The National Sleep Foundation reports:
The Food and Drug Administration’s (FDA) latest drug approval may provide significant symptom relief for narcolepsy patients. Researchers found that Xyrem® (sodium oxybate), a medication approved for treatment of cataplexy (the loss of muscle tone in narcolepsy patients) in 2002, abated symptoms of excessive daytime sleepiness in 4- and 8-week clinical trials. Participants reported a significant improvement in quality of life and the medication was generally well-tolerated. Researchers tested three doses of the drug – 4.5g, 6g, or 9g in divided doses (one at bedtime and the other 2.5 to 4 hours later) in the randomized, double-blind, placebo-controlled trial and found improvement in narcolepsy patients’ reports of excessive sleepiness for the individuals taking the 6g and 9g doses.
Narcolepsy is a neurological disorder caused by the brain’s inability to regulate sleep-wake cycles normally, and its prevalence in the developed world is approximately the same as Parkinson’s disease and multiple sclerosis. Researchers are hopeful that sodium oxybate will provide relief for the disabling effects of excessive daytime sleepiness in narcolepsy patients.
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Xyrem has been approved for several years for cataplexy. I have tried to prescribe it several times, but patients find it too inconvenient and don't want to try it. It has to be ordered from a central pharmacy (Another name for Xyrem is gamma-hydroxybutyrate, the "date rape" drug). Also, the patient has to awaken in the middle of the night to take the 2nd dose. From the data I've seen, it is no more effective than the tricyclic antidepressants for cataplexy. And it has the nasty side effect of enuresis (bedwetting).
Its effect on sleepiness is mild- less than the stimulants and provigil. It is thought to decrease sleepiness by improving nocturnal sleep. It consolidates sleep and increases slow wave sleep.
Xyrem may be worth a try in narcoleptics who are having trouble tolerating the traditional medications (stimulants, provigil, antidepressants) used for the symptoms of narcolepsy.
Wednesday, November 30, 2005
Friday, November 25, 2005
New Sleep Billing Codes
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?
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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?
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.
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