STUDY - Technical - New Dacian's Medicine
Sleep
and circadian rhythm disorders (1)
Translation Draft
Sleep disorders are among the most common accusations of those who go to the doctor, with a third of adults having occasional or persistent sleep disorders.
Absence of sleep or circadian rhythm disturbances can lead to serious changes in daytime activity. They are the sign of disorders that may be caused by associated medical or psychiatric conditions.
A short time ago (even though this practice is maintained in most cases), many of these disorders were treated with hypnotic medication without further diagnostic evaluation. But over time, in the medical world, a distinct class of sleep and wake-up disorders has been identified, and sleep disorders are already subject to clinical discipline.
The sleep-wake cycle is under the control of two main neurobiological systems: one that actively generates sleep and sleep-related processes and another that measures sleep within 25 hours. Sign or circadian rhythm disorders may be caused by intrinsic abnormalities of these two systems or by extrinsic abnormalities (environment, medication and disease).
It would be good to address (for starters) the physiology of sleep and wakefulness. Most adults sleep 7 to 8 hours a night, although the measurement, duration and internal structure of sleep vary in apparently healthy patients and by age. At the extremes, children and the elderly often have a interrupted sleep. Intermediate age adults tend to have a deep sleep episode over the day, although in some environments sleep can be divided into a reduced afternoon sleep and a short night sleep.
Although sleep duration varies greatly, studies suggest that adults who sleep less than 4 hours or more than 9 hours a night have an increased mortality rate compared to those who sleep 7 to 8 hours.
The stages and phases of human sleep are defined on the basis of characteristic patterns of encephalogram (EEG), electrooculogram (EOG - which measures the movement activity of the eyeballs) and surface electromyogram (RMG). Continuous recording of this multitude of physiological parameters to define sleep and wakefulness is called polysomnography.
With this, two sleep states were defined: 1. with rapid eye movements (REM) and 2. slow eye movements (NREM). NREM sleep is in turn divided into 4 stages characterized by increasing the threshold of awakening and slowing the activity of EEG. REM sleep is characterized by a low amplitude, with mixed frequency EEG similar to stage 1 of NREM sleep. EOG exhibits sudden changes in REM sleep similar to those observed during waking with open eyes. EMG activity is absent reflecting the complete muscle atonia mediated by the brain stem which is characteristic of this condition.
Let's see how human sleep is organized now. Normal night sleep in adults requires consistent night-to-night organization. After the onset of sleep, it usually progresses through the nREM stages 1 to 4 within 45 to 60 minutes.
Slow-wave sleep predominates in the first third of the night and includes 15 to 25% of total night sleep in young adults. The percentage of slow-wave sleep is influenced by several factors, the most important being age. Previous sleep deprivation increases both the rapidity of sleep onset and the intensity and amount of slow-wave sleep.
The first episode of REM sleep usually occurs within the second hour after the start of sleep. The faster onset of REM sleep in a young adult may (especially less than 30 minutes) suggest a pathology such as endogenous depression, narcolepsy, circadian rhythm disorders or drug withdrawal. REM and NREM alternate during the night with an average cycle of 90 to 110 minutes (ultradian cycle). Overall, REM sleep accounts for 20 to 25% of total sleep, and stages 1 and 2 of NREM sleep, 50 to 60% (by a higher percentage in older subjects).
Age has a big impact on the organization of sleep. Slow-wave sleep is more pronounced in childhood, falling sharply in puberty and over the 2nd and 3rd decades of life. After the age of 30 there is a progressive, almost linear decline in the amount of slow-wave sleep, and the amplitude of delta activity on the EEC, made up of slow-wave sleep, is reduced.
In people, otherwise healthy, in old age, slow-wave sleep may be completely absent, especially in men. For REM sleep there is a different age profile. In children, REM sleep can constitute 50% of total sleep time and the percentage is inversely proportional to the age of development. The amount of REM sleep decreases sharply during the first postnatal year as a mature REM-NREM cycle develops. In the rest of life, up to old age, REM sleep takes up a more constant percentage of total sleep time than slow-wave sleep.
Behavioural correlations of sleep stages and phases can help us understand more. Polysomnographic stages of sleep correlate with changes in behaviour during specific stages and phases. Awakenings from REM sleep are associated with the evocation of vivacious dreams more than 80% of the time.
The credibility of dream evocation increases with the late REM phases during the night. Images can also be rendered after nREM sleep interruption, although they are typically devoid of the details and vivacity of dreams in REM sleep. The incidence of dream rendering in NREM sleep can be increased by selective deprivation of REM sleep, suggesting that REM sleep and the dream itself are inevitably not related.
The onset of sleep is associated with marked decreases in perception of both auditory and visual stimuli and loss of consciousness. During stage 1 sleep, subjects may respond to weak auditory or visual signals without "awakening".
Furthermore, storage in memory is inhibited at the onset of stage 1 NREM and subjects awakened at this stage usually deny that they have fallen asleep. At the same time it is possible to continue performing routine or familiar motor tasks, such as driving a car, during the intermediate stage between wakefulness and sleep (stage 1 sleep) which often interferes with wakefulness behaviour in sleepy individuals.
During such disturbances, typically lasting a few seconds, but occasionally recognizing the persistence over longer durations, visual and auditory perception are attenuated and the reaction time is prolonged. Subsequently, the drowsy individual may experience amnesia of this event. Dramatic perception and cognitive deficits associated with frequent, short-stage 1 disturbances of sleep in the wakefulness behavioral state are a major component of psychomotor performance impairment observed in the drowsy.
Here are some physiological correlations of sleep stages and phases. All important physiological systems are influenced by sleep. In some cases, concomitant behavioral changes, such as the position of clinostatism or inactivity, are proximate causes of altered physiological function, but in most cases sleep itself is responsible.
Changes in cardiovascular activity during sleep include a decrease in blood pressure and heart rate during NREM sleep and especially in slow-wave sleep. During REM sleep, phase activity (sudden eye movements) is associated with variations in both blood pressure and heart rate, mediated mainly by the vagus nerve. Cardiac arrhythmias may occur selectively during REM sleep.
Changes also occur in respiratory functions. Compared to relaxed wakefulness, the respiratory frequency becomes more constant during NREM sleep (especially slow wave sleep) and REM tonic sleep and becomes very irregular during REM phasesleep. The per minute ventilation decreases during NREM sleep disproportionately compared to the decrease in metabolic rate at the onset of sleep, resulting in increased blood pressure of carbon dioxide.
Multiple factors contribute to these sleep-induced respiratory changes: 1. decrease in diameter and consequent increase in upper airway resistance, probably the result of sleep-associated relaxation, of a subset of active tonic muscles of the upper airways that lack a clear type of respiratory activation 2. change in the response of the respiratory system to chemical stimuli, i.e. to blood pressures of oxygen and carbon dioxide, 3. loss of respiratory responses to wake-up stimuli and 4. decrease in metabolic rate. In addition, the cough reflex is attenuated or absent during sleep. These changes in respiratory function may be relevant for the pathogenesis of obstructive sleep apnea and for sudden infant death syndrome.
Endocrine functions also change during sleep, the most important changes being evident in neuroendocrine parameters. Slow wave sleep is associated with growth hormone secretion, while sleep in general is associated with increased prolactin secretion.
Sleep has a complex effect on the secretion of luteinizing hormone (LH), during puberty sleep being associated with an increased secretion of LH, while the mature woman's sleep inhibits the secretion of LH in the early follicle phase of the menstrual cycle.
The onset of sleep (and probably slow-wave sleep) is associated with inhibition of thyroid-stimulating hormone (TSH) and the adenocorticotropic hormone (ACTH) axis - cortisol, an effect that overlaps circadian rhythm in the two systems. The pineal hormone, melatonin, is predominantly secreted at night in both active and night-time active species, reflecting the direct modulation of pineal activity by the circadian pacemaker in the anterior hypothalamus.
Melatonin secretion is not dependent on the appearance of sleep, persisting in people who stay awake at night. In addition, some recent data suggest that exogenous melatonin may increase drowsiness and may enhance sleep, especially when administered during daylight hours when endogenous melatonin levels are low. However, future studies are needed to verify and quantify the recognized properties of sleep-promoting melatonin.
That's it for today... It's just a holiday...
Sleep disorders are among the most common accusations of those who go to the doctor, with a third of adults having occasional or persistent sleep disorders.
Absence of sleep or circadian rhythm disturbances can lead to serious changes in daytime activity. They are the sign of disorders that may be caused by associated medical or psychiatric conditions.
A short time ago (even though this practice is maintained in most cases), many of these disorders were treated with hypnotic medication without further diagnostic evaluation. But over time, in the medical world, a distinct class of sleep and wake-up disorders has been identified, and sleep disorders are already subject to clinical discipline.
The sleep-wake cycle is under the control of two main neurobiological systems: one that actively generates sleep and sleep-related processes and another that measures sleep within 25 hours. Sign or circadian rhythm disorders may be caused by intrinsic abnormalities of these two systems or by extrinsic abnormalities (environment, medication and disease).
It would be good to address (for starters) the physiology of sleep and wakefulness. Most adults sleep 7 to 8 hours a night, although the measurement, duration and internal structure of sleep vary in apparently healthy patients and by age. At the extremes, children and the elderly often have a interrupted sleep. Intermediate age adults tend to have a deep sleep episode over the day, although in some environments sleep can be divided into a reduced afternoon sleep and a short night sleep.
Although sleep duration varies greatly, studies suggest that adults who sleep less than 4 hours or more than 9 hours a night have an increased mortality rate compared to those who sleep 7 to 8 hours.
The stages and phases of human sleep are defined on the basis of characteristic patterns of encephalogram (EEG), electrooculogram (EOG - which measures the movement activity of the eyeballs) and surface electromyogram (RMG). Continuous recording of this multitude of physiological parameters to define sleep and wakefulness is called polysomnography.
With this, two sleep states were defined: 1. with rapid eye movements (REM) and 2. slow eye movements (NREM). NREM sleep is in turn divided into 4 stages characterized by increasing the threshold of awakening and slowing the activity of EEG. REM sleep is characterized by a low amplitude, with mixed frequency EEG similar to stage 1 of NREM sleep. EOG exhibits sudden changes in REM sleep similar to those observed during waking with open eyes. EMG activity is absent reflecting the complete muscle atonia mediated by the brain stem which is characteristic of this condition.
Let's see how human sleep is organized now. Normal night sleep in adults requires consistent night-to-night organization. After the onset of sleep, it usually progresses through the nREM stages 1 to 4 within 45 to 60 minutes.
Slow-wave sleep predominates in the first third of the night and includes 15 to 25% of total night sleep in young adults. The percentage of slow-wave sleep is influenced by several factors, the most important being age. Previous sleep deprivation increases both the rapidity of sleep onset and the intensity and amount of slow-wave sleep.
The first episode of REM sleep usually occurs within the second hour after the start of sleep. The faster onset of REM sleep in a young adult may (especially less than 30 minutes) suggest a pathology such as endogenous depression, narcolepsy, circadian rhythm disorders or drug withdrawal. REM and NREM alternate during the night with an average cycle of 90 to 110 minutes (ultradian cycle). Overall, REM sleep accounts for 20 to 25% of total sleep, and stages 1 and 2 of NREM sleep, 50 to 60% (by a higher percentage in older subjects).
Age has a big impact on the organization of sleep. Slow-wave sleep is more pronounced in childhood, falling sharply in puberty and over the 2nd and 3rd decades of life. After the age of 30 there is a progressive, almost linear decline in the amount of slow-wave sleep, and the amplitude of delta activity on the EEC, made up of slow-wave sleep, is reduced.
In people, otherwise healthy, in old age, slow-wave sleep may be completely absent, especially in men. For REM sleep there is a different age profile. In children, REM sleep can constitute 50% of total sleep time and the percentage is inversely proportional to the age of development. The amount of REM sleep decreases sharply during the first postnatal year as a mature REM-NREM cycle develops. In the rest of life, up to old age, REM sleep takes up a more constant percentage of total sleep time than slow-wave sleep.
Behavioural correlations of sleep stages and phases can help us understand more. Polysomnographic stages of sleep correlate with changes in behaviour during specific stages and phases. Awakenings from REM sleep are associated with the evocation of vivacious dreams more than 80% of the time.
The credibility of dream evocation increases with the late REM phases during the night. Images can also be rendered after nREM sleep interruption, although they are typically devoid of the details and vivacity of dreams in REM sleep. The incidence of dream rendering in NREM sleep can be increased by selective deprivation of REM sleep, suggesting that REM sleep and the dream itself are inevitably not related.
The onset of sleep is associated with marked decreases in perception of both auditory and visual stimuli and loss of consciousness. During stage 1 sleep, subjects may respond to weak auditory or visual signals without "awakening".
Furthermore, storage in memory is inhibited at the onset of stage 1 NREM and subjects awakened at this stage usually deny that they have fallen asleep. At the same time it is possible to continue performing routine or familiar motor tasks, such as driving a car, during the intermediate stage between wakefulness and sleep (stage 1 sleep) which often interferes with wakefulness behaviour in sleepy individuals.
During such disturbances, typically lasting a few seconds, but occasionally recognizing the persistence over longer durations, visual and auditory perception are attenuated and the reaction time is prolonged. Subsequently, the drowsy individual may experience amnesia of this event. Dramatic perception and cognitive deficits associated with frequent, short-stage 1 disturbances of sleep in the wakefulness behavioral state are a major component of psychomotor performance impairment observed in the drowsy.
Here are some physiological correlations of sleep stages and phases. All important physiological systems are influenced by sleep. In some cases, concomitant behavioral changes, such as the position of clinostatism or inactivity, are proximate causes of altered physiological function, but in most cases sleep itself is responsible.
Changes in cardiovascular activity during sleep include a decrease in blood pressure and heart rate during NREM sleep and especially in slow-wave sleep. During REM sleep, phase activity (sudden eye movements) is associated with variations in both blood pressure and heart rate, mediated mainly by the vagus nerve. Cardiac arrhythmias may occur selectively during REM sleep.
Changes also occur in respiratory functions. Compared to relaxed wakefulness, the respiratory frequency becomes more constant during NREM sleep (especially slow wave sleep) and REM tonic sleep and becomes very irregular during REM phasesleep. The per minute ventilation decreases during NREM sleep disproportionately compared to the decrease in metabolic rate at the onset of sleep, resulting in increased blood pressure of carbon dioxide.
Multiple factors contribute to these sleep-induced respiratory changes: 1. decrease in diameter and consequent increase in upper airway resistance, probably the result of sleep-associated relaxation, of a subset of active tonic muscles of the upper airways that lack a clear type of respiratory activation 2. change in the response of the respiratory system to chemical stimuli, i.e. to blood pressures of oxygen and carbon dioxide, 3. loss of respiratory responses to wake-up stimuli and 4. decrease in metabolic rate. In addition, the cough reflex is attenuated or absent during sleep. These changes in respiratory function may be relevant for the pathogenesis of obstructive sleep apnea and for sudden infant death syndrome.
Endocrine functions also change during sleep, the most important changes being evident in neuroendocrine parameters. Slow wave sleep is associated with growth hormone secretion, while sleep in general is associated with increased prolactin secretion.
Sleep has a complex effect on the secretion of luteinizing hormone (LH), during puberty sleep being associated with an increased secretion of LH, while the mature woman's sleep inhibits the secretion of LH in the early follicle phase of the menstrual cycle.
The onset of sleep (and probably slow-wave sleep) is associated with inhibition of thyroid-stimulating hormone (TSH) and the adenocorticotropic hormone (ACTH) axis - cortisol, an effect that overlaps circadian rhythm in the two systems. The pineal hormone, melatonin, is predominantly secreted at night in both active and night-time active species, reflecting the direct modulation of pineal activity by the circadian pacemaker in the anterior hypothalamus.
Melatonin secretion is not dependent on the appearance of sleep, persisting in people who stay awake at night. In addition, some recent data suggest that exogenous melatonin may increase drowsiness and may enhance sleep, especially when administered during daylight hours when endogenous melatonin levels are low. However, future studies are needed to verify and quantify the recognized properties of sleep-promoting melatonin.
That's it for today... It's just a holiday...
Happy birthday to all the
Flowers in our lives! Sunday full of understanding, love and
gratitude! Don't forget the great celebration of Jesus' entry
into Jerusalem! Don't forget the week of passions begins! Be
loved by fate and by everyone in your life!
Dorin, Merticaru