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Classification of sleep disorders

The pathophysiology and main symptoms of sleep disorders form the basis of the approach to these conditions in this book (Table 1.5). The complaints of insomnia and excessive daytime sleepiness are covered in Chapters 6 and 7. The circadian rhythm disorders are separately identified since they form a physiological entity (Chapter 5). Abnormal experiences and events taking place during sleep are covered in Chapters 8 and 9 and the respiratory disorders of sleep, which are a subgroup of these, are discussed in Chapters 10 and 11. The links between the pathophysiology, clinical features and treatment of these sleep disorders are emphasized throughout these chapters. This approach has many similarities to, but also some differences from, the widely used 1997 third revision of the International Classification of Sleep Disorders (ICSD) produced by the American Sleep Disorders Association (ASDA) in association with other national and international sleep societies 25 (Table 1.6). This groups...

The Pineal Gland and Melatonin

The pineal gland is a neuroendocrine gland that synthesizes and secretes melatonin ( N-acetyl-5-methoxytryptamine). y The afferent input to the pineal gland is transmitted from the retinal photoreceptors through the SCN and sympathetic nervous system. The circadian rhythm of melatonin is controlled by the SCN but is strongly entrained by light. The two effects of light are, first, to regulate melatonin secretion in accordance with diurnal light-dark cycles and, second, to suppress melatonin if given in brief intense pulses. Melatonin secretion increases during the night, reaching a peak level between 2 00 and 4 00 am, then gradually falls during the latter part of the night, and is present at very low levels during the day. Exogenous melatonin has been used with some success to avoid jet lag and may be useful for treatment of phase-shifted sleep and sleep disturbance due to shift work. Melatonin is available through health food stores and has received strong public attention. However,...

Assessment of Sleep Disorders

The assessment of sleep disorders requires an understanding of normal sleep and how it may alter in abnormal circumstances, such as following sleep deprivation and with disorders that affect the nature of sleep. The details of the history obtained at interview with the patient, and often with a member of the family, partner, friend or carer, should be supplemented by a physical examination where this is applicable. The expanding range of investigative techniques is often invaluable, but they should only be used with clear aims. This chapter assesses the use of the sleep history and examination, and examines the principles underlying the most important investigations. The precise indications for these tests in different sleep disorders are discussed in Chapters 5-12. It can be more difficult to take a history of a sleep disorder than to enquire about a complaint that occurs during wakefulness. The patient often has little or no awareness of the problem and it is important to obtain the...

Indications in sleep disorders

Excessive daytime sleepiness due to central nervous system disorders. These include narcolepsy and idio-pathic hypersomnia. Amphetamines are effective, but their short action leads to a rapid return of sleepiness. Little benefit is obtained by increasing the dose above 60 mg dexamphetamine daily, and tolerance to amphetamines occurs in around one-third of subjects with narcolepsy. Their use is limited by side-effects, including psychosis and insomnia. There has been less experience of using amphetamines in neurological disorders other than narcolepsy, but they are probably as effective in idiopathic hypersomnia.

Sleep Problems and Remedies from Ambien to Zolpidem

The diagnosis of sleep problems is based on now standardized criteria summarized both in Diagnostic and statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and the more detailed classification of the ICSD (International Classification of Sleep Disorders) (Pressman and Orr, 1997). Unlike psychiatric diagnoses, which are typically obtained from a conversation with a psychiatrist through structured interview, sleep disorders have more objective criteria, consisting of electroencephalogram (EEG) measures of (i) sleep latency, (ii) REM latency (including REM latency minus awake), (iii) amount of SWS, (iv) amount of REM sleep, (v) eye movement density in REM sleep, and (vi) sleep efficiency (i.e., total number of minutes of sleep divided by the total time in bed). There is abundant data using these measures not only in standard nonpsychiatric sleep disorders, such as apnea, but also in many psychiatric disorders (Douglass, 1996). Objectively measured sleep problems allow...

Melatonin as a Circadian Hormone

FIGURE 1 Schematic organization of nervous network for circadian control. Light exerts its entrainment on SCN by the RHT. The nervous terminal of this pathway contains GLU and SP. Thanks to its autodepolarization property, the SCN represents the endogenous pacemaker. VIP, VP, and GABA are the main neurotrasmitters for the SCN efferents to VMN, SPZ, and PVN. SCN is also connected by a reciprocal innervation to IGL. SNC acts on PG through the multisynaptic retinohypothalamic-pineal pathway, which is represented in the figure by sketched line. Other inputs to PG are from IGL, LH, and HN. PG produces MLT, which reaches its targets via paracrine and endocrine secretion. MLT receptors are located in several neuronal and extraneuronal tissues. Abbreviations RT, retina GHT, geniculohypothalamic tract IGL, intergeniculate leaflet RHT, retino-hypothalamic tract SCN, suprachiasmatic nucleus VMN, ventromedialis nucleus SPZ, subparaventricular zone PVN, paraventricular nucleus CSC, cervical spinal...

Transient insomnia adjustment sleep disorder acute insomnia

The diagnosis of transient insomnia can only be firmly made retrospectively after it has been relieved. It is usually defined as insomnia that lasts for less than three weeks, and very often has a close temporal association to an event which is clearly recognized by the patient and is often stressful. It is equally common in males and females and is more likely if there is a history of previous poor sleep, or if there is a low threshold for emotional arousal. Recurrent episodes of transient insomnia are also common. Transient insomnia is usually triggered by one of the following factors.

Insomnia in children and adolescents

Insomnia or sleeplessness in children is a very common problem. Around 30 of 1 year olds wake at night and although the same number have a sleeping problem at the age of 5, this falls to around 10 in adolescence. Childhood sleepiness leads to parental sleep deprivation, mood changes, and frustration, which make it more difficult to cope with the child's disorder of sleep and can reinforce or help to perpetuate the problem. The causes of insomnia vary according to the age of the child (Table 7.3).

Insomnia in the elderly

As many as 3-4 of subjects develop insomnia each year, and the complaint becomes progressively more frequent in females rather than in males with age, although paradoxically sleep is objectively better preserved in elderly women than in elderly men. This may be because men under-report insomnia to a greater degree. Other medical conditions, such as dementia, may reduce awareness of insomnia, but, conversely, the increased burden placed on the carers by the elderly insomniac is often the trigger that precipitates referral for medical care or transfer to a residential institution. Insomnia in the elderly is usually multifactorial. Physiological arousals from sleep are more common and this increased fragility of sleep underlies the difficulty in maintaining sleep rather than initiating sleep which is particularly a problem in the elderly. Insomnia in the elderly is often associated with the following situations.

Optimize sleep hygiene

The quantity, quality and timing of sleep are affected by many everyday activities and attitudes (Table 1.4). Poor sleep hygiene is probably the most important cause of insomnia, but its significance is generally underestimated. In developed societies sleep is being increasingly squeezed into the time left over after family, social, work and recreational activities, with the result that insomnia, excessive daytime sleepiness and other sleep symptoms are becoming increasingly Treat the cause of insomnia The commonest treatable causes of secondary insomnia are shown on Fig. 7.1. It is important to treat depression and anxiety, which can both be either causes of insomnia or responses to it, before more complex aspects of management are considered. Antidepressants should only be used if features of depression are present and not as a routine treatment. Sedating tricyclic antidepressants, such as trimipramine, imipramine and doxepin, are particularly effective. Paroxetine is the most...

Fatal familial insomnia

This condition is equally common in males and females. It is usually familial but occasionally sporadic, and usually appears between the ages of 40 and 70 years. Progressively worsening insomnia is associated with vivid dreams and motor activity similar to that of the REM sleep behaviour disorder. The fall in total sleep time is associated with disintegration of the sleep structure with no discernible NREM or REM sleep. The normal 24-h rest-activity cycle is lost and the circadian cortisol rhythm disappears. Autonomic and motor abnormalities appear, but cognitive function is retained until stupor and eventually coma develop shortly before death. This usually occurs 6-24 months after the onset of the condition. The differential diagnosis includes the REM sleep behaviour disorder, although this does not have any autonomic abnormalities, dementia, particularly due to Alzheimer's disease, Creutzfeldt-Jakob disease and occasionally schizophrenia.

NREM sleepwakefulness transition movements arousal disorders

Quiet awakenings from stages 3 and 4 NREM sleep are common normal events. The subject may briefly sit up and then lie back and fall asleep again or make gross body movements. These postural movements are associated with a slight elevation of heart rate and blood pressure and the eyes may open briefly. There is no recall of the brief arousal and sleep is soon re-entered. These events usually occur at sleep onset, during stages 1 and 2 NREM sleep, or at the start or end of a REM sleep episode. They are most common in the second half of the night and often occur three to four times per hour.

Rapid Eye Movement Rem Sleep

The two major phases of sleep are rapid eye movement (REM) sleep and nonrapid eye movement (NREM) sleep (Gillin et al., 2000). REM sleep is often called dreaming (or D) sleep because dreams are reported by about 70-80 of persons awakened during this period. It also has been referred to as paradoxical sleep because the brain paradoxically seems to be in an activated state that is similar to, but not identical to, the waking state. For example, brain metabolism is normal or slightly increased during this period. REM sleep is characterized by an activated electroencephalogram (EEG) pattern (low-voltage, fast-frequency brain waves), muscular paralysis (with the exception of diaphragmatic and ocular muscles), periodic bursts of rapid eye movements, and instability of the autonomic nervous system (e.g., variable blood pressure, heart rate, and respiration). In men, penile erections occur during REM sleep, which can be evaluated in sleep studies to distinguish organic and psychological...

Respiration during REM sleep

The respiratory abnormalities are seen in REM before NREM sleep in all these disorders, apart for those, such as central alveolar hypoventilation and after cervical cordotomy, in which the medullary respiratory reflex control is directly affected 9 . REM sleep becomes fragmented and reduced in duration with frequent arousals, and only at a later stage is there loss of stages 3 and 4 NREM sleep. The main effects of REM sleep are as follows. Increase in upper airway resistance Weakness of the upper airway dilator muscles combines with the intense loss of muscle tone in REM sleep to predispose to upper airway obstruction. The risk of this is greater if the chest wall muscles are selectively spared and remain able to generate a sufficiently negative intra-airway pressure. Conversely, if the chest wall muscles, particularly the diaphragm, are involved then obstructive sleep apnoeas are less likely. The upper airway diameter is reduced through a reflex mechanism related to the loss of lung...

Respiration during NREM sleep

Increase in upper airway resistance This increases to a lesser extent than in REM sleep and obstructive sleep apnoeas are less common. They may, however, occur in degenerative disorders such as multiple system atrophy and motor neurone disease in which vocal cord adduction develops due to lesions in the nucleus ambiguus. Inactivation of chest wall muscles There is a global reduction in chest wall muscle activity in NREM sleep in contrast to REM sleep. Neuro-muscular disorders affecting these muscles accentuate this and predispose to hypoventilation. Disorders of the thoracic cage such as scoliosis which reduce its compliance may increase the work of breathing sufficiently for hypoventilation to occur even if the chest wall inspiratory muscles are intrinsically normal.

Clinical Assessment Of Sleep Disorders

A sleep disorder generally occurs for one of two reasons. It may represent a primary disorder of a mechanism controlling sleep or failure of a specific end organ, such as the upper airways and lungs. As in all of clinical medicine, testing must be ordered and interpreted within the context of the patient's clinical presentation, with a clear understanding of the questions to be answered and the inherent limitations of the study proposed. Most patients present with complaints of excessive daytime sleepiness, difficulty initiating or maintaining sleep, or some sort of unpleasant event that occurs during sleep. Detailed medical and sleep histories with careful attention to underlying medical and psychiatric illness, daytime schedules, lifestyle issues, medications, and drug use are prerequisites for the intelligent analysis of the problem and planning of the appropriate testing. A complete physical examination should always be obtained before referral for study. Sleep logs, which...

Sleep Disorders Classification

The Association of Sleep Disorders Centers initially classified sleep-wake disorders into four categories, including disorders of initiating and maintaining sleep disorders of excessive somnolence disorders of sleep-wake schedule and dysfunctions associated with sleep, sleep stages, or partial arousals. In 1990, the ICSD described a system, which was slightly revised in 1997, that divided the 84 sleep disorders into four classes dyssomnias, parasomnias, sleep disorders associated with medical or psychiatric disorders, and proposed sleep disorders. The latest ICSD was published in 2005 (63). ICSD-2 divides sleep disorders into eight categories insomnias sleep-related breathing disorders hypersomnias of central origin not due to a circadian rhythm sleep disorder, sleep-related breathing disorder, or other cause of disturbed nocturnal sleep circadian rhythm sleep disorders parasomnias sleep-related movement disorders isolated symptoms, apparently normal variants, and unresolved issues...

Pittsburgh Sleep Quality Index PSQI

Instructions The following questions relate to your usual sleep habits during the past month only. Your answers should indicate the most accurate reply for the majority of days and nights in the past month. Please answer all questions. 2. During the past month, how long has it usually taken you to fall asleep each night (a) Cannot get to sleep within 30 minutes (a) Cannot get to sleep within 30 minutes

REM Sleep Paradoxical Sleep Desynchronized Sleep

In a normal night of sleep, bouts of REM sleep lasting 5 to 30 minutes usually appear on the average every 90 minutes. When the person is extremely sleepy, each bout of REM sleep is short, and it may even be absent. Conversely, as the person becomes more rested through the night, the durations of the REM bouts increase. There are several important characteristics of REM sleep 2. The person is even more difficult to arouse by sensory stimuli than during deep slow-wave sleep, and yet people usually awaken spontaneously in the morning during an episode of REM sleep. 6. The brain is highly active in REM sleep, and overall brain metabolism may be increased as much as 20 per cent. The electroencephalogram (EEG) shows a pattern of brain waves similar to those that occur during wakefulness. This type of sleep is also called paradoxical sleep because it is a paradox that a person can still be asleep despite marked activity in the brain. In summary, REM sleep is a type of sleep in which the...

Sleepstate misperception pseudoinsomnia subjective insomnia

Sleep-state misperception is due to an inaccurate perception of the time spent asleep. There is a wide range of accuracy of perception of sleep in those with insomnia, but it is common for the sleep latency to be exaggerated and sleep efficiency to be underestimated. Sleep-state misperception probably represents the extreme end of the range of misperception and interestingly it may be associated with similar physiological changes to those seen in primary insomnia, despite apparently normal sleep. The diagnosis is made by a combination of the history of insomnia with normal polysomnography and the absence of any other sleep disorder. The condition should be distinguished from short sleepers, DSPS, psy-chophysiological insomnia and malingering, in which the subject is aware that there is no true insomnia. The demonstration of a normal sleep pattern, treatment of any associated anxiety or depression, and help in improving the accuracy of perception of sleep may be of benefit.

Maladaptive behaviour leading to poor sleep hygiene

A common sleep hygiene problem is lack of exposure to bright light. This is often reduced in the elderly because they remain indoors for longer and may have cataracts and macular degeneration which reduce the amount of light stimulating the retina. Exposure to bright light in the morning may also exacerbate the advanced sleep phase syndrome. Light exposure at night, even if it is brief, may reduce melatonin secretion and worsen insomnia. Lack of physical exercise, either due to a lack of opportunity, for instance in a residential home or because of physical restrictions, frequent daytime naps, particularly in the evenings, and excessive caffeine intake may all contribute to insomnia. Treatment of insomnia in the elderly includes the following.

REM sleep suppressant drugs

Both tricyclic antidepressants and selective serotonin re-uptake inhibitors (SSRIs) reduce the duration of REM sleep and are effective if OSA are confined or almost confined to REM sleep. Protriptyline 5-20 mg nocte has been most widely used, but has been withdrawn in the UK. It is non-sedating, but side-effects such as constipation and urinary retention are common with a dose of more than around 10 mg. Selective serotonin re-uptake inhibitor antidepressants, such as paroxetine, may also reduce the loss of upper airway muscle activity during NREM sleep. They reduce the frequency of OSA in NREM sleep slightly.

Melatonin estimations

Melatonin is affected by fewer confounding factors than most of the other indicators of circadian rhythms. Its secretion is not affected by sleep, physical activity, food or stress, but is modified by certain drugs and posture which need to be controlled for. Melatonin secretion is suppressed even by low light levels of around 10 lux. Salivary melatonin levels can be estimated at hourly intervals in the evening and overnight. The subject is exposed to a low light level of less than around 8 lux. The 'dim light melatonin onset' is taken as the point at which 25 of the peak value is reached. Salivary melatonin levels rise around 30 min later than those in the blood. It may be difficult to sleep when the samples are being acquired and diurnal changes may be difficult to detect since the concentration is only around one-third of that in the plasma. An alternative is estimation of 6-sulphatoxymelatonin concentration in the urine. This runs in parallel with the plasma levels, but around 1 h...

Normal Sleep Architecture And Sleep Stages

Sleep can be divided into two states nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. Each cycle of NREM and REM sleep lasts approximately 90 to 110 minutes, and about three to six cycles of NREM-REM sleep occur during a normal night of sleep (Fig. 1). Slow wave sleep (SWS), which will be discussed in more detail later, tends to dominate the first third of sleep, whereas REM sleep is most predominant in the last third of sleep. The first REM cycle is typically short the final cycle of REM tends to be the longest. In terms of arousa-bility, the deepest sleep occurs in the first third of the night, corresponding to SWS (NREM stages III and IV) an individual awakened during these stages of sleep is typically groggy and confused. If awakened during lighter stages of NREM sleep (stages I and II), there is the possibility that the individual may not be aware that he or she had fallen asleep. However, if one were awakened during REM sleep, a person may experience residual...

Melatonin

Melatonin is able to shift the circadian sleep rhythms and is also a sedative. It advances the sleep phase if it is given in the evening and, rather less reliably, delays it if it is administered in the morning. The phase response curve for melatonin is therefore the opposite of that for light exposure, although its inflection point is probably the same as that for light exposure at around 3-5 am. It is able to advance the onset of endogenous secretion and of sleep by 1.5 h per day. It does not alter sleep architecture 1 . Melatonin should be taken 1-2 h before the usual sleep onset time in DSPS and, as this becomes earlier, the timing of the melatonin dose is brought forward by intervals of 30 min. It acts in effect as an early night replacement treatment for endogenous melatonin, but its long-term efficacy is variable.

Sleep Disorders

The field of sleep medicine has grown to comprise a broad spectrum of syndromes, disorders, and diseases. The predominance of psychology and psychiatry in the field has given way to increasing neurology and pulmonary medicine involvement, and most centers prefer a multidisciplinary approach. Comprehensive sleep disorders centers, accredited by the American Academy of Sleep Medicine (AASM), provide clinical assessment, polysomnography, and treatment for patients. The AASM has developed a diagnostic and classification manual for sleep disorders, as well as evidence-based standards of practice. The polysomnogram provides objective evidence of sleep apnea. Airflow, chest and abdominal movement, and oxygen saturation are monitored continuously during the night. Sleep stages are identified by recording the electroencephalogram, eye movements, and chin muscle tone. Initially, breathing was assessed by counting the number of episodes of complete cessation of airflow lasting more than 10...

REM Sleep

The anatomical substrates for the different components of REM sleep are as follows 3. Muscle atonia, except for respiratory and ocular muscles, is a tonic event of REM sleep. Electrical stimulation studies have shown that muscle atonia occurs following activation of the medullary magnocellular reticular nucleus and the rostral nucleus pontis oralis. Muscle paralysis arises at the spinal cord level, from a centrally mediated hyperpolarization of the alpha motor neurons through the action of the inhibitory neurotransmitter glycine. 5. Rapid eye movements are another phasic event of REM sleep. Horizontal eye movements arise from burst neurons in the parabducens reticular formation in the pons, and vertical eye movements are associated with activation of the midbrain reticular formation. Positron emission tomography has shown that REM-related eye movements involve cortical areas similar to those used during wakefulness. 6. PGO activity is a phasic feature of REM sleep, generated in the...

Physiological Function of Sleep

Sleep evolves during life and changes with maturation and aging. During infancy, 16 to 18 hours a day are spent sleeping, with sleep-wake states initially occurring every 3 to 4 hours. By 6 months of age, a more prolonged sleep period occurs during the night. REM sleep time occupies as much as 80 percent of sleep time in the newborn, with a steady decrease until only approximately 20 percent of sleep is REM in the adult. Sleep spindles appear at approximately 2 years of age. During adolescence, sleep requirement increases, and the sleep pattern is one of phase delay. 8 Because school schedules do not allow for late awakening, the most common cause of daytime sleepiness in this age group is insufficient sleep. In adulthood, the need for sleep is relatively constant. With aging, sleep tends to become more fragmented, and night sleep may decrease with a corresponding increase of daytime napping. With aging, the amount of SWS decreases. Although REM sleep time remains stable with aging,...

Control of sleep and wakefulness

Whether an individual is awake or asleep depends on the balance of forces promoting and inhibiting each of these two states 11 . At times the balance can be almost equal and the subject may begin to fall asleep if he or she had previously been awake, or to lighten from sleep if previously asleep. The mechanisms determining whether sleep or wakefulness predominates are incompletely understood, but three processes interact with each other and with circadian rhythms (Fig. 2.3). This drive to enter sleep increases, probably exponentially, with the duration since the end of the previous episode of NREM sleep. It builds up during wakeful-ness and probably in REM sleep as well. The duration of NREM sleep in each sleep cycle is inversely related to the duration of REM sleep in the previous cycle.

Restorative Neural Functions

In the brain, there is evidence, although it is not yet conclusive, that overall RNA transcription and protein synthesis is relatively most prominent during deep SWS. This activity may have particular importance for synaptic function. Even considering the alternation of SWS and REM sleep, when brain activity is often as high as during the waking state, it has been suggested that SWS allows for a recovery from so-called activity debts. It has been hypothesized that the brain uses the materials produced and stored during SWS. The decline of cognitive function with sleep deprivation provides some evidence of these restorative or supportive functions of sleep. Other possible related functions are a restoration of balance at the synaptic level. Neurons relatively quiescent during the waking period can be activated at night during both NREM and REM sleep, so that the entire network does not become imbalanced. y Alternatively, SWS may be used to restore a functional balance, as of emotional...

Neurochemical Anatomy

The neurochemical constituents involved in the generation and maintenance of REM and NREM are listed in Iable 2 l . Neurochemically, REM sleep is associated with an increase in cholinergic activity and a reduction in noradrenergic and serotonergic activity. In contrast, SWS is associated with increased serotonergic activity .

Associated Medical Findings

The physical examination in a patient with a suspected sleep disorder focuses on several features. To assess for physical abnormalities associated with obstructive sleep apnea, particular attention is directed toward examination of height, weight, and blood pressure. Abnormalities of the upper airway, including enlarged tonsils, tongue, or low palate, can indicate possible airway obstruction. A reddened uvula and palate may be associated with loud snoring. Retrognathia and a small pharyngeal opening may also be seen in patients with sleep apnea.

Evaluation Guidelines

There are a variety of laboratory tests that directly or indirectly may apply to the evaluation of sleep and sleep disorders ( iiTable 2-2.). Neuroimaging. Neuroimaging is not usually necessary during the evaluation of a primary sleep disorder. If patients present with additional neurological symptoms and signs, or the clinical history is atypical, magnetic resonance imaging may be helpful. Insomnia PSG to indicate whether secondary to other sleep disorder EMG evidence of peripheral neuropathy in somepatients with RLS PSG assessing for nocturnal sleep disorder (sleep, apnea, PLMD) Multiple sleep latency test with shortened latency with or without REM onset naps who is present throughout the night. Videotaping abnormal sleep behaviors is possible. PSG testing provides objective data concerning sleep latency, sleep efficiency, sleep staging, severity and type of sleep apnea, periodic limb movements, and parasomnias. PSG is of more limited usefulness in the evaluation of insomnia, unless...

Affective Disorder Syndromes

Major depression has a lifetime prevalence of about 15 percent and is about 15 times as common as bipolar disorder (manic-depressive disorder). Major depression is about twice as common in women as in men in all countries and cultures and does not vary in occurrence among different races. It may occur at any age, but the majority of cases occur in adulthood. Studies suggest a genetic predisposition because there is an increased incidence of major depression and alcoholism in relatives of patients with this mood disorder. The diagnosis of depression is often overlooked, especially in patients with chronic neurological disease. The Diagnostic and Statistical Manual, 4th edition (DSM-IV) criteria for this diagnosis requires either that the patient have a depressed mood or that the patient have a sustained loss of interest and pleasure. Some depressed patients have a depressed affect or become withdrawn or irritable but do not admit to or complain of feelings of sadness. Almost all,...

Electrooculogram EOG recording

Movements of the eyes are important in diagnosing whether the subject is falling asleep and particularly whether REM sleep or wakefulness is present. The potential difference between the cornea and the retina is measured and it is movement of this electrical dipole, and not the activity of the extra-ocular muscles, that is recorded. One electrode is applied 1 cm above, but close to, the outer canthus of the right eye (ROC) and another electrode 1 cm below the outer canthus of the left eye (LOC). Reference (neutral) electrodes are connected to the contralateral ear (Fig. 3.3).

General Management Goals

It is also helpful to remind family members that memory-disordered patients retain many of their intellectual and emotional capacities and therefore need to have an active, regular schedule. Even patients with substantial memory or cognitive problems can slowly adapt to a regular, well-structured schedule. It is good to maintain a relatively normal sleep-wake cycle that ensures a good rest at night. This may require efforts to keep the patient awake during the day. Medications may be required to sustain a healthy sleep-wake cycle. Conversely, unexpected events can be exceptionally distressing to patients who cannot cope with novel circumstances.

We Didnt Take Any Preventive Measures

My lungs haven't got back to normal and I still feel tight in the chest. I suffer from a bad insomnia most nights I can only sleep for a couple hours. My muscles are so weak I can hardly lift anything, and my eyes are swollen and red. But the thing that disturbs me the most is my right leg. I can't walk, can't even move the leg without feeling an excruciating pain in my joints. I used to be very active, very physical.6

Penile erection monitoring

Normal values have been obtained for the frequency of erections during sleep, the total duration of the erections and the increase in penile circumference. Knowledge of the sleep structure is required to interpret these measurements, which should therefore only be carried out as part of polysomnography. Severe fragmentation of REM sleep, as in obstructive sleep apnoeas, may prevent erections from taking place.

Sleepspecific questionnaires

Other questionnaires are available to assess the overall degree of chronic sleepiness. The best known is the Epworth Sleepiness Scale (ESS) (Appendix 7), which assesses the probability of falling asleep in certain situations rather than how sleepy the subject feels 15, 16 . It has eight items, which the subject grades from 0 -3 according to the likelihood of falling asleep. Some of the situations are passive and some active, and it includes situations of which the subject may have no experience. Nevertheless it is a simple test which is repeatable and widely used in the assessment of excessive daytime sleepiness. Like the other self-administered assessment scales it correlates poorly with sleepiness as assessed by the MSLT and MWT (pages 73, 74), and in addition the wording of the questions of the ESS is imprecise.

Clinical Description and Course

Bipolar affective disorder, formerly known as manic-depressive illness, is a psychiatric disorder involving wideranging fluctuations in mood, activity, and cognition. It affects between 0.8 and 1.4 of the population. When depressed, bipolar persons experience a sad mood, loss of interests, fatigue, psychomotor retardation or agitation, loss of concentration, insomnia, feelings of worthlessness, and suicidality. During manias, patients experience euphoric, elevated or irritable mood states, racing of thoughts (or the verbal concomitant, flight of ideas), pressure of speech, increased activity and energy, impulsive and high-

Physiological Determinants Of Sleep

REM sleep generation is critically related to the pontomesencephalic region, as transection studies have demonstrated (55). When the mesopontine region is connected to rostral structures, REM sleep phenomena such as desynchronized EEG and ponto-geniculo-occipital (PGO) spikes are seen in the forebrain when this region is continuous with the medulla and the spinal cord, the REM sleep phenomenon of skeletal muscle atonia can be seen. The cholinergic ''REM-on'' nuclei, including the laterodorsal tegmental (LDT) nuclei and the pedunculopontine (PPT) nuclei, are found within the pontomesencephalic area (Fig. 3). The LDT and PPT nuclei project through the thalamus to the cortex, producing the EEG desynchronization of REM sleep. PGO spikes are a precursor to the REMs of REM sleep. They are formed in the cholinergic meso-pontine nuclei and propagate rostrally through the lateral geniculate and other thalamic nuclei to the occipital cortex (56). LDT and PPT nuclei project caudally via the...

Causal Inference Goes Beyond Covariation Tracking

Our consideration shows that, contrary to the causal mechanism view, prior knowledge of noncausality neither precludes nor refutes observation-based causal discovery. Thagard (2000) gave a striking historic illustration of this fact. Even though the stomach had been regarded as too acidic an environment for viruses to survive, a virus was inferred to be a cause of stomach ulcer. Prior causal knowledge may render a novel candidate causal relation more or less plausible but cannot rule it out definitively. Moreover, prior causal knowledge is often stochastic. Consider a situation in which one observes that insomia results whenever one drinks champagne. Now, there may be a straightforward physiological causal mechanism linking cause and effect, but it is also plausible that the relation is not causal it could easily be that drinking and insomnia are both caused by a third variable - for example, attending parties (cf. Gopnik et al., 2004).

Mechanisms of action

Modafinil is not known to have a direct action on any neurotransmitter system. It does not influence the suprachiasmatic nuclei or melatonin secretion. It does not have any direct effect on hypocretin-containing neurones in the lateral hypothalamus, although their activity increases indirectly as a consequence of the wakefulness induced by modafinil. In vitro in high doses it inhibits the dopamine re-uptake transporter, but this is probably of little clinical significance. Modafinil has a very low affinity for dopamine receptors and does not lead to dopamine release. Its action requires an intact alpha 1 adrenergic system, and there is some evidence that it selectively activates the locus coeruleus, leading to pupillary dilatation but not to other sympathetic effects such as tachycardia or hypertension.

Effects on wakefulness

Elimination of the drugs is slowed in the elderly, who are also more predisposed to sedation. The degree of sedation during the day also depends on the balance between the improvement in sleep quality and the 'hangover' effect of persisting sedation. Tolerance to the sedative effect often develops.

Summary Dopamine In State Control And Its Relevance To Restless Legs Syndrome Periodic Limb Movements

Pharmacologic agents that alter neural dopaminergic signaling are some of the most prescribed and effective agents for treating sleepiness and sleep disorders such as RLS PLMs. While this clinical experience argues that dopamine signaling is integral to the regulation of arousal state, a complete understanding is only beginning to emerge from recent scientific inquiries (32,33,81). To summarize very briefly, differential binding affinities and localizations of the various dopamine receptor subtypes likely account for the biphasic effects that dopaminomimetics have on behavioral state. Low doses promote sleep, including REM sleep that can be antagonized by nonsedating doses of neuroleptics, suggesting a presynaptic D2-like inhibitory mechanism on terminals or somata of dopaminergic VTA or sub-stantia nigra pars compacta neurons. Higher doses of nonspecific dopaminergic agonists increase locomotor activity, enhance wakefulness, and suppress SWS and REM sleep likely via D1-like...

Disorders of endogenous and exogenous linkage

These disorders lead to alterations in the timing of sleep so that there is a complaint of either insomnia or excessive sleepiness, or both. The sleep rhythm usually approximates to a free-running cycle of around 24.2 h which changes its relationship to the environment each day (non-24-h sleep-wake rhythm). The connection between the endogenous circadian rhythms and time givers, particularly light, is reduced or absent. Insomnia and excessive sleepiness fluctuate from day to day according to the degree of mismatch of the endogenous cycle and environmental time. The failure to link the circadian rhythms to the external environment also leads to internal desynchronization of the sleep, temperature and endocrine rhythms which may contribute to the sleep disorder.

Depression Description

Cal disorder, Major Depressive Disorder (MDD). In order to receive a diagnosis of MDD, a person must experience marked distress and a decrease in level of functioning. In addition, the 2 weeks preceding the examination must be characterized by the almost daily occurrence of a dysphoric mood (e.g., sadness) or a loss of interest or pleasure (anhe-donia) in almost all activities. The individual must also experience at least four (only three if both dysphoric mood and anhedonia are both present) of the following seven symptoms nearly every day for the 2-week period significant weight change or change in appetite Insomnia or Hypersomnia psychomotor agitation or retardation fatigue or loss of energy feelings of worthlessness or excessive or inappropriate guilt decreased concentration or indecisive-ness and suicidal ideation, plan, or attempt (Diagnostic and Statistical Manual of the American Psychiatric Association). Related disorders (i.e., other Mood Disorders) include Bipolar I and II...

Reliability and Validity of Dsmiv Diagnoses

Most data reported to date on the reliability and validity of DSM-IV categories have come from the field trials. They suggest modest increments in the reliability of a few diagnostic categories (e.g., Oppositional Defiant Disorder and Conduct Disorder in children and adolescents, Substance Abuse and Dependence) and in validity (e.g., Autistic Disorder Oppositional Defiant Disorder in childhood and adolescence). However, little progress was made in addressing the substantial reliability problems of the Personality Disorders, the Sleep Disorders, the disorders of childhood and adolescence, and some of the disorders within the schizophrenic spectrum.

Intrinsic advanced sleep phase syndrome

This syndrome is less common than intrinsic DSPS. It is often familial and it usually appears in late middle age or in the elderly. It may represent an exaggeration of the ASPS of the elderly and an extreme form of the 'lark' or 'morning types' who wake in the morning and are least alert in the evenings. It can be due to a genetic defect in the circadian sleep rhythms, or in the way in which they control the release of or respond to melatonin. An autosomal dominant mutation of per 2 gene has been demonstrated, but inheritance is probably usually polygenic.

Clinical features

This results from a failure of environmental factors to control the circadian sleep rhythm and melatonin secretion. The rhythm has an intrinsic cycle of around 24.2 h and if it becomes independent of the environment (free running) their relationship changes each day. At one point in the cycle the two are in phase, but the sleep rhythm then moves progressively forward, leading initially to what appears to be a DSPS, and then through sleep reversal with insomnia at night and sleepiness during the day to an ASPS, before returning temporarily to synchrony with the environment again. The rhythm may be partially entrained by cultural and social factors, depending on their intensity and the entrainability of the individual's circadian rhythm. The fluctuating insomnia and daytime sleepiness can be difficult to cope with, and while the same symptoms arise in partially entrained subjects as in those with free-running cycles, they are milder. Daytime naps tend to occur at the times of melatonin...

Beginnings of Empirical Research

Many view the scientific study of dreams beginning in 1953 with the discovery by Aserinsky and Kleitman of an association between dreaming and rapid eye movement (REM) sleep. Sleep generally is characterized by four different stages as reflected in the electroencephalogram (EEG). In contrast to the higher-voltage more-patterned EEG activity found in sleep, REM sleep appears to have an EEG pattern more like that of the waking state, also is referred to as paradoxical sleep, and is characterized by low-voltage random-appearing EEG activity. Awaking an individual during REM sleep is more likely to result in a dream report than any other sleep stage. Following the discovery of the association between REM sleep and dreams, a variety of labs examined the dream state. The work included a variety of foci including the nature of the dream itself, factors involved in dream recall, the influence of external factors on dreaming, and other factors associated with dreaming. For example, following a...

Factors that Promote and Impair Sleep

It is well known that satisfying basic bodily needs, from hunger to sexual urgency, promote sleepiness. Conversely, all kinds of emotional distress tend to reduce sleep onset and quality. This effect is very prominent in the difficulty that depressed individuals commonly experience in falling asleep and sustaining sleep, and also in the disrupted sleep patterns found in various anxiety disorders, mania, and schizophrenia (Kryger et al., 2000). It is well known that physical exertion during the day tends to increase SWS, while mental and emotional exertions, as long as they are not too extreme, tend to increase REM (Panksepp, 1998). Clearly there are several SWS generators in the brain, but one of the more prominent, highly localized, ones is in the lateral anterior lateral hypothalamus, which contains gamma-aminobutyric acid (GABA) as the main transmitter, which explains the utility of GABA facilitators (Table 4.1) to facilitate sleep (Kryger et al., 2000). The location of this...

Neurophysiological effects

The dorsolateral region of the prefrontal cortex is completely inactivated during both stages 3 and 4 NREM and REM sleep, and it is likely that this area is also under-active during the state of sleepiness. The dorsolateral region has a greater sensory input than the orbitomedial prefrontal cortex. Its under-activity

Insufficient duration of sleep sleep deprivation restriction

The development of artificial light sources has enabled the 24-h society to develop. The increased noise level caused by activities at night, such as driving, also hinders sleep, particularly in urban societies. The 24-h society has also had an impact on other time givers for sleep, such as meals, exercise and social activities, so that the endogenous circadian rhythms increasingly conflict with the often rapidly changing external factors that control sleep. These effects are magnified by any pre-existing insomnia, excessive daytime sleepiness or restriction of sleep duration. A careful history should elicit the nature and extent of sleep deprivation and the reasons for this. It is important to discuss methods of altering the balance between daytime activities and sleep in favour of the latter. Constraints, such as fixed working hours, may be difficult to change, but advice about regularity of sleep times and earlier onset of sleep, planning of naps during the day to compensate for...

Immunological effects

Acute sleep restriction reduces antibody production, for instance in response to influenza immunization, but also increases inflammatory mediators such as cytokines, including IL-6 and C reactive protein (CRP), which is a predictor of cardiovascular morbidity. Sleep deprivation increases the white blood count, reduces the production of interferon and increases the natural killer (NK) lymphocyte activity 25 and phagocytic activity. It may increase the frequency of infections. Sleep deprivation also affects melatonin secretion which influences immunological function.

Idiopathic narcolepsy

Narcolepsy has also been associated with physical trauma, particularly head injuries. Loss of consciousness at the time of the injury is usual, but not invariable, and narcolepsy may follow injuries to any part of the head. It usually appears immediately afterwards or within a few weeks or months of the injury. HLA DQB1*0602 is present in only around half of those with post-traumatic narcolepsy. This may be triggered by damage to the blood-brain barrier or by direct damage to structures controlling REM sleep, but more probably the injury initiates changes in neurotransmitters or an inflammatory response, which lead to symptoms of narcolepsy.

Disorders of motor control

Narcolepsy is associated with a variety of parasomnias due to fluctuations in the degree of motor inhibition in REM sleep. Sleep terrors, sleep talking and walking are common, and irregular jerking movements and periodic limb movements may be seen during REM sleep because of a failure of motor inhibition. This also underlies the appearance of REM sleep behaviour disorder. Obstructive sleep apnoeas are more common than in normal subjects, probably because of an alteration in the inhibition of the activity of the dilator muscles of the upper airway and also because of obesity. Recovery from an episode of cataplexy is usually sudden and complete. Cataplexy attacks usually last for a few seconds or up to 2 min, but can occur repetitively for up to 20-60 min (status cataplecticus) and are then usually followed by REM sleep.

Multiple sleep latency tests MSLTs

These should be carried out after a period of withdrawal from drugs such as amphetamines and anticat-aplectic agents, which may affect the results. MSLTs are not suitable for children under the age of around 6 years. They show a short sleep latency with a mean of less than 5 min in 80 of narcoleptics. Sleep-onset REM sleep in two or more of the four or five MSLTs is present in over 75 of narcoleptics, but may also be seen in depression, REM sleep deprivation due to sleep restriction or fragmentation due, for instance, to obstructive sleep apnoeas, and in REM suppressant drug and alcohol withdrawal. The hypocretin level is inversely related to body weight and fluctuates by around 40 in a diurnal pattern. It may double after exercise, is higher in wakefulness than in NREM sleep, lowest in REM sleep and is not affected by drugs, such as antidepressants and stimulant and wakefulness promoting agents. 2 There is difficulty in interpreting polysomnography or MSLT findings because of the...

Differential diagnosis

Before the widespread use of polysomnography and HLA typing, narcolepsy was often confused with or misdiagnosed as schizophrenia. The combination of an unusual affect and auditory and visual hallucinations led to this error, and the overlap of the symptoms of these two conditions led to the theory that schizophrenia was a REM sleep disorder. The two conditions are, however, unrelated 33 . The individual symptoms of narcolepsy can be confused with other disorders.

Myotonic dystrophy dystrophia myotonica

Polysomnography may confirm the diagnosis of central sleep apnoeas and occasionally reveal obstructive apnoeas or periodic limb movements in sleep. The sleep latency is shortened and sleep-onset REM sleep is common. The cerebrospinal fluid hypocretin concentration may be low and many subjects with EDS are also HLA DQB1*0602-positive, raising the pos-sibility that there may be an overlap with narcolepsy.

Human immunodeficiency virus infection HIV

A variety of sleep disorders occur with HIV infection. Patients who are HIV positive without features of the acquired immunodeficiency syndrome (AIDS) have an increased duration of stages 3 and 4 NREM sleep with reduction in REM sleep in the second half of the night so that REM sleep is more evenly distributed. As it advances, there is a decrease in sleep efficiency, an increase in the number of arousals, and a reduction in stages 3 and 4 NREM sleep which correlates with the fall in the CD4 lymphocyte count. Complaints of insomnia, daytime fatigue, drowsiness, poor concentration and memory are common.

Encephalitis lethargica

This has caused several large epidemics of which the last was between around 1915 and 1927. Cocksackie and Echo viruses have been isolated from some subsequent sporadic cases. Cerebral damage is extensive, but sleep disorders are most prominent when the inflammation involves the midbrain and hypothalamus.

Circadian Dysregulation

Abnormal sleep is a core symptom of major depressive disorder, with sleep disruption seen at all stages in the sleep cycle (Benca, 1994). Symptoms include difficulty falling asleep, or staying asleep, as well as early-morning awakening. Hypersomnia is also described. Electroencephalography (EEG) abnormalities in depressed patients include prolonged sleep latency, decreased slow-wave sleep, and reduced rapid eye movement (REM) latency with disturbances in the relative time spent in both REM (increased) and non-REM sleep (decreased slow-wave sleep).

Psychiatric disorders

Excessive daytime sleepiness is much less frequently caused by psychiatric problems than is insomnia 50 . It may develop as a protective psychological reaction to circumstances which are difficult to cope with. If it persists it may be difficult to distinguish from idio-pathic hypersomnia but MSLTs are usually normal. Excessive daytime sleepiness is common in younger subjects with depression, whereas later in life this more frequently causes insomnia. EDS may persist despite adequate treatment of low mood by anti-depressants and may even be worsened by sedative antidepressants. EDS in depression is usually associated with weight gain whereas depression and weight loss often lead to insomnia. EDS is also a feature of the seasonal affective disorder, which is associated with weight gain.

Psychological disturbances

These are common during the episode of insomnia, but are completely reversible once it is relieved. They include 2 Irritability and mood disturbance including anxiety and depression. Anxiety and depression are present in more than 50 of those with chronic insomnia and may be either a cause or a result of the insomnia. A vicious cycle of insomnia and worsening anxiety and depression often develops. If insomnia persists despite treatment of depression or alcoholism or following cessation of antipsychotic drugs and schizophrenia, it is more likely that the underlying psychiatric disorder will relapse. 4 Fear regarding long-term health effects of insomnia. 5 Intrusive ruminating thoughts at bedtime. These are often related to a fear of not sleeping or frustration or anger at the degree of insomnia and of not being able to function effectively, either at work or in family or social life.

Cognitive behavioural therapies

Insomnia responds much better to specific psychotherapy and behavioural therapies directed towards the aims, beliefs and behaviour about insomnia than it does to conventional psychotherapy. The aim is to reverse the maladaptive thoughts and behaviour patterns that perpetuate insomnia 6 . Treatment is often combined with sleep hygiene advice 7 . It is uncertain which modes of behavioural therapy are most effective for the different types of insomnia. Cognitive therapy requires a good relationship between the patient and the therapist and is most effective if the patient has an active and coping style. It may be best to combine cognitive behavioural therapy with a course of up to 1 month of hypnotic treatment in order to break the established patterns of thoughts and behaviour, as well as to give rapid relief of insomnia which can then be maintained by the cognitive behavioural therapy. A similar approach using a beta blocker such as propranolol, to reduce the

Stimulus control therapy

The principle of this treatment is to condition the patient to associate being in bed with successful attempts at falling asleep and maintaining sleep. It aims to interrupt the negative link between the patient's thoughts about sleep by encouraging sleep-promoting behaviour. Mental conditioning to associate the bedroom with

Precipitating factors

Seventy-five per cent of those with chronic insomnia link the onset of their sleep disorder to a stressful event. This may be a difficulty in a close relationship, bereavement, a change in school or employment, or the onset of a medical disorder. The stress leads to both physiological and psychological arousal, which is more likely to precipitate insomnia if the predisposing factors listed above are present. If they are absent, or if the patient adapts to the stress, insomnia may only be transient.

Monoamine Releasing Agents

Monoamine releasing agents are rapidly metabolized into inactive compounds and generally have relatively short half lives (4 to 8 hr). The most common side effects are insomnia, drowsiness, restlessness, nausea, weight loss, weight gain, and hypertension. At high doses these agents can cause a characteristic paranoid psychosis. These drugs are generally well tolerated in the clinical dose range (5 to 30 mg d-amphetamine day), with most patients experiencing no side effects and insomnia being the most common side effect reported.

Attention deficit hyperactivity disorder ADHD

The clinical features of ADHD can be mimicked by sleep fragmentation due to the restless legs syndrome, obstructive sleep apnoeas, and occasionally narcolepsy which leads to frequent awakenings during sleep. Polysomnography may be required to confirm these diagnoses. In ADHD it may be normal or show a low sleep efficiency, reduced total sleep time, an increased number of sleep cycles during the night and an increase in the duration of REM sleep. Limb movements are frequent in stages 1 and 2 NREM sleep.

Mania and manic depression bipolar disorder

Mania often leads to a feeling of being refreshed after only 3-4 h of sleep at night. It may even prevent sleep for several days, but the subject then becomes exhausted. The total sleep time is shortened, sleep latency is prolonged, there is a short REM sleep latency, the duration of stages 3 and 4 NREM sleep is often normal, but there can be a gross alteration in the sleep architecture. Abnormalities of circadian rhythms include changes in the diurnal cortisol secretion pattern. Sleep deprivation tends to elevate the mood, as in depression, and this may worsen the mania and lead to further sleep restriction. Treatment with benzodi-azepines or sedating antipsychotics improves the insomnia in bipolar disorder. This also improves with lithium, but more slowly.

Creutzfeldt Jakob disease

This is usually sporadic, but is occasionally familial. It is due to the same codon 178 mutation as in fatal familial insomnia, but polymorphism at other codons, such as 129, leads to a different phenotypic expression of the genetic abnormality. The cerebral cortex is usually predominantly affected, but in a subtype of the disease there is extensive thalamic atrophy. In these subjects insomnia is a prominent feature, in addition to the dementia and motor abnormalities. There is a progressive loss of both NREM and REM sleep with absence of spindles and K-complexes, and eventually there is no recognizable NREM or REM sleep.

Morvans fibrillary chorea

This rare condition is the result of abnormalities of the voltage gated potassium channels usually due to the production of auto-antibodies due to malignancy. It represents a form of limbic encephalitis. There is a reduction in sleep spindles and stages 3 and 4 NREM sleep, but muscle tone during REM sleep is retained and dream enactment similar to the REM sleep behaviour disorder is common. Insomnia, hallucinations, intense anxiety and delirium are characteristic. Hypertension, tachycardia, sweating and fever are common. The disorder may remit or progress and may respond to plasma exchange.

Dreams and Nightmares

Dreams appear to be initiated in REM sleep by pontine centres, particularly the LDT PPT. These are responsible for muscle atonia and project to the cerebral cortex, which in REM sleep, unlike NREM sleep, is receptive to input from the brainstem. The exception to this is that there is little activity in the ascending pain pathways during REM sleep. This is probably responsible for the rarity of the sensation of pain in dreams. The cerebral activity during REM sleep is largely independent of environmental stimuli and reflects the internal processing of information reaching the cortex from the brainstem, including the limbic system. The cerebral cortex is selectively active during REM sleep 1 . There is no primary sensory cortical activation and the dorsolateral prefrontal cortex is also inactive. In contrast the limbic system and orbitomedial prefrontal cortex are active. Retention of social awareness during dreams is due to persisting functioning of the orbito-medial frontal cortex. In...

Dreamlike hallucinations

The processes responsible for dreams can be activated outside sleep by, for instance, drugs and by sensory, food or sleep deprivation, as well as in psychiatric and neurological disorders. In these situations sensory processing is disordered, and leads to unusual perceptions. These may be primarily visual, as in peduncular hallucinosis due to midline lesions of the midbrain, or in the Charles Bonnet syndrome in which visual hallucinations occur despite blindness. Degenerative disorders such as fatal familial insomnia, Parkinson's disease and Lewy body disease are also associated with hallucinations during wakefulness which are analogous to dreaming in sleep.

Physical enactment of dreams

In REM sleep most of the skeletal muscles, except for instance the diaphragm, are intensely inhibited and the only movements that are seen are occasional twitches or jerks when the inhibition of muscle tone is temporarily lost. Motor inhibition prevents the dream experiences from being physically enacted. The exceptions are REM sleep behaviour disorder and status dissociatus when motor inhibition is lost and the aggressive content of the dreams is physically enacted. Dreams are also enacted in agrypnia excitata where the dreams represent REM sleep intrusion into wakefulness, and post-traumatic stress disorder when the 'nightmares' arise from NREM rather than REM sleep.

Posttraumatic stress disorder

'Nightmares' occur in around 75 of patients, particularly in stages 1 and 2 NREM sleep rather than REM sleep. They have a recurrent content, related to the previous traumatic event. They are experienced intensely and the frequency of the dreams is proportional to the intensity of the concern about the event. They occur particularly early in the night and are associated with gross body movements 11 .

Idiopathic Parkinsonism

Visual hallucinations also occur during wakefulness in around 25 of those with idiopathic Parkinsonism but especially in Lewy body disease. They often involve strangers, but are not frightening. They are probably due to brief episodes of REM sleep intruding into wakefulness and occur particularly in those who have sleep-onset REM during polysomnography 12 and REM sleep demonstrated during naps in the day. Cataplexy does not occur.

Disorders of Later Infancy with Recurrent Metabolic Crises

ASA synthetase deficiency was first reported in a 9- month-old girl with mental retardation. In Japan, a variant form of this disease is found to occur as late as 48 years of age. Ihe symptoms in such cases are nonspecific and include bizarre behavior, psychotic episodes, delusions, hallucinations, insomnia, and endocrine disturbances, such as delayed menarche. ASA lyase deficiency may also occur late in infancy or adults. Ihese cases present as mental retardation or ataxia, or the patient might be totally asymptomatic. This heterogeneity might be explained by the studies of McInnes and colleagues, which indicated at least 12 allelic mutations leading to extensive genetic heterogeneity. y Immunoblot analysis shows a wide variation in size and amount of enzyme protein in patients. Ihe presentation of arginase deficiency is heterogeneous. Early development is usually unremarkable, but developmental delay and psychomotor retardation will definitely appear by 3 years. Progressive spastic...

Practical Conclusions

It should be emphasized that, in practice, there is no sharp border between the relaxing states and the relaxation response only. During meditation, according to rules described by Benson (1975), the reduction of interoceptive stimuli reception may not occur and eventually the relaxing state or sleepiness may appear. Similarly, during relaxing exercises it is possible to counteract the tendency to fall asleep by switching attention from interoceptive experiences to monotonous stimuli (i.e., observing or counting breaths). This may lead to the relaxation response by cutting off the reception of stimuli from the external sources of stimulation.

Aetiology of periodic limb movements

2 REM sleep disorders, e.g. narcolepsy, REM sleep behaviour disorder. The periodic limb movement disorder (PLMD) is defined as the presence of an abnormal number of PLMS for the subject's age in the absence of RLS or any other disorder or drug that causes PLMS and with symptoms, particularly insomnia or excessive daytime sleepiness, due to the limb movements (Table 9.10). PLMD can be graded as mild (PLMI 5-24), moderate (PLMI 25-49) or severe (PLMI 50 or more or a PLMAI of 25 or more per hour).

Effects of movement disorders on sleep

2 There may be associated sleep disorders. Huntington's disease, for instance, is associated with periodic limb movements in sleep and RLS, and multiple system atrophy is associated with the REM sleep behaviour disorder. Children with tics are predisposed to sleep walk and talk. 5 Drugs used therapeutically may help to relieve the movement disorder, but may induce other sleep disorders.

Upper airway compliance

The other important factor is the activity of the pharyngeal dilator and constrictor muscles. Tonic activity in both these muscle groups is less during sleep, especially REM sleep, than during wakefulness. These changes in the sequence or relative force of contraction in the upper airway and chest wall muscles vary according to, for instance, the Pco2, stage of sleep, and the individual response to factors such as sleep deprivation, the nasal cycle, and changes in position. There is also breath-to-breath variability within REM sleep which may predispose to apnoeas developing intermittently.

Chest wall muscle activity

The pressure within the upper airway is determined by the activity of the chest wall muscles and the extent to which this is transmitted to the upper airway. During NREM sleep, the diaphragm, intercostal and accessory respiratory muscles are all active, but in REM sleep the diaphragm alone is responsible for inspiration. The pressure that these muscles generate in the upper airway depends on their contractility, mass, length, rate of shortening and mechanical advantage as well as the compliance and resistance of the lungs and chest wall.

And Preoperative Evaluation

General guidelines for surgical intervention include significant symptoms of snoring and daytime somnolence documented failure in continuous positive airway pressure (CPAP) trials and documented failure of conservative measures, such as dental appliances, changes in sleeping position, and sleep hygiene in general. Apparent obstruction at the level of the soft palate must be determined by fiberoptic nasopharyngo-laryngoscopy, and M ller maneuver or sleep endoscopy. Adequate medical clearance and a thorough review with the patient of the procedure, its implications, and potential outcomes and complications are essential components of the preoperative workup.

Neurophysiological Bases Of Evoked Electrical Brain Activity

Evoked potentials are systematic changes of the EEG induced by incoming information to the brain. Every sensory stimulus elicits electrical activity that is projected by selective and specialized afferent fiber systems to the corresponding cortical sensory areas, where it induces changes of the ongoing electrical activity. These changes depend on (1) the function state of the brain (information processing is different during various sleep stages and in differ

Prior oxygen saturation

The sigmoid shape of the oxyhaemoglobin dissociation curve dictates that at a normal Po2 of around 13.3 kPa the oxygen saturation is above 95 , and a fall in the Po2 of as much as 4 kPa will only reduce the saturation to around 90 . If, however, the initial Po2 is 8 kPa, the oxygen saturation is around 90 , but will fall to as low as 60 when the Po2 falls by 4 kPa. Patients with a lower initial Po2 will have greater desaturation for any fall in Po2 than those in whom initial oxygenation is normal. In REM sleep the impaired ventilation-perfusion matching reduces the baseline oxygen saturation and predisposes to deeper dips.

Heart rate and dysrhythmias

The heart rate initially slows during an OSA and then rises towards the end of it and early in the postapnoea phase. This alternating bradycardia and tachycardia may be mistaken for the brady-tachy syndrome and pacemakers have been implanted unnecessarily on the basis of this erroneous diagnosis. Bradycardias can be profound with heart rates of less than 30 per minute and asystole lasting for more than 2.5 s. First and second degree atrioventricular heart block may appear in otherwise normal subjects, especially in REM sleep. Inspiratory efforts against a closed airway increase the parasympathetic activity and contribute to the brady-cardias. The degree of the subsequent tachycardia is proportional to the fall in Po2.

Pulmonary artery pressure

If the apnoeas cause severe oxygen desaturation and are frequent there will be insufficient time between the apnoeas for the arterial Po2 to return to normal. The pulmonary artery pressure will then be raised not only during apnoeas but between them. This is seen particularly during REM sleep in which the arousal threshold is higher, apnoeas are more prolonged and pulmonary vascular reactivity to hypoxia may be more pronounced than in NREM sleep.

Hormones Mood and Cognition

Most hormones play a significant role in affect and cognition. An example is cortisol, which is secreted by the adrenal cortex under the influence of the anterior pituitary peptide adrenocorticotropin hormone (ACTH). Cortisol hypersecretion, such as in Cushing's disease, produces psychological changes ranging from hyperphagia, insomnia, and euphoria to anxiety, panic, and mania. On the other hand, a significant number of individuals diagnosed with major depression present signs of adrenal hypertrophy and increased circulating levels of cortisol. The mechanisms hypothesized to mediate increased cortisol levels in clinically depressed patients have implicated increased activity at the level of the hypothalamus, and dysregulation of brain serotonergic and noradrenergic systems. A reduction of circulating cortisol levels, observed in patients with Addison's disease (adrenal atrophy and insufficiency), is itself correlated with irritability, apprehension, mild anxiety, and inability to...

Formulation Applications

Melanotan I is a tridecapeptide analog of a-MSH with melanotropic activity (Bhardwaj and Blanchard, 1996). It has been evaluated in clinical trials for its chemopreventative activity for sunlight-induced skin cancers (Bhardwaj and Blanchard, 1996). Melatonin I (pH 7.4) was formulated as a controlled release

Other daytime symptoms

These occur on waking, possibly related to the increased intracranial pressure during OSA, particularly in REM sleep, and occasionally to hypercapnia. 3 Reduced libido and impotence. This is partly due to EDS resulting from sleep fragmentation and partly to reduced testosterone levels due to a reduction in gonadotrophin secretion during sleep. There are also fewer penile erections during sleep because of REM sleep fragmentation.

Nervous and Endocrine Cooperation

We all have internal clocks governing the times we feel sleepy, wake up without alarm clocks, are hungry, and so on. Because they are on a roughly 24-hour cycle, the clocks are called circadian. The clocks vary somewhat in individuals and can be reset by exposure to new patterns of light and darkness. Blind people, who have no external visual cues, may suffer from insomnia for this reason. A recent study of blind people showed that the hormone melatonin produced within the brain by the pineal gland can reset those clocks. When given either a placebo or melatonin, only the subjects who received melatonin reset their clocks to a normal cycle. At one time melatonin was expected to be a miracle cure for jet lag, but that has not proved to be the case. With the new results in blind people, scientists have new hope of finding melatonin's exact role in circadian cycles.7 Like melatonin, many hormones alter brain functions, so that the brain adjusts its own performance and control of the...

Sleep hypoventilation

Impaired respiratory mechanics or to widespread respiratory muscle weakness so that even a normal respiratory drive cannot be translated into detectable respiratory movements (Fig. 11.3). This latter group are better considered as 'pseudocentral' or 'peripheral' apnoeas, rather than due to any central abnormality 8 . They are characteristic of neuromuscular disorders that cause diaphragmatic weakness so that in REM sleep no functioning inspiratory chest wall muscles are left (Table 11.1). Impaired respiratory mechanics in, for instance, emphysema may also cause even a normal drive only to be able to develop a small tidal volume (hypopnoea) or even no detectable airflow.

Serotonin 5hydroxytryptamine 5ht

Serotonin is an evolutionarily old neurotransmitter. All metazoan species with organized nervous systems appear to use serotonin as a neurotransmitter. Serotonergic neurons, receptors, and serotonin-mediated behaviors have been described in the nematode C. elegans, fruit fly D. melanogaster, crayfish, mouse, rat, cat, pig, chimpanzee, and humans, among others. Serotonin has been shown to participate in many different behaviors, including feeding and satiety behaviors, mating and copulatory behaviors, nociception, circadian rhythmicity, arousal, sleep and REM sleep production, perception, temperature regulation, aggression, and seizure vulnerability.

Neuromuscular disorders

Generalized respiratory muscle weakness reduces the lung volumes, including the vital capacity. The maximal inspiratory and expiratory pressures are reduced and the respiratory frequency increases and tidal volume falls. Hypoventilation occurs in sleep when the vital capacity falls below around 30 predicted or to around 1-1.5 l. It is seen in REM sleep before NREM sleep 11 .

Regulation of Growth Hormone Secretion

Growth hormone is secreted in a pulsatile pattern, increasing and decreasing. The precise mechanisms that control secretion of growth hormone are not fully understood, but several factors related to a person's state of nutrition or stress are known to stimulate secretion (1) starvation, especially with severe protein deficiency (2) hypoglycemia or low concentration of fatty acids in the blood (3) exercise (4) excitement and (5) trauma. Growth hormone also characteristically increases during the first 2 hours of deep sleep, as shown in Figure 75-6. Table 75-3 summarizes some of the factors that are known to influence growth hormone secretion.

Neurodevelopmental disorders

Many of these disorders have abnormalities of sleep, such as an absence of sleep spindles or a reduction in REM sleep duration. In autism and Asperger's syndrome there is an increased number of REM sleep episodes, but they are briefer than normal. There is also an increased prevalence of sleep terrors and an awareness of poor sleep at night. Primary sleep disorders such as the restless legs syndrome and obstructive sleep apnoeas may exacerbate developmental problems and cause excessive daytime sleepiness, manifested as hyperactivity, aggression and poor cognitive development. Around 20 of those with attention deficit hyperactivity disorder are said to have the restless legs syndrome. In Down's syndrome and cerebral palsy there is a predisposition to sleep apnoeas. Sleep disorders may also be the result of the care and care environment. Children with developmental disorders often live in residential and nursing homes and are inactive for much of the day with little exposure to bright...

Cluster headaches migrainous neuralgia

These are often intense, occur unilaterally around the eye, and are associated with lachrymation, nasal discharge and facial vasodilatation. They are 10 times more common in males than in females, occur particularly between the ages of 40 and 60 years and last for 30-180 min. They are most frequent in spring and autumn when the change in the length of exposure to light is greatest, and are also associated with low plasma peak melatonin and cortisol concentrations. Seventy-five per cent of cluster headaches occur during sleep and they often appear at the same time each night for several weeks before going into remission. They are most common in REM sleep, and at the transition between REM and NREM sleep. Metabolic activity is increased during these episodes in the cingulate gyrus and hypothalamus close to the supra-chiasmatic nuclei. This probably alters the balance between parasympathetic and sympathetic systems to cause the unilateral vascular and secretory changes which underlie the...

Suggested Readings

American Sleep Disorders Association. (1997). ICSD International classification of sleep disorders Diagnostic and coding manual (Rev. ed.). Rochester, MN Author. Chokroverty, S. (Ed.). (1999). Sleep disorders medicine Basic science, technical considerations, and clinical aspects (2nd ed.). Boston Butterworth, Heinemann. Hauri, P.J. (Ed.). (1991). Case studies in insomnia. New York Plenum. Young, T., Palta, M., Dempsey, J., Skatrud, J., Weber, S., & Badr, S. (1993). The occurrence of sleep-disordered breathing among middle-aged adults. New England Journal of Medicine, 328, 1230-1235.

Natural Cures For Insomnia

Natural Cures For Insomnia

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