted to certain mammalian species, the effects on neural functioning appear more conserved 10,91-93 . Generally speaking, sleep loss results in cognitive deficits in animals as diverse as the fruit-fly 93 to man 10 . These findings strongly suggest that the core function of sleep concerns the brain. As originally proposed at the beginning of the twentieth century, the hypnotoxin theory of sleep function posited that...

Definitions and methodological issues

It is important to notice that dreaming as a mental activity during sleep is not directly measurable two boundaries have to be crossed (sleep-wake transition and time) before the person can report the subjective experiences which occurred during sleep. This leads to the problem of validity, i.e. is the dream report an appropriate account of the actual dream experience (see Dream content analysis section). The second question which has been raised by Maury 11 is whether the dream report reflects mental activity during sleep or is merely produced during the awakening process. Modern research combining physiological approaches with dream content analysis, however, has been able to demonstrate that dream reports are accounts of mental activity during sleep since physiological parameters (e.g. eye movements, heart rate) during REM sleep at least partially match with dream contents elicited upon awakening (cf. 12 ). In addition, the incorporation of stimuli applied during sleep into dreams...

Dreams and psychopathology

Regarding dream recall, many studies failed to show marked differences among various diagnostic groups, such as schizophrenia, eating disorders, etc., and healthy controls 61 . An exception is depression where patients have a reduced dream recall frequency 69,70 the reduction was again related to symptom severity 71 . The explanations for the reduced dream recall in depressed patients, however, remain unclear. The question of whether the typical sleep architecture of depressive patients (decreased latency to REM sleep), cognitive impairment often found in severely disturbed patients, or intrinsic alterations related to depression is responsible has yet to be answered.

Dream content and sleep physiology

First of all, researchers were interested in whether the typical eye movements of REM sleep are related to gaze shifts within the dream. The studies yielded inconsistent results (for a review see 12 ), but Herman et al. 86 who carried out the most sophisticated study concluded that there is a small but substantial relationship, i.e. some eye movements correspond to dream content and some do not. For deliberately carried out gaze shifts during lucid dreams, the results are more clear. Proficient lucid dreamers can carry out prearranged eye movements while dreaming, e.g. right-left-right-left. These patterns can be identified in the EOG pattern with high reliability (see 87 ). Previous studies investigated the relationship between other peripheral parameters, like EMG, heart rate, respiratory rate, and sexual excitement (cf. 12 ). Wolpert 88 , for example, found that dreams which included many dreamed movements are associated Even though the findings regarding peripheral parameters and...

Daytime habits and behaviors

Daytime behaviors can adversely affect nocturnal sleep and aggravate insomnia. The patient's daytime activities and their timing should, therefore, be systematically explored. Intense exercise too close to bedtime can disrupt sleep 18 . Long periods of bed rest, inactivity, and excessive napping can foment circadian rhythm disturbances and aggravate insomnia. Exposure to bright light can be helpful in establishing circadian cycling and, conversely, lack of sufficient light exposure during the morning hours can disrupt sleep timing. Frequent travel and shift work can also disrupt sleep and contribute to both insomnia and daytime sleepiness. It is useful to understand the patient's preferred social and occupational activities as this information can be helpful in devising a daily structure that promotes consistent sleep scheduling.

Sleeprelated habits and behaviors

Although not typically explored in the routine psychiatric evaluation, the behaviors in which the patient engages during the few hours prior to bedtime, during bedtime hours, and just after morning awakening can cause or significantly intensify existing insomnia. These are listed in Table 6.2. Although t. Fl ise rate (he tunen (i e.r last 2 widrs) SEVERITY of your insomnia problemis). Total score ranges from 0-2B 0-7 No clinically significant iisoiiuiia S-t-4 Subthreshold iiisomrifl i5-ll CUcd insomnia(moderate severity) 32-21 Clinical insomnia (severe) Figure 6.1 The insomnia severity index. Reprinted, with permission, from 17 . Copyright Charles M. Morin, these factors are seldom the lone cause of an insomnia complaint, a lack of awareness of them can lead to a failure in other treatment modalities. Similarly, the patient's attitude towards their insomnia can itself have an important influence on dysfunctional beliefs and attitudes as well as sleep-related anxiety as bedtime...

Parasomnias history of the chief complaint

The time of night that they occur, whether the patient remembers the event, whether there is associated dreaming, and age of onset should be evaluated. For example, disorders of arousal such as sleepwalking and night terrors usually occur during the first third of night since they arise from slow-wave sleep, are associated with amnesia for the event or a vague sense of imminent danger, are not associated with reports of dreaming, are common in childhood, and decrease in incidence with increasing age. On the other hand, REM sleep behavior disorder (RBD) is more likely to occur in the latter portions of the night since it arises from REM sleep, is often associated with intense dreaming and later memory of the dream and associated behaviors, and is more common in middle and older age 28 . A good approximation of the frequency of the episodes and their potential danger or other consequences (e.g. daytime sleepiness) is helpful, as this will help guide the...

Past medical psychiatric and surgical history

Co-morbid disorders should be reviewed, along with their dates of onset, types of treatment, and results of treatment. Surgeries and hospitalizations should also be evaluated. Major medical disorders can affect sleep by virtue of their psychological impact, through pain and discomfort, as well as direct effects on sleep and wakefulness. It is important to note that myriad psychiatric illnesses are associated with sleep disturbance, and careful evaluation of the timing of the sleep complaint in relation to psychiatric symptoms may be of high value in patients with psychiatric illness. For a review of psychiatric disorders and their effects on sleep, please see Section VI of this book. Additionally, the patient may have a history of a primary sleep disorder, and review of prior documentation including results of polysomnographic studies and other laboratory tests may be extremely helpful. For a review of primary sleep disorders, please see Section IV of this volume.

Differential diagnosis

Table 6.3 outlines some of the more commonly encountered sleep disorders that are related to insomnia and ES. The differential diagnosis of the parasom-nias is discussed in Chapter 10 Parasomnias. Several disorders may present with either insomnia and or ES, which may complicate the differential diagnosis. Thus, it is important for the practicing clinician to be familiar with some common symptoms of sleep disorders, to aid in the evaluation and management of sleep complaints.

Symptoms of specific disorders

The existence of certain symptoms in addition to insomnia and or ES can indicate the presence of specific disorders as a cause of these complaints. Defining symptoms for a selected list of sleep disorders are listed in Table 6.4. Defining symptoms for the para-somnias is discussed in Chapter 10 Parasomnias. These symptoms should be systematically explored to refine the diagnostic possibilities. Readers are referred to Sections IV and VI of this book for a more detailed discussion of each disorder and its hallmark symptoms.

Scales and inventories

A few of the more commonly utilized inventories have already been described, including the insomnia severity index, the fatigue severity scale, the Epworth sleepiness scale, sleep diaries, and the Mallampati airway classification. The STOP-bang scoring model 35 is a method that was recently introduced, which strives to predict the risk of OSA without the use of polysomno-graphy, the gold-standard procedure for the diagnosis of the disorder (Figure 6.6). It includes elements of the history and physical examination, and was validated in preoperative patients. Yes answers to three or more questions place the patient at high risk for OSA. The questionnaire was validated in a mixed group of preoperative patients against in-lab polysomnography. Sensitivities and specificities of the questionnaire are, respectively, as follows for mild OSA (apnea-hypopnea index, or AHI, between 6 and 15), 83.6 and 56.4 for moderate OSA (AHI between 16 and 29), 92.9 and 43.0 for severe OSA (AHI greater than...

Tests and consultations

Serum laboratory tests have not been systematically explored in the evaluation of insomnia and ES. However, it seems reasonable that, providing they have not been performed in the past 6 months to 1 year, general serum laboratory tests including thyroid function insomnia or ES and associated RLS symptoms, and a level of 50 mg L or less is considered significant. Actigraphy utilizes small, wristwatch-like devices to record movement. It assumes that lack of movement is equivalent to sleep, and is not, therefore, useful to measure exact sleep times. Although it is not appropriate for the routine diagnosis of sleep disorders, it can be useful as an adjunct to other procedures for the assessment of sleep-wake patterns when such information is not reliably available by other means such as sleep logs. It can be appropriate for the documentation of changes in sleep patterns over prolonged diagnosis and treatment periods for the assessment of whether an insomniac follows certain sleep hygiene...

Epidemiology of restless legs syndrome and periodic limb movement disorder

RLS is generally divided into primary (idiopathic) and secondary forms, the latter of which will be discussed later in the chapter. Several studies have shown that the overall prevalence of RLS is roughly 5-10 of the general population (e.g. 10 ), though the prevalence of persons in which medical treatment is indicated is estimated to be one-fifth to one-third of affected individuals 11 . Population studies have revealed two potential subtypes of primary RLS. One RLS subtype is characterized by onset of symptoms in early life, with a significantly higher prevalence of affected relatives 12 . These patients are believed to have a relatively low rate of small-fiber neuropathy 13 , compared to those with a later age at symptom onset. A second subtype consists of patients without a family history of the disease, have a later age of symptom onset, higher incidence of neuropathy 14 , and lower serum ferritin levels 15,16 . One study found that patients with a later onset of RLS are more...

General considerations

Patients with sporadic or only mild RLS symptoms without significant impairment in daily life are likely not to need pharmacological treatment. No data is yet available on the prevalence of RLS requiring pharmacological treatment. It is estimated that approximately 2-3 of the population have RLS leading to reduced quality of life 10 . A recent epidemiological study in Germany reported an 8.8 prevalence of RLS, and 1.6 of the whole study population had a wish for treatment 11 . Before starting pharmacological treatment, sleep hygiene measures should be

Affective disorders in RLS

Sustained sleep disturbances in RLS may have particular relevance in the development of affective disorders, especially depression. RLS symptoms appear in a circadian manner with maximum severity between midnight and 4 a.m. and disturb sleep in patients with moderate to severe symptoms, and as such are likely to cause insomnia symtoms. There is a strong relationship between insomnia and depression and studies have shown that subjects with chronic insomnia are at a high risk of developing major depressive disorder (MDD) later in life 101,102 . On the other hand, sleep disruption might not exclusively account for the relationship between RLS and depression in a large cohort of patients with chronic kidney disease, the presence of RLS was significantly associated with depressive symptoms independent of insomnia as well as other relevant socio-demographic and clinical factors 103 . The treatment of co-morbid depression and RLS has some unique aspects of which practicing clinicians should...

Other sleeprelated movement disorders

Sleep-related bruxism is the grinding or clenching of teeth during sleep, which may lead to abnormal wear of the teeth, jaw muscle discomfort, temporomandibu-lar disorder, insomnia, orofacial pain, and hypertrophy of the masseter muscle. The tooth-grinding sound may also disrupt the sleep of the bed partner. The prevalence of bruxism is reported to be around 8 and declines with age 110 . The etiology is unknown, though anxiety and stress are generally regarded as potential predisposing factors. Serotonin may be involved in its development, since SSRIs have been reported to exacerbate sleep-related bruxism 111,112 .

Behaviorally induced insufficient sleep

Voluntary lifestyle choices, job or school demands, shift work, or poor sleep hygiene. Although insufficient sleep might be expected to lead to frank EDS, a constellation of other subjective complaints are more commonly seen, including tiredness, lack of energy, or fatigue. Decrements in attention, learning capacity, short-term memory, and psychomotor performance, with or without EDS, also may be present. Moreover, irritability, poor impulse control, or other forms of mood instability may exist alone or in combination with these features in individuals with insufficient sleep. While it is obvious that complete sleep deprivation compromises performance and well-being, until the last decade an erroneous belief has persisted that people adapt to chronic sleep loss without significant compromise. This is being challenged by a rapidly expanding literature suggesting a wide range of adverse medical, cognitive, and socioeconomic effects of sleep loss and untreated sleep disorders 21 . The...

Psychiatric disorders

Insomnia to a primary sleep disorder thus, attention to both psychiatric and potential sleep disorders provides the most comprehensive and appropriate care in the excessively sleepy patient (Box 9.2). While it is true that tiredness, fatigue, and or lack of energy are reported by a majority of patients with major depression, evaluation of EDS with subjective rating scales and objective measures suggests that frank sleepiness or a high sleep propensity may be less common than the complaint of fatigue or lack of energy 79 . Only a few studies have evaluated objective measures of sleepiness, such as the MSLT, in depression. These produce somewhat conflicting results, but overall suggest that most patients with depression maintain a normal level of daytime alertness and sleep propensity on MSLT 80 . Decreased sleep latency, shortened REM latency, and increased REM percentages are reported on overnight polysom-nography in both sleep-deprived, non-depressed patients and suicidal patients...

Medications and sleepiness

Side-effects from some psychiatric medications and non-prescription substances must be considered in the evaluation of a patient complaining of EDS. Special consideration should be given to sedating antidepressants, antipsychotics, antiepileptics, hypnotics, or sleep aids. Many psychotropic medications involve antidopaminergic, antiadrenergic, anticholin-ergic, or antihistaminic activity, all of which can contribute to sleepiness or fatigue. While side-effects are typically worse at drug initiation or during dose escalations, patients on stable dosing may continue to have sedation or fatigue related to their medication regimen. Many of the medications used in psychiatry have half-lives which lead to drug accumulation, and it is thus not surprising that even medications used at bedtime can produce EDS, as daytime serum levels of sedating medications can be many times higher than the maximum serum concentration immediately after drug initiation. For shorter-acting agents, one potential...

Sleepwalking and sleep terrors overview and clinical description

Though often unnecessary in typical, benign cases of SW and ST, PSG is indicated when they have an adult onset (as this may indicate another underlying precipitating sleep disorder), when there is risk of significant injury to oneself or another person, or when there is substantial disruption of one's sleep or the sleep of the bed partner. Such studies should include an expanded seizure montage of EEG channels, electromyographic (EMG) monitoring of four limbs to detect movement, and continuous audiovisual monitoring (that is time-synchronized to the PSG), in order to rule out seizure disorder, REM sleep behavior disorder (RBD), OSA, PLMS, or other primary sleep disorders 25,26 . Electrocardiogram More recent reports provide no basis for a psychiatric etiology of parasomnias. In a retrospective review of 11 cases of ST, though 7 11 patients reported an influence of stress on their disturbance, none had a diagnosis of panic disorder and the course of the sleep disorders did not overlap...

Somatic theories of sleep function

The cycling of leptin and ghrelin in humans reflects the influence of sleep, or independent circadian rhythms in the release of these peptides 8 . Studies in rodents have produced mixed results. The putative associations between leptin and ghrelin release and sleep observed in humans do not occur in rats 73 . Constitutive knock-out of leptin (ob ob) 74 or leptin (db db) receptors 75 in mice results in abnormal sleep patterns (increases in NREM sleep, sleep fragmentation), but it is not clear if these changes are secondary to other abnormalities, developmental or otherwise, in these mouse lines. For example, ob ob mice do not thermoregulate normally 74 , and ob ob and db db mice both display abnormal levels of motor activity 74,75 either abnormality would be expected to impact sleep expression, if only indirectly. Ghrelin knock-out mice display even fainter sleep phenotypes, displaying modest increases in NREM sleep time versus wild-type mice both in the baseline and following recovery...

Summary and conclusions

The discovery of REM sleep, and its association with dreaming by Aserinsky and Kleitman in 1953, was first greeted by many in the psychiatric community as an opportunity to confirm Freud. But as the second half of the twentieth century evolved, it become more and more clear that REM sleep likely has biological significance that transcends dreaming. During this same period, the field of sleep medicine exponentially developed, with many biologically oriented psychiatrists contributing significantly to this nascent medical specialty. Significant progress in basic sleep and dreaming research has yielded new insights previously unimaginable at the dawn of psychiatry. Now, in the twenty-first century, psychiatric sleep medicine continues to move forward with developments in sleep genetics, bioenergetics, neurophysiology, and neuro-pharmacology. Within modern paradigms, it seems more likely that REM sleep (and dreaming) are the handmaidens of waking consciousness, rather than the royal road...

Evaluation of the patient with EDS

Thorough screening for primary sleep disorders includes assessment of the presence of snoring, witnessed apneas, symptoms of restless legs syndrome, periodic limb movements, and restless sleep or non-refreshing sleep. Medical conditions and alcohol or drug use can be significant contributors to EDS if any of these are suspected, appropriate evaluation should ensue. Any chronic sedating medications should also be noted. If a thorough history and physical examination raises suspicion of disorders such as periodic limb movements, obstructive sleep apnea, nocturnal seizure, or parasomnia, then nocturnal polysomnography (PSG) - overnight sleep study - may be indicated to either rule out sleep disturbances or to quantify their severity. This is typically related to sleep disorders that produce sleep fragmentation or sleep inefficiency including sleep-related breathing disorders, periodic limb movement disorder, REM sleep behavior disorder, other sleep-related movement disorders,...

Conclusions and recommendations

Insomnia, ES, and parasomnias are commonly encountered in psychiatric practice. They are the hallmark symptoms of a variety of sleep disorders, many of which will be discussed in greater detail in the ensuing chapters. This chapter has focused on the critical first steps in bridging symptom with disorder, namely the history and examination. These represent the cornerstones of the evaluation process. Below are some key recommendations that emerge from this chapter 8. Ask for symptoms of specific sleep disorders

The reciprocal interaction model

McCarley and Hobson proposed the reciprocal interaction model to explain the transitions into and out of REM sleep states, described by the Lotka-Volterra equations, derived from population models of predator prey interaction 136 . The limit cycle model, an update of the reciprocal interaction model, incorporated circadian and local GABAergic influences on REM sleep regulation 118,137 . As reviewed in Figure 2.5, select cholinergic neurons of LDT PPT increase firing prior to and during REM sleep. These cholinergic neurons specifically direct the firing of reticular formation neurons (SubC, parabrachial nucleus, and PnO), whose glutam-atergic output is responsible for the activation of the various components of REM sleep described above, including muscle atonia, PGO wave generation, and hippocampal theta activity. LDT PPT neurons also project to GABAergic interneurons of RF. Therefore, inhibition of these GABAergic RF neurons, which inhibit REM-on RF neurons, provides positive...

Idiopathic hypersomnia

Headache, anxiety, irritability, hypertension, palpitations, appetite suppression, tremor, insomnia Lifestyle and behavioral modifications, including good sleep hygiene, are appropriate first steps. As with narcolepsy, treatment with traditional stimulants or modafinil is usually necessary and often provides some benefit. Unfortunately, response to these treatments is often unsatisfactory. None of these medications are FDA approved for the treatment of idiopathic hypersomnia.

Excessive sleepiness ES history of the chief complaint

Sleepiness, the tendency to fall asleep, is a normal phenomenon when it occurs at the desired time of the day. ES is the tendency to fall asleep at inappropriate times or settings 4 . ES should be distinguished from fatigue, which is classically defined as the inability to sustain performance over time and is typically associated with subjective reports of tiredness, weariness, exhaustion, and lack of energy 21 . Even though fatigued patients can perceive themselves as being excessively sleepy, in its pure form, fatigue does not result in an increased propensity to fall asleep. Fatigue is a symptom of a wide variety of medical, psychiatric, and neurological disorders and less specific for sleep disorders than is ES. It has been most widely examined in the context of multiple sclerosis, autoimmune disorders, and psychiatric conditions (Figure 6.3). Also, a complaint of ES may co-occur with that of hypersomnia, which is an abnormal increase in time spent asleep or trying to sleep. In...

Social and occupational history

Several social or occupational factors can contribute to sleep-related complaints, necessitating evaluation. For example, ES and insomnia are common in shift workers and individuals whose occupations require frequent travel across time zones. Exposure to industrial toxins and chemicals can also produce sleep wake symptoms. Job loss and retirement can result in the loss of regularity in daily schedule, which is important in maintaining circadian rhythm consistency in some individuals, leading to erratic sleep wake hours and the complaints of insomnia and ES. Disruption in interpersonal relationships, family, job, and hobbies can cause anxiety and subsequent insomnia.

Cognitive theories of sleep function memory synaptic plasticity and neurodevelopment

Early critics pointed out that the effects of sleep on various forms of animal learning were inconsistent and confounded by the use of stressful forms of sleep deprivation 61,160 . Nor were the results of early human studies particularly encouraging. Many studies found no effect of sleep loss (generally REM sleep) on verbal learning tasks (e.g. word association), and those that did reported relatively marginal effects 61,160 . Therefore, after a flurry of interest, many scientists concluded that sleep had nothing to do with memory and the search for sleep function shifted elsewhere 61,160 . Beginning in the late 1980s several investigators have shown that sleep states influence tetany-induced LTP in animal models (reviewed in 13,177 ). Overall, it appears that hippocampal LTP can be induced during REM sleep, whereas similar stimulus protocols during NREM sleep have no effect or produce LTD 178-180 . Subsequent investigations have shown that sleep and...

Functions of dreaming

Prior to reviewing the major theories regarding dream function, two very important issues have to be discussed. First, it is crucial to differentiate between the physiological level (REM sleep) and the psychological level (dreaming). This was not clarified in one of the first publications on REM sleep deprivation 113 . Since dreaming as subjective experience which is recallable after awakening does not reflect the total brain activity during REM sleep or other sleep stages, the functions of sleep and particularly REM sleep must not parallel the functions of dreaming. REM sleep, for example, is important for memory consolidation, especially procedural and emotional memory (cf. 114 ), but whether dreams are related to this memory consolidation has not been Despite these problems, a variety of researchers have proposed different functions of dreaming which are listed in Table 5.7. Flanagan 118 , for example, put forward the idea that dreams are a pure epiphe-nomenon of sleep, especially...

Editors introduction

Sleep and psychiatric illnesses are powerfully linked in numerous ways. This is likely because, at both the observable and neurobiological levels, what and how we think and behave influences our sleep, and conversely, how we sleep influences our thinking and behavior. The most prevalent sleep complaint, insomnia, is frequently co-morbid with mental illness and is linked to a host of neuropsychiatric symptoms. In fact, insomnia may be present across the entire history of psychiatric disorders as a risk factor for the development of incident mood, anxiety, and substance use disorders, as well as a symptom of active illness, an iatrogenic response to psychotropic medications, and risk factor for symptomatic relapse in a number of psychiatric disorders. The value to psychiatrists of understanding sleep medicine has become increasingly evident over the past 20 years. The neuropsychiatric sequelae of primary sleep disorders such as sleep-related breathing disorders, sleep-related movement...

Dream deprivation

William Dement, widely recognized as a pioneer in the field of sleep medicine, and a graduate student and psychiatrist working in Kleitman's laboratory at that time, was more interested in the dream story than his physiologist colleagues 6,7 . Dement was motivated by the conviction that he could test Freud's dream theory rigorously using the burgeoning knowledge of sleep physiology and REM sleep. By preventing subjects from entering REM with enforced awakenings, he and the neurobiologically educated psychoanalyst, Charles Fisher, theorized they could prevent dreaming and thus cause psychological distress in their subjects 8 . Although their subjects did become psychologically distressed, they were perhaps more importantly increasingly difficult to awaken from sleep. By the fifth night of the experiment, subjects made no less than 50 attempts to enter REM (up tenfold from five such attempts on the first night). This observation indicated that REM sleep, if not dreaming, was carefully...

Dream consciousness

Figure 1.4 Physiologicalsigns and regionalbrain mechanisms of REM sleep dreaming separated into the activation (A), input source (I), and modulation (M) functionalcomponents of the AIM model. Dynamic changes in A, I, and M during REM sleep dreaming are noted adjacent to each figure. Note that these are highly schematized depictions which illustrate globalprocesses and do not attempt to comprehensively detailallthe brain structures and their interactions which may be involved in REM sleep dreaming. From Hobson JA, Pace Schott EF, Stickgold R. Dreaming and the brain toward a cognitive neuroscience of conscious states. Behav Brain Sci. 2000 Dec 23(6) 793 842,2001 Cambridge Journals, reproduced with permission. I would argue that this dogma has outlived its utility. If dreaming is not so much unconscious mental activity in a Freudian sense but is, instead, an intensely conscious experience that is not remembered, our theoretical perspective changes dramatically. Dream consciousness is...

Acetylcholine

Neuroanatomical studies have defined the BF, including cholinergic neurons, as a principal relay for ascending activation of neocortical regions in the ventral arousal pathway. Double-labeling experiments (employing immunohistochemistry techniques to determine the cholinergic phenotypes of BF neurons, in combination with retrograde tract tracing techniques) have demonstrated BF cholinergic projections to widespread cortical regions 15,16 . This technique has also been used to describe the more specific projections of the medial septum vertical limb of the diagonal band of Broca to the hippocampus, including both GABAergic and cholinergic input (for review, see 17,18 ). These septo-hippocampal projections are part of the brain circuitry involved in the generation of the EEG theta wave, recorded in the hippocampus during REM sleep, as well as Unlike other wakefulness-related neurotransmit-ter systems that are described in this chapter that are typically decreased in both NREM and REM...

Serotonin

Several midbrain brainstem regions rich in serotonin (5-HT), i.e. the dorsal, median, magnus, obscurus, and pallidus raphe nuclei 35,36 , are involved in vigilance state regulation. Serotonin plays a complex role in vigilance state regulation, due to its actions in different brain regions, as well as the complexity of the multiple serotonergic auto- and heteroreceptors distributed throughout the arousal circuitry. Serotonergic neurons send projections to many areas involved in vigilance state regulation. These neurons are most active during wakefulness, have considerably decreased firing during NREM sleep, and cease activity during REM sleep 37,38 . Correspondingly, 5-HT levels in various brain regions, including the neocortex, significantly rise during wakefulness, and decrease considerably during NREM and REM sleep 39,40 . Recent neurochemical and electrophysiological investigations conclude that serotonin promotes wakefulness and inhibits REM sleep, complementing the action of...

Noradrenaline NA

The locus coeruleus, located bilaterally in the dorsolateral pons, contains a large group of noradren-ergic neurons. Similar to serotonergic neurons, noradrenergic neurons of LC project to widespread areas of the neuraxis, and are most active during wakefulness, minimally active during NREM sleep, and cease activity during REM sleep 53,54,55 . Non-specific lesions of the LC lead to a minimal decrease in wakefulness behavior and attenuation of the cortical EEG indicative of wakefulness 56 . This may be due to the redundancy of systems involved in vigilance state regulation, for the many wakefulness-related neurotransmitter systems described here act similarly on the brain nuclei comprising the dorsal and ventral arousal pathways, as well as in the cortex. Emotional states that involve an increase of NA activity (e.g. stress) may lead to overexcitation of arousal regions, causing vigilance state dysregulation, such as that seen in insomnia 57 .

Histamine

Older generation antihistamines, known to cross the blood brain barrier, have sedating effects, acting as antagonists largely on the histamine 1 (H1) receptor of wakefulness-related nuclei 69 . Histaminergic neurons are located in the tuberomammillary nucleus of the posterior hypothalamus (TMN), and project to a number of the arousal-related brain nuclei, as well as directly to the cortex 70,71 . The discharge profile of these neurons matches that of noradrenergic and sero-tonergic neurons, where most action potential firing occurs during wakefulness, considerably less firing is observed during NREM sleep, and firing ceases during REM sleep 72,73,74 . Histamine release in the posterior hypothalamus is highest during wake, lower during NREM sleep, and minimal during REM sleep 75 , matching the discharge profile. An investigation by Siegel and colleagues recently revealed a unique role of histaminergic neurons in the maintenance of wakefulness 74 . Cataplexy is a sudden loss of muscle...

Orexin hypocretin

Neurons containing the neuropeptide orexin (also called hypocretin) are located largely in the periforni-cal region (near the fornix) of the lateral hypothalamus. Recent investigations reveal a unique role of orexin neurons in vigilance state regulation, as well as in the sleep disorder narcolepsy, by means of their extensive input to a number of sleep wake-related nuclei 79,80 . Direct application of wake-promoting agents into the LH increases orexinergic neuronal activity 91 . Similar to the majority of wakefulness-related nuclei, orexinergic cell firing largely occurs during wakeful-ness, decreases considerably during NREM sleep, and ceases during REM sleep, except for some activity during REM-related muscle twitches 92 . Microdia-lysis sampling in the lateral hypothalamus found highest orexin levels during wakefulness 93 , and following examination of c-Fos protein expression it was concluded that orexinergic neurons were wake-fulness-active 94 . The unique role orexin may play in...

Conclusion

The field of sleep medicine has seen a recent investiga-tional surge, due to the development of novel experimental techniques, as well as an increased public awareness of sleep disorders and their implications. Only within the last century have investigations attempted to explain the neural mechanisms responsible for vigilance state regulation. This chapter provides a review of both the neurobiological mechanisms generating wakefulness, NREM sleep, and REM sleep, as well as the major homeostatic and circadian factors that influence the timing of these states. All human life, and indeed the life of most animals, is shaped by periods of wakefulness and sleep, and thus knowledge of the underlying mechanisms is of great biological, social, and medical significance. By furthering understanding of the neural circuitry involved in vigilance state regulation, pharmacological and behavioral treatments may then be developed to reverse the symp-tomology of a number of sleep-related disorders.

Definition of sleep

Sleep is defined by a combination of behavioral and physiological characteristics. Behaviorally, sleeping humans tend to lie still in stereotypical postures. This condition, which is characterized by a markedly reduced awareness of the outside world, is different, however, from other unconscious states like coma or anesthesia because of its prompt reversibility 10 . Using electrophysiological criteria, human sleep can be divided into two types, REM and NREM sleep. During REM sleep, bursts of eye movement activity frequently occur. REM sleep is also called paradoxical sleep because of EEG activity similar to that observed during wakefulness. On the other hand, during NREM sleep, which is also described as orthodox sleep, the EEG shows low-frequency activity.

Sleep and the body

Ontogenetic considerations are difficult to address as very little is known about the interrelationship between sleep and endocrine biology, energy metabolism, or immune function, in developing humans or animals. However, as discussed by Feinberg, peak GH release and amounts of the deeper NREM sleep stages are inversely related across development in human children 241 . One might also expect that if sleep function was tied to GH release, this would be especially true in neonates, as this a period of rapid physical growth. Yet, in both animals and humans, NREM sleep is at its nadir and REM sleep instead predominates in newborns 190,192 .

Summary

Dreams have been studied from different perspectives psychoanalysis, academic psychology, and neurosciences. After presenting the definition of dreaming and the methodological tools of dream research, the major findings regarding the phenomenology of dreaming and the factors influencing dream content have been reviewed. The so-called continuity hypothesis stating that dreams reflect waking-life experiences is supported by studies investigating the dreams of psychiatric patients and patients with sleep disorders, i.e. their daytime symptoms and problems are reflected in their dreams. Dreams also play an important role in psychotherapy the efficiency of nightmare treatment strategies in particular has been demonstrated in randomized controlled trials. The question about the functions of dreaming is still unanswered and open to future research.

Daytime symptoms

An assessment of daytime symptoms is useful in understanding the impact of insomnia on an individual's functioning. Additionally, the correction of daytime impairment is an important measure of treatment efficacy. Typically, the severity of daytime symptoms in insomnia co-varies with the degree of impairment in the quality and quantity in nocturnal sleep. At times, however, despite minimal apparent difficulty with sleep latency or nocturnal awakenings, patients can complain that sleep is unproductive and non-restorative. It is, therefore, important to independently explore daytime symptoms. As a group, insomniacs obtain less sleep than non-complaining individuals. Interestingly, however, they are generally not excessively sleepy during the course of the day, where sleepiness is defined as the tendency to fall asleep. In fact, most complain that they are unable to fall asleep during attempts at napping. This is supported by objective evidence that insomniacs are less prone to falling...

Related symptoms

How likely are you to doze off or fall asleep in the following situations, in contrast to feeling just tired This refers to your usual way of life in recent times. Even if you have not done some of these things recently try to work out how they would have affected you. Use the following scale to choose the most appropriate number for each situation Other components in the history-taking of ES are described in the section on insomnia these include daytime habits and behaviors, sleep-related habits and behaviors, and sleep patterns.

Medications

A history ofcurrent and prior medications is an integral part of the history. The list should include not only prescribed medications, but over-the-counter agents, nutraceuticals, herbal substances, dietary supplements, and even foods. Their effects, side-effects, dosages or quantities, and timing of administration should be recorded. If the use of a medication correlates temporally with the onset of the sleep complaint, a medication-induced sleep disorder should be suspected. Medications can also have secondary effects by virtue of their exacerbation of underlying conditions. For example, weight gain associated with medication use can lead to the development of symptoms of OSA, such as ES, snoring, and breathing pauses during sleep. Allergies to medications should also be recorded. The effects of commonly used medications on sleep are reviewed in Chapter 3 Neurophysiology and neuroimaging of human sleep.

Substances

Insomnia, ES, and parasomnias can be related to substance use. Chronic and excessive use of substances may lead to substance use disorders, which are characterized by either abuse or dependence. Stimulants such as caffeine, amphetamines, and cocaine classically disrupt sleep. Sedatives such as opiates and analgesics cause ES. Alcohol, at low dosages, can help with sleep initiation, yet chronic and excessive use can lead to disturbed sleep and the complaint of insomnia 29 . The effects of substances on sleep are reviewed in greater detail in Chapter 19 Sleep in substance use disorders.

ADHDandOSA

Attention-deficit hyperactivity disorder (ADHD) is a common childhood illness with prevalence between 3 and 16 . It is characterized by hyperactivity, impulsiveness, impairment in academic, social, and occupational functioning, and short attention span. OSA is also a common medical problem in children with a prevalence rate of 2 in general pediatric populations 130 . Several studies have reported a relationship between ADHD and sleep problems 131,132 . Parents of children with ADHD report decreased nocturnal sleep efficiency and sleep fragmentation in their children as compared to parents of healthy controls 133 . Experimental sleep restriction, leading to daytime somnolence, is associated with ADHD-like behavior and poor cognitive functioning. Golan and colleagues found that children with ADHD had a high prevalence of primary sleep disorders and objective daytime somnolence 134 . Thus, in evaluating children with ADHD symptoms, it is wise to consider the possibility that undiagnosed...

Antidepressants

Administration of paroxetine increased activity of upper airway dilator muscle during wakefulness in normal subjects 139 and during non-REM sleep in patients with OSA 140 , which suggested that the SSRI may be effective in treating OSA. However, in clinical studies, serotonergic drugs such as protrypti-line, fluoxetine, paroxetine, and mirtazapine have been tested as treatments for OSA, with limited improvement and significant side-effects 141,142 . Administration of the serotonin precursor, L-tryptophan, was reported to be effective in decreasing obstructive apneas in non-REM sleep in an uncontrolled study of 12 patients with OSA 143 . However, L-tryptophan was previously SSRIs are widely used to treat depressive mood and anxiety in OSA patients. Moreover, SSRIs may be at least partially (and theoretically) effective in OSA by virtue of their REM sleep suppression (as OSA tends to worsen during REM sleep when muscle tone is lowest and the upper airway is most prone to obstruct) and...

Synopsis

Excessive daytime sleepiness (EDS), hypersomno-lence, or pathological sleepiness is a complaint of increased sleep propensity occurring at inappropriate times that adversely affects vigilance, performance, and daytime function. Psychiatric, medical, or primary sleep disorders and medications can all produce complaints of EDS or fatigue. Insufficient sleep is by far the most common cause of EDS in the general population. Fatigue will not be addressed specifically in this chapter as it is a broader symptom relating to a variety of conditions of tiredness or mental or physical exhaustion and is often independent of sleepiness. This chapter summarizes the clinical presentation, diagnostic criteria, and initial treatment options for the specific subtype of EDS known as hypersomnias of central origin.

Excessive sleepiness

EDS in narcoleptic patients manifests as an increased propensity to fall asleep in relaxed or sedentary situations or a struggle to avoid sleeping in these situations. These so-called sleep attacks are often mistakenly believed to be unique to narcolepsy, but actually represent sleepiness that is identical to that of other sleep disorders such as untreated obstructive sleep apnea or sleep deprivation 17 . Epworth sleepiness scale scores of > 15 are common in untreated patients 4,17,20 . The irresistible urge to sleep commonly occurs in inappropriate or dangerous situations and thus produces significant social and occupational dysfunction. While the ICSD-2 specifies an MSLT mean sleep latency of less than 8 minutes as support for the diagnosis of narcolepsy, narcolepsy patients commonly evidence much shorter mean sleep latencies of less than 5 minutes (Table 9.1).

Endocrine disorders

Patients with chronic endocrine disorders may complain of EDS. Sleepiness is a well-recognized symptom of hypothyroidism. Additionally, hypothyroidism has been reported as a risk factor for the development of obstructive sleep apnea 75 . It is not clear in some patients with hypothyroidism whether the sleepiness they experience is due to a direct effect of the hypothy-roid state or to a co-existing SRBD. Patients with acromegaly have also been shown to have an increased prevalence of sleep apnea, with reported rates from 39 to 58.8 76,77 . On the other hand, patients with growth hormone deficiency consistently report low energy, fatigue, and impaired sleep quality 78 .

Treatment of SWST

The earliest pharmacological agents offered to individuals at serious risk of injury were diazepam 65 and imipramine 66 . Clonazepam has been reported to be effective in doses of 0.25-2.0 mg taken about 30-120 minutes before sleep. When given to 28 54 (51.9 ) patients with SW ST, it produced substantial benefit in over 80 19 . Other agents anecdotally effective include other benzodiazepines, carbamazepine, paroxetine, doxe-pin, trazodone 57 , and melatonin 67 . In cases with less imminent risk of injury, non-pharmacological therapy with clinical hypnosis may be preferred. This can also be offered initially in combination with medication, which can be gradually withdrawn. Patients are instructed in the induction of a relaxed, meditative state, with visual imagery of quiet, restful sleep associated with comfort, safety, and reinforcement of possible but minimally probable need for physical mobilization. With self-hypnosis utilized before retiring to bed, benefit has been reported in 20...

Sleep architecture

Sleep architecture refers to the organization of sleep across the recording period. Sleep recording is divided into 30-second epochs across the night, and each epoch is classified into a stage based on the predominant pattern (> 50 of the epoch). Sleep stage scoring is a standardized procedure established about 40 years ago 12 and is still routinely employed, with some recent modifications 13 , in clinical and research settings. Sleep scoring provides several measures of sleep quality and quantity. For example, sleep scoring quantifies the amount of time spent in each sleep stage. In a healthy young adult, NREM stage N1 Waking REM Sleep NREM Stage N1 NREM Stage N2 NREM Stage N3 Waking REM Sleep NREM Stage N1 NREM Stage N2 NREM Stage N3 occupies about 5 of the total sleep time, stage N2 50-60 , and stage N3 20-25 , while REM sleep (stage R) accounts for the remaining 20-25 . Periods of NREM and REM alternate in a relatively predictable temporal pattern (approximately 90-120-minute...

Physical examination

The physical examination can contribute essential information to the process of understanding the etiology of the sleep complaint. Vital signs should include the measurement of neck circumference a thick and or muscular neck, as well as a neck circumference of 16 inches or greater in women and 17 inches or greater in men, are associated with an increased risk for sleep-related breathing disorders 33 . Body habitus should be inspected obesity with fat distribution around the neck or midriff suggests the diagnosis of OSA. Other contributors to sleep-related breathing disorders include nasal obstruction, mandibular hypoplasia, and retro-gnathia. Oropharyngeal abnormalities can also be involved, including enlarged tonsils and tongue, an elongated uvula and soft palate, diminished pharyngeal patency, and redundant pharyngeal mucosa. The Mallampati airway classification score should be determined (Figure 6.5), which is useful in assessing the risk for OSA. On average, for every 1-point...

The AIM model

As the reciprocal interaction and activation-synthesis hypotheses evolved, they metamorphosed into the AIM model based on findings in sleep and dream research 23 . Basic sleep research has identified three factors that interact to determine brain-mind state. Whether we are awake (with waking consciousness), in NREM asleep (with little or no consciousness), or in REM asleep (with dream consciousness) depends upon (1) activation level (A) (which is high in wake and REM) (2) input-output gates (I) (which are open in wake but closed in REM) and (3) aminergic modu-latory ratio (M) (which is high in wake and low in REM). Thus, the AIM (Activation, Input Source, and Modulation) model proposes that conscious states can be defined and distinguished from one another by the values of these three parameters. The three factors can be used to construct a three-dimensional AIM state space as shown in Figure 1.3. Waking, NREM, and REM occupy discreetly different domains in the state space. The...

Depression in OSA

Depression is the most commonly encountered affective disorder associated with OSA 68 . The prevalence of depression in OSA has ranged from 7 to 63 69 . Early investigations by Guilleminault and colleagues reported that 24 of male patients with OSA had previously seen a psychiatrist for anxiety and depression 70 . A recent epidemiological study of 18 980 subjects representative of the general population in the UK, Germany, Italy, Portugal, and Spain found that 17.6 of subjects with a Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV) breathing-related sleep disorder diagnosis (by history, without sleep study) have major depressive disorder (MDD) 71 . Thus, some co-morbidity between SRBD and depression has long been observed. The variations in the prevalence of depression are thought to be affected by sampling characteristics, mood assessment methods, and diagnostic difficulty due to an overlap of symptoms across depression and OSA. of UARS is nocturnal esophageal...

Sleep patterns

Although the assessment of bedtime and sleep patterns is important in the evaluation of any sleep-related complaint, it is a particularly essential component of the evaluation of insomnia (Table 6.1). Patients should be asked regarding these parameters on initial and follow-up visits. These patterns can also be assessed by utilizing patient-completed sleep logs or diaries that track sleep-wake patterns over time (Figure 6.2). Sleep logs and diaries may be more useful than subjective summaries since insomniacs tend to underestimate total sleep time and overestimate sleep latency, possibly resulting from a preferential recall bias for particularly bad nights of sleep that do not reflect the longitudinal course of their complaints 19 . Ideally, individuals retire and emerge from bed at consistent times day to day, including weekends. The time spent in bed between retiring and falling asleep would preferably be less than 20 minutes, and individuals would emerge from bed soon after...

Cancer

Patients with cancer also have an elevated likelihood of EDS. Studies indicate prevalence rates of 54-68 for feeling drowsy and 21-40 for being overly sleepy in this population 72,73 . Causes of EDS in this population may be related to an increased risk of primary sleep disorders due to age alone (the average age at onset of cancer is 55 years) or a complex combination of etiologies. These include insufficient sleep due to insomnia, depression, or pain disruption or erratic hormone secretion due to the malignancy or chemotherapy, with subsequent sleep disruption or shortened sleep periods effects of cytokines and inflammatory mediators induced by cancer cells, biotherapy, or radiotherapy and side-effects from chemotherapy or other adjunctive medications 74 .

Counselling of patients after perinatal death

When a woman and her family experience a loss associated with pregnancy, special attention must be given to the grieving that they are going to undergo. Mourning is an extremely important part of coping and the clinical signs and symptoms of grief are important to recognize so that the healthcare workers can be sympathetic to this grieving process. These symptoms include sleeplessness, fatigue, poor eating habits, preoccupation with pictures of the baby, feelings of guilt, hostility and anger and a general disruption in the normal pattern of daily life. Unless the clinicians are aware of these changes, misunderstanding may occur and the ability to help the process of grieving will be lost. These families require a sympathetic person so that they have the opportunity to express and discuss their feelings in an open way. The establishment of identified individuals who are trained to deal with perinatal death is extremely important and centres should have doctors, midwives and...

Early signs and symptoms

The clinical presentation of overt thyrotoxicosis can be subtle and nonspecific. Some patients may complain of classic symptoms such as nervousness, sweating, fatigue, heat intolerance, weakness, tremor, hyperactivity, changes in weight or appetite, insomnia, exertional dyspnea, hyperdefecation, or palpitations. Oligomenorrhea occurs in about one in four women with thyrotoxicosis (25). Thyrotoxic patients, especially among the elderly, may have higher rates of depression than their euthyroid counterparts (26). Although subclinical thyrotoxicosis is usually assumed to be asymptomatic, some studies suggest it may be possible to elicit subtle physical and psychiatric symptoms in these patients (27).

NOC Child Development Infant

Promotes longer periods of alert and or deep sleep which will enhance the body's own natural defenses providing rest periods will allow infant to recover prior to initiation of additional caregiving prevents sudden disruptions in sleep promotes stability and adaptive behaviors.

What is the role of qualitative studies

Randomized clinical trials and observational studies rarely consider individual patients' perceptions or preferences. Qualitative studies fill this void. One must not forget that patients may regard risks and benefits very differently, and patients with the same medical condition may have very different symptoms, as well as completely different thresholds of tolerance for these symptoms. Some patients with asthma may suffer primarily from exertion dyspnea, while others have difficulty coping with dry cough or insomnia due to nocturnal attacks. Any trial evaluating asthma interventions for symptomatic relief ought to focus especially on what is most important to individual patients. Patient perspectives and expectations should be taken into account when designing trials to evaluate interventions.

Clinical Note continued

The middle-aged working population, and can occur in 35-50 of some groups, such as diabetics, the morbidly obese, or the elderly (> 65 years of age). Snoring is a mild form of upper airway obstruction, where the soft palate vibrates during inspiration at 40-60 Hz and impedes airflow. Obstructive apneas can occur during all sleep stages, however, often they are longer and result in more severe hypoxemia during REM (rapid eye movement) sleep. REM sleep is also called active sleep and is the sleep stage during which dreaming occurs. During REM, there is atonia (lack of muscle tone) and a general inhibition of sensory input, which inhibits afferent information from the lungs and ventilatory muscles, causing breathing to be more irregular. Obstructive apnea can occur when reflexes do not respond to the normal negative pressure in the upper airways during inspiratory flow and induce the normal contractions of upper airway muscles to support the airways in an open position. Increased...

Pharmacologic Highlights

If the patient develops signs of alcohol withdrawal (restlessness, insomnia, thirst, and tremors progressing to fever, hallucinations, and combative and irrational behavior), notify the physician and decrease stimulation as much as possible. Place the patient in a quiet, darkened room with a cool temperature. Provide frequent sips of water and fruit juices, but avoid fluids with caffeine. Place the patient in a room where she or he can be monitored frequently to decrease the risk of injury.

Duplications Of 17p112

Estimated prevalence of 1 20,000, is characterized by mental retardation, neurobehavioral abnormalities, sleep disorders, speech and motor delays, midface hypoplasia, short stature, and brachydactyly. 3 The same deletion is seen in 90 of patients. Only recently has it been recognized that a reciprocal duplication also exists. The dup(17)(p11.2p11.2) syndrome is characterized by borderline to mild mental retardation, behavioral problems, short stature, dental anomalies, normal facies, and lack of major organ malformations 4,5 This syndrome typifies a milder phenotype that was not recognized as a syndrome until connected to the microduplication.

The Postsynaptic Cell

Receptor complexity of the postsynaptic membrane. Synaptosomes - preparation - physiology - contents. Postsynaptic density - preparation - biochemistry - cadherins, PSD-95-attachment of receptors to cytoskeleton - intricate multimolecular architecture. Electrophysiology excitatory synapses ionic bases of EPSPs - local circuits to IS - initiation of AP - significance of size and site of synapses - graded characteristic - spatial and temporal summation inhibitory synapses ionic bases of IPSPs - local circuits to IS - inhibition of AP -significance of size and site of synapses - graded characteristic - spatial and temporal summation. Algebraic summation of EPSPs and IPSPs at IS. Biophysics of channels in postsynaptic membranes single-channel biophysics - operational complexity - populations of channels - comparison with AP - subtlety of response of postsynaptic membrane. Second messenger control of ion channels Ca2+ channels - K+ channels - physiological significance. Second messenger...

Description Medical Nonmalignant Breast

In reviewing breastfeeding history, note if the frequency or regularity of feedings has changed. Fully investigate (1) the length of time the infant spends feeding (2) the time between feedings (3) if the infant is falling asleep at the breast (4) if the infant is sleeping through the night (5) if the infant receives supplementary water, juice, or formula and (6) if the infant receives bottled breast milk.

Restless Legs Syndrome

Restless legs syndrome (RLS) features nocturnal involuntary limb movements that can cause insomnia because of frequent sleep disruption, and often affects bed partners because of frequent myoclonic-type jerking. It generally begins in early adulthood and affects from 2 to 5 of the population. RLS may run in families, with susceptibility genes identified on chromosomes 12q and 14q. RLS has also been associated with Parkinson's disease, pregnancy, end-stage renal disease, iron deficiency anemia, peripheral neuropathy, and diabetes.

Minimal criteria B plus C or A plus D plus E plus G Severity criteria

Adapted from The International Classification of Sleep Disorders, Revised Diagnostic and Coding Manual. Rochester American Sleep Disorders Association, 1997. criteria for both obstructive and varieties of central sleep apnea are located in the section on sleep in the criteria adapted from the American Sleep Disorders Associations International Classification of Sleep Disorders Diagnosis and Coding Manual.

Menopausal Ovarian Failure

The first symptom of menopause is often vasomotor instability (hot flashes, warm flushes). These may begin after an interval of amenorrhea but usually surface earlier in the presence of irregular or even seemingly normal menstrual function. In most cases these episodes pass within 1-2 yr, but in a significant number of patients they may last for decades or disappear only to reappear years later. Although hot flashes are frequently considered a minor nuisance that will eventually pass, they may interfere significantly with normal REM sleep, thereby creating a state of relative sleep deprivation. Estrogen replacement therapy (ERT) represents the most effective approach to eliminating hot flashes. Relief is usually observed within 7-10 d after beginning such treatment. Other medications such as megestrol acetate (Megace ) (2), clonidine (3), selective serotonin reuptake inhibitors (4), and veralipride (5), have been reported to be effective in some but not all patients who are not able...

Diagnostic Criteria for Central Sleep Apnea Syndrome

Complaint of insomnia or excessive sleepiness. The patient may occasionally be unaware of clinical facts that are nevertheless apparent to others. c. Oxygen desaturation associated with the apneic episodes (criteria included in the International Classification of Sleep Disorders).

The Insomnia Battle

The Insomnia Battle

Who Else Wants To Sleep From Lights Out 'Til Sunrise Without Staring At The Ceiling For Hours Leaving You Feeling Fresh And Ready To Face A New Day You know you should be asleep. You've dedicated the last three hours in the dark to trying to get some sleep. But you're wide awake.

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