5/24/2011
Why sleep cause cardiovascular disease
Poor sleep is prospectively linked to all-cause and cardiovascular mortality. So why. Recently, Motivala from UCLA Semel Institute in USA found that sleep loss is associated with increase cytokines in sleep deprivation studies and in primary insomnia patients. He said bidirectional communication between the brain and the inmmune system is carried out through a complex network of autonomic nerves, endocrine hormones and cytokines. Disturbed sleep appears to perturb the functioning of this network and therefore contribute to elevations in inflammatory mediators linked to cardiovascular disease.
5/23/2011
Sleep disorders in medical disease
Insomnia and hypersomnia are highly comorbid with medical conditions, such as chronic pain and diabetes, as well as with various cardiovascular, respiratory, gastrointestinal, urinary and neurological disorders. Restless legs syndrome and periodic leg movement syndrome have been associated with iron deficiency, kidney disease, diabetes, and neurological, autoimmune, cardiovascular and respiratory disorders. Rapid eye movement behaviour disorder has been described as an early manifestation of serious central nervous system diseases; thus, close neurological monitoring of patients referring with this complaint is indicated.
Therefore, identification and management of any sleep disorder in medical patients is important for optimizing the course and prognosis. Of equal importance is the search for undetected medical disorder in patients presenting with sleep disorders.
Therefore, identification and management of any sleep disorder in medical patients is important for optimizing the course and prognosis. Of equal importance is the search for undetected medical disorder in patients presenting with sleep disorders.
5/19/2011
Psychological Flexibility is effective to treat Insomnia in Persons with Chronic Pain
Sleep disturbance is a common complaint in people with chronic pain, and is associated with a range of adverse outcomes including reports of greater pain and disability. Most of these people usually use pain killer to help them reduce insomnia. Recently, McCracken et al from King's college in UK found psychological flexibity, a process from acceptance and commitment therapy is helpful for the insomniac with chronic pain. They found the components of psychological flexibility, particularly acceptance of pain and values-based action is positive correlations with sleep quality. They said the psychological flexibity may be a new candidate to treat insomnia in persons with chronic pain.
5/18/2011
Sleep and primary headaches
The relationship between sleep and primary headaches has been known for over a century, particularly for headaches occurring during the night or early morning. Migraine, tension-tyre headache, and cluster headache may cause sleep fragmentation, insomnia, and hypersomnia, causing considerable social and economical costs and several familial problems. By contrast, sleep disorders may themselves trigger headache attacks. Finally, headaches and sleep disorders can also be symptoms of other underlying pathologies. Despite this background, there is still no clarity about the mechanism that links these two entities and their interdependence remains to be defined. Patients with primary headache should undergo a careful assessment of sleep habits.
Placebo is effective to treat insomnia?
In clinical trial, sometime we may found placebo administration significantly decreased subjective sleep latency and increased subjective total sleep time. So is placebo effective to treat insomnia?
Recently, Ogawa et al from Kyoto University in Japan investigate the association between subjective sleep latency fluctuation and the placebo response. They found higher fluctuation of subjective sleep latency was associated with a greater decrease in subjective sleep latency in placebo treatment. Multivariate analysis suggested that a wider standard deviation for daily subjective sleep latency and a higher weekly mean sSL were independent predictors of greater improvement in mean subjective sleep latency during the subsequent weeks of placebo treatment. Likewise, a wider standard deviation and lower mean of subjective total sleep time were independent predictors of greater improvement in mean subjective total sleep time in the subsequent weeks.
So, placebo is effective to treat the insomniac with high fluctuation of subjective sleep latency and total sleep time.
Recently, Ogawa et al from Kyoto University in Japan investigate the association between subjective sleep latency fluctuation and the placebo response. They found higher fluctuation of subjective sleep latency was associated with a greater decrease in subjective sleep latency in placebo treatment. Multivariate analysis suggested that a wider standard deviation for daily subjective sleep latency and a higher weekly mean sSL were independent predictors of greater improvement in mean subjective sleep latency during the subsequent weeks of placebo treatment. Likewise, a wider standard deviation and lower mean of subjective total sleep time were independent predictors of greater improvement in mean subjective total sleep time in the subsequent weeks.
So, placebo is effective to treat the insomniac with high fluctuation of subjective sleep latency and total sleep time.
5/16/2011
cognitive-behaviour therapy for behavioural insomnia of school-aged children.
Chronic sleep problems can lead to the development of behavioural insomnia of Childhood - a sleep disorder involving problematic sleep-onset associations (i.e., parental presence), and resulting in impairments for children and family members.
Recently, Paine et al from Flinders University in Australia perform a controlled evaluation of cognitive-behaviour therapy (CBT) for behavioural insomnia. 42 children (M = 9.3 ± 1.9 yrs, range 7-13 yrs, 18f, 24m) were randomised to CBT (N = 21) or waitlist control (N = 21). CBT consisted of 6 sessions, and combined behavioural sleep medicine techniques (e.g., sleep restriction) with anxiety treatment techniques (e.g., cognitive restructuring). Compared to waitlist controls, children receiving CBT showed significant improvements in sleep latency, wake after sleep onset, and sleep efficiency (all p ≤ .003), but not total sleep time (p > .05). CBT was also associated with a reduction in problematic sleep associations (p ≤ .001), child-reported total and separation anxiety (both p ≤ .01), with all gains being maintained 6 months post-treatment.
This is the first controlled study to demonstrate that multi-component CBT can be effective for the sleep, insomnia, and anxiety symptoms of Behavioural Insomnia of Childhood in school-aged children.
Recently, Paine et al from Flinders University in Australia perform a controlled evaluation of cognitive-behaviour therapy (CBT) for behavioural insomnia. 42 children (M = 9.3 ± 1.9 yrs, range 7-13 yrs, 18f, 24m) were randomised to CBT (N = 21) or waitlist control (N = 21). CBT consisted of 6 sessions, and combined behavioural sleep medicine techniques (e.g., sleep restriction) with anxiety treatment techniques (e.g., cognitive restructuring). Compared to waitlist controls, children receiving CBT showed significant improvements in sleep latency, wake after sleep onset, and sleep efficiency (all p ≤ .003), but not total sleep time (p > .05). CBT was also associated with a reduction in problematic sleep associations (p ≤ .001), child-reported total and separation anxiety (both p ≤ .01), with all gains being maintained 6 months post-treatment.
This is the first controlled study to demonstrate that multi-component CBT can be effective for the sleep, insomnia, and anxiety symptoms of Behavioural Insomnia of Childhood in school-aged children.
Melatonin receptor agonists are new options for insomnia
The circadian nature of melatonin secretion, coupled with the localization of melatonin receptors to the suprachiasmatic nucleus, has led to numerous studies of the role of melatonin in modulation of the sleep-wake cycle and circadian rhythms in humans. Although much more needs to be understood about the various functions exerted by melatonin and its mechanisms of action, three therapeutic agents (ramelteon, prolonged-release melatonin, and agomelatine) are already in use, and melatonin receptor agonists are now appearing as new promising treatment options for sleep and circadian-rhythm related disorders.
Recently, Spadoni et al reviewed the medicinal chemistry strategies leading to MLT receptor agonists, and the evidence supporting therapeutic efficacy of compounds undergoing clinical evaluation.
A wide range of clinical trials demonstrated that ramelteon, prolonged-release melatonin and tasimelteon have sleep-promoting effects, providing an important treatment option for insomnia and transient insomnia, even if the improvements of sleep maintenance appear moderate.
Despite a large number of high affinity nonselective melatonin receptor agonists, only limited data on MT(1) or MT(2) subtype-selective compounds are available up to now. Administration of the MT(2)-selective agonist IIK7 to rats has proved to decrease NREM sleep onset latency, suggesting that MT(2) receptor subtype is involved in the acute sleep-promoting action of melatonin; rigorous clinical studies are needed to demonstrate this hypothesis. Further clinical candidates based on selective activation of MT(1) or MT(2) receptors are expected in coming years.
Recently, Spadoni et al reviewed the medicinal chemistry strategies leading to MLT receptor agonists, and the evidence supporting therapeutic efficacy of compounds undergoing clinical evaluation.
A wide range of clinical trials demonstrated that ramelteon, prolonged-release melatonin and tasimelteon have sleep-promoting effects, providing an important treatment option for insomnia and transient insomnia, even if the improvements of sleep maintenance appear moderate.
Despite a large number of high affinity nonselective melatonin receptor agonists, only limited data on MT(1) or MT(2) subtype-selective compounds are available up to now. Administration of the MT(2)-selective agonist IIK7 to rats has proved to decrease NREM sleep onset latency, suggesting that MT(2) receptor subtype is involved in the acute sleep-promoting action of melatonin; rigorous clinical studies are needed to demonstrate this hypothesis. Further clinical candidates based on selective activation of MT(1) or MT(2) receptors are expected in coming years.
5/12/2011
Overview of cognitive behavioral therapy for insomnia
A recent study found that Cognitive Behavioral Therapy for Insomnia (CBT-I) is more effective than hypnotic medications in controlling insomnia.
In Cognitive Behavioral Therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include:
1. Unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night).
2. Misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia).
3. Amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep).
4. Performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process.
Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.
In Cognitive Behavioral Therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include:
1. Unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night).
2. Misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia).
3. Amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep).
4. Performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process.
Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.
5/11/2011
Sleep Restriction for insomniac
Sleep restriction is a component of stimulus control therapy. It aims to match the time spent in bed with actual time spent asleep. It involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation.
It is achieved by averaging the time in bed that the patient spends only sleeping. Rigid bedtime and rise time are set, and the patient is forced to get up at the rising time even if they feel sleepy. This may help the patient sleep better the next night because of the sleep deprivation from the previous night.
Complete treatment usually lasts up to 3 weeks. At the begining, make oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock.
Sleep restriction has been helpful in some cases.
It is achieved by averaging the time in bed that the patient spends only sleeping. Rigid bedtime and rise time are set, and the patient is forced to get up at the rising time even if they feel sleepy. This may help the patient sleep better the next night because of the sleep deprivation from the previous night.
Complete treatment usually lasts up to 3 weeks. At the begining, make oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock.
Sleep restriction has been helpful in some cases.
5/08/2011
Stimulus control therapy for insomnia
Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene.
Examples of stimulus control therapy include:
1. Go to bed when you feel sleepy and when there is a high likelihood that sleep will occur.
2. Do not watch TV, read, eat, or worry in bed. Your bed should be used only for sleep and sexual activity.
3. If you do not fall asleep 30 minutes after going to bed, get up and go to another room and resume your relaxation techniques.
4. Reduce the subjective effort and energy expended trying to fall asleep.
5. Set your alarm clock to get up at a certain time each morning, even on weekends. Do not oversleep.
6. Avoid exposure to bright light during nighttime hours.
7. Avoid taking naps in the daytime.
Examples of stimulus control therapy include:
1. Go to bed when you feel sleepy and when there is a high likelihood that sleep will occur.
2. Do not watch TV, read, eat, or worry in bed. Your bed should be used only for sleep and sexual activity.
3. If you do not fall asleep 30 minutes after going to bed, get up and go to another room and resume your relaxation techniques.
4. Reduce the subjective effort and energy expended trying to fall asleep.
5. Set your alarm clock to get up at a certain time each morning, even on weekends. Do not oversleep.
6. Avoid exposure to bright light during nighttime hours.
7. Avoid taking naps in the daytime.
5/06/2011
Sleep hygiene for insomniac
Sleep hygiene is a variety of different practices that are necessary to have normal, quality nighttime sleep and full daytime alertness.
Good sleep hygiene practices include:
1. Sleep and wake pattern
The most important sleep hygiene measure is to maintain a regular sleep and wake pattern seven days a week. It is also important to spend an appropriate amount of time in bed, not too little, or too excessive. This may vary by individual; for example, if someone has a problem with daytime sleepiness, they should spend a minimum of eight hours in bed, if they have difficulty sleeping at night, they should limit themselves to 7 hours in bed in order to keep the sleep pattern consolidated.
2. Regular relaxing bedtime routine
Try to avoid emotionally upsetting conversations and activities before trying to go to sleep. Don't dwell on, or bring your problems to bed.
3. Associate your bed with sleep
It's not a good idea to use your bed to watch TV, listen to the radio, or read.
4. Good sleep environment
Make sure that the sleep environment is pleasant and relaxing. The bed should be comfortable, the room should not be too hot or cold, or too bright.
5. Exercise
Exercise can promote good sleep. Vigorous exercise should be taken in the morning or late afternoon. A relaxing exercise, like yoga, can be done before bed to help initiate a restful night's sleep.
6. Light
Ensure adequate exposure to natural light. This is particularly important for older people who may not venture outside as frequently as children and adults. Light exposure helps maintain a healthy sleep-wake cycle.
6. No napping
Avoid napping during the day; it can disturb the normal pattern of sleep and wakefulness.
7. No stimulants
Avoid stimulants such as caffeine, nicotine, and alcohol too close to bedtime. While alcohol is well known to speed the onset of sleep, it disrupts sleep in the second half as the body begins to metabolize the alcohol, causing arousal.
8. No food before sleep
Food can be disruptive right before sleep; stay away from large meals close to bedtime. Also dietary changes can cause sleep problems, if someone is struggling with a sleep problem, it's not a good time to start experimenting with spicy dishes. And, remember, chocolate has caffeine.
Good sleep hygiene practices include:
1. Sleep and wake pattern
The most important sleep hygiene measure is to maintain a regular sleep and wake pattern seven days a week. It is also important to spend an appropriate amount of time in bed, not too little, or too excessive. This may vary by individual; for example, if someone has a problem with daytime sleepiness, they should spend a minimum of eight hours in bed, if they have difficulty sleeping at night, they should limit themselves to 7 hours in bed in order to keep the sleep pattern consolidated.
 |
| Do not disturb your biological clock |
2. Regular relaxing bedtime routine
Try to avoid emotionally upsetting conversations and activities before trying to go to sleep. Don't dwell on, or bring your problems to bed.
 |
| Do not think when going to bed. Sleep like a baby. |
3. Associate your bed with sleep
It's not a good idea to use your bed to watch TV, listen to the radio, or read.
 |
| Make you bed comfortable |
4. Good sleep environment
Make sure that the sleep environment is pleasant and relaxing. The bed should be comfortable, the room should not be too hot or cold, or too bright.
5. Exercise
Exercise can promote good sleep. Vigorous exercise should be taken in the morning or late afternoon. A relaxing exercise, like yoga, can be done before bed to help initiate a restful night's sleep.
 |
| Yoga is good for your sleep |
6. Light
Ensure adequate exposure to natural light. This is particularly important for older people who may not venture outside as frequently as children and adults. Light exposure helps maintain a healthy sleep-wake cycle.
 |
| Light is good. |
6. No napping
Avoid napping during the day; it can disturb the normal pattern of sleep and wakefulness.
 |
| No nap for insomniac |
7. No stimulants
Avoid stimulants such as caffeine, nicotine, and alcohol too close to bedtime. While alcohol is well known to speed the onset of sleep, it disrupts sleep in the second half as the body begins to metabolize the alcohol, causing arousal.
 |
| Smoking is bad for your sleep |
8. No food before sleep
Food can be disruptive right before sleep; stay away from large meals close to bedtime. Also dietary changes can cause sleep problems, if someone is struggling with a sleep problem, it's not a good time to start experimenting with spicy dishes. And, remember, chocolate has caffeine.
 |
| Do not eat spicy food |
5/05/2011
Treatment of Insomnia
It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia. The treatment of insomnia is including:
1. Non-pharmacological strategies:
Non-pharmacological strategies are superior to hypnotic medication for insomnia because tolerance develops to the hypnotic effects. In addition, dependence can develop with rebound withdrawal effects developing upon discontinuation. Hypnotic medication is therefore only recommended for short-term use, especially in acute or chronic insomnia. Non pharmacological strategies however, have long lasting improvements to insomnia and are recommended as a first line and long term strategy of managing insomnia.
Non pharmacological strategies include:
(1). Sleep hygiene
(2). Stimulus control
(3). Behavioral interventions
(4). Sleep-restriction therapy
(5). Paradoxical intention
(6). Patient education
(7). Relaxation therapy
(8). Cognitive behavioral therapy for insomnia
2. Medications
Many insomniacs rely on sleeping tablets and other sedatives to get rest, with research showing that medications are prescribed to over 95% of insomniac cases.
The medications for insomnia include:
(1). Benzodiazepines
(2). Non-benzodiazepines
(3). Opioids
(4). Antidepressants
(5). Melatonin and melatonin agonists
(6). Antihistamines
(7). Atypical antipsychotics
(8). Other substances, for example, Some insomniacs use herbs such as valerian, chamomile, lavender, hops, and passion-flower.
1. Non-pharmacological strategies:
Non-pharmacological strategies are superior to hypnotic medication for insomnia because tolerance develops to the hypnotic effects. In addition, dependence can develop with rebound withdrawal effects developing upon discontinuation. Hypnotic medication is therefore only recommended for short-term use, especially in acute or chronic insomnia. Non pharmacological strategies however, have long lasting improvements to insomnia and are recommended as a first line and long term strategy of managing insomnia.
Non pharmacological strategies include:
(1). Sleep hygiene
(2). Stimulus control
(3). Behavioral interventions
(4). Sleep-restriction therapy
(5). Paradoxical intention
(6). Patient education
(7). Relaxation therapy
(8). Cognitive behavioral therapy for insomnia
2. Medications
Many insomniacs rely on sleeping tablets and other sedatives to get rest, with research showing that medications are prescribed to over 95% of insomniac cases.
The medications for insomnia include:
(1). Benzodiazepines
(2). Non-benzodiazepines
(3). Opioids
(4). Antidepressants
(5). Melatonin and melatonin agonists
(6). Antihistamines
(7). Atypical antipsychotics
(8). Other substances, for example, Some insomniacs use herbs such as valerian, chamomile, lavender, hops, and passion-flower.
Causes of Insomnia
Symptoms of insomnia can be caused by:
1. Environmental factors, e.g., noise
2. Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.
3. Life events, such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, birth of a child and bereavement.
4. Hormone shift, such as those that precede menstruation and those during menopause.
5. Diseases:
(1). Restless legs syndrome, which can cause sleep onset insomnia due to discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.
(2). Periodic limb movement disorder, which occurs during sleep and can cause arousals that the sleeper is unaware of.
(3). Pain. An injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep, and can in addition cause awakening.
(4). Parasomnias, which include such disruptive sleep events as nightmares, sleepwalking, night terrors, violent behavior while sleeping, and REM behavior disorder, in which the physical body moves in response to events within dreams.
(5). Medical disorders, such as hyperthroidism and rheumatoid arthritis.
(6). Neurological disorders, like brain lession, or a history of traumatic brain injury.
(7). Mental disorders, such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive complusive disorder, Dementia or excessive alcohol intake.
6. Drugs:
(1). Certain psychoactive drugs or stimulants, including certain medications, herbs, caffeine, cocaine, amphetamines, methylphenidate, MDMA and modafinil.
(2). Fluoroquinolone antibiotic drugs
(3). Abuse of over-the counter or prescription sleep aids can produce rebound insomnia.
7. A rare genetic condition can cause a prion-based, permanent and eventually fetal form of insomnia called fetal familial insomnia.
1. Environmental factors, e.g., noise
2. Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.
3. Life events, such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, birth of a child and bereavement.
4. Hormone shift, such as those that precede menstruation and those during menopause.
5. Diseases:
(1). Restless legs syndrome, which can cause sleep onset insomnia due to discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.
(2). Periodic limb movement disorder, which occurs during sleep and can cause arousals that the sleeper is unaware of.
(3). Pain. An injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep, and can in addition cause awakening.
(4). Parasomnias, which include such disruptive sleep events as nightmares, sleepwalking, night terrors, violent behavior while sleeping, and REM behavior disorder, in which the physical body moves in response to events within dreams.
(5). Medical disorders, such as hyperthroidism and rheumatoid arthritis.
(6). Neurological disorders, like brain lession, or a history of traumatic brain injury.
(7). Mental disorders, such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive complusive disorder, Dementia or excessive alcohol intake.
6. Drugs:
(1). Certain psychoactive drugs or stimulants, including certain medications, herbs, caffeine, cocaine, amphetamines, methylphenidate, MDMA and modafinil.
(2). Fluoroquinolone antibiotic drugs
(3). Abuse of over-the counter or prescription sleep aids can produce rebound insomnia.
7. A rare genetic condition can cause a prion-based, permanent and eventually fetal form of insomnia called fetal familial insomnia.
5/04/2011
ICD-10 Diagnostic Criteria for Non-Organic Insomnia
The diagnostic criteria for Non-Organic Insomnia is as follows:
A. The complaint is either of difficulty falling asleep or maintaining sleep, or of poor
quality sleep;
Same items as in DSM-IV
B. The sleep disturbance has occurred at least three times per week for at least 1
month;
The 3 days a week part is met in the coding above for Criterion A
The 1 month part is operationalized in the same way as DSM-IV, namely:
SL21 ≥ 30 days (For how many weeks, months, or years have you had at least one of these problems?)
C. There is preoccupation with the sleeplessness and excessive concern over its
consequences at night and during the day;
SL36A = 3-4 (R has moderate or severe concerns about the sleep problems)
OR
SL36B = 4-5 (R has much or very much worries or distress about the sleep problems)
D. The unsatisfactory quantity and/or quality of sleep either causes marked distress or interferes with ordinary activities in daily living.
We created a count of responses to all the daytime impairment items to operationalize this criterion.
SUM the number of responses in the SL28-34 series that were coded 3-4 plus whether or not SL35 was coded 4 plus the sum of the SL41-44 series that were coded 7-10.
Impairment is initialized to zero.
28. reduced motivation mod/sev - If SL28=3 or 4 then impairment=impairment + 1
29. reduced performance at work, school, or social activities mod/sev - IF SL29=3 or 4 then impairment = impairment + 1
30. errors or accidents mod/sev - If SL30=3 or 4 then impairment=impairment + 1
31. irritability, nerves, mood disturbance mod/sev - If SL31=3 or 4 then impairment=impairment + 1
32. daytime attention, concentration, or memory problems mod/sev - If SL32=3 or 4 then impairment=impairment + 1
33. daytime fatigue mod/sev - If SL33=3 or 4 then impairment=impairment + 1
34. daytime sleepiness mod/sev - If SL34=3 or 4 then impairment=impairment + 1
35. tension headaches or digestive problems SEVERE (NOT MOD/SEV) - If SL35=4 then impairment=impairment + 1
41. sleep probs interfered with home management 7-10/0-10 - If SL41 ≥ 7 then impairment=impairment +1
42. sleep probs interfered with ability to work 7-10/0-10 - If SL42 ≥ 7 then impairment=impairment +1
43. sleep probs interfered with social life 7-10/0-10 - If SL43 ≥ 7 then impairment=impairment +1
44. sleep probs interfered with close relationships 7-10/0-10 - If SL44 ≥ 7 then impairment=impairment +1
We say that Criterion D is met if impairment ≥ 2
DSM-IV-TR Diagnostic Criteria for Primary Insomnia
DSM is short for Diagnostic and Statistical Manual of Mental Disorders. It is published by the American Psychiatric Association and privides a common language and standard criteria for the classification of mental disorders. It is used in the United States and in varying degrees around the world. DSM-IV-TR is the "test revision" of its fifth edition.Primary insomnia is defined as follows in DSM-IV-TR.
A. The predominant complaint is difficulty initiating or maintaining sleep, or nonrestorative sleep, for at least 1 month.
A1.1. The predominant complaint is difficulty initiating sleep
SL1 = 3-7 (problems getting to sleep ≥3 and ≤7 nights a week) AND
SL3 ≥ 30 minutes (it takes 30 or more minutes to get to sleep those nights)
OR
A1.2. The predominant complaint is difficulty maintaining sleep
A1.2a. Waking multiple times (waking 3 or more times at night)
SL4 = 3-7 (problems staying asleep ≥3 and ≤7 nights a week) AND EITHER
[(SL6 ≥ 3: waking 3 or more times)
OR
A1.2b. Taking a long time to get back to sleep after awakening at night (30 or more minutes awake)
SL4 = 3-7 (problems staying asleep ≥3 and ≤7 nights a week) AND EITHER
[(SL5.1 ≥ 30 minutes awake at night) OR (SL7: Number of minutes it takes to get back to sleep) x (SL6: Number of awakenings) ≥ 30 minutes]
OR
A1.2c. Waking too early in the AM (30 or more minutes early)
SL8 = 3-7 (problems waking too early in the morning ≥3 and ≤7 days a week) AND
SL10 ≥ 30 minutes (R wakes 30 or more minutes early those mornings)
OR
A1.3. The predominant complaint is nonrestorative sleep
SL11 = 3-7 (problems feeling unrefreshed in the morning ≥3 and ≤7 days a week) AND
SL13 = 2-4 (the severity of the problem waking up feeling nonrefreshed is either moderate, severe, or very severe) AND
SS5+SS6 >= 7 hours (R has adequate opportunity for sleep) AND
A1.1 = No and A1.2a= No and A1.2b=No and A1.2c=No (R doesn’t have any other sleep problem)
AND
A2. The complaint has lasted at least one month
SL21 ≥ 30 days (For how many weeks, months, or years have you had at least one of these problems?)
B. The sleep disturbance (or associated daytime fatigue) causes clinically significant
distress or impairment in social, occupational, or other important areas of
functioning.
We created a count of responses to all the daytime impairment items to operationalize this criterion.
SUM the number of responses in the SL28-34 series that were coded 3-4 plus whether or not SL35 was coded 4 plus whether or not 36A was coded 3-4 plus whether or not SL36B was coded 4-5 (you only get 1 point if either 36A or 36B was in the range) plus the sum of the SL41-44 series that were coded 7-10.
Impairment is initialized to zero.
28. reduced motivation mod/sev - If SL28=3 or 4 then impairment=impairment + 1
29. reduced performance at work, school, or social activities mod/sev - IF SL29=3 or 4 then impairment = impairment + 1
30. errors or accidents mod/sev - If SL30=3 or 4 then impairment=impairment + 1
31. irritability, nerves, mood disturbance mod/sev - If SL31=3 or 4 then impairment=impairment + 1
32. daytime attention, concentration, or memory problems mod/sev - If SL32=3 or 4 then impairment=impairment + 1
33. daytime fatigue mod/sev - If SL33=3 or 4 then impairment=impairment + 1
34. daytime sleepiness mod/sev - If SL34=3 or 4 then impairment=impairment + 1
35. tension headaches or digestive problems SEVERE (NOT MOD/SEV) - If SL35=4 then impairment=impairment + 1
36A. concerns or worries about your sleep mod/sev
36B. worried or distressed about sleep problems much/very much – If SL36a OR SL36b=3 or 4 then impairment=impairment+1
41. sleep probs interfered with home management 7-10/0-10 - If SL41 ≥ 7 then impairment=impairment +1
42. sleep probs interfered with ability to work 7-10/0-10 - If SL42 ≥ 7 then impairment=impairment +1
43. sleep probs interfered with social life 7-10/0-10 - If SL43 ≥ 7 then impairment=impairment +1
44. sleep probs interfered with close relationships 7-10/0-10 - If SL44 ≥ 7 then impairment=impairment +1
We say that Criterion B is met if impairment ≥ 2.
C. The sleep disturbance does not occur exclusively during the course of narcolepsy,
breathing-related sleep disorder, circadian rhythm sleep disorder, or parasomnia.
NOT OPERATIONALIZED
D. The disturbance does not occur exclusively during the course of another mental
disorder (e.g., major depressive disorder, generalized anxiety disorder, a delirium).
NOT OPERATIONALIZED
E. The disturbance is not due to the direct physiological effects of a substance.
NOT OPERATIONALIZED
5/03/2011
What is insomnia
Insomnia (from Latin "in" meaning "not", and "Somnus" meaning "sleep") is most often defined by an individual's report of sleeping difficulties.[1] While the term is sometimes used in sleep literature to describe a disorder demonstrated by polysomnographic evidence of disturbed sleep, insomnia is often defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"[1]
Thus, insomnia is most often thought of as both a sign [2] and a symptom[1][3] that can accompany several sleep, medical, and psychiatric disorders, characterized by persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. One definition of insomnia is difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month."[4]
Insomnia can be grouped into primary and secondary, or comorbid, insomnia.[5][6][7] Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause.[8] A complete diagnosis will differentiate between:
Thus, insomnia is most often thought of as both a sign [2] and a symptom[1][3] that can accompany several sleep, medical, and psychiatric disorders, characterized by persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. One definition of insomnia is difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month."[4]
Insomnia can be grouped into primary and secondary, or comorbid, insomnia.[5][6][7] Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause.[8] A complete diagnosis will differentiate between:
- insomnia as secondary to another condition,
- primary insomnia co-morbid with one or more conditions, or
- free-standing primary insomnia.
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