STUDY - Technical - New Dacian's Medicine
Sleep
and circadian rhythm disorders (4)
Translation Draft
As I said in the past post, let's talk about insomnia!
Persistent psychophysiological insomnia is a behavioural disorder in which patients are concerned about perceived inability to sleep properly during the night. Sleep disorders are often triggered by stressful emotional events but, however, the habit of sleeping little acquired during the stressful period lasts even after the initial incident.
Such patients are stressed, stressed, as a result of their own effort to sleep and/ or due to the sleep environment, and insomnia is a conditioned or learned response. Patients with psychophysiological insomnia fall asleep much more easily at unscheduled hours (when not trying to fall asleep) or outside the environment.
In such cases, polysomnographic records reveal objective sleep disorders often with abnormally long latency of sleep, with frequent nocturnal awakenings and a stage 1 transition sleep with increased volume. Extrinsic factors can contribute to this situation. Particular attention should be paid to sleep hygiene and correction of suressitation before bedtime. Behavioural therapy (i.e. sleep hygiene, relaxation training, stimuli control therapy, sleep restriction therapy) is the way of selection of treatment for psychophysiological insomnia and such therapy seems best instituted without medication.
Extrinsic insomnia is the following... A number of sleep disorders are the result of extrinsic factors that interfere with sleep. Adaptive sleep disorder, also called transient situational insomnia, can occur after changing the sleeping environment (e.g. at an unknown hotel, hospital bed) or before or after a significant life event, such as changing profession, workplace, loss of a nearby person, illness or fear near a deadline or examination.
Increased sleep latency, frequent sleep awakenings and early morning awakenings may also occur. Recovery is generally rapid, within 2 to 3 weeks. Inadequate sleep hygiene is characterized by a pattern of behaviour prior to sleep and/ or environmental conditions in the bedroom that are not conducive to sleep.
Noise and/ or light in the bedroom may interfere with sleep or the patient may be disturbed by the bed partner who moves his limbs in his sleep or who snores hard. Bright clocks can wake the patient, accentuating his fear of the time it takes to fall asleep. CNS-acting medicines, rich meals, special exercise or hot showers just before sleep can occur in the onset of sleep. Instead of taking hypnotic medications, patients should be advised to have their own soporific bedtime rituals, prepare and reserve their bedroom for sleep. Regular, consistent waking hours should be noted daily (total time spent in bed should be restricted to actual sleep hours).
A few words about altitude insomnia (easily interpretable as an insomnia of hypoxia, lack of oxygenation)... Sleep disorders are a common consequence of high altitude exposure. Cheyne-Stokes periodic breathing is generally installed during NREM sleep at twice as low intervals at altitude, with the return of normal breathing to REM sleep.
Central sleep apnea, rather than obstructive sleep apnea, appears to be responsible for this, characterized by regular respiratory breaks. It is believed that both hypoxia and hypocapnia are involved in the development of periodic breathing. Frequent awakenings and an unrestful sleep characterize the altitude insomnia, which is generally stronger in the first nights at high altitude, but can persist. Sleep duration is unchanged, but more awakenings may occur after the onset of sleep and shorter time of slow wave sleep (stages 3 and 4). Treatment with acetazolamide may decrease the time during which periodic breathing occurs and may substantially reduce hypoxia during sleep.
Medroxiprogesteroneacetate (MPA) also reduces hypoxia, but does not significantly reduce periodic breathing in sleep at altitude.
Let's move on to alcohol-dependent sleep disorders and medications! Sleep with disorders may be the result of an ingestion of highly varied agents. Caffeine is probably the most common pharmacological cause of insomnia in sensitive patients. It produces an increased latency of sleep onset and more frequent awakenings during the night, as well as a reduction in total sleep duration to 8 to 14 hours after ingestion.
Some patients are surprised to learn that their insomnia may be related to coffee consumption. 3 - 5 cups (33 - 50 ml a cup) can disturb the sleep of some patients significantly (this is why abstinence from caffeine of 1 to 2 months is required in these patients for a return to normal sleep). Similarly, alcohol and nicotine can interfere with sleep, although many patients use them for relaxation or to induce sleep.
Although alcohol can increase dizziness and short sleep latency, even moderate amounts of alcohol can increase awakenings after the onset of sleep, interfering with the brain's ability to maintain sleep. In addition, ingestion of alcohol before bedtime is contraindicated in patients with sleep apnea, due to the inhibitory effect of alcohol on the tone of the upper airway muscles.
Amphetamine and cocaine acutely suppress REM sleep as well as total sleep time, which return to normal with the use of high doses of benzodiazepines with short half-life. For this reason, hypnotics should be rarely prescribed for current use and the dose should be low to moderate, the duration of therapy being limited to 2 to 3 weeks, and the dosage of medication gradually reduced to suppression.
Narcolepsy has as symptoms (most common) excessive daytime sleepiness with episodes of involuntary sleep during the day, night sleep with disorders and cataplexy (sudden weakness or loss of muscle tone, without loss of consciousness, caused by emotions). Some patients may also experience muscle paralysis and/ or hallucinations at the onset of sleep or upon awakening.
The severity of the shapes differs. Patients may experience 2 to 3 cataplectic attacks per day or 10 days, and the extent and duration of the attack may range from transient paresis of the jaw lasting a few seconds to flaccid paralysis of the entire voluntary muscle for 20 to 30 minutes, in rare cases. Experiments in narcolepsy (on canine subjects) suggest an autosomal recessive pattern of inheritance.
In humans, first-degree relatives of narcoleptic patients have a much higher incidence of narcolepsy than the rest of the population. In addition, almost all narcoleptics are positive to the human leukocytic antigen DR15 and the presence of a high rate of discord in monozigotic twins indicates that one or more non-hereditary factors contribute to the development of narcolepsy. Symptoms begin to appear typically in the second decade, although the onset varies between the age of 5 to 50 years. Once installed, the disease is chronic, with no remissions.
Classically, the diagnosis of narcolepsy requires the presence of "narcoleptic tetrade", which consists of: 1. excessive daytime sleepiness, 2. cataplexy, 3. hypnagogic hallucinations (the presence of terrifying dreams at the onset of sleep) and 4. sleep paralysis (the finding that voluntary muscles is paralyzed coincides with the onset of sleep).
The last three symptoms of the tetrade are all manifestations of normal REM sleep regulation, inherent in the syndrome. All patients with narcolepsy have verifiable objective sleepiness during the day, but the other 3 symptoms are variablely present and only cataplexy is unique in narcolepsy.
At least half of patients have cataplexy of some degree and a similar percentage report hypnagogic hallucinations and/ or sleep paralysis. Other associated symptoms are useful for diagnosis, but not specifically. A history of "automatic wake-up" behavior (a trance-like state during which simple motor behaviors persist) mainly serves to corroborate it with the presence of daytime sleepiness, but is not specific to the mechanism.
Patients with narcolepsy also routinely report severe nocturnal sleep disorders. A family history is important to assess the patient with excessive daytime sleepiness. Careful observation of children and siblings suffering from narcolepsy, especially at the typical age of onset (second decade of life), can lead to early diagnosis.
The diagnosis of narcolepsy in a patient with a suggestive history depends on 1. objective check of excessive daytime sleepiness (typically using TLSM after recording night sleep) of 2. an unequivocal history of catalexia, of 3. recording of abnormal REM sleep adjustment evidenced by the onset of REM sleep 10 minutes after the onset of sleep, either by nocturnal recordings or by one or more TLSM and 4 determinations. exclusion of other disorders, such as sleep apnea that causes excessive sleepiness.
Treatment of narcolepsy is symptomatic. Drowsiness is treated with stimulants. Methylphenidate is considered to be the preferred drug of most clinicians. Pemolina, the second substance commonly used in narcoleptic patients, has a longer half-life and is associated with fewer side effects, but may not be as effective. Dextroamphetamine and methamphetamine are also commonly used. Treatment of cataplexy, hypnagogic hallucinations and sleep paralysis require the administration of antidepressants, which are effective in part due to the strong suppressive effects of REM sleep.
That's enough for today! We still have quite discussed insomnia and circadian rhythm disorders: sleep apnea syndromes, dyssomnia, parasomnias, sleep disorders associated with medical/psychiatric disorders... and then the circadian rhythm disturbances... But all in their time (at least two more posts)!
As I said in the past post, let's talk about insomnia!
Persistent psychophysiological insomnia is a behavioural disorder in which patients are concerned about perceived inability to sleep properly during the night. Sleep disorders are often triggered by stressful emotional events but, however, the habit of sleeping little acquired during the stressful period lasts even after the initial incident.
Such patients are stressed, stressed, as a result of their own effort to sleep and/ or due to the sleep environment, and insomnia is a conditioned or learned response. Patients with psychophysiological insomnia fall asleep much more easily at unscheduled hours (when not trying to fall asleep) or outside the environment.
In such cases, polysomnographic records reveal objective sleep disorders often with abnormally long latency of sleep, with frequent nocturnal awakenings and a stage 1 transition sleep with increased volume. Extrinsic factors can contribute to this situation. Particular attention should be paid to sleep hygiene and correction of suressitation before bedtime. Behavioural therapy (i.e. sleep hygiene, relaxation training, stimuli control therapy, sleep restriction therapy) is the way of selection of treatment for psychophysiological insomnia and such therapy seems best instituted without medication.
Extrinsic insomnia is the following... A number of sleep disorders are the result of extrinsic factors that interfere with sleep. Adaptive sleep disorder, also called transient situational insomnia, can occur after changing the sleeping environment (e.g. at an unknown hotel, hospital bed) or before or after a significant life event, such as changing profession, workplace, loss of a nearby person, illness or fear near a deadline or examination.
Increased sleep latency, frequent sleep awakenings and early morning awakenings may also occur. Recovery is generally rapid, within 2 to 3 weeks. Inadequate sleep hygiene is characterized by a pattern of behaviour prior to sleep and/ or environmental conditions in the bedroom that are not conducive to sleep.
Noise and/ or light in the bedroom may interfere with sleep or the patient may be disturbed by the bed partner who moves his limbs in his sleep or who snores hard. Bright clocks can wake the patient, accentuating his fear of the time it takes to fall asleep. CNS-acting medicines, rich meals, special exercise or hot showers just before sleep can occur in the onset of sleep. Instead of taking hypnotic medications, patients should be advised to have their own soporific bedtime rituals, prepare and reserve their bedroom for sleep. Regular, consistent waking hours should be noted daily (total time spent in bed should be restricted to actual sleep hours).
A few words about altitude insomnia (easily interpretable as an insomnia of hypoxia, lack of oxygenation)... Sleep disorders are a common consequence of high altitude exposure. Cheyne-Stokes periodic breathing is generally installed during NREM sleep at twice as low intervals at altitude, with the return of normal breathing to REM sleep.
Central sleep apnea, rather than obstructive sleep apnea, appears to be responsible for this, characterized by regular respiratory breaks. It is believed that both hypoxia and hypocapnia are involved in the development of periodic breathing. Frequent awakenings and an unrestful sleep characterize the altitude insomnia, which is generally stronger in the first nights at high altitude, but can persist. Sleep duration is unchanged, but more awakenings may occur after the onset of sleep and shorter time of slow wave sleep (stages 3 and 4). Treatment with acetazolamide may decrease the time during which periodic breathing occurs and may substantially reduce hypoxia during sleep.
Medroxiprogesteroneacetate (MPA) also reduces hypoxia, but does not significantly reduce periodic breathing in sleep at altitude.
Let's move on to alcohol-dependent sleep disorders and medications! Sleep with disorders may be the result of an ingestion of highly varied agents. Caffeine is probably the most common pharmacological cause of insomnia in sensitive patients. It produces an increased latency of sleep onset and more frequent awakenings during the night, as well as a reduction in total sleep duration to 8 to 14 hours after ingestion.
Some patients are surprised to learn that their insomnia may be related to coffee consumption. 3 - 5 cups (33 - 50 ml a cup) can disturb the sleep of some patients significantly (this is why abstinence from caffeine of 1 to 2 months is required in these patients for a return to normal sleep). Similarly, alcohol and nicotine can interfere with sleep, although many patients use them for relaxation or to induce sleep.
Although alcohol can increase dizziness and short sleep latency, even moderate amounts of alcohol can increase awakenings after the onset of sleep, interfering with the brain's ability to maintain sleep. In addition, ingestion of alcohol before bedtime is contraindicated in patients with sleep apnea, due to the inhibitory effect of alcohol on the tone of the upper airway muscles.
Amphetamine and cocaine acutely suppress REM sleep as well as total sleep time, which return to normal with the use of high doses of benzodiazepines with short half-life. For this reason, hypnotics should be rarely prescribed for current use and the dose should be low to moderate, the duration of therapy being limited to 2 to 3 weeks, and the dosage of medication gradually reduced to suppression.
Narcolepsy has as symptoms (most common) excessive daytime sleepiness with episodes of involuntary sleep during the day, night sleep with disorders and cataplexy (sudden weakness or loss of muscle tone, without loss of consciousness, caused by emotions). Some patients may also experience muscle paralysis and/ or hallucinations at the onset of sleep or upon awakening.
The severity of the shapes differs. Patients may experience 2 to 3 cataplectic attacks per day or 10 days, and the extent and duration of the attack may range from transient paresis of the jaw lasting a few seconds to flaccid paralysis of the entire voluntary muscle for 20 to 30 minutes, in rare cases. Experiments in narcolepsy (on canine subjects) suggest an autosomal recessive pattern of inheritance.
In humans, first-degree relatives of narcoleptic patients have a much higher incidence of narcolepsy than the rest of the population. In addition, almost all narcoleptics are positive to the human leukocytic antigen DR15 and the presence of a high rate of discord in monozigotic twins indicates that one or more non-hereditary factors contribute to the development of narcolepsy. Symptoms begin to appear typically in the second decade, although the onset varies between the age of 5 to 50 years. Once installed, the disease is chronic, with no remissions.
Classically, the diagnosis of narcolepsy requires the presence of "narcoleptic tetrade", which consists of: 1. excessive daytime sleepiness, 2. cataplexy, 3. hypnagogic hallucinations (the presence of terrifying dreams at the onset of sleep) and 4. sleep paralysis (the finding that voluntary muscles is paralyzed coincides with the onset of sleep).
The last three symptoms of the tetrade are all manifestations of normal REM sleep regulation, inherent in the syndrome. All patients with narcolepsy have verifiable objective sleepiness during the day, but the other 3 symptoms are variablely present and only cataplexy is unique in narcolepsy.
At least half of patients have cataplexy of some degree and a similar percentage report hypnagogic hallucinations and/ or sleep paralysis. Other associated symptoms are useful for diagnosis, but not specifically. A history of "automatic wake-up" behavior (a trance-like state during which simple motor behaviors persist) mainly serves to corroborate it with the presence of daytime sleepiness, but is not specific to the mechanism.
Patients with narcolepsy also routinely report severe nocturnal sleep disorders. A family history is important to assess the patient with excessive daytime sleepiness. Careful observation of children and siblings suffering from narcolepsy, especially at the typical age of onset (second decade of life), can lead to early diagnosis.
The diagnosis of narcolepsy in a patient with a suggestive history depends on 1. objective check of excessive daytime sleepiness (typically using TLSM after recording night sleep) of 2. an unequivocal history of catalexia, of 3. recording of abnormal REM sleep adjustment evidenced by the onset of REM sleep 10 minutes after the onset of sleep, either by nocturnal recordings or by one or more TLSM and 4 determinations. exclusion of other disorders, such as sleep apnea that causes excessive sleepiness.
Treatment of narcolepsy is symptomatic. Drowsiness is treated with stimulants. Methylphenidate is considered to be the preferred drug of most clinicians. Pemolina, the second substance commonly used in narcoleptic patients, has a longer half-life and is associated with fewer side effects, but may not be as effective. Dextroamphetamine and methamphetamine are also commonly used. Treatment of cataplexy, hypnagogic hallucinations and sleep paralysis require the administration of antidepressants, which are effective in part due to the strong suppressive effects of REM sleep.
That's enough for today! We still have quite discussed insomnia and circadian rhythm disorders: sleep apnea syndromes, dyssomnia, parasomnias, sleep disorders associated with medical/psychiatric disorders... and then the circadian rhythm disturbances... But all in their time (at least two more posts)!
Have a good day!
Dorin, Merticaru