A recent study published in BMJ Open found that the prescription of sleeping pills (hypnotics) was associated with a greater than threefold increase in the risk of death. The abstract and full article are available (free) here:
http://bmjopen.bmj.com/content/2/1/e000850.full
There are a number of problems with this study, as mentioned by Dr. Nancy Collop, President of the American Academy of Sleep Medicine:
"Although the study found that the use of hypnotic medication, or sleeping pills, was associated with an increased risk of mortality, a cause-and-effect relationship could not be established because the study only analyzed an insurance database... it was impossible for them to control for psychiatric conditions and anxiety, which is an area of significant concern to this study population..." http://www.medscape.com/viewarticle/759336?src=mpnews&spon=17
The major problem that I have with the study is that, as I far as I can see looking at the full article, the presence of insomnia was not controlled for (most of the comparison group did not have insomnia). Insomnia itself is associated with increased mortality (in some but not all studies) and morbidity (illness). To further illustrate why this is a problem, consider a hypothetical study in which the use of insulin was associated with an increased death rate. It is well known that dibetes itself increases the risk of death. If the comparison group in this hypothetical study did not have diabetes, I don't think much if anything could be learned from the study.
This new sleeping pill study doesn't add much new information to the field of sleep medicine, although it does add to the literature suggesting that insomnia is a serious problem. I did find this earlier editorial by Dr. Kripke (primary author of the current study) which sums up the problem with this current study:
"Numerous previous studies have shown an association of hypnotic use to mortality, which can become confounded with insomnia. Was mortality controlled for hypnotic usage in examining the association with insomnia?" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079930/?tool=pubmed
To fully apply to the current study, that last statement can be changed to: Was mortality controlled for insomnia in examining the association with hypnotic usage?
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Edit: The association between insomnia and death is a complex issue. It is clearly associated with illness/morbidity. This abstract sums up the issues: http://www.ncbi.nlm.nih.gov/pubmed/15600216
Some studies have found that while a subjective complaint of insomnia is not associated with an increased risk of death, short sleep time is.
Showing posts with label insomnia. Show all posts
Showing posts with label insomnia. Show all posts
Saturday, March 03, 2012
Saturday, April 10, 2010
Sleeping Pills and Obstructive sleep apnea
This question was recently posted on Medscape's Physician connect:
I am treating a man who has sleep apnea and uses CPAP. He is on Trileptal and Lamictal. Recent problems with insomnia has made me suggest Sonata. Are there any concerns about this? Contraindications?
This is my answer (which also includes a response to a few of the comments posted on Physician Connect):
If a person is on an effective cpap pressure, the adverse effects of hypnotics should be no different than in someone without osa. I have treated thousands of patients with osa; some of them require ambien/lunesta/Sonata. I occasionally use benzodiazepines, especially restoril. There have been several studies showing that moderate doses of alcohol do not effect cpap requirements (not that I recommend alcohol). I do agree with having the patient check with the sleep clinic, however. What the patient is calling "insomnia" may be a sign of problems with cpap and should be addressed by his sleep physician.
I am treating a man who has sleep apnea and uses CPAP. He is on Trileptal and Lamictal. Recent problems with insomnia has made me suggest Sonata. Are there any concerns about this? Contraindications?
This is my answer (which also includes a response to a few of the comments posted on Physician Connect):
If a person is on an effective cpap pressure, the adverse effects of hypnotics should be no different than in someone without osa. I have treated thousands of patients with osa; some of them require ambien/lunesta/Sonata. I occasionally use benzodiazepines, especially restoril. There have been several studies showing that moderate doses of alcohol do not effect cpap requirements (not that I recommend alcohol). I do agree with having the patient check with the sleep clinic, however. What the patient is calling "insomnia" may be a sign of problems with cpap and should be addressed by his sleep physician.
Friday, January 02, 2009
Sleep and coronary artery calcification
Several medical bloggers have posted about a recent study in which increased sleep time was associated with a decreased incidence of coronary artery disease (as measured by coronary artery calcification).
The problem with these observational studies looking at sleep duration and mortality/morbidity is that they don't distinguish between 1) voluntary sleep deprivation, 2) primary insomnia, and 3) insomnia secondary to medical/sleep disorders.
How is a doctor to use the data from this study???
I doubt writing a prescription for a sleeping pill would improve someone's coronary artery calcification score. However, advising someone with voluntary sleep deprivation (due to work pressures, etc) to extend their sleep hours might (if they take your advice)- I base this conclusion on prior studies which demonstrated that voluntary sleep restriction does lead to adverse metabolic consequences. And of course, treating any obstructive sleep apnea present is important, especially in patients with pre-existing coronary artery disease, atrial fibrillation, or congestive heart failure.
The problem with these observational studies looking at sleep duration and mortality/morbidity is that they don't distinguish between 1) voluntary sleep deprivation, 2) primary insomnia, and 3) insomnia secondary to medical/sleep disorders.
How is a doctor to use the data from this study???
I doubt writing a prescription for a sleeping pill would improve someone's coronary artery calcification score. However, advising someone with voluntary sleep deprivation (due to work pressures, etc) to extend their sleep hours might (if they take your advice)- I base this conclusion on prior studies which demonstrated that voluntary sleep restriction does lead to adverse metabolic consequences. And of course, treating any obstructive sleep apnea present is important, especially in patients with pre-existing coronary artery disease, atrial fibrillation, or congestive heart failure.
Wednesday, August 20, 2008
Treating Resistant Insomnia
I posted this on the Medscape message boards today:
I see a lot of pts who have failed the standard hypnotics (Rozerem, Ambien, Ambien CR, Lunesta, Sonata). It's important to screen for secondary causes, including restless legs. If they haven't taken Restoril yet, that's sometimes effective. I have found chloral hydrate effective for short term use (no more than 1 month), for breaking the cycle of insomnia. I have one patient on Xyrem for insomnia (and several who take it for narcolepsy). Before prescribing xyrem, it's important to rule out obstructive sleep apnea. I'll occasionally use Seroquel for insomnia, but only if there is comorbid psychiatric illness. I'll also sometimes use neurontin, but usually only if there are also neuropathic/RLS symptoms present.
I see a lot of pts who have failed the standard hypnotics (Rozerem, Ambien, Ambien CR, Lunesta, Sonata). It's important to screen for secondary causes, including restless legs. If they haven't taken Restoril yet, that's sometimes effective. I have found chloral hydrate effective for short term use (no more than 1 month), for breaking the cycle of insomnia. I have one patient on Xyrem for insomnia (and several who take it for narcolepsy). Before prescribing xyrem, it's important to rule out obstructive sleep apnea. I'll occasionally use Seroquel for insomnia, but only if there is comorbid psychiatric illness. I'll also sometimes use neurontin, but usually only if there are also neuropathic/RLS symptoms present.
Thursday, November 22, 2007
Duloxetine may improve sleep in patients with diabetic neuropathy
Clinical Psychiatry News reports on a poster presentation suggesting that duloxetine improves sleep in in patients with diabetic neuropathy:
WASHINGTON – Not only does duloxetine appear to reduce the severity of pain, especially during the night, but it may also help patients with diabetic peripheral neuropathy get a better night's sleep, according to a poster presentation at the annual meeting of the American Pain Society.
After 12 weeks of treatment, patients on 60 mg of duloxetine once or twice daily had improvements in average daily pain severity, night pain severity, and pain-related sleep interference, wrote Dr. David A. Fishbain, professor of psychiatry and behavioral sciences at the University of Miami, and his colleagues at Eli Lilly, maker of duloxetine (Cymbalta).
Although causality cannot be demonstrated between duloxetine and better sleep, the findings suggest that improvements in pain will be associated with less interference in sleep, the authors wrote.
The researchers pooled data from three double-blind, placebo-controlled trials of duloxetine in patients with diabetic peripheral neuropathic pain (DPNP). In the first study, 457 patients were randomized to receive 20 mg of duloxetine once daily, 60 mg of duloxetine once or twice daily, or placebo. In studies two and three, 334 and 348 patients, respectively, were randomized to receive 60 mg of duloxetine once daily, 60 mg of duloxetine twice daily, or placebo. Although the primary efficacy measure for the studies was the reduction in the weekly mean of the 24-hour average pain score, secondary end points included average daily night pain severity (measured on an 11-point Likert scale) and the Brief Pain Inventory sleep interference item.
Patients were included in the trials if they were 18 years or older with pain because of bilateral peripheral neuropathy caused by type 1 or type 2 diabetes mellitus. Pain had to have begun in the feet with relatively symmetric onset. Diagnosis was confirmed by a score of at least three on the Michigan Neuropathy Screening Instrument. Daily pain had to be present for at least 6 months. Patients also had to have at least a 4 on the 24-hour average pain severity (11-point Likert) scale and stable glycemic control. Notably, patients with a current or recent (within the last year) diagnosis of major depressive disorder as defined by the DSM-IV were excluded from the studies.
The researchers identified a subset of nonsomnolent patients by excluding those who reported treatment-emergent somnolence or who were on concomitant sedating medications. Treatment-emergent somnolence included reports of daytime sleepiness, drowsiness, being drowsy upon awakening, excessive daytime sleepiness, a feeling of residual sleepiness, groggy, groggy and sluggish, groggy on awakening, hard to awaken, less alert on rising, sleepiness, sleepy, and somnolence.
In all three studies, 339 patients received placebo. Of these, 307 met the criteria for the nonsomnolent subset. A total of 685 patients received 60 mg or 120 mg per day of duloxetine in all three studies. Of these, 607 met the criteria for the nonsomnolent subset. Patients in the nonsomnolent/nonsedating subgroup who were on duloxetine showed improvements in daily average pain and night pain severity, compared with those on placebo. The improvements started as early as 1 week and were maintained for 12 weeks. At 12 weeks, subset patients on 60 mg of duloxetine once and twice daily had improvements in daily average pain severity of 47% and 50%, compared with 29% for those on placebo.
Also at 12 weeks, subset patients on 60 mg of duloxetine once and twice daily had improvements in night pain severity of 47% and 51%, respectively, compared with 34% for those on placebo.
Most of the SSRI's and dual reuptake antidepressants can cause insomnia when used to treat major depressive disorder. This study suggests that by improving pain, duloxetine (which increases synaptic levels of serotonin and norepinephrine by inhibiting their reuptake) improves sleep in non-depressed patients with diabetic neuropathy. One limitation to this study is that patients who developed somnolence were excluded from analysis.
WASHINGTON – Not only does duloxetine appear to reduce the severity of pain, especially during the night, but it may also help patients with diabetic peripheral neuropathy get a better night's sleep, according to a poster presentation at the annual meeting of the American Pain Society.
After 12 weeks of treatment, patients on 60 mg of duloxetine once or twice daily had improvements in average daily pain severity, night pain severity, and pain-related sleep interference, wrote Dr. David A. Fishbain, professor of psychiatry and behavioral sciences at the University of Miami, and his colleagues at Eli Lilly, maker of duloxetine (Cymbalta).
Although causality cannot be demonstrated between duloxetine and better sleep, the findings suggest that improvements in pain will be associated with less interference in sleep, the authors wrote.
The researchers pooled data from three double-blind, placebo-controlled trials of duloxetine in patients with diabetic peripheral neuropathic pain (DPNP). In the first study, 457 patients were randomized to receive 20 mg of duloxetine once daily, 60 mg of duloxetine once or twice daily, or placebo. In studies two and three, 334 and 348 patients, respectively, were randomized to receive 60 mg of duloxetine once daily, 60 mg of duloxetine twice daily, or placebo. Although the primary efficacy measure for the studies was the reduction in the weekly mean of the 24-hour average pain score, secondary end points included average daily night pain severity (measured on an 11-point Likert scale) and the Brief Pain Inventory sleep interference item.
Patients were included in the trials if they were 18 years or older with pain because of bilateral peripheral neuropathy caused by type 1 or type 2 diabetes mellitus. Pain had to have begun in the feet with relatively symmetric onset. Diagnosis was confirmed by a score of at least three on the Michigan Neuropathy Screening Instrument. Daily pain had to be present for at least 6 months. Patients also had to have at least a 4 on the 24-hour average pain severity (11-point Likert) scale and stable glycemic control. Notably, patients with a current or recent (within the last year) diagnosis of major depressive disorder as defined by the DSM-IV were excluded from the studies.
The researchers identified a subset of nonsomnolent patients by excluding those who reported treatment-emergent somnolence or who were on concomitant sedating medications. Treatment-emergent somnolence included reports of daytime sleepiness, drowsiness, being drowsy upon awakening, excessive daytime sleepiness, a feeling of residual sleepiness, groggy, groggy and sluggish, groggy on awakening, hard to awaken, less alert on rising, sleepiness, sleepy, and somnolence.
In all three studies, 339 patients received placebo. Of these, 307 met the criteria for the nonsomnolent subset. A total of 685 patients received 60 mg or 120 mg per day of duloxetine in all three studies. Of these, 607 met the criteria for the nonsomnolent subset. Patients in the nonsomnolent/nonsedating subgroup who were on duloxetine showed improvements in daily average pain and night pain severity, compared with those on placebo. The improvements started as early as 1 week and were maintained for 12 weeks. At 12 weeks, subset patients on 60 mg of duloxetine once and twice daily had improvements in daily average pain severity of 47% and 50%, compared with 29% for those on placebo.
Also at 12 weeks, subset patients on 60 mg of duloxetine once and twice daily had improvements in night pain severity of 47% and 51%, respectively, compared with 34% for those on placebo.
Most of the SSRI's and dual reuptake antidepressants can cause insomnia when used to treat major depressive disorder. This study suggests that by improving pain, duloxetine (which increases synaptic levels of serotonin and norepinephrine by inhibiting their reuptake) improves sleep in non-depressed patients with diabetic neuropathy. One limitation to this study is that patients who developed somnolence were excluded from analysis.
Thursday, October 18, 2007
Fish can get Insomnia too
Yahoo News reports that Zebrafish lacking a hypocretin receptor sleep 30% less than fish without this mutation:
LOS ANGELES (Reuters) - Fish might not have eyelids, but they do sleep, and some suffer from insomnia, scientists reported on Monday.
California scientists studying sleep disorders in humans found that some zebrafish, a common aquarium pet, have a mutant gene that disrupts their sleep patterns in a way similar to insomnia in humans.
Zebrafish with the mutant gene slept 30 percent less than fish without the mutation. When they finally drifted off they remained asleep half as long as the normal fish, the researchers at the Stanford University School of Medicine said.
The mutant fish lacked a working receptor for hypocretin, a neuropeptide that is secreted in normal fish by neurons in the region of the brain that controls hunger, sex and other basic behaviors.
The researchers, led by Emmanuel Mignot, said they would look for fish that have a mutation that causes them to oversleep or never sleep in the hope of discovering if sleep-regulating molecules and brain networks developed through evolution.
The study was published in Tuesday's edition of the Public Library of Science-Biology.
Hypocretin is the neurochemical linked to the narcolepsy-cataplexy syndrome; human narcoleptics (with cataplexy) have a hypocretin deficiency. Disturbed, fragmented nocturnal sleep is a common, underrecognized symptom of narcolepsy.
Narcolepsy without cataplexy is a poorly understood condition and we sleep doctors have no idea what causes most cases of this condition.
LOS ANGELES (Reuters) - Fish might not have eyelids, but they do sleep, and some suffer from insomnia, scientists reported on Monday.
California scientists studying sleep disorders in humans found that some zebrafish, a common aquarium pet, have a mutant gene that disrupts their sleep patterns in a way similar to insomnia in humans.
Zebrafish with the mutant gene slept 30 percent less than fish without the mutation. When they finally drifted off they remained asleep half as long as the normal fish, the researchers at the Stanford University School of Medicine said.
The mutant fish lacked a working receptor for hypocretin, a neuropeptide that is secreted in normal fish by neurons in the region of the brain that controls hunger, sex and other basic behaviors.
The researchers, led by Emmanuel Mignot, said they would look for fish that have a mutation that causes them to oversleep or never sleep in the hope of discovering if sleep-regulating molecules and brain networks developed through evolution.
The study was published in Tuesday's edition of the Public Library of Science-Biology.
Hypocretin is the neurochemical linked to the narcolepsy-cataplexy syndrome; human narcoleptics (with cataplexy) have a hypocretin deficiency. Disturbed, fragmented nocturnal sleep is a common, underrecognized symptom of narcolepsy.
Narcolepsy without cataplexy is a poorly understood condition and we sleep doctors have no idea what causes most cases of this condition.
Sunday, September 02, 2007
CBT for Insomnia
Clinical Psychiatry News recently published a nice summary on the use of cognitive behavioral treatments for insomnia. The article focuses on secondary/comorbid insomnia, but the techniques discussed can also be utilized in primary insomnia:
Cognitive-behavioral treatments can help people overcome chronic insomnia, even when a medical or psychiatric disorder appears to be the primary cause of sleeplessness, Edward J. Stepanski, Ph.D., said at a meeting on sleep medicine sponsored by the American College of Chest Physicians.
Traditionally, behavioral treatments have been reserved for primary insomnia and not recommended for people whose lack of sleep is secondary to other conditions, said Dr. Stepanski, vice president for scientific affairs of the Accelerated Community Oncology Research Network (ACORN) in Memphis, Tenn.
The underlying assumptions—both of which he challenged—are that insomnia will remit if the primary condition is resolved and that cognitive-behavioral treatment (CBT) approaches will not be effective against an etiology such as pain or depression. People continue to sleep poorly after successful treatment of posttraumatic stress disorder, he said, and randomized controlled trials have shown that people with a primary condition such as arthritis or chronic obstructive pulmonary disease can sleep better after CBT.
Sometimes secondary insomnia does remit with treatment of the underlying condition, and optimal treatment of the underlying condition is important.
“Use [CBT] in any chronic insomnia,” Dr. Stepanski said, suggesting comorbid insomnia would be a better name than secondary insomnia when diagnosed in patients with other conditions. “CBT has its place,” he said. “There are always behavioral and cognitive features to a chronic patient with insomnia.”
For most patients, he recommended that behavioral treatments come before cognitive therapy. Many worry that they will have a mental breakdown or lose their jobs if they don't get more sleep. Once they are sleeping better, he suggested they may be more open to cognitive restructuring—in particular, to considering how their lives would be different without insomnia. Not everyone will embrace the possibility.
“If every failure in their entire life is due to insomnia, they are not going to give that up,” warned Dr. Stepanski. “Some personality disorder patients don't really want help.”
For insomniacs who do want better sleep, he recommended trying a variety of behavioral treatments, as there is no way to predict which would be the most beneficial to a particular patient. These include:
▸ Sleep hygiene education. For example, telling patients that they can't drink coffee before bedtime or nap 3 hours in the afternoon and then expect to sleep through the night.
Sleep hygiene alone is not very helpful, but can be useful when combined with other CBT techniques.
▸ Stimulus control therapy. The patient should only go to bed when sleepy and not use the bedroom for activities, such as television viewing or aerobic exercises, that are incompatible with sleep. If the patient can't sleep, he should get up and leave the bedroom. “If you force yourself to lie in bed wide awake, you are doing damage to yourself. [There's] nothing else to do but ruminate and catastrophize,” he said.
▸ Sleep restriction therapy. The goal is to use partial sleep deprivation to increase homeostatic sleep drive. Use a sleep log to reduce time in bed to the amount of time the patient actually sleeps. Five hours of good sleep is better than 8 hours of intermittent sleep, said Dr. Stepanski: “Excess time in bed is death to normal sleep.”
I have found that sleep restriction is a powerful behavioral method for treating insomnia. The basic concepts are rather simple, but it does take time to explain to the patient and get them to comply- many are hesitant to use this technique.
▸ Relaxation training. Examples include progressive muscle relaxation, guided imagery, biofeedback, and self-hypnosis.
As none of these techniques work quickly, Dr. Stepanski said practitioners should devote time early on to educating, reassuring, and encouraging patients—and preparing them for relapse. Patients “must understand the rationale for the treatment approach,” he said. “Sleep is a biological rhythm. It doesn't change right away.”
Medication works faster than CBT, but is not as effective, said Dr. Stepanski. Combining the two approaches can relieve panic about sleep deprivation while giving CBT more time to work. Studies have shown, however, that CBT alone is more effective than CBT combined with medication.
Cognitive-behavioral treatments can help people overcome chronic insomnia, even when a medical or psychiatric disorder appears to be the primary cause of sleeplessness, Edward J. Stepanski, Ph.D., said at a meeting on sleep medicine sponsored by the American College of Chest Physicians.
Traditionally, behavioral treatments have been reserved for primary insomnia and not recommended for people whose lack of sleep is secondary to other conditions, said Dr. Stepanski, vice president for scientific affairs of the Accelerated Community Oncology Research Network (ACORN) in Memphis, Tenn.
The underlying assumptions—both of which he challenged—are that insomnia will remit if the primary condition is resolved and that cognitive-behavioral treatment (CBT) approaches will not be effective against an etiology such as pain or depression. People continue to sleep poorly after successful treatment of posttraumatic stress disorder, he said, and randomized controlled trials have shown that people with a primary condition such as arthritis or chronic obstructive pulmonary disease can sleep better after CBT.
Sometimes secondary insomnia does remit with treatment of the underlying condition, and optimal treatment of the underlying condition is important.
“Use [CBT] in any chronic insomnia,” Dr. Stepanski said, suggesting comorbid insomnia would be a better name than secondary insomnia when diagnosed in patients with other conditions. “CBT has its place,” he said. “There are always behavioral and cognitive features to a chronic patient with insomnia.”
For most patients, he recommended that behavioral treatments come before cognitive therapy. Many worry that they will have a mental breakdown or lose their jobs if they don't get more sleep. Once they are sleeping better, he suggested they may be more open to cognitive restructuring—in particular, to considering how their lives would be different without insomnia. Not everyone will embrace the possibility.
“If every failure in their entire life is due to insomnia, they are not going to give that up,” warned Dr. Stepanski. “Some personality disorder patients don't really want help.”
For insomniacs who do want better sleep, he recommended trying a variety of behavioral treatments, as there is no way to predict which would be the most beneficial to a particular patient. These include:
▸ Sleep hygiene education. For example, telling patients that they can't drink coffee before bedtime or nap 3 hours in the afternoon and then expect to sleep through the night.
Sleep hygiene alone is not very helpful, but can be useful when combined with other CBT techniques.
▸ Stimulus control therapy. The patient should only go to bed when sleepy and not use the bedroom for activities, such as television viewing or aerobic exercises, that are incompatible with sleep. If the patient can't sleep, he should get up and leave the bedroom. “If you force yourself to lie in bed wide awake, you are doing damage to yourself. [There's] nothing else to do but ruminate and catastrophize,” he said.
▸ Sleep restriction therapy. The goal is to use partial sleep deprivation to increase homeostatic sleep drive. Use a sleep log to reduce time in bed to the amount of time the patient actually sleeps. Five hours of good sleep is better than 8 hours of intermittent sleep, said Dr. Stepanski: “Excess time in bed is death to normal sleep.”
I have found that sleep restriction is a powerful behavioral method for treating insomnia. The basic concepts are rather simple, but it does take time to explain to the patient and get them to comply- many are hesitant to use this technique.
▸ Relaxation training. Examples include progressive muscle relaxation, guided imagery, biofeedback, and self-hypnosis.
As none of these techniques work quickly, Dr. Stepanski said practitioners should devote time early on to educating, reassuring, and encouraging patients—and preparing them for relapse. Patients “must understand the rationale for the treatment approach,” he said. “Sleep is a biological rhythm. It doesn't change right away.”
Medication works faster than CBT, but is not as effective, said Dr. Stepanski. Combining the two approaches can relieve panic about sleep deprivation while giving CBT more time to work. Studies have shown, however, that CBT alone is more effective than CBT combined with medication.
Saturday, June 02, 2007
Treatment of Alcohol-related sleep disorders
The following is from an article I wrote for Medlink Neurology on "Sleep disorders associated with alcohol use and abuse." It is copyrighted by Medlink Neurology:
For the sleep disorders occurring during alcohol intake, cessation of alcohol use is often the only necessary treatment. Treatment of the sleep apnea exacerbated by alcohol requires avoidance of alcohol intake at least for 4 hours to 6 hours before going to bed. If the apnea does not resolve with alcohol cessation, then standard treatments for obstructive sleep apnea, such as nasal continuous positive airway pressure, are required. The hypersomnia that can occur with alcohol use is usually eliminated after 1 day or 2 days without alcohol, but insomnia may actually worsen for the first 2 weeks to 7 weeks off alcohol. It is important not to restart the alcohol even at a low dose to ameliorate this problem; similarly, use of hypnotics is contraindicated because of the cross-tolerance with alcohol and the potential for both abuse and dependence. Sedating antihistamines or low doses of sedating antidepressants can be used for temporary relief when insomnia episodes are particularly severe. Patients should be reassured that in most cases the insomnia gradually gets better.
Behavioral treatments for insomnia with good sleep hygiene, relaxation training, desensitization, or sleep restriction should be used during the withdrawal period. If evidence develops for depression then a sedating antidepressant (eg, amitriptyline or mirtazapine) may be helpful for both sleep and depression.
As mentioned above, sleep abnormalities in alcoholics can persist for several years after alcohol cessation; this sleep disturbance may contribute to relapse of alcoholism. Various medications and psychotherapy techniques have been used to treat this sleep disturbance. Gabapentin, at doses of 300 mg to 1800 mg at bedtime, is useful in treating insomnia in abstinent alcohol-dependent outpatients and appears to be more effective than trazodone (Karam-Hage and Brower 2003). Although quetiapine is of potential benefit for this condition (Monnelly et al 2004; Sattar et al 2004), the risk of tardive dyskinesia and metabolic abnormalities associated with the use of atypical antipsychotics suggests that they should be used cautiously, if at all, for insomnia. Cognitive-behavioral treatments, including stimulus control, sleep restriction, and cognitive restructuring, have been shown to improve subjective sleep quality in recovering alcoholics (Currie et al 2004).
The melatonin receptor agonist Ramelteon (Rozerem-Takeda) is an option for treating insomnia in recovering alcoholics, though controlled trials are lacking. Ramelteon is not a controlled substance, and has essentially no abuse liability (Anonymous 2005; Griffiths and Johnson 2005). It is approved for the treatment of insomnia characterized by difficulty with sleep onset (Laustsen and Andersen 2006). The standard dose is 8 mg, taken within 30 minutes of going to bed. It is metabolized by cytochrome p450 enzyme 1A2 but does not appear to inhibit or induce this enzyme (Laustsen and Andersen 2006). It should not be used in combination with fluvoxamine, a strong 1A2 inhibitor (Takeda Pharmaceuticals 2005).
Acamprosate (Campral- Forest Pharmaceuticals) is a glutamate modulator that is FDA-approved for the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation (Forest Pharmaceuticals 2005). A recent parallel double-blind placebo-controlled study found that acamprosate improved sleep quality during early abstinence (Staner et al 2006).
disclaimer: this is not the final edited version that will appear in Medlink Neurology. I encourage you to check out the website for Medlink Neurology for the full version of this article as well as numerous other articles about sleep (a few written by me).
For the sleep disorders occurring during alcohol intake, cessation of alcohol use is often the only necessary treatment. Treatment of the sleep apnea exacerbated by alcohol requires avoidance of alcohol intake at least for 4 hours to 6 hours before going to bed. If the apnea does not resolve with alcohol cessation, then standard treatments for obstructive sleep apnea, such as nasal continuous positive airway pressure, are required. The hypersomnia that can occur with alcohol use is usually eliminated after 1 day or 2 days without alcohol, but insomnia may actually worsen for the first 2 weeks to 7 weeks off alcohol. It is important not to restart the alcohol even at a low dose to ameliorate this problem; similarly, use of hypnotics is contraindicated because of the cross-tolerance with alcohol and the potential for both abuse and dependence. Sedating antihistamines or low doses of sedating antidepressants can be used for temporary relief when insomnia episodes are particularly severe. Patients should be reassured that in most cases the insomnia gradually gets better.
Behavioral treatments for insomnia with good sleep hygiene, relaxation training, desensitization, or sleep restriction should be used during the withdrawal period. If evidence develops for depression then a sedating antidepressant (eg, amitriptyline or mirtazapine) may be helpful for both sleep and depression.
As mentioned above, sleep abnormalities in alcoholics can persist for several years after alcohol cessation; this sleep disturbance may contribute to relapse of alcoholism. Various medications and psychotherapy techniques have been used to treat this sleep disturbance. Gabapentin, at doses of 300 mg to 1800 mg at bedtime, is useful in treating insomnia in abstinent alcohol-dependent outpatients and appears to be more effective than trazodone (Karam-Hage and Brower 2003). Although quetiapine is of potential benefit for this condition (Monnelly et al 2004; Sattar et al 2004), the risk of tardive dyskinesia and metabolic abnormalities associated with the use of atypical antipsychotics suggests that they should be used cautiously, if at all, for insomnia. Cognitive-behavioral treatments, including stimulus control, sleep restriction, and cognitive restructuring, have been shown to improve subjective sleep quality in recovering alcoholics (Currie et al 2004).
The melatonin receptor agonist Ramelteon (Rozerem-Takeda) is an option for treating insomnia in recovering alcoholics, though controlled trials are lacking. Ramelteon is not a controlled substance, and has essentially no abuse liability (Anonymous 2005; Griffiths and Johnson 2005). It is approved for the treatment of insomnia characterized by difficulty with sleep onset (Laustsen and Andersen 2006). The standard dose is 8 mg, taken within 30 minutes of going to bed. It is metabolized by cytochrome p450 enzyme 1A2 but does not appear to inhibit or induce this enzyme (Laustsen and Andersen 2006). It should not be used in combination with fluvoxamine, a strong 1A2 inhibitor (Takeda Pharmaceuticals 2005).
Acamprosate (Campral- Forest Pharmaceuticals) is a glutamate modulator that is FDA-approved for the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation (Forest Pharmaceuticals 2005). A recent parallel double-blind placebo-controlled study found that acamprosate improved sleep quality during early abstinence (Staner et al 2006).
disclaimer: this is not the final edited version that will appear in Medlink Neurology. I encourage you to check out the website for Medlink Neurology for the full version of this article as well as numerous other articles about sleep (a few written by me).
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