STUDY - Technical - New Dacian's Medicine
Sleep
and circadian rhythm disorders (2)
Translation Draft
We're going on yesterday...
Sleep is also associated with alterations in thermoregulatory function. Sleep, NREM is associated with a softening of thermoregulatory responses to both heat and cold stress, and animal studies on thermosensitive neurons in the hypothalamus show a reduction dependent on NREM from the initial thermoregulator point.
REM sleep is associated with the total absence of the thermoregulatory response, effectively consisting of functional poikilotermy. However, the impact of the opposite effect of this thermoregulation failure is dimmed by the inhibition of REM sleep in the case of extreme ambient temperatures.
Let's analyze sleep neuroanatomy now. Animal injury and neurological disease studies have suggested distinct neuroanatomical localizations in the generation of normal sleep and awakening. Studies in patients with lethargic encephalitis have suggested that a "sleep center" is found in the anterior hypothalamus, while in the posterior hypothalamus there is a "wakefulness centre".
Experimental animal studies have differently involved medullary reticular formations, thalamus and antero-basal brains in sleep generation, while the reticulated formation of the brain stem, the mesencephalus, the subtalamus and the anterobasal brain appear to have a role in the generation of wakefulness or in the recorded awakening of EEG.
Despite numerous studies, there is little evidence of either a "discreet sleep centre" or a discreet "wake-up" centre. More recent hypotheses suggest that this ability to generate sleep and wakefulness is distributed along an axial "core" of neurons that extend rosral from the brain stem to the previously basal brain.
The complex mixture of neural groups occurs at different points along this axis: brain stem - antero-basal brain. However, the neuroanatomical correlations of REM sleep appear to be discretely localized. Specific regions of the deck are associated with each of the neurophysiological correlations of REM sleep.
These experimental studies are based on the miming of pathological conditions in humans and animals. In narcolepsy, for example, a partial (catalepsy) or complete, sudden paralysis occurs in response to a variety of stimuli. In dogs with this condition, physiostigmine, a central cholinesterase inhibitor, increases the frequency of cataleptic attacks, while atropine decreases their frequency. On the contrary, in REM sleep disorders, patients suffer from incomplete motor inhibition during REM sleep, resulting ininvoluntary, sometimes violent movements during REM sleep.
In terms of sleep neurochemistry, the first experimental studies on brain stem rafe nuclei appeared to involve serotonin as a neurotransmitter that induces primary sleep, while catecholamines were considered responsible for wakefulness.
Subsequent studies have shown that the serotonin-rafeu system can facilitate sleep, but it is not necessary for its expression. Extensive pharmacology of sleep and wakefulness also suggests that other neurotransmitters play a certain role.
Cholinergic neurotransmission is known to play a role in the generation of REM sleep. The exerting influence of caffeine involves adenosine, while the hypnotic effect of benzodiazepines and barbiturates suggests a role as endogenous ligands of the GABA-A receptor complex.
A wide variety of sleep-inducing substances have been identified. These include prostaglandin D2, sleep-inducing delta peptides, muramil dipeptide, interleukin 1, primary fatty acid amides and melatonin, but the hypnotic effect is generally limited to NREM or slow-wave sleep, although peptides that accentuate REM sleep were also. Reported. Many recognized "sleep factors", including interleukin 1 and prostaglandin D2, are also immunologically active, suggesting a link between immune function and sleep-wake states.
Let me move on to the physiology of circadian rhythmicity now. The sleep-wake cycle is evident in many individuals within 24 hours. Significant daily variations also occur in endocrine, thermoretitor, cardiac, pulmonary, renal, gastrointestinal and cognitive functions.
However, it is important in assessing a daily variation to distinguish between those rhythmic components passively highlighted by environmental changes and behavioural changes (e.g. increased blood pressure and heart rate in vertical posture) and those actively induced by an endogenous oscillator process (e.g. circadian variation of plasma cortisol that persists in a variety of behavioural and environmental conditions).
The suprachiasmatic (NSC) of the hypothalamus acts as pacemakers that conduct endogenous circadian rhythm in mammals. Bilateral destruction of these nuclei results in the loss of endogenous circadian rhythmicity, which can only be restored by transplanting the same (same) structures from a donor animal. The periods and phases of the endogenous neural oscillator are synchronized normally over a 24-hour night-day, dark-light cycle period. The adaptation of circadian rhythms in mammals to the dark-light cycle is mediated by the retino-talamic tract, a monosynaptic pathway linking the retina to the NSC.
The main properties that characterize the circadian endogenous pacemaker are the intrinsic period, the maintained phase, the amplitude and the capacity for restoration. In human subjects living in controlled laboratory environments without time indicators (free-uninterrupted) the duration of the behavioral cycle of activity-rest is on average 25 hours.
However, the timing of the dark-light cycle was generally unchecked in these studies with subjects who choose to be exposed to light in their "subjective days". Recent studies have suggested that when the dark-light cycle is controlled, the period observed on the human circadian pacemaker is closer to 24 hours. However, the synchronization of the endogenous circadian pacemaker at 24 hours requires its restoration every day, which is normally achieved by exposure to the light-dark ambient cycle.
Exposure to light can change the phase of the endogenous circadian pacemaker, but both the intensity and direction of light-induced phase changes depend on the time of day, the duration, amplitude and intensity of light. Appropriately timed exposure to a light of sufficient intensity can, within 2 to 3 days, restore the human circadian pacemaker (assumed NSC) at any desired time.
Exposure to ordinary room light can also change the circadian phase, but not to as large a magnitude as outdoor light. The timing and internal structure of sleep are coupled directly to the capacity of the endogenous pacemaker. Spontaneous sleep duration, drowsiness, rem sleep inclination, and ability and tendency to sleep vary depending on the circadian phase.
The tendency to sleep, drowsiness and inclination to sleep REM peak just after the nadir (temporary point and opposite setup) of the endogenous circadian cycle of temperature (approximately 1 to 3 hours before awakening). In addition, 85% of all awakenings of subjects living in constant environmental conditions take place on the upward slope of the temperature cycle.
Moreover, there are certain times (wakefulness areas) when it is very difficult to fall asleep, even in the case of subjects who are deprived of sleep. The wrong correlation of the command of the endogenous circadian pacemaker with the desired sleep-wake cycle is considered to be responsible for certain states of insomnia, as well as for the decrease of wakefulness and performance in the case of workers during the night shift and after the time zone change.
The time has come when they can actually switch to sleep and wakefulness disorders. An international classification of sleep disorders divides these disorders into three major groups: dyssomnias, parasomnias and medical-psychiatric sleep disorders.
Dyssomnias are represented by: 1. intrinsic sleep disorders (psychophysiological insomnia, idiopathic insomnia, narcolepsy, idiopathic or recurrent hypersomnia, posttraumatic hypersomnia, sleep apnea syndromes, periodic disorders of limb movement and restless leg syndrome), 2. extrinsic sleep disorders (inadequate sleep hygiene, sleep disturbances caused by ambient factors, altitude insomnia, sleep adjustment disorders, sleep-related disorders, insomnia caused by food allergies, night hunger/thirst syndrome, alcohol or drug dependence disorders) and 3. circadian rhythm disorders (time zone change syndrome, shift activity disorders, delayed and advanced sleep phase syndromes, and sleep-wake disorders at intervals other than 24 hours).
Parasomnias are represented by: 1. awakening disorders (confused awakenings, sleepwalking, restless sleep, terrifying dreams), 2. sleep-wake transition disorders (rhythmic movement disorders, talked in sleep and nocturnal cramps in the lower limbs), 3. parasomnias usually associated with REM sleep (nightmares, sleep paralysis, erection disorders of the penis in sleep/ painful erections, cardiac arrhythmias in REM sleep and behavioral disorders in REM sleep) and 4. other parasomnias (nocturnal bruxism, nocturnal enuresis and nocturnal paroxysmal dystonia). Sleep disorders associated with medical/psychiatric disorders represented by: 1. disorders associated with mental disorders, 2. disorders associated with neurological disorders (brain degenerative disorders, parkinsonism, fatal family insomnia, sleep-related epilepsy, sleep-related migraines) and 3. disorders associated with other medical disorders (sleep sickness, nocturnal cardiac ischemia, chronic obstructive pulmonary disease, sleep-related asthma, sleep-related gastroesophageal reflux, peptic ulcerative disease and fibrosis syndrome). Note that we have highlighted the most common pathological conditions encountered in the evaluation of a patient with various accusations related to sleep or circadian rhythm.
That's enough for today!
We're going on yesterday...
Sleep is also associated with alterations in thermoregulatory function. Sleep, NREM is associated with a softening of thermoregulatory responses to both heat and cold stress, and animal studies on thermosensitive neurons in the hypothalamus show a reduction dependent on NREM from the initial thermoregulator point.
REM sleep is associated with the total absence of the thermoregulatory response, effectively consisting of functional poikilotermy. However, the impact of the opposite effect of this thermoregulation failure is dimmed by the inhibition of REM sleep in the case of extreme ambient temperatures.
Let's analyze sleep neuroanatomy now. Animal injury and neurological disease studies have suggested distinct neuroanatomical localizations in the generation of normal sleep and awakening. Studies in patients with lethargic encephalitis have suggested that a "sleep center" is found in the anterior hypothalamus, while in the posterior hypothalamus there is a "wakefulness centre".
Experimental animal studies have differently involved medullary reticular formations, thalamus and antero-basal brains in sleep generation, while the reticulated formation of the brain stem, the mesencephalus, the subtalamus and the anterobasal brain appear to have a role in the generation of wakefulness or in the recorded awakening of EEG.
Despite numerous studies, there is little evidence of either a "discreet sleep centre" or a discreet "wake-up" centre. More recent hypotheses suggest that this ability to generate sleep and wakefulness is distributed along an axial "core" of neurons that extend rosral from the brain stem to the previously basal brain.
The complex mixture of neural groups occurs at different points along this axis: brain stem - antero-basal brain. However, the neuroanatomical correlations of REM sleep appear to be discretely localized. Specific regions of the deck are associated with each of the neurophysiological correlations of REM sleep.
These experimental studies are based on the miming of pathological conditions in humans and animals. In narcolepsy, for example, a partial (catalepsy) or complete, sudden paralysis occurs in response to a variety of stimuli. In dogs with this condition, physiostigmine, a central cholinesterase inhibitor, increases the frequency of cataleptic attacks, while atropine decreases their frequency. On the contrary, in REM sleep disorders, patients suffer from incomplete motor inhibition during REM sleep, resulting ininvoluntary, sometimes violent movements during REM sleep.
In terms of sleep neurochemistry, the first experimental studies on brain stem rafe nuclei appeared to involve serotonin as a neurotransmitter that induces primary sleep, while catecholamines were considered responsible for wakefulness.
Subsequent studies have shown that the serotonin-rafeu system can facilitate sleep, but it is not necessary for its expression. Extensive pharmacology of sleep and wakefulness also suggests that other neurotransmitters play a certain role.
Cholinergic neurotransmission is known to play a role in the generation of REM sleep. The exerting influence of caffeine involves adenosine, while the hypnotic effect of benzodiazepines and barbiturates suggests a role as endogenous ligands of the GABA-A receptor complex.
A wide variety of sleep-inducing substances have been identified. These include prostaglandin D2, sleep-inducing delta peptides, muramil dipeptide, interleukin 1, primary fatty acid amides and melatonin, but the hypnotic effect is generally limited to NREM or slow-wave sleep, although peptides that accentuate REM sleep were also. Reported. Many recognized "sleep factors", including interleukin 1 and prostaglandin D2, are also immunologically active, suggesting a link between immune function and sleep-wake states.
Let me move on to the physiology of circadian rhythmicity now. The sleep-wake cycle is evident in many individuals within 24 hours. Significant daily variations also occur in endocrine, thermoretitor, cardiac, pulmonary, renal, gastrointestinal and cognitive functions.
However, it is important in assessing a daily variation to distinguish between those rhythmic components passively highlighted by environmental changes and behavioural changes (e.g. increased blood pressure and heart rate in vertical posture) and those actively induced by an endogenous oscillator process (e.g. circadian variation of plasma cortisol that persists in a variety of behavioural and environmental conditions).
The suprachiasmatic (NSC) of the hypothalamus acts as pacemakers that conduct endogenous circadian rhythm in mammals. Bilateral destruction of these nuclei results in the loss of endogenous circadian rhythmicity, which can only be restored by transplanting the same (same) structures from a donor animal. The periods and phases of the endogenous neural oscillator are synchronized normally over a 24-hour night-day, dark-light cycle period. The adaptation of circadian rhythms in mammals to the dark-light cycle is mediated by the retino-talamic tract, a monosynaptic pathway linking the retina to the NSC.
The main properties that characterize the circadian endogenous pacemaker are the intrinsic period, the maintained phase, the amplitude and the capacity for restoration. In human subjects living in controlled laboratory environments without time indicators (free-uninterrupted) the duration of the behavioral cycle of activity-rest is on average 25 hours.
However, the timing of the dark-light cycle was generally unchecked in these studies with subjects who choose to be exposed to light in their "subjective days". Recent studies have suggested that when the dark-light cycle is controlled, the period observed on the human circadian pacemaker is closer to 24 hours. However, the synchronization of the endogenous circadian pacemaker at 24 hours requires its restoration every day, which is normally achieved by exposure to the light-dark ambient cycle.
Exposure to light can change the phase of the endogenous circadian pacemaker, but both the intensity and direction of light-induced phase changes depend on the time of day, the duration, amplitude and intensity of light. Appropriately timed exposure to a light of sufficient intensity can, within 2 to 3 days, restore the human circadian pacemaker (assumed NSC) at any desired time.
Exposure to ordinary room light can also change the circadian phase, but not to as large a magnitude as outdoor light. The timing and internal structure of sleep are coupled directly to the capacity of the endogenous pacemaker. Spontaneous sleep duration, drowsiness, rem sleep inclination, and ability and tendency to sleep vary depending on the circadian phase.
The tendency to sleep, drowsiness and inclination to sleep REM peak just after the nadir (temporary point and opposite setup) of the endogenous circadian cycle of temperature (approximately 1 to 3 hours before awakening). In addition, 85% of all awakenings of subjects living in constant environmental conditions take place on the upward slope of the temperature cycle.
Moreover, there are certain times (wakefulness areas) when it is very difficult to fall asleep, even in the case of subjects who are deprived of sleep. The wrong correlation of the command of the endogenous circadian pacemaker with the desired sleep-wake cycle is considered to be responsible for certain states of insomnia, as well as for the decrease of wakefulness and performance in the case of workers during the night shift and after the time zone change.
The time has come when they can actually switch to sleep and wakefulness disorders. An international classification of sleep disorders divides these disorders into three major groups: dyssomnias, parasomnias and medical-psychiatric sleep disorders.
Dyssomnias are represented by: 1. intrinsic sleep disorders (psychophysiological insomnia, idiopathic insomnia, narcolepsy, idiopathic or recurrent hypersomnia, posttraumatic hypersomnia, sleep apnea syndromes, periodic disorders of limb movement and restless leg syndrome), 2. extrinsic sleep disorders (inadequate sleep hygiene, sleep disturbances caused by ambient factors, altitude insomnia, sleep adjustment disorders, sleep-related disorders, insomnia caused by food allergies, night hunger/thirst syndrome, alcohol or drug dependence disorders) and 3. circadian rhythm disorders (time zone change syndrome, shift activity disorders, delayed and advanced sleep phase syndromes, and sleep-wake disorders at intervals other than 24 hours).
Parasomnias are represented by: 1. awakening disorders (confused awakenings, sleepwalking, restless sleep, terrifying dreams), 2. sleep-wake transition disorders (rhythmic movement disorders, talked in sleep and nocturnal cramps in the lower limbs), 3. parasomnias usually associated with REM sleep (nightmares, sleep paralysis, erection disorders of the penis in sleep/ painful erections, cardiac arrhythmias in REM sleep and behavioral disorders in REM sleep) and 4. other parasomnias (nocturnal bruxism, nocturnal enuresis and nocturnal paroxysmal dystonia). Sleep disorders associated with medical/psychiatric disorders represented by: 1. disorders associated with mental disorders, 2. disorders associated with neurological disorders (brain degenerative disorders, parkinsonism, fatal family insomnia, sleep-related epilepsy, sleep-related migraines) and 3. disorders associated with other medical disorders (sleep sickness, nocturnal cardiac ischemia, chronic obstructive pulmonary disease, sleep-related asthma, sleep-related gastroesophageal reflux, peptic ulcerative disease and fibrosis syndrome). Note that we have highlighted the most common pathological conditions encountered in the evaluation of a patient with various accusations related to sleep or circadian rhythm.
That's enough for today!
So, a good week, full of
understanding, love and gratitude!
Dorin, Merticaru