Does anyone have any experience with the new ICD-9 billing codes for sleep, especially the codes for obstructive sleep apnea (OSA)??
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780.53-0 used to be the code for OSA. Now there are 2 main codes for OSA:
780.53 (hypersomnia with sleep apnea, unspecified) and 327.23 (obstructive sleep apnea).
What I have been doing is using 780.53 for suspected cases of OSA, and 327.23 for confirmed cases. For upper airway resistance syndrome, I usually code 780.53. Does anyone know if this is correct?? Does anyone have any references?? I bought my copy of The International Classification of Sleep Disorders-2nd edition this summer, before the new ICD-9 codes were available. Have ICD-9 codes been added to the International Classification of Sleep Disorders yet?
Friday, November 25, 2005
Sunday, November 20, 2005
Cardiovascular Disease and Sleep Apnea
The Nov 10 issue of the New England Journal of Medicine had several interesting articles about sleep apnea.
Obstructive sleep apnea (OSA) is a risk factor for the development of hypertension. Increasing evidence also links OSA to ischemic heart disease and stroke. Yaggi HK and colleagues (N Engl J Med 2005;353:2034-41), in an observational cohort study, found that OSA significantly increases the risk of stroke or death from any cause. This increase in risk is independent of other risk factors, including hypertension.
Both obstructive and central sleep apnea are common in patients with CHF; central sleep apnea is present in up to 40% of patients with chronic heart failure. Bradley TD et al. (N Engl J Med 2005;353:2025-33) randomly assigned 258 patients with CHF and central sleep apnea to receive either CPAP or no CPAP. CPAP decreased apnea, increased the injection fraction, and improved nocturnal oxygenation, but did not increase survival.
Nasal CPAP is the standard treatment for OSA; other treatment modalities include oral appliances and ENT surgery. The first step in the management of central sleep apnea associated with heart failure is optimization of cardiac functioning. Other possible treatments include CPAP, BiPAP, supplemental oxygen, and theophylline.
Obstructive sleep apnea (OSA) is a risk factor for the development of hypertension. Increasing evidence also links OSA to ischemic heart disease and stroke. Yaggi HK and colleagues (N Engl J Med 2005;353:2034-41), in an observational cohort study, found that OSA significantly increases the risk of stroke or death from any cause. This increase in risk is independent of other risk factors, including hypertension.
Both obstructive and central sleep apnea are common in patients with CHF; central sleep apnea is present in up to 40% of patients with chronic heart failure. Bradley TD et al. (N Engl J Med 2005;353:2025-33) randomly assigned 258 patients with CHF and central sleep apnea to receive either CPAP or no CPAP. CPAP decreased apnea, increased the injection fraction, and improved nocturnal oxygenation, but did not increase survival.
Nasal CPAP is the standard treatment for OSA; other treatment modalities include oral appliances and ENT surgery. The first step in the management of central sleep apnea associated with heart failure is optimization of cardiac functioning. Other possible treatments include CPAP, BiPAP, supplemental oxygen, and theophylline.
Tuesday, November 15, 2005
Adolescent Insomnia
The New York Times reports that the use of medication to treat insomnia in adolescents is increasing:
In 2004, more than 180,000 people under age 20 in the United States - most of them 10 or older took sleep medications, according to estimates released last month by Medco Health Solutions, a large managed-care company.
Although that represents only about one child in 500, Medco found that usage was up by 85 percent since 2000.
The numbers reported by Medco were somewhat mysterious: the company's report did not indicate why the pills were prescribed for the patients under 18, or which pills were prescribed for them.
That makes some doctors worry that the large increase may reflect a certain amount of unnecessary prescribing.
It's a fairly good article, but I disagree with one of the statements made by a sleep specialist in the article:
"The last thing we want to suggest is that it's O.K. to throw a medication at something without understanding the problem," said Dr. Judith Owens, the director of the Pediatric Sleep Disorders Clinic at Hasbro Children's Hospital, in Providence, R.I. "Insomnia is a symptom, not a disorder. It's like pain. You're not going to give a patient pain medication without figuring out what's causing the pain."
At least in adults, considering insomnia to be just a symptom is outdated. To quote from the new book Cognitive Behavioral Treatment of Insomnia (Perlis ML et al, 2005), "In the early 1980's...there was perhaps no rallying cry as popular as 'insomnia is a symptom, not a disorder'....After more than two decades of sleep research...Insomnia is once again considered a distinct nosological entity." The "NIH State of the Science Conference Statement on Manifestations and Management of Chronic Insomnia in Adults Statement" moves away from the concept of 'secondary insomnia'. It uses the term 'comorbid insomnia'. For example, in the case of depression associated with insomnia, it is often impossible to tell if depression is causing the insomnia, or if insomnia is causing the depression. According to the conference statement, "the limited understanding of mechanistic pathways in chronic insomnia precludes drawing firm conclusions about the nature of these associations or direction of causality."
In 2004, more than 180,000 people under age 20 in the United States - most of them 10 or older took sleep medications, according to estimates released last month by Medco Health Solutions, a large managed-care company.
Although that represents only about one child in 500, Medco found that usage was up by 85 percent since 2000.
The numbers reported by Medco were somewhat mysterious: the company's report did not indicate why the pills were prescribed for the patients under 18, or which pills were prescribed for them.
That makes some doctors worry that the large increase may reflect a certain amount of unnecessary prescribing.
It's a fairly good article, but I disagree with one of the statements made by a sleep specialist in the article:
"The last thing we want to suggest is that it's O.K. to throw a medication at something without understanding the problem," said Dr. Judith Owens, the director of the Pediatric Sleep Disorders Clinic at Hasbro Children's Hospital, in Providence, R.I. "Insomnia is a symptom, not a disorder. It's like pain. You're not going to give a patient pain medication without figuring out what's causing the pain."
At least in adults, considering insomnia to be just a symptom is outdated. To quote from the new book Cognitive Behavioral Treatment of Insomnia (Perlis ML et al, 2005), "In the early 1980's...there was perhaps no rallying cry as popular as 'insomnia is a symptom, not a disorder'....After more than two decades of sleep research...Insomnia is once again considered a distinct nosological entity." The "NIH State of the Science Conference Statement on Manifestations and Management of Chronic Insomnia in Adults Statement" moves away from the concept of 'secondary insomnia'. It uses the term 'comorbid insomnia'. For example, in the case of depression associated with insomnia, it is often impossible to tell if depression is causing the insomnia, or if insomnia is causing the depression. According to the conference statement, "the limited understanding of mechanistic pathways in chronic insomnia precludes drawing firm conclusions about the nature of these associations or direction of causality."
Saturday, November 12, 2005
Sleep in Animals
The NY Times has a nice article about how scientists are studying sleep in animals in order to better understand the mysteries of human sleep:
It has been almost 600 million years since human ancestors diverged from those of flies. As those ancestors evolved, their sleep evolved as well. Human sleep, for example, features not only slow-wave sleep, but bouts of sleep when the eyes make rapid movements and when we dream. Rapid eye movement, or REM sleep, as it is known, generally comes later in the night, after periods of intense slow-wave sleep.
Other mammals also experience a mix of REM and non-REM sleep, as do birds. Sleep researchers would like to know whether this pattern existed in the common ancestors of birds and mammals, reptilian animals that lived 310 million years ago. It is also possible that birds and mammals independently evolved this sleep pattern, just as birds and bats independently evolved wings.
Answering that question may help scientists understand why REM sleep exists. Scientists have long debated its function, suggesting that it may play important roles in memory or learning. In the Oct. 27 issue of Nature, Jerome Siegel, a sleep expert at the University of California, Los Angeles, argues that REM does not play a vital physiological role like slow-wave sleep. He points out that brain injuries and even medications like antidepressants can drastically reduce REM without any apparent ill effect.
"People who don't have REM sleep are remarkably normal," Dr. Siegel said. "There's no evidence for any intellectual or emotional problems."
So why do mammals and birds have REM sleep at all? "The best answer I can come up with is that it's there to prepare you for waking," Dr. Siegel said. "When the important work of sleep is done, REM sleep just makes you as alert as you can be while you're asleep."
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Circadiana blogged about this topic on Nov 1st.
It has been almost 600 million years since human ancestors diverged from those of flies. As those ancestors evolved, their sleep evolved as well. Human sleep, for example, features not only slow-wave sleep, but bouts of sleep when the eyes make rapid movements and when we dream. Rapid eye movement, or REM sleep, as it is known, generally comes later in the night, after periods of intense slow-wave sleep.
Other mammals also experience a mix of REM and non-REM sleep, as do birds. Sleep researchers would like to know whether this pattern existed in the common ancestors of birds and mammals, reptilian animals that lived 310 million years ago. It is also possible that birds and mammals independently evolved this sleep pattern, just as birds and bats independently evolved wings.
Answering that question may help scientists understand why REM sleep exists. Scientists have long debated its function, suggesting that it may play important roles in memory or learning. In the Oct. 27 issue of Nature, Jerome Siegel, a sleep expert at the University of California, Los Angeles, argues that REM does not play a vital physiological role like slow-wave sleep. He points out that brain injuries and even medications like antidepressants can drastically reduce REM without any apparent ill effect.
"People who don't have REM sleep are remarkably normal," Dr. Siegel said. "There's no evidence for any intellectual or emotional problems."
So why do mammals and birds have REM sleep at all? "The best answer I can come up with is that it's there to prepare you for waking," Dr. Siegel said. "When the important work of sleep is done, REM sleep just makes you as alert as you can be while you're asleep."
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Circadiana blogged about this topic on Nov 1st.
Tuesday, October 25, 2005
Brief Update
I have left the University of Mississippi Medical Center. Somnus Sleep Clinic will be opening in several weeks.
Tuesday, August 30, 2005
Restless Leg Syndrome
Below is a collumn about restless leg syndrome that I wrote for the newsletter of the Mississippi Psychiatric Association newsletter:
It’s summer and time for vacation! Although the time spent at the vacation destination is usually pleasant, long car and airplane trips can be tedious. For those with restless leg syndrome, these trips can be pure misery.
Restless leg syndrome (RLS) is characterized by an urge to move the legs, usually accompanied by disagreeable/uncomfortable leg sensations. These sensations, often described as "creeping" or "crawling," are typically perceived in the calves, but can also involve other parts of the lower extremities, and in more severe cases, can involve the upper extremities. RLS is worse in the evening/night and in sedentary situations such as long car rides. The symptoms often interfere with sleep. Vigorous movement improves RLS symptoms. Response to a dopaminergic drug is considered to be supportive of the diagnosis.
Approximately 10% of the population has at least mild, intermittent symptoms of RLS; about 3% of the population has moderate to severe symptoms.
RLS can be idiopathic, familial (often inherited in an autosomal dominant pattern), or secondary. Common secondary causes of RLS include iron deficiency, pregnancy, uremia, and neuropathy. RLS has also been reported to occur in association with folate, B12, and magnesium deficiencies. Many psychiatric medications, including dopamine antagonists, serotonergic antidepressants, and lithium, can unmask or worsen RLS. Wellbutrin, however, does not worsen RLS. Wellbutrin, due to its dopaminergic properties, has been speculated to improve RLS, but data is lacking.
RLS is diagnosed based on history; polysomnography is not necessary or indicated for diagnosis, though in most cases periodic leg movements occur during sleep. The differential diagnosis includes nocturnal leg cramps, neuropathy, akathisia, and vascular disease. The most important lab test to check in someone with restless leg syndrome is a ferritin level. Iron supplementation should be administered to keep the ferritin level above 50.
RLS is commonly treated with dopaminergic agents. Requip (ropinirole) is the first and only FDA-approved medication for the treatment of moderate-to-severe primary RLS. Mirapex (pramipexole) is also commonly used. Ergot-derived medications, such as pergolide, should be avoided due to the risk of cardiac valvuopathy. Sinemet can be used for short-term treatment or to confirm the diagnosis, but has a higher risk of augmentation than the other dopaminergic medications. Augmentation is the shifting of symptoms to several hours earlier than was typical before pharmacologic intervention. Other medications used to treat RLS include benzodiazepines, opioids, and gabapentin.
RLS is a common, unpleasant condition that can be unmasked or worsened by many psychiatric medications. Its prevalence in the psychiatric population is probably higher than in the general population. In cases in which the diagnosis is uncertain or in which the psychiatrist feels uncomfortable treating RLS, referral to a sleep specialist or a neurologist is indicated.
It’s summer and time for vacation! Although the time spent at the vacation destination is usually pleasant, long car and airplane trips can be tedious. For those with restless leg syndrome, these trips can be pure misery.
Restless leg syndrome (RLS) is characterized by an urge to move the legs, usually accompanied by disagreeable/uncomfortable leg sensations. These sensations, often described as "creeping" or "crawling," are typically perceived in the calves, but can also involve other parts of the lower extremities, and in more severe cases, can involve the upper extremities. RLS is worse in the evening/night and in sedentary situations such as long car rides. The symptoms often interfere with sleep. Vigorous movement improves RLS symptoms. Response to a dopaminergic drug is considered to be supportive of the diagnosis.
Approximately 10% of the population has at least mild, intermittent symptoms of RLS; about 3% of the population has moderate to severe symptoms.
RLS can be idiopathic, familial (often inherited in an autosomal dominant pattern), or secondary. Common secondary causes of RLS include iron deficiency, pregnancy, uremia, and neuropathy. RLS has also been reported to occur in association with folate, B12, and magnesium deficiencies. Many psychiatric medications, including dopamine antagonists, serotonergic antidepressants, and lithium, can unmask or worsen RLS. Wellbutrin, however, does not worsen RLS. Wellbutrin, due to its dopaminergic properties, has been speculated to improve RLS, but data is lacking.
RLS is diagnosed based on history; polysomnography is not necessary or indicated for diagnosis, though in most cases periodic leg movements occur during sleep. The differential diagnosis includes nocturnal leg cramps, neuropathy, akathisia, and vascular disease. The most important lab test to check in someone with restless leg syndrome is a ferritin level. Iron supplementation should be administered to keep the ferritin level above 50.
RLS is commonly treated with dopaminergic agents. Requip (ropinirole) is the first and only FDA-approved medication for the treatment of moderate-to-severe primary RLS. Mirapex (pramipexole) is also commonly used. Ergot-derived medications, such as pergolide, should be avoided due to the risk of cardiac valvuopathy. Sinemet can be used for short-term treatment or to confirm the diagnosis, but has a higher risk of augmentation than the other dopaminergic medications. Augmentation is the shifting of symptoms to several hours earlier than was typical before pharmacologic intervention. Other medications used to treat RLS include benzodiazepines, opioids, and gabapentin.
RLS is a common, unpleasant condition that can be unmasked or worsened by many psychiatric medications. Its prevalence in the psychiatric population is probably higher than in the general population. In cases in which the diagnosis is uncertain or in which the psychiatrist feels uncomfortable treating RLS, referral to a sleep specialist or a neurologist is indicated.
Tuesday, August 23, 2005
Missouri Medicaid Cuts CPAP coverage
From the National Sleep Foundation:
Effective September 1, 2005, Missouri Medicaid will no longer cover many kinds of durable medical equipment (DME), including positive airway pressure (PAP or CPAP) devices which are the mainstay of treatment for obstructive sleep apnea.
NSF Chairman, Barbara Phillips, MD, MSPH, explained, "This is a dangerous public health decision, not just for the 1 in 20 Missourians who have sleep apnea, but also for those on the roads and in the cars with them." Sleep apnea causes adverse or worsens many health problems, including hypertension, cardiovascular disease, diabetes, cognitive impairment and cerebrovascular accidents. CPAP treatment is effective in reversing these consequences. More important for all Missourians, however, is the fact that untreated sleep apnea results in automobile crashes; the risk of this is normalized with CPAP treatment. Budgetary limitations are a sad fact of life, but it's important to know that the cost of care of patients with sleep apnea goes down after CPAP treatment is initiated. The decision to eliminate coverage of DME passed by the Missouri State Legislature in Senate Bill 539 endangers the health of all Missourians, and will likely cost more money in the long run if enacted. Sleep Health Advocates are urged to contact their legislators if they are Missourians (www.moga.state.mo.us/) as well as the Missouri Medicaid Offices.
Learn more here.
Effective September 1, 2005, Missouri Medicaid will no longer cover many kinds of durable medical equipment (DME), including positive airway pressure (PAP or CPAP) devices which are the mainstay of treatment for obstructive sleep apnea.
NSF Chairman, Barbara Phillips, MD, MSPH, explained, "This is a dangerous public health decision, not just for the 1 in 20 Missourians who have sleep apnea, but also for those on the roads and in the cars with them." Sleep apnea causes adverse or worsens many health problems, including hypertension, cardiovascular disease, diabetes, cognitive impairment and cerebrovascular accidents. CPAP treatment is effective in reversing these consequences. More important for all Missourians, however, is the fact that untreated sleep apnea results in automobile crashes; the risk of this is normalized with CPAP treatment. Budgetary limitations are a sad fact of life, but it's important to know that the cost of care of patients with sleep apnea goes down after CPAP treatment is initiated. The decision to eliminate coverage of DME passed by the Missouri State Legislature in Senate Bill 539 endangers the health of all Missourians, and will likely cost more money in the long run if enacted. Sleep Health Advocates are urged to contact their legislators if they are Missourians (www.moga.state.mo.us/) as well as the Missouri Medicaid Offices.
Learn more here.
Tuesday, July 26, 2005
A New Medication for Insomnia
Rozerem (ramelteon), a new hypnotic medication that is "indicated for the treatment of insomnia characterized by difficulty with sleep onset," was approved by the U.S. Food and Drug Administration (FDA) last Friday (July 22). Because of its unique characteristics, ramelteon is considered to be the first of a new class of sleep aids.
In clinical trials conducted with 4,200 patients, most with chronic insomnia, researchers for Takeda Pharmaceuticals North America were able to demonstrate that ramelteon reduced the time to fall asleep and resulted in a modest increase in total sleep time of patients, but did not decrease nocturnal awakenings, a significant factor for persons whose insomnia causes them to have frequent or prolonged awakenings during the night. 472 patients took ramelteon nightly for one year. After cessation, ramelteon did not cause “rebound insomnia,” a worsening of symptoms that can occur after treatment is halted.
Unlike other prescription sleep aids, ramelteon is thought to work by selectively affecting melatonin receptors (neurons) in the suprachiasmatic nucleus, a part of the brain that functions to regulate times for sleep and times for optimal alertness or wakefulness. This contrasts with other hypnotic medications that work by binding to GABA receptors, which reduce central nervous system (CNS) activity.
Other studies found no evidence that ramelteon has a potential for abuse or dependence. As a result, ramelteon has not been designated as a scheduled substance by the U.S. Drug Enforcement Administration (DEA), the first prescription sleep aid to not be controlled. Additionally, the FDA will allow physicians to prescribe ramelteon for long-term use in adults.
Like other medications, ramelteon does come with precautions. Its use should be preceded by a thorough health evaluation and consideration of alternatives. Labeling information should be read and discussed with a physician or pharmacist to learn about drug interactions and side effects. To date, the effectiveness of ramelteon has not been studied in patients with severe sleep apnea or COPD, nor was it compared in clinical trials to cognitive behavioral therapy, a non-pharmacological treatment method that was identified by a recent National Institutes of Health "State of the Science" panel as effective for treatment of chronic insomnia. Ramelteon is not recommended for use during pregnancy, during nursing or for pediatric use.
From the National Sleep Foundation
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As the first non-addictive, non-controlled hypnotic approved by the FDA, Ramelteon should be a popular drug.
In clinical trials conducted with 4,200 patients, most with chronic insomnia, researchers for Takeda Pharmaceuticals North America were able to demonstrate that ramelteon reduced the time to fall asleep and resulted in a modest increase in total sleep time of patients, but did not decrease nocturnal awakenings, a significant factor for persons whose insomnia causes them to have frequent or prolonged awakenings during the night. 472 patients took ramelteon nightly for one year. After cessation, ramelteon did not cause “rebound insomnia,” a worsening of symptoms that can occur after treatment is halted.
Unlike other prescription sleep aids, ramelteon is thought to work by selectively affecting melatonin receptors (neurons) in the suprachiasmatic nucleus, a part of the brain that functions to regulate times for sleep and times for optimal alertness or wakefulness. This contrasts with other hypnotic medications that work by binding to GABA receptors, which reduce central nervous system (CNS) activity.
Other studies found no evidence that ramelteon has a potential for abuse or dependence. As a result, ramelteon has not been designated as a scheduled substance by the U.S. Drug Enforcement Administration (DEA), the first prescription sleep aid to not be controlled. Additionally, the FDA will allow physicians to prescribe ramelteon for long-term use in adults.
Like other medications, ramelteon does come with precautions. Its use should be preceded by a thorough health evaluation and consideration of alternatives. Labeling information should be read and discussed with a physician or pharmacist to learn about drug interactions and side effects. To date, the effectiveness of ramelteon has not been studied in patients with severe sleep apnea or COPD, nor was it compared in clinical trials to cognitive behavioral therapy, a non-pharmacological treatment method that was identified by a recent National Institutes of Health "State of the Science" panel as effective for treatment of chronic insomnia. Ramelteon is not recommended for use during pregnancy, during nursing or for pediatric use.
From the National Sleep Foundation
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As the first non-addictive, non-controlled hypnotic approved by the FDA, Ramelteon should be a popular drug.
Tuesday, June 28, 2005
The Future of Sleep Medicine
It is an exciting time for the field of sleep medicine. ICSD-2, the 2nd edition of the International Classification of Sleep Disorders, was introduced at the 19th Annual Meeting of the Associated Professional Sleep Societies. In many ways the ICSD-2 is a big improvement over the original ICSD. For example, there are now separate criteria for adult and pediatric obstructive sleep apnea- this is important since adult and pediatric OSA usually have different etiologies (adenotonsilar hypertrophy in kids and obesity/craniofacial abnormalities in adults). Unfortunately, where to draw the line between children and adults is unclear, though most sleep specialists draw it at puberty.
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Another development in sleep medicine is a revision of the R+K scoring manual. There was a lot of debate about the proposed revisions at the 19th Annual Meeting. The new manual should be available in late 2006. The committee revising R+K hopes to simplify the criteria for the ending and beginning of REM sleep. Stage 3+4 will probably be combined into one stage. The scoring of periodic limb movements may be revised. Unfortunately, no one is able to agree on what exactly a "hypopnea" is; and there is little consensus about what if any degree of saturation should be required to score a hypopnea. The lack of a standard definition of a hypopnea limits research into Obstructive sleep apnea, it would be easier to compare studies if there was a standard definition.
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Another development in sleep medicine is a revision of the R+K scoring manual. There was a lot of debate about the proposed revisions at the 19th Annual Meeting. The new manual should be available in late 2006. The committee revising R+K hopes to simplify the criteria for the ending and beginning of REM sleep. Stage 3+4 will probably be combined into one stage. The scoring of periodic limb movements may be revised. Unfortunately, no one is able to agree on what exactly a "hypopnea" is; and there is little consensus about what if any degree of saturation should be required to score a hypopnea. The lack of a standard definition of a hypopnea limits research into Obstructive sleep apnea, it would be easier to compare studies if there was a standard definition.
Friday, June 17, 2005
I am going on vacation
I am leaving tomorrow morning for the 19th Annual Meeting of the Associated Professional Sleep Societies.
I will be getting back late on June 23rd. I don't know if I will have internet access at the meeting. Blogging will be light until the 24th.
I will be getting back late on June 23rd. I don't know if I will have internet access at the meeting. Blogging will be light until the 24th.
Sleep Medicine is now an Official Subspecialty
Sleep medicine gained approval from the American Board of Medical Specialties as an official subspecialty for physicians practicing psychiatry, neurology, internal medicine, and pediatrics in March. This development is expected to further delivery of care to millions of individuals with sleep disorders and foster research and education in the field, said Michael Sateia, M.D., president of the American Academy of Sleep Medicine. Sateia, a professor of psychiatry, directs sleep medicine at Dartmouth Medical School.
The Accreditation Council for Graduate Medical Education (ACGME) approved program requirements for sleep medicine fellowship training programs in psychiatry, neurology, internal medicine, otolaryngology, and pediatrics in 2004. Information and application forms for ACGME-approved sleep medicine fellowships are posted online at <www.aasmnet.org/News.aspx?ArticleID=53>.
From Psychiatric News
The Accreditation Council for Graduate Medical Education (ACGME) approved program requirements for sleep medicine fellowship training programs in psychiatry, neurology, internal medicine, otolaryngology, and pediatrics in 2004. Information and application forms for ACGME-approved sleep medicine fellowships are posted online at <www.aasmnet.org/News.aspx?ArticleID=53>.
From Psychiatric News
Thursday, June 16, 2005
Sleep Fellowship
As of yesterday, I am the new program director of the University of Mississippi Medical Center Sleep Disorders Fellowship. I will be using this blog as the official web site of the fellowship, and will be posting the sleep conference schedule on it, as well as tips for passing the sleep boards. The Sleep Fellowship accepts 1 full time fellow per year; requirements include board elgibility in neurology, psychiatry, internal medicine, pediatrics, or otolaryngology. If any physicians have a question about the fellowship or sleep medicine in general, they can post a comment or e-mail me at michaelrack@msn.com. An application for the 2006/2007 academic year can be requested by e-mailing me your (snail-mail) address.
Sunday, May 22, 2005
Reader Questions
A reader asks about/speculates that there "might be one form of “ADD” that is simply a phenotype of ADD but that is actually caused by narcolepsy and the patient's attempt to compensate for it. This might explain why modafinil has been occasionally known to improve ADD symptoms - the reasons to engage inthe ADD behavior are abolished by the absence of sleepiness."
The new edition of Principles and Practice of Pediatric Sleep Medicine has a good chapter on "Attention Deficit, Hyperactivity, and Sleep Disorders." Conditions such as obstructive sleep apnea that present with sleepiness in adults often present with inattention and hyperactivity in children. From Principles and Practice: "...increasing evidence suggests that a variety of childhood sleep disorders are associated with inattention, hyperactivity, and cognitive impairment that could have significantly adverse effects on such important outcomes as development and school performance."
Obstructive sleep apnea and restless legs syndrome are the 2 sleep disorders that have the most evidence linking them to ADHD symptoms.
As far as narcolepsy, Principles and Practice of Pediatric Sleep Medicine mentions that "Children with narcolepsy often have problems with inattention and hyperactivity that may improve upon treatment" and "Adults who have been diagnosed with narcolepsy frequently give a history of 'attention deficit disorder' in childhood."
I have never used Modafinil (Provigil) to treat ADHD, but a quick Medline search suggests that it is effective for ADHD symptoms.
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Inattention and hyperactivity can be symptoms of psychiatric disorders (including ADHD) and can be symptoms of sleep disorders. Multiple studies have linked inattention and hyperactivity to sleep disorders in children, but research is lacking in adults. However, I think it is quite possible for inattention to be a symptom of a sleep disorder in an adult.
The new edition of Principles and Practice of Pediatric Sleep Medicine has a good chapter on "Attention Deficit, Hyperactivity, and Sleep Disorders." Conditions such as obstructive sleep apnea that present with sleepiness in adults often present with inattention and hyperactivity in children. From Principles and Practice: "...increasing evidence suggests that a variety of childhood sleep disorders are associated with inattention, hyperactivity, and cognitive impairment that could have significantly adverse effects on such important outcomes as development and school performance."
Obstructive sleep apnea and restless legs syndrome are the 2 sleep disorders that have the most evidence linking them to ADHD symptoms.
As far as narcolepsy, Principles and Practice of Pediatric Sleep Medicine mentions that "Children with narcolepsy often have problems with inattention and hyperactivity that may improve upon treatment" and "Adults who have been diagnosed with narcolepsy frequently give a history of 'attention deficit disorder' in childhood."
I have never used Modafinil (Provigil) to treat ADHD, but a quick Medline search suggests that it is effective for ADHD symptoms.
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Inattention and hyperactivity can be symptoms of psychiatric disorders (including ADHD) and can be symptoms of sleep disorders. Multiple studies have linked inattention and hyperactivity to sleep disorders in children, but research is lacking in adults. However, I think it is quite possible for inattention to be a symptom of a sleep disorder in an adult.
Monday, May 02, 2005
Grand Rounds 32
Grand Rounds 32, A Day in the Life of a Medical Student, is up at MudFud.
This carnival celebrates every aspect of medicine, from the student,to the surgeon and the patient on the table.
This carnival celebrates every aspect of medicine, from the student,to the surgeon and the patient on the table.
Sunday, May 01, 2005
Narcolepsy 3
Part 1, Part 2
This is 3rd in a series about narcolepsy.
In the last 5-6 years there has been a revolution in our understanding of narcolepsy. In 1999 hypocretin (orexin) was discovered. Most cases of human narcolepsy are due to a loss of hypocretin cells in the lateral hypothalamus, which results in very low levels of hypocretin in the cerebrospinal fluid. In contrast, narcolepsy in animal models (e.g. Doberman pinschers) is usually due to dysfunction of the hypocretin receptors.
Hypocretin neurons project to multiple areas in the brainstem and hypothalamus involved in the regulation of the alternation of sleep/wake and REM/non-REM cycles. There are 2 main theories about the function of hypocretin: 1) hypocretin promotes wakefulness and 2) hypocretin promotes stability of sleep/wake/REM/non-REM states. These 2 theories are not mutually exclusive.
Thus narcolepsy, a hypocretin deficient state, can be thought of as 1) a disorder of excessive daytime sleepiness in which a person has irresistable episodes of sleep and/or 2) a disorder of unstable sleep/wake/REM/non-REM states in which daytime wakefulness is interrupted by periods of sleep and nighttime sleep is frequently restless and fragmented (intrusion of wakefulness). Cataplexy can be explained in this model as a mixture of REM sleep and wakefulness- cataplexy is the intrusion of the muscle atonia (decreased/absent muscle tone) of REM sleep into wakefulness.
Hypocretin is also involved in appetite, feeding and metabolism. This is an area I know very little about, so I won't mention it further.
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That's it for now. I know I've been promising to talk more about Xyrem- I'll try to do this in part 4.
This is 3rd in a series about narcolepsy.
In the last 5-6 years there has been a revolution in our understanding of narcolepsy. In 1999 hypocretin (orexin) was discovered. Most cases of human narcolepsy are due to a loss of hypocretin cells in the lateral hypothalamus, which results in very low levels of hypocretin in the cerebrospinal fluid. In contrast, narcolepsy in animal models (e.g. Doberman pinschers) is usually due to dysfunction of the hypocretin receptors.
Hypocretin neurons project to multiple areas in the brainstem and hypothalamus involved in the regulation of the alternation of sleep/wake and REM/non-REM cycles. There are 2 main theories about the function of hypocretin: 1) hypocretin promotes wakefulness and 2) hypocretin promotes stability of sleep/wake/REM/non-REM states. These 2 theories are not mutually exclusive.
Thus narcolepsy, a hypocretin deficient state, can be thought of as 1) a disorder of excessive daytime sleepiness in which a person has irresistable episodes of sleep and/or 2) a disorder of unstable sleep/wake/REM/non-REM states in which daytime wakefulness is interrupted by periods of sleep and nighttime sleep is frequently restless and fragmented (intrusion of wakefulness). Cataplexy can be explained in this model as a mixture of REM sleep and wakefulness- cataplexy is the intrusion of the muscle atonia (decreased/absent muscle tone) of REM sleep into wakefulness.
Hypocretin is also involved in appetite, feeding and metabolism. This is an area I know very little about, so I won't mention it further.
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That's it for now. I know I've been promising to talk more about Xyrem- I'll try to do this in part 4.
Tuesday, April 26, 2005
Sleeping on the job
From a Fox News story about Michael Jackson's attorneys:
Oxman had come to the case as Randy Jackson's lawyer from previous domestic skirmishes within the Jackson family. But he had no experience in criminal defense matters, and often slept through crucial sessions in Jackson's child molestation case.
Not enough info in the story to determine if he has a sleep disorder.
Oxman had come to the case as Randy Jackson's lawyer from previous domestic skirmishes within the Jackson family. But he had no experience in criminal defense matters, and often slept through crucial sessions in Jackson's child molestation case.
Not enough info in the story to determine if he has a sleep disorder.
Thursday, April 14, 2005
Insomnia Increases Falls in the Elderly
According to this report from the National Sleep Foundation, insomnia increases the risk for falls in the elderly:
Falling is a significant cause of health problems and injury among older adults. According to the Centers for Disease Control, in 2001, more than 1.6 million seniors were treated in emergency departments for fall-related injuries and nearly 388,000 were hospitalized. The problem is even worse among nursing home residents where as many as 75% of residents fall annually, twice the rate of seniors living in the community. Despite prevalent sleep problems experienced by many nursing home residents, use of sleeping pills has been contraindicated due to a concern that their use might contribute to falls. A recent study in Journal of the American Geriatrics Society shows that contrary to common beliefs, it may not be sleeping medication but rather insomnia that increases nursing home residents' risk of falling. The study included more than 34,000 Michigan nursing home residents over age 65. Participants who had untreated insomnia at the start of the study were 90% more likely to fall in the next six months compared with those who did not have insomnia. In contrast, those who were taking hypnotic drugs to treat their insomnia at the start were only 29% more likely to fall. Alon Avidan, MD, MPH, first author of the study, explained, "Our findings suggest that people whose insomnia is effectively treated are less likely to fall than untreated insomniacs."
Falling is a significant cause of health problems and injury among older adults. According to the Centers for Disease Control, in 2001, more than 1.6 million seniors were treated in emergency departments for fall-related injuries and nearly 388,000 were hospitalized. The problem is even worse among nursing home residents where as many as 75% of residents fall annually, twice the rate of seniors living in the community. Despite prevalent sleep problems experienced by many nursing home residents, use of sleeping pills has been contraindicated due to a concern that their use might contribute to falls. A recent study in Journal of the American Geriatrics Society shows that contrary to common beliefs, it may not be sleeping medication but rather insomnia that increases nursing home residents' risk of falling. The study included more than 34,000 Michigan nursing home residents over age 65. Participants who had untreated insomnia at the start of the study were 90% more likely to fall in the next six months compared with those who did not have insomnia. In contrast, those who were taking hypnotic drugs to treat their insomnia at the start were only 29% more likely to fall. Alon Avidan, MD, MPH, first author of the study, explained, "Our findings suggest that people whose insomnia is effectively treated are less likely to fall than untreated insomniacs."
Wednesday, April 13, 2005
More about Narcolepsy
As I mentioned in the April 11 post about narcolepsy, the two main symptoms of narcolepsy are sleepiness and cataplexy. The sleepiness is usually treated with stimulants or Modafinil. Treatment improves the sleepiness, but it usually does not entirely go away.
The stimulants, but not modafinil, also slightly reduce cataplexy.
Cataplexy is " a sudden weakness of the muscles of the body, especially the legs but also the face and neck, that is brought on by strong emotion, especially laughing. " Cataplexy can be very effectively treated by the antidepressants that increase brain levels of norepinephrine, including venlafaxine (effexor), protryptiline (vivactil) and fluoxetine (prozac). (although prozac is a selective serotonin reuptake inhibitor, it has a metabolite that increases norepinephrine).
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Xyrem is a novel treatment for cataplexy. Xyrem is gamma hydroxybutyrate (one of the "date rape"/club drugs). It improves night-time sleep, reduces cataplexy, and mildly improves daytime sleepiness. It is FDA approved for the treatment of cataplexy.
From the National Sleep Foundation: This medication is usually administered in two doses, at bedtime and 4 hours later. It produces consolidation of sleep and improvement of disturbed nocturnal sleep characteristic of narcolepsy. This improvement may contribute to decreased daytime drowsiness and diminished cataplexy (Broughton and Mamelak, 1980; Scharf et al.,1985). The dosing makes it very inconvenient to take. Also, because of its history as a date rape drug, it must be ordered from a central pharmacy and mailed to the patient.
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In my opinion, Xyrem is faily worthless drug. Cataplexy is usually fairly easy to control with antidepressants. For disturbed night-time sleep in narcolepsy, I prefer to use a hypnotic such as Ambien rather than Xyrem. The only reason to prescribe xyrem, in my opinion, is if someone can not tolerate antidepressants
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In my next post about narcolepsy, I will more about how xyrem works, and will also discuss the reconceptualization of narcolepsy from a disorder of sleepiness to a disorder of instability of the sleep/wake systems.
The stimulants, but not modafinil, also slightly reduce cataplexy.
Cataplexy is " a sudden weakness of the muscles of the body, especially the legs but also the face and neck, that is brought on by strong emotion, especially laughing. " Cataplexy can be very effectively treated by the antidepressants that increase brain levels of norepinephrine, including venlafaxine (effexor), protryptiline (vivactil) and fluoxetine (prozac). (although prozac is a selective serotonin reuptake inhibitor, it has a metabolite that increases norepinephrine).
-
Xyrem is a novel treatment for cataplexy. Xyrem is gamma hydroxybutyrate (one of the "date rape"/club drugs). It improves night-time sleep, reduces cataplexy, and mildly improves daytime sleepiness. It is FDA approved for the treatment of cataplexy.
From the National Sleep Foundation: This medication is usually administered in two doses, at bedtime and 4 hours later. It produces consolidation of sleep and improvement of disturbed nocturnal sleep characteristic of narcolepsy. This improvement may contribute to decreased daytime drowsiness and diminished cataplexy (Broughton and Mamelak, 1980; Scharf et al.,1985). The dosing makes it very inconvenient to take. Also, because of its history as a date rape drug, it must be ordered from a central pharmacy and mailed to the patient.
-
In my opinion, Xyrem is faily worthless drug. Cataplexy is usually fairly easy to control with antidepressants. For disturbed night-time sleep in narcolepsy, I prefer to use a hypnotic such as Ambien rather than Xyrem. The only reason to prescribe xyrem, in my opinion, is if someone can not tolerate antidepressants
-
In my next post about narcolepsy, I will more about how xyrem works, and will also discuss the reconceptualization of narcolepsy from a disorder of sleepiness to a disorder of instability of the sleep/wake systems.
Tuesday, April 12, 2005
Dreaming and Schizophrenia
I just read an interesting article from the Neuroscience Education Institute comparing schizophrenia to the dream state.
In both REM (dream) sleep and in wakefulness in schizophrenia, the dorsolateral prefrontal cortex is relatively deactivated. This may be why the dreams of normal subjects and the delusions of schizophrenics seem real. In normal wakefulness, the dorsolateral prefrontal cortex is fully engaged.
"Dreams are brief madness and madness a long dream"
-Arthur Schopenhauer
In both REM (dream) sleep and in wakefulness in schizophrenia, the dorsolateral prefrontal cortex is relatively deactivated. This may be why the dreams of normal subjects and the delusions of schizophrenics seem real. In normal wakefulness, the dorsolateral prefrontal cortex is fully engaged.
"Dreams are brief madness and madness a long dream"
-Arthur Schopenhauer
Monday, April 11, 2005
Narcolepsy
Shrinkette (http://www.shrinkette.blogspot.com/) recently forwarded me a question about narcolepsy from another blogger. I am posting some info about narcolepsy from the National Sleep Foundation (in italics) along with my comments:
What is narcolepsy?
Narcolepsy is a chronic (long-lasting) neurological (affecting the brain or nerves) disorder that involves your body's central nervous system. The central nervous system is the "highway" of nerves that carries messages from your brain to other parts of your body. For people with narcolepsy, the messages about when to sleep and when to be awake sometimes hit roadblocks or detours and arrive in the wrong place at the wrong time. This is why someone who has narcolepsy, not managed by medications, may fall asleep while eating dinner or engaged in social activities - or at times when he or she wants to be awake.
The major symptoms of narcolepsy are:
Excessive daytime sleepiness is usually the first symptom to appear, and often the most troubling. It is an overwhelming and recurring need to sleep at times when you want to be awake. In addition to sleepiness, key symptoms of narcolepsy can include regular episodes of:
cataplexy - a sudden loss of muscle control ranging from slight weakness (head droop, facial sagging, jaw drop, slurred speech, buckling of knees) to total collapse. It is commonly triggered by intense emotion (laughter, anger, surprise, fear) or strenuous athletic activity. Most persons with narcolepsy have some degree of cataplexy.
sleep paralysis - being unable to talk or move for a brief period when falling asleep or waking up. Many persons with narcolepsy suffer short-lasting partial or complete sleep paralysis.
hypnagogic hallucinations - vivid and often scary dreams and sounds reported when falling asleep. People without narcolepsy may experience hypnagogic hallucinations and sleep paralysis as well.
automatic behavior - familiar, routine or boring tasks performed without full awareness or later memory of them.
Cataplexy is one of the main symptoms that a sleep specialist looks for in diagnosing narcolepsy- this symptom is specific to narcolepsy. Unfortunately, it can take up to 10 years after sleepiness first occurs for cataplexy to develop. Excessive daytime sleepiness is common to a wide variety of sleep disorders, including obstructive sleep apnea.
The diagnosis of narcolepsy:
In addition to a medical history and physician examination, a diagnosis is made from polysomnogram tests in an overnight sleep laboratory to measure brain waves and body movements as well as nerve and muscle function. A diagnosis also includes the results of the Multiple Sleep Latency Test (MSLT), which measures the time it takes to fall asleep and to go into deep sleep while taking several naps over a period of time.
The major medications for sleepiness are the stimulants and Modafinil. Cylert is not used anymore due to liver toxicity:
Common stimulants include: dextroamphetamine sulfate (DexedrineTM), methylphenidate hydrochloride (RitalinTM), and pemoline (CylertTM). Methamphetamine hydrochloride (DesoxynTM) is prescribed less frequently for narcolepsy.
Some of the most common side effects of stimulants are headache, irritability, nervousness, insomnia, irregular heart beat, and mood changes.
A wake-promoting drug, modafinil (ProvigilTM) was approved by the U.S. Food and Drug Administration (FDA) in 1999 for use in treating the excessive daytime sleepiness associated with narcolepsy. It does not act as a stimulant for other body systems and studies have shown that modafinil is effective in improving alertness with few side effects and low abuse potential.
Modafinil is less effective than the stimulants. It is often better tolerated, though it can cause headaches. Modafinil interacts with birth control pills and decreases their efficacy.
Antidepressants are usually used to treat cataplexy:
Several classes of antidepressants are prescribed to treat cataplexy, hypnagogic hallucinations and sleep paralysis. One class, multicyclics, includes imipramine (TofranilTM), desimpramine (NorpraminTM), clomipramine (AnafranilTM), and protriptyline (VivactilTM). Another class are selective serotonin re-uptake inhibitors (SSRIs). These include fluoxetine (ProzacTM), paroxetine (PaxilTM), and sertraline (ZoloftTM).
The multicyclics (tricyclics) can have cardiac side effects, including fast heart rate and heart arrhythmias. They can also cause dry mouth and constipation. They are more effective, in my opinion, than the SSRI's for cataplexy. The only SSRI that has been well studied for cataplexy is Prozac. The tricyclics increase norepinephrine and serotonin levels. The SSRI's increase serotonin levels; Prozac also has a norepinephrine-increasing metabolite. Norepinephrine-increasing effects are thought to be necessary for treatment of cataplexy. I am not aware of evidence that the serotonin selective reuptake inhibitors (other than prozac) are effective for cataplexy (I'd be interested in hearing any comments on this).
Xyrem is a relatively new drug for cataplexy; it also decreases sleepiness:
Sodium oxybate (XyremTM) is the first and only FDA-approved medication for the treatment of cataplexy associated with narcolepsy. It produces consolidation of sleep and improvement of disturbed nighttime sleep characteristic of narcolepsy. It is sedating and should only be used at night. Xyrem is a Schedule III controlled drug substance with abuse potential that is available by prescription.
That's it about narcolepsy today; more later.
What is narcolepsy?
Narcolepsy is a chronic (long-lasting) neurological (affecting the brain or nerves) disorder that involves your body's central nervous system. The central nervous system is the "highway" of nerves that carries messages from your brain to other parts of your body. For people with narcolepsy, the messages about when to sleep and when to be awake sometimes hit roadblocks or detours and arrive in the wrong place at the wrong time. This is why someone who has narcolepsy, not managed by medications, may fall asleep while eating dinner or engaged in social activities - or at times when he or she wants to be awake.
The major symptoms of narcolepsy are:
Excessive daytime sleepiness is usually the first symptom to appear, and often the most troubling. It is an overwhelming and recurring need to sleep at times when you want to be awake. In addition to sleepiness, key symptoms of narcolepsy can include regular episodes of:
cataplexy - a sudden loss of muscle control ranging from slight weakness (head droop, facial sagging, jaw drop, slurred speech, buckling of knees) to total collapse. It is commonly triggered by intense emotion (laughter, anger, surprise, fear) or strenuous athletic activity. Most persons with narcolepsy have some degree of cataplexy.
sleep paralysis - being unable to talk or move for a brief period when falling asleep or waking up. Many persons with narcolepsy suffer short-lasting partial or complete sleep paralysis.
hypnagogic hallucinations - vivid and often scary dreams and sounds reported when falling asleep. People without narcolepsy may experience hypnagogic hallucinations and sleep paralysis as well.
automatic behavior - familiar, routine or boring tasks performed without full awareness or later memory of them.
Cataplexy is one of the main symptoms that a sleep specialist looks for in diagnosing narcolepsy- this symptom is specific to narcolepsy. Unfortunately, it can take up to 10 years after sleepiness first occurs for cataplexy to develop. Excessive daytime sleepiness is common to a wide variety of sleep disorders, including obstructive sleep apnea.
The diagnosis of narcolepsy:
In addition to a medical history and physician examination, a diagnosis is made from polysomnogram tests in an overnight sleep laboratory to measure brain waves and body movements as well as nerve and muscle function. A diagnosis also includes the results of the Multiple Sleep Latency Test (MSLT), which measures the time it takes to fall asleep and to go into deep sleep while taking several naps over a period of time.
The major medications for sleepiness are the stimulants and Modafinil. Cylert is not used anymore due to liver toxicity:
Common stimulants include: dextroamphetamine sulfate (DexedrineTM), methylphenidate hydrochloride (RitalinTM), and pemoline (CylertTM). Methamphetamine hydrochloride (DesoxynTM) is prescribed less frequently for narcolepsy.
Some of the most common side effects of stimulants are headache, irritability, nervousness, insomnia, irregular heart beat, and mood changes.
A wake-promoting drug, modafinil (ProvigilTM) was approved by the U.S. Food and Drug Administration (FDA) in 1999 for use in treating the excessive daytime sleepiness associated with narcolepsy. It does not act as a stimulant for other body systems and studies have shown that modafinil is effective in improving alertness with few side effects and low abuse potential.
Modafinil is less effective than the stimulants. It is often better tolerated, though it can cause headaches. Modafinil interacts with birth control pills and decreases their efficacy.
Antidepressants are usually used to treat cataplexy:
Several classes of antidepressants are prescribed to treat cataplexy, hypnagogic hallucinations and sleep paralysis. One class, multicyclics, includes imipramine (TofranilTM), desimpramine (NorpraminTM), clomipramine (AnafranilTM), and protriptyline (VivactilTM). Another class are selective serotonin re-uptake inhibitors (SSRIs). These include fluoxetine (ProzacTM), paroxetine (PaxilTM), and sertraline (ZoloftTM).
The multicyclics (tricyclics) can have cardiac side effects, including fast heart rate and heart arrhythmias. They can also cause dry mouth and constipation. They are more effective, in my opinion, than the SSRI's for cataplexy. The only SSRI that has been well studied for cataplexy is Prozac. The tricyclics increase norepinephrine and serotonin levels. The SSRI's increase serotonin levels; Prozac also has a norepinephrine-increasing metabolite. Norepinephrine-increasing effects are thought to be necessary for treatment of cataplexy. I am not aware of evidence that the serotonin selective reuptake inhibitors (other than prozac) are effective for cataplexy (I'd be interested in hearing any comments on this).
Xyrem is a relatively new drug for cataplexy; it also decreases sleepiness:
Sodium oxybate (XyremTM) is the first and only FDA-approved medication for the treatment of cataplexy associated with narcolepsy. It produces consolidation of sleep and improvement of disturbed nighttime sleep characteristic of narcolepsy. It is sedating and should only be used at night. Xyrem is a Schedule III controlled drug substance with abuse potential that is available by prescription.
That's it about narcolepsy today; more later.
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