STUDY - Technical - New Dacian's Medicine
Sleep
and circadian rhythm disorders (6)
Translation Draft
I'm going to start presenting some things about sleep disorders associated with medical/psychiatric disorders.
I'm going to start presenting some things about sleep disorders associated with medical/psychiatric disorders.
In schizophrenia there are
changes in the appearance and physiology of sleep (a decrease in
stage 4 and a lack of REM sleep augmentation following REM sleep
deprivation) - patients with chronic schizophrenia usually
experience reversal of nictemeral rhythm, sleep fragmentation
and insomnia.
Also, patients with other psychiatric disorders (anxiety, affective disorders, obsessive-compulsive diseases and chronic alcoholism) often sleep little. In the nature of sleep disorders heterogeneity is considerable both between the conditions that generate them and between patients with the same problems.
Depression may be associated with insomnia at the onset of sleep, insomnia in sleep maintenance and/ or waking up very early in the morning. However, hypersomnia is characteristic for some depressed patients, especially adolescents and those with either bipolar or seasonal depression (autumn/winter).
Indeed, sleep disorders are an important vegetative sign of depression and may begin before the patient perceives any mood swings. Polysomnographic results found in depression include low REM sleep latency, prolongation of the first NREM sleep episode, even if these results are not specific to depression, and the extent of these changes varies with age and symptomatology.
In mania and hypomania, sleep latency is increased and total sleep duration may be reduced. Patients with anxiety disorders tend not to experience changes in REM sleep and slow-wave sleep changes observed in patients with endogenous depression. Finally, chronic alcoholics do not show slow-wave sleep, have a low REM sleep and frequently wake up at night. These symptoms are associated with wakefulness disorders during the day. the sleep of chronic alcoholics remains disturbed for years after the cessation of alcohol abuse.
Sleep disorders associated with neurological disorders are represented by a variety of neurological diseases resulting from sleep disruption, both by non-specific indirect mechanisms (pain in cervical spondylosis or lower spine pain) or by damage to the central neural structures involved in sleep generation and control.
For example, dementias have long been associated with disorders in sleep-wake synchronization, often characterized by nocturnal wanderings and an exacerbation of symptomatology at night (so-called sunset). These clinical observations are consistent with neuropathological studies showing that 80% of cells in the hypothalamic circadian pacemaker (NSC) are lost in patients with senile dementia (Alzheimer's disease), although studies have not been replicated and causal association is still unproven. Sleep disorders rarely occur in epilepsy.
Often the history is abnormal behavior, occasionally with convulsive movements during sleep, and differential diagnosis includes behavioral disorders in REM sleep, sleep apnea syndrome and periodic movements in sleep. Diagnosis requires nocturnal EEG records.
Other neurological diseases associated with abnormal movements such as Parkinson's disease, hemibalism, Huntington's Korea and Gilles de la Tourette's syndrome are also associated with interrupted sleep, perhaps through secondary mechanisms. Headache syndrome may indicate sleep-related exacerbations (migraine or headache). The mechanisms of association of headache with sleep is unknown.
I will end with fatal familial insomnia which is a rare hereditary disorder caused by bilateral degeneration of the anterior and dorsomedial nuclei of the thalamus. Insomnia is a prominent early symptom. Progressively, the syndrome causes vegetative dysfunction, dysartria, myoclonia, coma and death. pathogenesis of thalamic destruction is unknown.
Sleep disorders associated with other medical disorders follow. A number of medical conditions is associated with sleep disruptions. The association may be non-specific, for example, between sleep interruptions and chronic pain caused by rheumatological conditions.
It is important to pay attention to these symptoms associated with sleep, as they are accused by many patients. In addition, sleep interruptions may occur due to the proper use of drugs, such as steroids, or are symptoms of other diseases.
Among the most important associations is that between sleep disorders and asthma. In many asthmatics there is an important daily variation in airway resistance, which results in a significant increase in symptoms, especially during sleep. In addition, the treatment of asthma with theophylline-based compounds, adrenergic agonists or glucocorticoids may independently interrupt sleep.
When sleep disruption is a marked side effect of asthma treatment, inhaled steroids (e.g. betaclomethasone) that do not interrupt sleep can provide an effective alternative. Cardiac ischemia may also be associated with sleep disruption. Variability in the function of the vegetative nervous system in REM sleep may justify the association of sleep with angina, although this remains unproven.
Patients may have restless nightmares or dreams, almost real, with or without the appearance of classic symptoms of angina. Recent studies suggest that patients with nocturnal angina most likely have obstructive sleep apnea, whose treatment can substantially relieve symptoms of nocturnal angina.
Nocturnal paroxysmal dyspnea may also be present as a consequence of sleep-associated cardiac ischemia, which causes pulmonary congestion exacerbated by the horizontal position. Chronic obstructive pulmonary disease is also associated with sleep disruption. Other conditions associated with sleep disruption include: cystic fibrosis, menopause, hyperthyroidism, gastroesophageal reflex, chronic renal failure and liver failure.
We've finally reached circadian rhythm disturbances.
A subcategory of patients who experience either insomnia or hypersomnia may have a sleep coordination disorder rather than sleep-inducing. Sleep coordination disorders can be organic (due to an intrinsic defect in the circadian pacemaker or its response to related stimuli) or environmental (due to a disruption of exposure to related environmental stimuli). Regardless of etiology, symptoms reflect the influence of the background circadian pacemaker on sleep-wake function. Thus, effective therapeutic approaches must aim to load the oscillator at a suitable stage.
The syndrome of rapid time zone changes occurs, in particular, due to the fact that especially many people experience long air travel (which involve significant time zone changes) which is often associated with excessive daytime sleepiness, insomnia at the onset of sleep and frequent sleep awakenings especially in the second half of the night.
Gastrointestinal discomfort is also common. The syndrome is transient, typically lasting 2 to 14 days, depending on the number of time zones crossed, the direction of the journey, the age of the traveller and the ability to adapt to change. It is said that those travelers who spend a lot of time outdoors adapt more easily than those who stay longer in hotel rooms, probably due to exposure to natural light.
Sleep disorders in shift work occur because a large number of people work constantly at night, either in permanent hours or in rotation. In addition, every week, millions of people choose to stay awake at night to achieve the deadline, to drive long distances or to participate in recreational activities, leading to a reversal of their own sleep-wake cycle.
Studies carried out in the case of workers in night shifts indicate that the circadian timer system fails to successfully adapt to such an inverted work schedule. This leads to an inadequate adjustment between the desired work-rest schedule and the pacemaker's yield and a troubled daytime sleep.
As a result, sleep deprivation, increased pre-work wake time and inadequate adjustment of the circadian phase produce low wakefulness and lead to an increased risk of safety for workers on night shifts. Routine activities, such as motorway driving, are particularly subject to sleep-related accidents.
There is a significant increase in the risk of fatal road accidents to provide between midnight and 6 a.m., even when alcohol is eliminated from the causative factors. In addition, workers who work at night are believed to have an increased heart rate, gastrointestinal and reproductive disorders. Interventions should promote increased awareness of the dangers associated with night work and should aim to minimize both circadian disruption and sleep deprivation.
The working hours must be minimized: 1. exposure to night work, 2. frequency of shift shifts so that changes are not made before 2 to 3 weeks, 3. the number of consecutive night shifts worked from 7 (which is characteristic) to 4-5 and 4. duration of the night shift. In addition, the strategic use of exposure to bright light can facilitate rapid adaptation to night shift work where possible. These steps can lead to marked improvement in the employee's health and performance and reduced accident rates among shift employees.
Late sleep phase syndrome is characterized by: 1. the onset of sleep reported as late, and the hours of awakening in refractory delay edup later than desired, 2. the actual periods of sleep almost at the same hours daily, 3. polysomnography throughout the night is generally normal, except for the onset of delayed sleep.
Patients have an abnormally delayed endogenous circadian phase with a minimum body temperature during the observed routine that occurs later than normal. This delayed phase may be due to: 1. an abnormally long intrinsic period of endogenous circadian pacemaker, 2. the pacemaker's ability to advance the abnormally reduced phase or 3. an irregular previous sleep-wake program, characterized by numerous nights in which the patient chooses to stay awake well above midnight program (for school, work or social reasons).
In most cases, it is difficult to distinguish between these factors, given that patients with an abnormally long intrinsic period prefer to voluntarily choose these late nocturnal activities, because at that time they cannot sleep. Patients tend to be young adults. This self-perpetuating state can persist for years and does not usually respond to attempts to restore normal sleep hours.
Patients respond to a reprogramming regimen in which sleep hours are successively delayed by approximately 3 hours a day until the desired sleep time (and earlier). Treatment methods involving high-light phototherapy during the morning hours prove promising in these patients.
Advanced sleep phase syndrome is the opposite of delayed sleep phase syndrome and tends to manifest itself in the elderly. In this situation patients report excessive daytime sleepiness until evening hours, when they have a great weight in staying awake even in social circumstances. Patients wake up from 3-5 in the morning every day, often a few hours earlier than the desired time. Although these patients have not been studied for a long time, some of them may benefit from bright light therapy during evening hours, designed to reprogram the circadian pacemaker to a later hour.
There are also non-circadian sleep-wake disorders. This may occur when the maximum ability to advance the sleep phase of the circadian pacemaker is not appropriate to accommodate the difference between the 24-hour geographic day and the intrinsic period of the patient's pacemaker. As a result, intentional exposure of patients to artificial light may induce the circadian pacemaker a program longer than 24 hours.
Affected patients are unable to maintain a stable phase relationship between pacemaker yield and 24-hour day. Such patients typically exhibit an increasing pattern of successive delays in the onset of sleep and waking hours, oscillating in phase and out of phase with local time. When the endogenous rhythms of the patients are out of the environment, insomnia coexists with excessive daytime sleepiness. On the contrary, when endogenous rhythms oscillate in phase with the environment, the symptoms subside.
Periods of alternation between symptomatic and asymptomatic intervals can last from a few weeks to a few months. Blind subjects unable to perceive light are particularly susceptible to these disorders.
I will complete this post and this "group" of signs of the disease with the medical implications of circadian rhythmicity. Understanding the role of circadian rhythmicity in the physiology of the disease can lead to improvements in diagnosis and treatment. For example, marked circadian variations have been reported in the incidence of acute myocardial infarction, sudden cardiac death and stroke, some of the main causes leading to deaths.
Platelet aggregation is increased in the early hours of the morning after waking, and coincides with the peak incidence of these cardiovascular episodes. A better understanding of the possible role of circadian rhythmicity in the acute destabilization of a chronic condition, such as atherosclerotic disease, could improve the understanding of physiopathology.
Diagnostic and therapy procedures may also be affected by the time of day the data is collected. Examples include blood pressure, body temperature, dexmethasone suppression test and plasma cortisol levels. The schedule of chemotherapy has been reported to have an effect on the outcome of treatment. Few doctors realize how much the results of routine tests are influenced during (or the state of sleep/wakefulness) at which they are performed.
In addition, both the toxicity and effectiveness of medicines may vary during the day. For example, a 5-fold difference was observed in the mortality rate following the administration of toxic agents in animal experiments at different times of the day. Anaesthetic agents are particularly sensitive to the effects of the time of day.
Also, patients with other psychiatric disorders (anxiety, affective disorders, obsessive-compulsive diseases and chronic alcoholism) often sleep little. In the nature of sleep disorders heterogeneity is considerable both between the conditions that generate them and between patients with the same problems.
Depression may be associated with insomnia at the onset of sleep, insomnia in sleep maintenance and/ or waking up very early in the morning. However, hypersomnia is characteristic for some depressed patients, especially adolescents and those with either bipolar or seasonal depression (autumn/winter).
Indeed, sleep disorders are an important vegetative sign of depression and may begin before the patient perceives any mood swings. Polysomnographic results found in depression include low REM sleep latency, prolongation of the first NREM sleep episode, even if these results are not specific to depression, and the extent of these changes varies with age and symptomatology.
In mania and hypomania, sleep latency is increased and total sleep duration may be reduced. Patients with anxiety disorders tend not to experience changes in REM sleep and slow-wave sleep changes observed in patients with endogenous depression. Finally, chronic alcoholics do not show slow-wave sleep, have a low REM sleep and frequently wake up at night. These symptoms are associated with wakefulness disorders during the day. the sleep of chronic alcoholics remains disturbed for years after the cessation of alcohol abuse.
Sleep disorders associated with neurological disorders are represented by a variety of neurological diseases resulting from sleep disruption, both by non-specific indirect mechanisms (pain in cervical spondylosis or lower spine pain) or by damage to the central neural structures involved in sleep generation and control.
For example, dementias have long been associated with disorders in sleep-wake synchronization, often characterized by nocturnal wanderings and an exacerbation of symptomatology at night (so-called sunset). These clinical observations are consistent with neuropathological studies showing that 80% of cells in the hypothalamic circadian pacemaker (NSC) are lost in patients with senile dementia (Alzheimer's disease), although studies have not been replicated and causal association is still unproven. Sleep disorders rarely occur in epilepsy.
Often the history is abnormal behavior, occasionally with convulsive movements during sleep, and differential diagnosis includes behavioral disorders in REM sleep, sleep apnea syndrome and periodic movements in sleep. Diagnosis requires nocturnal EEG records.
Other neurological diseases associated with abnormal movements such as Parkinson's disease, hemibalism, Huntington's Korea and Gilles de la Tourette's syndrome are also associated with interrupted sleep, perhaps through secondary mechanisms. Headache syndrome may indicate sleep-related exacerbations (migraine or headache). The mechanisms of association of headache with sleep is unknown.
I will end with fatal familial insomnia which is a rare hereditary disorder caused by bilateral degeneration of the anterior and dorsomedial nuclei of the thalamus. Insomnia is a prominent early symptom. Progressively, the syndrome causes vegetative dysfunction, dysartria, myoclonia, coma and death. pathogenesis of thalamic destruction is unknown.
Sleep disorders associated with other medical disorders follow. A number of medical conditions is associated with sleep disruptions. The association may be non-specific, for example, between sleep interruptions and chronic pain caused by rheumatological conditions.
It is important to pay attention to these symptoms associated with sleep, as they are accused by many patients. In addition, sleep interruptions may occur due to the proper use of drugs, such as steroids, or are symptoms of other diseases.
Among the most important associations is that between sleep disorders and asthma. In many asthmatics there is an important daily variation in airway resistance, which results in a significant increase in symptoms, especially during sleep. In addition, the treatment of asthma with theophylline-based compounds, adrenergic agonists or glucocorticoids may independently interrupt sleep.
When sleep disruption is a marked side effect of asthma treatment, inhaled steroids (e.g. betaclomethasone) that do not interrupt sleep can provide an effective alternative. Cardiac ischemia may also be associated with sleep disruption. Variability in the function of the vegetative nervous system in REM sleep may justify the association of sleep with angina, although this remains unproven.
Patients may have restless nightmares or dreams, almost real, with or without the appearance of classic symptoms of angina. Recent studies suggest that patients with nocturnal angina most likely have obstructive sleep apnea, whose treatment can substantially relieve symptoms of nocturnal angina.
Nocturnal paroxysmal dyspnea may also be present as a consequence of sleep-associated cardiac ischemia, which causes pulmonary congestion exacerbated by the horizontal position. Chronic obstructive pulmonary disease is also associated with sleep disruption. Other conditions associated with sleep disruption include: cystic fibrosis, menopause, hyperthyroidism, gastroesophageal reflex, chronic renal failure and liver failure.
We've finally reached circadian rhythm disturbances.
A subcategory of patients who experience either insomnia or hypersomnia may have a sleep coordination disorder rather than sleep-inducing. Sleep coordination disorders can be organic (due to an intrinsic defect in the circadian pacemaker or its response to related stimuli) or environmental (due to a disruption of exposure to related environmental stimuli). Regardless of etiology, symptoms reflect the influence of the background circadian pacemaker on sleep-wake function. Thus, effective therapeutic approaches must aim to load the oscillator at a suitable stage.
The syndrome of rapid time zone changes occurs, in particular, due to the fact that especially many people experience long air travel (which involve significant time zone changes) which is often associated with excessive daytime sleepiness, insomnia at the onset of sleep and frequent sleep awakenings especially in the second half of the night.
Gastrointestinal discomfort is also common. The syndrome is transient, typically lasting 2 to 14 days, depending on the number of time zones crossed, the direction of the journey, the age of the traveller and the ability to adapt to change. It is said that those travelers who spend a lot of time outdoors adapt more easily than those who stay longer in hotel rooms, probably due to exposure to natural light.
Sleep disorders in shift work occur because a large number of people work constantly at night, either in permanent hours or in rotation. In addition, every week, millions of people choose to stay awake at night to achieve the deadline, to drive long distances or to participate in recreational activities, leading to a reversal of their own sleep-wake cycle.
Studies carried out in the case of workers in night shifts indicate that the circadian timer system fails to successfully adapt to such an inverted work schedule. This leads to an inadequate adjustment between the desired work-rest schedule and the pacemaker's yield and a troubled daytime sleep.
As a result, sleep deprivation, increased pre-work wake time and inadequate adjustment of the circadian phase produce low wakefulness and lead to an increased risk of safety for workers on night shifts. Routine activities, such as motorway driving, are particularly subject to sleep-related accidents.
There is a significant increase in the risk of fatal road accidents to provide between midnight and 6 a.m., even when alcohol is eliminated from the causative factors. In addition, workers who work at night are believed to have an increased heart rate, gastrointestinal and reproductive disorders. Interventions should promote increased awareness of the dangers associated with night work and should aim to minimize both circadian disruption and sleep deprivation.
The working hours must be minimized: 1. exposure to night work, 2. frequency of shift shifts so that changes are not made before 2 to 3 weeks, 3. the number of consecutive night shifts worked from 7 (which is characteristic) to 4-5 and 4. duration of the night shift. In addition, the strategic use of exposure to bright light can facilitate rapid adaptation to night shift work where possible. These steps can lead to marked improvement in the employee's health and performance and reduced accident rates among shift employees.
Late sleep phase syndrome is characterized by: 1. the onset of sleep reported as late, and the hours of awakening in refractory delay edup later than desired, 2. the actual periods of sleep almost at the same hours daily, 3. polysomnography throughout the night is generally normal, except for the onset of delayed sleep.
Patients have an abnormally delayed endogenous circadian phase with a minimum body temperature during the observed routine that occurs later than normal. This delayed phase may be due to: 1. an abnormally long intrinsic period of endogenous circadian pacemaker, 2. the pacemaker's ability to advance the abnormally reduced phase or 3. an irregular previous sleep-wake program, characterized by numerous nights in which the patient chooses to stay awake well above midnight program (for school, work or social reasons).
In most cases, it is difficult to distinguish between these factors, given that patients with an abnormally long intrinsic period prefer to voluntarily choose these late nocturnal activities, because at that time they cannot sleep. Patients tend to be young adults. This self-perpetuating state can persist for years and does not usually respond to attempts to restore normal sleep hours.
Patients respond to a reprogramming regimen in which sleep hours are successively delayed by approximately 3 hours a day until the desired sleep time (and earlier). Treatment methods involving high-light phototherapy during the morning hours prove promising in these patients.
Advanced sleep phase syndrome is the opposite of delayed sleep phase syndrome and tends to manifest itself in the elderly. In this situation patients report excessive daytime sleepiness until evening hours, when they have a great weight in staying awake even in social circumstances. Patients wake up from 3-5 in the morning every day, often a few hours earlier than the desired time. Although these patients have not been studied for a long time, some of them may benefit from bright light therapy during evening hours, designed to reprogram the circadian pacemaker to a later hour.
There are also non-circadian sleep-wake disorders. This may occur when the maximum ability to advance the sleep phase of the circadian pacemaker is not appropriate to accommodate the difference between the 24-hour geographic day and the intrinsic period of the patient's pacemaker. As a result, intentional exposure of patients to artificial light may induce the circadian pacemaker a program longer than 24 hours.
Affected patients are unable to maintain a stable phase relationship between pacemaker yield and 24-hour day. Such patients typically exhibit an increasing pattern of successive delays in the onset of sleep and waking hours, oscillating in phase and out of phase with local time. When the endogenous rhythms of the patients are out of the environment, insomnia coexists with excessive daytime sleepiness. On the contrary, when endogenous rhythms oscillate in phase with the environment, the symptoms subside.
Periods of alternation between symptomatic and asymptomatic intervals can last from a few weeks to a few months. Blind subjects unable to perceive light are particularly susceptible to these disorders.
I will complete this post and this "group" of signs of the disease with the medical implications of circadian rhythmicity. Understanding the role of circadian rhythmicity in the physiology of the disease can lead to improvements in diagnosis and treatment. For example, marked circadian variations have been reported in the incidence of acute myocardial infarction, sudden cardiac death and stroke, some of the main causes leading to deaths.
Platelet aggregation is increased in the early hours of the morning after waking, and coincides with the peak incidence of these cardiovascular episodes. A better understanding of the possible role of circadian rhythmicity in the acute destabilization of a chronic condition, such as atherosclerotic disease, could improve the understanding of physiopathology.
Diagnostic and therapy procedures may also be affected by the time of day the data is collected. Examples include blood pressure, body temperature, dexmethasone suppression test and plasma cortisol levels. The schedule of chemotherapy has been reported to have an effect on the outcome of treatment. Few doctors realize how much the results of routine tests are influenced during (or the state of sleep/wakefulness) at which they are performed.
In addition, both the toxicity and effectiveness of medicines may vary during the day. For example, a 5-fold difference was observed in the mortality rate following the administration of toxic agents in animal experiments at different times of the day. Anaesthetic agents are particularly sensitive to the effects of the time of day.
A weekend full of Easter
holiday light!
Dorin, Merticaru