*2.2.1 Relationship of sleep with body systems and diseases*

*Cardiovascular system*: known hemodynamic measurements "heart rate, heart rate variations, blood pressure, cardiac output, baroreflex activity and peripheral vascular resistance" provides us important information as to how the cardiovascular system functions in sleep as well as in wakefulness. In NREM and REM stages of sleep, due to parasympathetic system activation heart rate, blood pressure, cardiac output and peripheral vascular resistance decreases. Lowest levels of arterial blood pressure are seen during Stage N3. The decrease in the heart rate is related to the decrease in the sympathetic motor tone. During NREM sleep; blood pressure, respiratory rate and basal metabolic rate decrease by 10–30%, this is the most comforting and most restful period of deep sleep. In the hemodynamic changes in sleep, arterial baroreflex mechanism is thought to play a regulating role. Baroreflex arch consists of peripheral receptors (sinus caroticus and arcus aorta), central neurons (tractus solitorius and medulla oblongata) and afferent and efferent (sympathetic, parasympathetic) neurons. The decrease in blood pressure is compensated with an increase in the heart rate centrally through this reflex arch, or vice versa. From a cardiovascular perspective, during NREM sleep, there is relative autonomic stability, sympathetic inhibition, and increase of vagal (parasympathetic) tone. It is also the stage where bradycardia

**15**

*Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine*

and respiratory sinus arrhythmia is seen. Despite the fact that there is parasympathetic predominance during REM sleep, due to bursting in sympathetic

rate. During this stage, first degree or Wenckebach type second degree AV blocks, and sinus blockage can take place due to increased vagal tone. During Stage N3 blood pressure decreases by 10–20% and heart rate by 5–10% (dipper). The absence of the expected nocturnal decrease in blood pressure is called non-dipper, while a decrease of extreme scale is called extreme dipper and both can lead to cardiovascular events. Compared to NREM, blood pressure is higher during REM sleep; myocardial infarction, unstable angina, cardiac death, ventricular tachyarrhythmias, pulmonary embolism, cerebrovascular incidents and sudden cardiac death can take place during REM stage of sleep that intensifies during early hours of the day during which there is autonomic instability (sudden sympathetic discharge) triggering platelet aggregation, plaque rupture and coronary spasm [19–25]. *Respiratory system*: control mechanisms for respiration during sleep: (1) homeostatic and metabolic control; O2 and CO2 sensitivity mechanisms on carotid bodies through chemoreceptors provide for the regularity of breathing. (2) Behavioral (cortical) control; during activities like speaking or swallowing breathing is controlled voluntarily. (3) Wakefulness warning; during wakefulness reticular activating system sends non-tonic stimuli to the respiratory center in the brain stem resulting in an increase in breathing. NREM and REM stages are controlled with metabolic stimuli. It is shown that respiratory response by chemoreceptors decreases during NREM and this decrease gets more significant during REM. The main stimulus for respiration is PaCO2, the effector organ is the lungs, and the chemoreceptors that regulate the response to stimuli are located on carotid bodies and brain stem. The system operates with stimuli and feedback mechanisms. For example, during heart failure the response to stimulus is delayed as a result of lengthened circulatory time. Likewise, a minor change in ventilation can result in a significant change in CO2 and can cause impairment in respiratory balance. Instances where the tendency to central apnea increases in the organism are: (1) During transition to sleep; when CO2 is at a level that is lower than that is required to stimulate respiration and the number of

respiration becomes insufficient. (2) When the ratio between respiratory

response and respiratory stimuli is high; idiopathic sleep apnea is an example for this. (3) Lengthened circulatory time; for example during cardiac failure typically Cheyne-Stokes breathing develops. (4) Instances where respiratory control gets out of order; in conditions pertaining to the brain, in patients with decreased or disappeared chemosensitivity, hypercapnia is seen during wakefulness. These patients experience hypoventilation especially during REM stage. That is why in patients having central alveolar hypoventilation and obesity hypoventilation syndrome, the ventilation is further hindered during sleep; so hypoxia, hypercapnia, both central and obstructive apneas are observed [26–30]. *Upper respiratory tract*: it is a multipurpose conduit. As it allows for the passage of liquids and food, it is where activities like talking, swallowing and breathing take place. It contains the following structures: "Extrathoracic trachea, larynx, pharynx and nose". The segment with the highest tendency to collapse in the respiratory system is the pharynx. The pharynx consists of three parts: (1) Nasopharynx is the part that extends from the nasal passage to the hard palate. (2) Oropharynx is divided into two parts as retropalatal and retroglossal fields. (3) Hypopharynx starts from the root of the tongue and extends to the larynx. In most of the patients with Obstructive Sleep Apnea Syndrome (OSAS), narrowing or closure of the airways that happen throughout the sleep takes place in the retropalatal and retroglossal region. For the preservation of the patency of the upper airways,

nervous system, blood pressure increases and variations are observed in the heart

*DOI: http://dx.doi.org/10.5772/intechopen.82754*

#### *Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine DOI: http://dx.doi.org/10.5772/intechopen.82754*

and respiratory sinus arrhythmia is seen. Despite the fact that there is parasympathetic predominance during REM sleep, due to bursting in sympathetic nervous system, blood pressure increases and variations are observed in the heart rate. During this stage, first degree or Wenckebach type second degree AV blocks, and sinus blockage can take place due to increased vagal tone. During Stage N3 blood pressure decreases by 10–20% and heart rate by 5–10% (dipper). The absence of the expected nocturnal decrease in blood pressure is called non-dipper, while a decrease of extreme scale is called extreme dipper and both can lead to cardiovascular events. Compared to NREM, blood pressure is higher during REM sleep; myocardial infarction, unstable angina, cardiac death, ventricular tachyarrhythmias, pulmonary embolism, cerebrovascular incidents and sudden cardiac death can take place during REM stage of sleep that intensifies during early hours of the day during which there is autonomic instability (sudden sympathetic discharge) triggering platelet aggregation, plaque rupture and coronary spasm [19–25]. *Respiratory system*: control mechanisms for respiration during sleep: (1) homeostatic and metabolic control; O2 and CO2 sensitivity mechanisms on carotid bodies through chemoreceptors provide for the regularity of breathing. (2) Behavioral (cortical) control; during activities like speaking or swallowing breathing is controlled voluntarily. (3) Wakefulness warning; during wakefulness reticular activating system sends non-tonic stimuli to the respiratory center in the brain stem resulting in an increase in breathing. NREM and REM stages are controlled with metabolic stimuli. It is shown that respiratory response by chemoreceptors decreases during NREM and this decrease gets more significant during REM. The main stimulus for respiration is PaCO2, the effector organ is the lungs, and the chemoreceptors that regulate the response to stimuli are located on carotid bodies and brain stem. The system operates with stimuli and feedback mechanisms. For example, during heart failure the response to stimulus is delayed as a result of lengthened circulatory time. Likewise, a minor change in ventilation can result in a significant change in CO2 and can cause impairment in respiratory balance. Instances where the tendency to central apnea increases in the organism are: (1) During transition to sleep; when CO2 is at a level that is lower than that is required to stimulate respiration and the number of respiration becomes insufficient. (2) When the ratio between respiratory response and respiratory stimuli is high; idiopathic sleep apnea is an example for this. (3) Lengthened circulatory time; for example during cardiac failure typically Cheyne-Stokes breathing develops. (4) Instances where respiratory control gets out of order; in conditions pertaining to the brain, in patients with decreased or disappeared chemosensitivity, hypercapnia is seen during wakefulness. These patients experience hypoventilation especially during REM stage. That is why in patients having central alveolar hypoventilation and obesity hypoventilation syndrome, the ventilation is further hindered during sleep; so hypoxia, hypercapnia, both central and obstructive apneas are observed [26–30]. *Upper respiratory tract*: it is a multipurpose conduit. As it allows for the passage of liquids and food, it is where activities like talking, swallowing and breathing take place. It contains the following structures: "Extrathoracic trachea, larynx, pharynx and nose". The segment with the highest tendency to collapse in the respiratory system is the pharynx. The pharynx consists of three parts: (1) Nasopharynx is the part that extends from the nasal passage to the hard palate. (2) Oropharynx is divided into two parts as retropalatal and retroglossal fields. (3) Hypopharynx starts from the root of the tongue and extends to the larynx. In most of the patients with Obstructive Sleep Apnea Syndrome (OSAS), narrowing or closure of the airways that happen throughout the sleep takes place in the retropalatal and retroglossal region. For the preservation of the patency of the upper airways,

*Updates in Sleep Neurology and Obstructive Sleep Apnea*

Based on respiratory effort, there are three types of apnea: (1) Obstructive apnea: apnea during a respiratory effort. (2) Central apnea: apnea criteria and the absence of respiratory effort during the period where air flow stops. (3) Mixed apnea: apnea criteria that start with an absence of respiratory effort and follows with a continuing increase in respiratory effort. *Hypopnea scoring*: It is performed based on following criteria: (1) More than 30% of a decrease in the signal amplitude of the nasal cannula compared to the baseline. (2) The episode lasting for at least 10 seconds. (3) 4% or more of a decrease in the O2 saturation compared to the baseline saturation. (4) At least 90% of the incident should satisfy the amplitude decrease parameters accepted for hypopnea. *Apnea index (AI)*: defines the number of apneas that occur within an hour while sleeping. *Apnea-hypopnea index (AHI)*: defines the total number of apneas and hypopneas combined during an hour while sleeping. *Respiratory effort related arousal (RERA) scoring*: arousal resulting from 10 seconds or longer of flattening of the inspiratory portion of nasal pressure which does not fulfill the criteria for hypopnea or apnea. *Respiratory disturbance index (RDI)*: it defines the summation of apnea, hypopnea and RERA incidents that appear in an hour during sleep. *Hypoventilation scoring*: if PaCO2 increases more than 10 mmHg during sleep compared to levels obtained in supine position during wakefulness this is scored as hypoventilation. *Cheyne-Stokes breathing is score*: when there are at least three consecutive crescendo and decrescendo breathing changes, with at least one of the following criteria: (1) five or more central apnea or hypopnea during an hour of sleep (2) breathing amplitude changes in crescendo-decrescendo style in a consecutive manner lasting at least 10 minutes (3) Cheyne-Stokes breathing cycle lasting for 60 seconds in general, but variable. *O2 saturation measurement*: measurement of O2 saturation is generally performed with pulse oximetry. It detects the O2 saturation of hemoglobin in the capillary blood through the emission and absorption of light generated from a source. *O2 desaturation index (ODI)*: it defines the number of oxyhemoglobin desaturation incidents per hour

**14**

seen during sleep [15–18].

**2.2 Physiopathology and symptomatology in sleep medicine**

*Cardiovascular system*: known hemodynamic measurements "heart rate, heart rate variations, blood pressure, cardiac output, baroreflex activity and peripheral vascular resistance" provides us important information as to how the cardiovascular system functions in sleep as well as in wakefulness. In NREM and REM stages of sleep, due to parasympathetic system activation heart rate, blood pressure, cardiac output and peripheral vascular resistance decreases. Lowest levels of arterial blood pressure are seen during Stage N3. The decrease in the heart rate is related to the decrease in the sympathetic motor tone. During NREM sleep; blood pressure, respiratory rate and basal metabolic rate decrease by 10–30%, this is the most comforting and most restful period of deep sleep. In the hemodynamic changes in sleep, arterial baroreflex mechanism is thought to play a regulating role. Baroreflex arch consists of peripheral receptors (sinus caroticus and arcus aorta), central neurons (tractus solitorius and medulla oblongata) and afferent and efferent (sympathetic, parasympathetic) neurons. The decrease in blood pressure is compensated with an increase in the heart rate centrally

through this reflex arch, or vice versa. From a cardiovascular perspective, during NREM sleep, there is relative autonomic stability, sympathetic inhibition, and increase of vagal (parasympathetic) tone. It is also the stage where bradycardia

*2.2.1 Relationship of sleep with body systems and diseases*

two important physiological mechanisms need to be in balance: (a) Forces that cause the collapse of the pharyngeal airways (the amount of soft tissue that covers the airways and the size of the airways). (b) Forces that dilate the pharyngeal airways (the activity of a muscle group that work in a coordinated manner to keep the airways open). Predisposing factors that would impair this balance are: "Mainly age and gender and then race, obesity, neck circumference, cigarettealcohol-sedative use, genetic factors, co-morbid diseases (acromegaly, hypothyroidism, Down Syndrome, storage diseases like amyloidosis and mucopolysaccharidosis), body posture and gravity, anatomic factors, genetic factors and hormones influence the patency of upper airways and constitute the risk factors for OSAS [31–35]. *Sleep and immune system*: among the substances that are both sleep inducing and immunologically active we can list; Interleukin-1 (IL-1), IL-2, alpha interferon, Factor-S, muramyl peptides, tumor necrosis factor (TNF) and prostaglandin D2 (PGD2). We know that people who are sleep deprived can get sick more easily and when they pay attention to sleeping properly and resting, they heal faster. Several factors play a role in sleep regulation. TNF-alpha, IL-1-beta, growth hormone releasing hormone (GHRH), PGD2 and adenosine affect NREM sleep, whereas vasoactive intestinal peptide (VIP), nitric oxide (NO) and prolactin exert their effects on REM sleep. In the regulation of sleep-wakefulness, elements of immune system that are of significant value are; IL-1, IL-6 and TNF. When the endogenous production of IL-1-beta and TNFalpha increases (overnutrition, infectious disease states) NREM sleep increases. The effects of certain cytokines on sleep can be summarized as follows: *Prosomnogenic cytokines*: IL-1-beta, IL-1-alpha, TNF-alpha, IL-2, IL-6, IL-15, IL-18, epidermal growth factor, nerve growth factor, interferon-gamma, neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3, and 4 have been observed in elevated concentrations in allergic diseases, and they cause swelling and tenderness in the joints, and increase the tendency for autoimmune diseases like rheumatoid arthritis. The secretion of such factors by the immune system peaks during the early hours of the night and with gradual decreases they reach their lowest levels during morning hours. Short term sleep deprivation lead to decreases in natural killer (NK) cell activity, when this deprivation lasts longer there is an increase in NK cell activity. Experimental studies on laboratory animals have shown that, in instances of lengthened sleep deprivation fatal bacterial infections stemming from the gastrointestinal system can turn fatal within 3 days. In narcolepsy cases increases have been observed in TNF-alpha levels. In OSAS patients the circadian rhythm of secretion for TNF-alpha deteriorates significantly [36–40]. *Endocrine Physiology during Sleep*: Circadian rhythm and homeostatic balance provide for the control of hormonal and metabolic changes during sleep. Sleep deprivation studies analyze the effects of sleep and circadian rhythm on hormones. Based on these studies, growth hormone (GH) and prolactin (PRL) secretion increases during normal sleep, cortisol and thyroid stimulating hormone (TSH) secretions decrease. If sleep is interrupted by wakefulness, GH and PRL decrease while TSH and cortisol increase. Physiologically cortisol decreases starting from early hours of the morning towards the evening by reaching its lowest levels during the late hours of the day and initial hours of sleep. A couple of hours before waking up, there are reactivation of cortisol secretion. Low levels of cortisol is associated with slow wave sleep. During sleep deprivation the amplitude of cortisol rhythm decreases 15% compared to normal. Especially in elderly individuals who have fragmented sleep patterns, as deep sleep decreases as well, there is an increase in cortisol levels during night time and this is associated with decreased memory and increases in insulin resistance. In Cushing syndrome patients, due to bad

**17**

*Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine*

sleep quality decreases have been shown in REM latency, increases in first REM intensity and decreases of deep sleep. There are three basic processes coming into play in sleep regulation: (1) Homeostatic process: it tells us the relationship between last sleep and wakefulness periods. Sleep deprivation in the organism increases the duration and depth of sleep as a compensatory mechanism. (2) Circadian process: it is also defined as the biological clock. (3) Ultradian process: it defines the duration of REM—NREM sleep cycles and the interactions between

them. Melatonin is the neuroendocrine modulator of day-night rhythm. Melatonin receptors are densely located at the suprachiasmatic nucleus (SCN). The endogenous circadian rhythm of melatonin secretion is in parallel to the endogenous rhythm of sleep tendency. Secretion of melatonin from the pineal gland is under the control of SCN. This pathway is multisynaptic and has contributions from the sympathetic nervous system. Melatonin has three important physiological features: (1) Hypnotic effect: the ability to initiate sleep when

homeostatic effect is inadequate to initiate or to maintain sleep. (2)

significant lengthening of REM sleep was identified [46].

*2.2.2 Basic signs in sleep disorders and pathophysiological causes (semiology, propedeutics, preliminary instruction, introduction to further study)*

The first step in the evaluation of a patient with a sleep disorder is to identify the main symptom. A detailed history of the sleep and wakefulness cycle constitutes the second step. This is followed by the medical history of the patient, a list of previously used medications, family history, detailed information about school, work, family and social life and a physical exam of bodily systems. Relevant laboratory tests are performed for differential diagnosis.

Chronohypnotic effect: it is the ability to inhibit the time of waking-up that is normally regulated by the circadian center. (3) Chronobiotic effect: concerning the regulation of the circadian rhythm, it is the ability to initiate phase shifts and to do this during desired hours. The light that an individual is exposed to during night hours causes sudden decreases in melatonin levels. Beta blockers used for the prophylaxis of hypertension, cardiac arrhythmias and headaches block the sympathetic activity both at the heart and at the pineal gland. On the other hand, antidepressant drug fluvoxamine prevents the degradation of melatonin and increases its plasma concentrations. Neurotransmitter imbalance has been shown to be present in SCN of essential hypertension patients and there is a decrease in the secretion of melatonin in coronary artery disease that follows. These findings bring forward the possibility of using melatonin in hypertensive patients. At the beginning of sleep norepinephrine and epinephrine levels decrease and they reach their lowest levels within an hour. In patients with OSAS there is an increase in the levels of nocturnal catecholamines. Despite long hours of fasting during sleep, blood glucose levels have been shown to remain stable. Leptin that plays an important role in energy balance by suppressing appetite (produced by adipose tissue), increases significantly during sleep at night and thus increases slow wave sleep. In lengthened sleep deprivation, there is suppression of the night increases of leptin [41–45]. *Gastrointestinal System*: Gastric acid secretion has a circadian rhythm. Basal acid secretion is at its lowest during the hours of the day where there is no food intake, while it is at its highest during midnight. In healthy individuals, there is no relationship between gastric acid secretion and the stages of sleep. Together with the inhibition of acid secretion throughout the night (with H2 receptor blockers and proton pump inhibitors) the healing of duodenum ulcers could be shown. Small bowel and colon motility decrease during sleep. In studies conducted on patients with irritable bowel syndrome,

*DOI: http://dx.doi.org/10.5772/intechopen.82754*

#### *Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine DOI: http://dx.doi.org/10.5772/intechopen.82754*

sleep quality decreases have been shown in REM latency, increases in first REM intensity and decreases of deep sleep. There are three basic processes coming into play in sleep regulation: (1) Homeostatic process: it tells us the relationship between last sleep and wakefulness periods. Sleep deprivation in the organism increases the duration and depth of sleep as a compensatory mechanism. (2) Circadian process: it is also defined as the biological clock. (3) Ultradian process: it defines the duration of REM—NREM sleep cycles and the interactions between them. Melatonin is the neuroendocrine modulator of day-night rhythm. Melatonin receptors are densely located at the suprachiasmatic nucleus (SCN). The endogenous circadian rhythm of melatonin secretion is in parallel to the endogenous rhythm of sleep tendency. Secretion of melatonin from the pineal gland is under the control of SCN. This pathway is multisynaptic and has contributions from the sympathetic nervous system. Melatonin has three important physiological features: (1) Hypnotic effect: the ability to initiate sleep when homeostatic effect is inadequate to initiate or to maintain sleep. (2) Chronohypnotic effect: it is the ability to inhibit the time of waking-up that is normally regulated by the circadian center. (3) Chronobiotic effect: concerning the regulation of the circadian rhythm, it is the ability to initiate phase shifts and to do this during desired hours. The light that an individual is exposed to during night hours causes sudden decreases in melatonin levels. Beta blockers used for the prophylaxis of hypertension, cardiac arrhythmias and headaches block the sympathetic activity both at the heart and at the pineal gland. On the other hand, antidepressant drug fluvoxamine prevents the degradation of melatonin and increases its plasma concentrations. Neurotransmitter imbalance has been shown to be present in SCN of essential hypertension patients and there is a decrease in the secretion of melatonin in coronary artery disease that follows. These findings bring forward the possibility of using melatonin in hypertensive patients. At the beginning of sleep norepinephrine and epinephrine levels decrease and they reach their lowest levels within an hour. In patients with OSAS there is an increase in the levels of nocturnal catecholamines. Despite long hours of fasting during sleep, blood glucose levels have been shown to remain stable. Leptin that plays an important role in energy balance by suppressing appetite (produced by adipose tissue), increases significantly during sleep at night and thus increases slow wave sleep. In lengthened sleep deprivation, there is suppression of the night increases of leptin [41–45]. *Gastrointestinal System*: Gastric acid secretion has a circadian rhythm. Basal acid secretion is at its lowest during the hours of the day where there is no food intake, while it is at its highest during midnight. In healthy individuals, there is no relationship between gastric acid secretion and the stages of sleep. Together with the inhibition of acid secretion throughout the night (with H2 receptor blockers and proton pump inhibitors) the healing of duodenum ulcers could be shown. Small bowel and colon motility decrease during sleep. In studies conducted on patients with irritable bowel syndrome, significant lengthening of REM sleep was identified [46].

### *2.2.2 Basic signs in sleep disorders and pathophysiological causes (semiology, propedeutics, preliminary instruction, introduction to further study)*

The first step in the evaluation of a patient with a sleep disorder is to identify the main symptom. A detailed history of the sleep and wakefulness cycle constitutes the second step. This is followed by the medical history of the patient, a list of previously used medications, family history, detailed information about school, work, family and social life and a physical exam of bodily systems. Relevant laboratory tests are performed for differential diagnosis.

*Updates in Sleep Neurology and Obstructive Sleep Apnea*

two important physiological mechanisms need to be in balance: (a) Forces that cause the collapse of the pharyngeal airways (the amount of soft tissue that covers the airways and the size of the airways). (b) Forces that dilate the pharyngeal airways (the activity of a muscle group that work in a coordinated manner to keep the airways open). Predisposing factors that would impair this balance are: "Mainly age and gender and then race, obesity, neck circumference, cigarettealcohol-sedative use, genetic factors, co-morbid diseases (acromegaly, hypothy-

mucopolysaccharidosis), body posture and gravity, anatomic factors, genetic factors and hormones influence the patency of upper airways and constitute the risk factors for OSAS [31–35]. *Sleep and immune system*: among the substances that are both sleep inducing and immunologically active we can list; Interleukin-1 (IL-1), IL-2, alpha interferon, Factor-S, muramyl peptides, tumor necrosis factor

(TNF) and prostaglandin D2 (PGD2). We know that people who are sleep deprived can get sick more easily and when they pay attention to sleeping properly and resting, they heal faster. Several factors play a role in sleep regulation. TNF-alpha, IL-1-beta, growth hormone releasing hormone (GHRH), PGD2 and adenosine affect NREM sleep, whereas vasoactive intestinal peptide (VIP), nitric oxide (NO) and prolactin exert their effects on REM sleep. In the regulation of sleep-wakefulness, elements of immune system that are of significant value are; IL-1, IL-6 and TNF. When the endogenous production of IL-1-beta and TNFalpha increases (overnutrition, infectious disease states) NREM sleep increases.

The effects of certain cytokines on sleep can be summarized as follows: *Prosomnogenic cytokines*: IL-1-beta, IL-1-alpha, TNF-alpha, IL-2, IL-6, IL-15, IL-18, epidermal growth factor, nerve growth factor, interferon-gamma, neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3, and 4 have been observed in elevated concentrations in allergic diseases, and they cause swelling and tenderness in the joints, and increase the tendency for autoimmune diseases like rheumatoid arthritis. The secretion of such factors by the immune system peaks during the early hours of the night and with gradual decreases they reach their lowest levels during morning hours. Short term sleep deprivation lead to decreases in natural killer (NK) cell activity,

when this deprivation lasts longer there is an increase in NK cell activity. Experimental studies on laboratory animals have shown that, in instances of lengthened sleep deprivation fatal bacterial infections stemming from the gastrointestinal system can turn fatal within 3 days. In narcolepsy cases increases have been observed in TNF-alpha levels. In OSAS patients the circadian rhythm

of secretion for TNF-alpha deteriorates significantly [36–40]. *Endocrine Physiology during Sleep*: Circadian rhythm and homeostatic balance provide for the control of hormonal and metabolic changes during sleep. Sleep deprivation studies analyze the effects of sleep and circadian rhythm on hormones. Based on these studies, growth hormone (GH) and prolactin (PRL) secretion increases during normal sleep, cortisol and thyroid stimulating hormone (TSH) secretions decrease. If sleep is interrupted by wakefulness, GH and PRL decrease while TSH and cortisol increase. Physiologically cortisol decreases starting from early hours of the morning towards the evening by reaching its lowest levels during the late hours of the day and initial hours of sleep. A couple of hours before waking up, there are reactivation of cortisol secretion. Low levels of cortisol is associated with slow wave sleep. During sleep deprivation the amplitude of cortisol rhythm decreases 15% compared to normal. Especially in elderly individuals who have fragmented sleep patterns, as deep sleep decreases as well, there is an increase in cortisol levels during night time and this is associated with decreased memory and increases in insulin resistance. In Cushing syndrome patients, due to bad

roidism, Down Syndrome, storage diseases like amyloidosis and

**16**

PSG establishes the definitive diagnosis. Despite developments in the field of sleep medicine, we see that neither the society nor the physicians are adequately informed about sleep and sleep disturbances. However, diseases associated with sleep are frequent in the population and can have significant consequences: they can negatively influence the individual's "work or school success, social life, marriage and other relationships as well as leading to occupational and traffic accidents. Sleep disturbances can hinder the cognitive functions of an individual and can increase the risk of having psychiatric and other system related diseases. Sleep apnea syndrome has a role in the etiology of severe diseases namely hypertension, myocardial infarction, heart failure, stroke and diabetes. Sleep deprivation can result in an increase in the number of seizures in a patient with epilepsy. Complaints of patients with diseases of other systems can be related to sleep disorders: in a patient having a follow-up with a Holter recording for hypertension, the reason behind an increase in blood pressure during sleep can be sleep apnea syndrome. Frequent arousals during the night, chest pain, not being able to climb the stairs during the day, tiredness, complaints about sleepiness are evaluated as angina by cardiologists and angiograms are performed. However, a PSG to be performed on this patient can establish the correct diagnosis of central apnea syndrome. In a patient with goiter disease, during an overnight sleep test, it is possible to diagnose sinusal bradycardia. Likewise, patients having severe OSAS can have predominant depression symptoms and can therefore admit to psychiatry outpatient departments. Children admitting to pediatric neurology outpatient departments with sleep episodes are valuated multidimensionally and then treated for epilepsy. However, if these children were to undergo PSG and MSLT (multiple sleep latency test), correct diagnoses of underlying sleep apnea syndrome, central hypersomnia and narcolepsy could have been established.

*Insomnia*: it is described as "difficulty falling asleep or staying asleep"; short, inadequate, superficial, easily disruptable and non-restorative sleep. The amount of sleep an individual needs changes from one person to the other based on genetic traits. Some people carry out their daily functions with 5 hours of sleep a day, whereas others who do not sleep nine to 10 hours can feel bad the next day. Sleeplessness can be related to a primary disturbance related to mechanisms of sleep or can develop due to an underlying disease. Acute insomnia develops due to an abrupt change in environmental, physical or cognitive factors that initiate sleeplessness. Sleep complaints only disappear when the individual gets used to this new condition. There are different diseases underlying primary insomnia; circadian rhythm disturbances, drug-substance use or sudden discontinuation of their use. Acquisition of behavior that hinders sleep hygiene can result in chronic insomnia. Psychophysiological insomnia is learned insomnia; the patient starts getting tense as the time for going bed approaches. This effort to get asleep and tension cause a performance anxiety and ends up being the main reason of insomnia. As the patient searches for behavioral changes to relieve herself of this anxiety, insomnia becomes inextricable: inadequate sleep hygiene, night eating (drinking) syndrome, alcohol-hypnoticstimulant related insomnia are examples to insomnia for which such behavioral changes and habits lay the foundation. Causes of pain that increase during the night that negatively affect sleep and trigger insomnia are: "entrapment neuropathies, cluster headaches, arthritis, rheumatic pain, pain and paresthesia of the legs that are seen before falling asleep in restless leg syndrome. Most of the psychiatric diseases have a relationship with sleep: "In depression and anxiety disorder, insomnia might have started years ahead and likewise insomnia might

**19**

*Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine*

foreshadow psychosis or manic episodes." Examinations of physical neurological and cognitive functioning of the patient might reveal important clues about insomnia. In anxiety, tachycardia, rapid breathing and cold hands; in sleep apnea syndrome, short and thick neck, obesity and narrow upper respiratory tract; in endocrine system pathologies hyperthyroidism characterized by excessive sweating and tachycardia, round face and buffalo hump in Cushing syndrome and neurological examination might reveal causes of insomnia like neuropathy and parkinsonism. It should be kept in mind that women with iron deficiency anemia may complain of insomnia. *Excessive sleepiness*: having somnolence at inappropriate times and in inappropriate environments and being unable to prevent it. Although somnolence might be related to the nature of the individual, to the wearisomeness of his daily life or to depression, it is an important symptom that forecasts sleep disorders. In its mild forms it is seen during rest, in advanced cases the patient might fall asleep during a conversation, while doing work, during eating or while driving. Hypersomnia leads to important work and traffic accidents. In differential diagnosis, daytime excessive sleepiness due to chronic sleep deprivation should be kept in mind; additionally, excessive sleepiness can be seen during heart, kidney and liver failure, rheumatic, endocrinological and neurological diseases. Slowing down of responses, frequent yawning, closing of the eye lids, hesitance during speech or movements are the physical signs for excessive sleepiness. In people with chronic hypersomnia, round dark circles underneath the eyes attract one's attention. Sleep disturbances where one can see hypersomnolence are: "sleep apnea syndrome, narcolepsy, idiopathic hypersomnia, parasomnias"; however, certain complaints that are obtained during history help in the differential diagnosis of these disease states. Such complaints are; "snoring, apnea episodes observed by close ones, morning headaches, nocturia, sleep paralysis, hypnogogic hallucinations, cataplexy and confusion while waking up from sleep". Idiopathic hypersomnia is characterized by increased sleep time and despite there is nothing that would hinder the quality of sleep, the individual feels himself sleepy which differentiates this condition from insomnia associated with sleep deprivation. *Tiredness*: patients who have excessive sleepiness also complain about tiredness and lack of energy. However, tiredness is not associated with tendency to fall asleep. Tiredness is an important symptom for many diseases. Especially in women, tiredness due to iron deficiency anemia is usually ignored and mostly confused with sleepiness and that is why women come to sleep laboratories. Endocrine and metabolic diseases, heart, kidney and liver failures and psychiatric conditions like depression can as well lead to tiredness and fatigue. *Snoring*: it is the sound generated during sleep due to the resonance of the tissues of the upper respiratory tract which is mostly heard during inspiration, rarely during expiration and sometimes during both phases. Due to narrowed upper respiratory tract the speed of the flowing air increases, this creates turbulence and increases the intensity of the sound. Patients are usually not aware of this and they are guided to a doctor by close ones who are bothered by the noise. Sometimes the patient wakes up with his own snoring or his own effort to breathe. Characteristic features of the snoring sound give clues as to whether the patient has sleep apnea or not. In patients who had undergone surgery for upper respiratory airways, apnea episodes might as well be seen in the absence of snoring. *Sleep apnea*: it is the stopping of respiration for 10 seconds or longer during sleep. The patient's partner or close ones describe it as an interruption of snoring, as patient holding his/her breath during sleep. During apnea the snoring stops, while the apnea ends the patient has a deep inhalation,

*DOI: http://dx.doi.org/10.5772/intechopen.82754*

#### *Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine DOI: http://dx.doi.org/10.5772/intechopen.82754*

foreshadow psychosis or manic episodes." Examinations of physical neurological and cognitive functioning of the patient might reveal important clues about insomnia. In anxiety, tachycardia, rapid breathing and cold hands; in sleep apnea syndrome, short and thick neck, obesity and narrow upper respiratory tract; in endocrine system pathologies hyperthyroidism characterized by excessive sweating and tachycardia, round face and buffalo hump in Cushing syndrome and neurological examination might reveal causes of insomnia like neuropathy and parkinsonism. It should be kept in mind that women with iron deficiency anemia may complain of insomnia. *Excessive sleepiness*: having somnolence at inappropriate times and in inappropriate environments and being unable to prevent it. Although somnolence might be related to the nature of the individual, to the wearisomeness of his daily life or to depression, it is an important symptom that forecasts sleep disorders. In its mild forms it is seen during rest, in advanced cases the patient might fall asleep during a conversation, while doing work, during eating or while driving. Hypersomnia leads to important work and traffic accidents. In differential diagnosis, daytime excessive sleepiness due to chronic sleep deprivation should be kept in mind; additionally, excessive sleepiness can be seen during heart, kidney and liver failure, rheumatic, endocrinological and neurological diseases. Slowing down of responses, frequent yawning, closing of the eye lids, hesitance during speech or movements are the physical signs for excessive sleepiness. In people with chronic hypersomnia, round dark circles underneath the eyes attract one's attention. Sleep disturbances where one can see hypersomnolence are: "sleep apnea syndrome, narcolepsy, idiopathic hypersomnia, parasomnias"; however, certain complaints that are obtained during history help in the differential diagnosis of these disease states. Such complaints are; "snoring, apnea episodes observed by close ones, morning headaches, nocturia, sleep paralysis, hypnogogic hallucinations, cataplexy and confusion while waking up from sleep". Idiopathic hypersomnia is characterized by increased sleep time and despite there is nothing that would hinder the quality of sleep, the individual feels himself sleepy which differentiates this condition from insomnia associated with sleep deprivation. *Tiredness*: patients who have excessive sleepiness also complain about tiredness and lack of energy. However, tiredness is not associated with tendency to fall asleep. Tiredness is an important symptom for many diseases. Especially in women, tiredness due to iron deficiency anemia is usually ignored and mostly confused with sleepiness and that is why women come to sleep laboratories. Endocrine and metabolic diseases, heart, kidney and liver failures and psychiatric conditions like depression can as well lead to tiredness and fatigue. *Snoring*: it is the sound generated during sleep due to the resonance of the tissues of the upper respiratory tract which is mostly heard during inspiration, rarely during expiration and sometimes during both phases. Due to narrowed upper respiratory tract the speed of the flowing air increases, this creates turbulence and increases the intensity of the sound. Patients are usually not aware of this and they are guided to a doctor by close ones who are bothered by the noise. Sometimes the patient wakes up with his own snoring or his own effort to breathe. Characteristic features of the snoring sound give clues as to whether the patient has sleep apnea or not. In patients who had undergone surgery for upper respiratory airways, apnea episodes might as well be seen in the absence of snoring. *Sleep apnea*: it is the stopping of respiration for 10 seconds or longer during sleep. The patient's partner or close ones describe it as an interruption of snoring, as patient holding his/her breath during sleep. During apnea the snoring stops, while the apnea ends the patient has a deep inhalation,

*Updates in Sleep Neurology and Obstructive Sleep Apnea*

PSG establishes the definitive diagnosis. Despite developments in the field of sleep medicine, we see that neither the society nor the physicians are adequately informed about sleep and sleep disturbances. However, diseases associated with sleep are frequent in the population and can have significant consequences: they can negatively influence the individual's "work or school success, social life, marriage and other relationships as well as leading to occupational and traffic accidents. Sleep disturbances can hinder the cognitive functions of an individual and can increase the risk of having psychiatric and other system related diseases. Sleep apnea syndrome has a role in the etiology of severe diseases namely hypertension, myocardial infarction, heart failure, stroke and diabetes. Sleep deprivation can result in an increase in the number of seizures in a patient with epilepsy. Complaints of patients with diseases of other systems can be related to sleep disorders: in a patient having a follow-up with a Holter recording for hypertension, the reason behind an increase in blood pressure during sleep can be sleep apnea syndrome. Frequent arousals during the night, chest pain, not being able to climb the stairs during the day, tiredness, complaints about sleepiness are evaluated as angina by cardiologists and angiograms are performed. However, a PSG to be performed on this patient can establish the correct diagnosis of central apnea syndrome. In a patient with goiter disease, during an overnight sleep test, it is possible to diagnose sinusal bradycardia. Likewise, patients having severe OSAS can have predominant depression symptoms and can therefore admit to psychiatry outpatient departments. Children admitting to pediatric neurology outpatient departments with sleep episodes are valuated multidimensionally and then treated for epilepsy. However, if these children were to undergo PSG and MSLT (multiple sleep latency test), correct diagnoses of underlying sleep apnea syndrome, central hypersomnia and narcolepsy could

*Insomnia*: it is described as "difficulty falling asleep or staying asleep"; short,

amount of sleep an individual needs changes from one person to the other based on genetic traits. Some people carry out their daily functions with 5 hours of sleep a day, whereas others who do not sleep nine to 10 hours can feel bad the next day. Sleeplessness can be related to a primary disturbance related to mechanisms of sleep or can develop due to an underlying disease. Acute insomnia develops due to an abrupt change in environmental, physical or cognitive factors that initiate sleeplessness. Sleep complaints only disappear when the individual gets used to this new condition. There are different diseases underlying primary insomnia; circadian rhythm disturbances, drug-substance use or sudden discontinuation of their use. Acquisition of behavior that hinders sleep hygiene can result in chronic insomnia. Psychophysiological insomnia is learned insomnia; the patient starts getting tense as the time for going bed approaches. This effort to get asleep and tension cause a performance anxiety and ends up being the main reason of insomnia. As the patient searches for behavioral changes to relieve herself of this anxiety, insomnia becomes inextricable: inadequate sleep hygiene, night eating (drinking) syndrome, alcohol-hypnoticstimulant related insomnia are examples to insomnia for which such behavioral changes and habits lay the foundation. Causes of pain that increase during the night that negatively affect sleep and trigger insomnia are: "entrapment neuropathies, cluster headaches, arthritis, rheumatic pain, pain and paresthesia of the legs that are seen before falling asleep in restless leg syndrome. Most of the psychiatric diseases have a relationship with sleep: "In depression and anxiety disorder, insomnia might have started years ahead and likewise insomnia might

inadequate, superficial, easily disruptable and non-restorative sleep. The

**18**

have been established.

and the snoring restarts with a loud sound like roaring or snorting. These episodes can repeat hundreds of times through the night depending on the severity of the disease. The ending of apnea goes together with wakefulness reactions. This divides the sleep and hinders its quality. It might result in hypersomnia or insomnia. There are two main types of apnea: In central apnea air flow stops together with the effort of respiration. In obstructive apnea, air flow stops because of a narrowing in the upper respiratory tract but the effort of respiration still continues. Obstructive apnea is mainly accompanied by snoring and other complaints like night sweats, feeling of suffocation, nocturia, morning headaches, irritability, forgetfulness and depression and hypertension might follow. The patients are generally obese with short and thick necks; they also have narrow upper respiratory tracts. This body composition is not a rule though; people from all age groups including children might have obstructive apnea. Central apnea might be due to lesions of the brain stem and regions associated with the regulation of breathing. Furthermore, heart failure, metabolic and toxic encephalopathies might lead to central apnea. Central apnea might happen both in sleep and during wakefulness. *Night and morning headaches*: their relationship with sleep disturbances and neurological diseases is important. In the presence of morning headaches, one should consider problems related to sleep and respiration. This headache is diffuse and blunt in nature and is related to a decrease in O2 saturation. Cluster headaches typically appear during REM sleep. *Cataplexy*: It is the sudden loss of muscular tonus triggered by intense emotional stimuli and physical exercise. It is described as muscular atonia or hypotonia ranging from couple of seconds to couple of minutes in duration. If this symptom is together with sleepiness during the day, then it is always related to narcolepsy. The fact that consciousness and memory are preserved during the incident differentiates cataplexy from syncope and epileptic seizures. *Sleep paralysis*: it is the carrying over of REM sleep related atonia to wakefulness. The duration of the incident is limited to seconds or minutes. When the episodes become more frequent and they last longer, this disturbs the patient significantly and even be frightening. Despite the patient is awake, visual and auditory hallucinations might be present. In order not to experience this situation during sleep, the individual avoids to sleep and develops insomnia. Narcolepsy, depression, alcohol use, sleep deprivation and shift changes are instances where this symptom might be seen. *Hypnagogic and hypnopompic hallucinations*: hallucinations taking place during the beginning of sleep are called hypnagogic, those appearing while the individual is about to wake up are called hypnopompic. These hallucinations might have visual, auditory and tactile components; they can either be pleasing or frightening. Other than being seen during narcolepsy, they can happen in instances of sleep deprivation or when there are changes in sleep patterns as well as following alcohol consumption. *Parasomnias and movement during sleep*: parasomnias are involuntary physical events that take place when an individual is about to fall asleep, during sleeping and when he/she is about to wake up. the activation of the central nervous system during parasomnias results in features caused by activation of autonomic nervous system and motor activity. NREM parasomnias are disturbances in waking up from NREM sleep and the most common are confusional arousals, sleep terror, and sleepwalking. They mainly appear during deep slow wave sleep especially during the first 1/3 of the night. Familial characteristics are prominent. Despite the patient might seem like awake during the incident, arousal is not complete and he does not interact with his surroundings, does not respond to external stimuli, is not easily arousable, resists to

**21**

be considered [47–54].

*Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine*

consideration in children coming with the following complaints:

"Developmental delay, decrease in school performance, distractibility, hyperactivity, moodiness, stubbornness and aggression". School-age children can admit to doctors with complaints of feeling themselves not rested throughout the day, not having slept enough, difficulty in concentrating, adenoid hypertrophy, lack of attention and sleepiness during classes. In the presence of such symptoms, diagnoses of sleep apnea, insomnia, RLS, hypersomnia and narcolepsy should

efforts of waking him up and can show agitation. Patients are difficult to arouse during the event but if awaken they are confused; when episode ends, he can easily fall asleep after going to bed and does not remember the episode the next day. *Movements associated with sleep*: during REM sleep, muscle tonus disappears. REM sleep behavioral disturbance (RBD) is a parasomnia associated with REM sleep during which muscle tonus does not disappear but increases. As a result of this, the patient starts playing her/his dreams. It is characterized by aggressive behavior like speaking, shouting, kicking, punching or slapping, jumping, running which include violence and might harm the patient herself and her bed partners. The most important difference of arousal disturbances from NREM parasomnias is the development of episodes towards morning hours when REM sleep intensifies, when the patient wakes up after the episode, he is not confused and can remember a dream that can explain her/him behavior during which s/he has frequently felt threatened. Most of the patients are in the advanced age group and are idiopathic cases. Associated neurological diseases are "Parkinson's, Multisystem Atrophies and Dementia with Levy Bodies". The condition can also be seen in individuals using tricyclic antidepressants, monoamine oxidase inhibitors and serotonin reuptake inhibitors and in those who have recently stopped consuming alcohol. *Talking during sleep*: these are vocalizations ranging from murmuring to meaningful conversation during superficial NREM sleep. They can rarely be seen during REM stage as well. Stress, febrile diseases and frequent sleep deprivation can result in this. There is no need for treatment if there is not any underlying sleep disturbance. *Bruxism*: it is a movement disorder characterized by repetitive rhythmical jaw clenching and ensuing teeth grinding. It increases with stress and can result in face pain, jaw pain, teeth pain and damage to the teeth and even breaking of teeth as well as jaw dislocation. *Rhythmical movement disorder*: these are stereotypical movements that start immediately before falling asleep and continue during superficial sleep. The most known one is to rhythmically knock the head on the pillow or the headboard. It is a phenomenon usually encountered during infancy or early childhood and it disappears with increasing age by decreasing in intensity. *Restless leg syndrome (RLS) and periodical leg movements (PLM) during sleep*: RLS usually appears during evening hours and mostly after going to bed. These are unpleasant leg symptoms that cannot be well expressed by the patients. The disturbing sensation leading to an irresistible need to move the legs is the most important feature. As symptoms disappear with movement, patients constantly move their legs while in bed and they can even stand up and start walking around after a while. When patients come to see a physician with the complaint of insomnia, antidepressants that might be prescribed for treatment can increase the severity of RLS. Other causes that can increase the severity of the symptoms can be listed as: "Iron deficiency anemia, B12 and folate deficiencies, uremia, spinal cord lesions, diabetes mellitus, peripheral neuropathies, excessive exercise and caffeinated beverages". *Signs in children*: although they might be non-specific, the physician should definitely take sleep disturbances into

*DOI: http://dx.doi.org/10.5772/intechopen.82754*

#### *Sleep Physiology and Polysomnogram, Physiopathology and Symptomatology in Sleep Medicine DOI: http://dx.doi.org/10.5772/intechopen.82754*

efforts of waking him up and can show agitation. Patients are difficult to arouse during the event but if awaken they are confused; when episode ends, he can easily fall asleep after going to bed and does not remember the episode the next day. *Movements associated with sleep*: during REM sleep, muscle tonus disappears. REM sleep behavioral disturbance (RBD) is a parasomnia associated with REM sleep during which muscle tonus does not disappear but increases. As a result of this, the patient starts playing her/his dreams. It is characterized by aggressive behavior like speaking, shouting, kicking, punching or slapping, jumping, running which include violence and might harm the patient herself and her bed partners. The most important difference of arousal disturbances from NREM parasomnias is the development of episodes towards morning hours when REM sleep intensifies, when the patient wakes up after the episode, he is not confused and can remember a dream that can explain her/him behavior during which s/he has frequently felt threatened. Most of the patients are in the advanced age group and are idiopathic cases. Associated neurological diseases are "Parkinson's, Multisystem Atrophies and Dementia with Levy Bodies". The condition can also be seen in individuals using tricyclic antidepressants, monoamine oxidase inhibitors and serotonin reuptake inhibitors and in those who have recently stopped consuming alcohol. *Talking during sleep*: these are vocalizations ranging from murmuring to meaningful conversation during superficial NREM sleep. They can rarely be seen during REM stage as well. Stress, febrile diseases and frequent sleep deprivation can result in this. There is no need for treatment if there is not any underlying sleep disturbance. *Bruxism*: it is a movement disorder characterized by repetitive rhythmical jaw clenching and ensuing teeth grinding. It increases with stress and can result in face pain, jaw pain, teeth pain and damage to the teeth and even breaking of teeth as well as jaw dislocation. *Rhythmical movement disorder*: these are stereotypical movements that start immediately before falling asleep and continue during superficial sleep. The most known one is to rhythmically knock the head on the pillow or the headboard. It is a phenomenon usually encountered during infancy or early childhood and it disappears with increasing age by decreasing in intensity. *Restless leg syndrome (RLS) and periodical leg movements (PLM) during sleep*: RLS usually appears during evening hours and mostly after going to bed. These are unpleasant leg symptoms that cannot be well expressed by the patients. The disturbing sensation leading to an irresistible need to move the legs is the most important feature. As symptoms disappear with movement, patients constantly move their legs while in bed and they can even stand up and start walking around after a while. When patients come to see a physician with the complaint of insomnia, antidepressants that might be prescribed for treatment can increase the severity of RLS. Other causes that can increase the severity of the symptoms can be listed as: "Iron deficiency anemia, B12 and folate deficiencies, uremia, spinal cord lesions, diabetes mellitus, peripheral neuropathies, excessive exercise and caffeinated beverages". *Signs in children*: although they might be non-specific, the physician should definitely take sleep disturbances into consideration in children coming with the following complaints: "Developmental delay, decrease in school performance, distractibility, hyperactivity, moodiness, stubbornness and aggression". School-age children can admit to doctors with complaints of feeling themselves not rested throughout the day, not having slept enough, difficulty in concentrating, adenoid hypertrophy, lack of attention and sleepiness during classes. In the presence of such symptoms,

diagnoses of sleep apnea, insomnia, RLS, hypersomnia and narcolepsy should be considered [47–54].

*Updates in Sleep Neurology and Obstructive Sleep Apnea*

and the snoring restarts with a loud sound like roaring or snorting. These episodes can repeat hundreds of times through the night depending on the severity of the disease. The ending of apnea goes together with wakefulness reactions. This divides the sleep and hinders its quality. It might result in hypersomnia or insomnia. There are two main types of apnea: In central apnea air flow stops together with the effort of respiration. In obstructive apnea, air flow stops because of a narrowing in the upper respiratory tract but the effort of respiration still continues. Obstructive apnea is mainly accompanied by snoring and other complaints like night sweats, feeling of suffocation, nocturia, morning headaches, irritability, forgetfulness and depression and hypertension might follow. The patients are generally obese with short and thick necks; they also have narrow upper respiratory tracts. This body composition is not a rule though; people from all age groups including children might have obstructive apnea. Central apnea might be due to lesions of the brain stem and regions associated with the regulation of breathing. Furthermore, heart failure, metabolic and toxic encephalopathies might lead to central apnea. Central apnea might happen both in sleep and during wakefulness. *Night and morning headaches*: their relationship with sleep disturbances and neurological diseases is important. In the presence of morning headaches, one should consider problems related to sleep and respiration. This headache is diffuse and blunt in nature and is related to a decrease in O2 saturation. Cluster headaches typically appear during REM sleep. *Cataplexy*: It is the sudden loss of muscular tonus triggered by intense emotional stimuli and physical exercise. It is described as muscular atonia or hypotonia ranging from couple of seconds to couple of minutes in duration. If this symptom is together with sleepiness during the day, then it is always related to narcolepsy. The fact that consciousness and memory are preserved during the incident differentiates cataplexy from syncope and epileptic seizures. *Sleep paralysis*: it is the carrying over of REM sleep related atonia to wakefulness. The duration of the incident is limited to seconds or minutes. When the episodes become more frequent and they last longer, this disturbs the patient significantly and even be frightening. Despite the patient is awake, visual and auditory hallucinations might be present. In order not to experience this situation during sleep, the individual avoids to sleep and develops insomnia. Narcolepsy, depression, alcohol use, sleep deprivation and shift changes are instances where this symptom might be seen. *Hypnagogic and hypnopompic hallucinations*: hallucinations taking place during the beginning of sleep are called hypnagogic, those appearing while the individual is about to wake up are called hypnopompic. These hallucinations might have visual, auditory and tactile components; they can either be pleasing or frightening. Other than being seen during narcolepsy, they can happen in instances of sleep deprivation or when there are changes in sleep patterns as well as following alcohol consumption. *Parasomnias and movement during sleep*: parasomnias are involuntary physical events that take place when an individual is about to fall asleep, during sleeping and when he/she is about to wake up. the activation of the central nervous system during parasomnias results in features caused by activation of autonomic nervous system and motor activity. NREM parasomnias are disturbances in waking up from NREM sleep and the most common are confusional arousals, sleep terror, and sleepwalking. They mainly appear during

deep slow wave sleep especially during the first 1/3 of the night. Familial

characteristics are prominent. Despite the patient might seem like awake during the incident, arousal is not complete and he does not interact with his surroundings, does not respond to external stimuli, is not easily arousable, resists to

**20**

*Updates in Sleep Neurology and Obstructive Sleep Apnea*
