Home Sleep Testing: New Respect at AASM?

When it comes to respecting home sleep testing, the CEO of Itamar Medical believes the American Academy of Sleep Medicine (AASM) has finally come around. Evidence for the belief can be found in the AASM’s Accreditation of Out of Center Sleep Testing for Adult Patients, a program announced in February 2011.

With the stated purpose “to meet the changing needs of our members, sleep disorders centers, and the sleep medicine field,” the new program signals what Dov Rubin, PhD, believes is a growing acceptance of home sleep testing on the part of AASM.

“The potential patient benefits are enormous,” says Rubin. “The AASM is now actively preparing their members to capitalize on home testing and use it to their advantage. This occurred at the recent winter meeting in La Jolla [Calif] where they told membership that it is not a question of ‘if’ home sleep testing will come around, but ‘when’ and, more importantly, how the membership should capitalize on these developments.”

The newfound clinical respect coincides with a growing realization that home sleep testing can peacefully coexist with the business interests of in-lab testing. Working together to see and ultimately help more people is the idea, and the AASM’s new stance could go a long way toward this goal.

The 50% Rule

Rubin suspects that the AASM’s friendlier approach is likely driven by a realization that sleep laboratories have inherent limitations. “I like to say that 50% of the population would not walk into a sleep lab if their life depended on it,” says Rubin, who holds a doctorate in biomedical engineering from the University of Southern California. “The AASM realizes that they can now provide vital medical help for a larger percentage of the population just as we also know that home sleep testing is not for everyone. For more difficult cases, it is obvious that an in-lab sleep center will be more appropriate. This will convert the sleep lab into a true sleep health center. It took the leadership of the AASM to give the blessing, and they have really turned the corner.”

A shift in AASM philosophy is no small matter, and the change of heart could presage a day when many more CPAP prescriptions are given out based on home results alone. “That is always a question that concerns the insurance companies, because they are afraid of an explosion in the use of CPAP,” says Rubin. “I don’t know whether more home sleep testing acceptance will bring an increase in cost. Quite the opposite. Statistics show that for every dollar spent on preventive medicine, $12.50 is saved 10 years down the road. If insurance companies are looking at this as a long-term cost savings, it is well worth it.”

Devoted Following

DME providers with long-standing sleep lab partnerships have relied on the PAT® (peripheral arterial tone) signal technology found in Itamar’s WatchPAT device for a long time. Rubin attributes the loyalty to ease of use. “You get logical and simple usage with the WatchPAT,” says Rubin. “It makes good intuitive sense. It is not some sort of a tethered medical device, and it is not intimidating.”

Right now, WatchPAT is FDA-cleared only for people age 17 and above. Company officials have fielded a lot of requests from lab directors and sleep physicians, and they are providing data to regulators in an effort to expand the age range to include younger patients. Rubin estimates approval could materialize in the next 6 months, but it depends on the FDA.

Home Sleep Harmony

These days, there is a realization that sleep labs and home testing can work together harmoniously. For example, savvy DME providers can bring in those undiagnosed sleep apnea sufferers, and send the more complex cases to sleep labs. “My estimate is that home sleep testing will increase sleep lab business by at least 30% because there will be referrals,” explains Rubin. “To this, add Board-certified interpretation of results, patient treatment, and testing which will ultimately add up to more business for sleep labs.”

Reimbursement for home sleep testing has gone down, as has reimbursement for in-lab sleep tests. PAT technology received its own code (95800) this year, and with it what Rubin deems a “fairly good price” of about $205 per test. Since it is a new code, providers can count on this Medicare dollar amount remaining fixed for the next 2 years. Private payers, on the other hand, may be lower or higher depending on the company.

Future is Bright

The massive potential of the sleep market is now considered all but a sure thing among sleep labs and sleep industry manufacturers. And, as patient awareness grows, clinical knowledge and infrastructure inevitably rises to meet the challenge. Rubin believes the modern age of sleep medicine is quickly developing into an era where turf battles are tossed aside and patients take center stage. Telemedicine and physician- friendly, web-based access to sleep studies, as offered by WatchPAT, becomes yet another modality for patient ease of use and treatment.

Reimbursement wars have largely focused on the diagnostic utility of ambulatory sleep studies, but innovations such as the PAT signal technology have a distinct place among a variety of options. With hypertension affecting roughly 50 million Americans, and sleep apnea pegged as one of the causes, the stakes are high and cooperation is essential. “We want to start with the common understanding among sleep physicians that ambulatory sleep monitoring is their friend, not their enemy,” says Rubin. “We are trying to show sleep physicians that there is nothing to be afraid of here, and these ambulatory sleep studies are an adjunct to what they do — not much different from what they do today. Sleep physicians still have the 6 to 8 channels of polysomnographic data, and they analyze it just as they would any other polysomnogram.”

In a recent issue of Sleep Diagnosis and Therapy, Koby Sheffy, PhD, essentially agreed with Rubin, writing that the role of unattended sleep studies in the management of sleep apnea patients has substantially evolved in recent years. While PSG will continue to be recognized as the most comprehensive sleep study paradigm, Sheffy believes it will probably not remain as the only testing modality. “Increased clinical demands, shifts in health care environment, and technological developments will contribute to a growing acceptance of simpler diagnostic options,” writes Sheffy in a 2009 article entitled Shattering the Black Box Myth: PAT Technology in Action. “Thus, over the next few years, sleep labs will be required to assess their services and determine how to adapt to and benefit from the shifting landscape.”

Part of this landscape will undoubtedly include the physiological signals generated by PAT. “At first glance, systems incorporating PAT signals might be perceived as yet another black box,” adds Sheffy. “Understanding the simple physiological rationale upon which it is based shows that it is far from being a mystery.”


Dov Rubin is President & CEO of Itamar Medical Caesarea, Israel.
For more information visit http://www.itamar-medical.com


Out of Center Sleep Testing

AASM officials say that sleep service entities interested in obtaining accreditation as a provider of out of center sleep testing can go to http://www.aasmnet.org and download an application. Accompanying Standards for Accreditation of Out of Center Sleep Testing are also available for download at the Web site. The AASM’s accreditation department can be reached via e-mail: ocstaccreditation@aasmnet.org

Sleep 2011 June 11-15 Preliminary Program

The Preliminary Program for SLEEP 2011, the 25th annual meeting of the Associated Professional Sleep Societies (APSS) is available online. View PDF of full program

This program includes comprehensive information about scheduled sessions and courses, continuing education, registration, hotel and travel.


The following SLEEP 2011 sessions do not have any remaining seats available and are sold-out: the APSS does not maintain waiting lists for sold-out sessions

Meet the Professor Sessions:

M01: Genetic Basis of Sleep and Circadian Rhythms
Fred Turek, PhD

M03: Perioperative Assessment and Management of Patients with OSA: Impact and Outcomes
Peter Gay, MD

M04: Predicting and Improving CPAP Adherence
Christopher Lettieri, MD

M05: Sleep and the Failing Heart
Virend Somers, MD, PhD

M07: When Does a Child Become an Adult? How to Apply the AASM Scoring Rules in Adolescents
Lee Brooks, MD

M09: Basics of Portable Monitoring
Max Hirshkowitz, PhD

M12: Oral Appliances in Sleep Medicine
Dennis Bailey, DDS

M16: Treatment of Narcolepsy – Cataplexy across the Lifespan
Emmanuel Mignot, MD, PhD

M17: Beyond Dopamine Therapy: Causes and Management of Refractory RLS
Michael Silber, MBChB

M19: Designing a PAP Compliance Program
Lawrence Epstein, MD

M22: Portable Monitor Testing: Ready or Not Here It Comes
Samuel Kuna, MD

Lunch and Learn:

L01: Hypnotic Induced Sleep Is As Good As Natural Sleep
Michael Perlis, PhD; and Thomas Roth, PhD

L02: Should Mild Sleep Apnea Be Treated?
Michael Littner, MD; and Terri Weaver, PhD

View the full program

American Thoracic Society Sleep Program, May 13-18 Annual Meeting

Sleep, both adult and pediatric, is the third pillar of the American Thoracic Society.  At the International Conference, clinical and research experts provide insights into all areas of sleep medicine, though a particular focus at the conference is obstructive sleep apnea and the affect of sleep problems on people with lung disease.  Below is a select list of topics that will be presented during ATS 2011 (return mid-January to review individual session details, including session topics and speakers):


  • Clinical Year in Review: Sleep Apnea
  • Clinical Impact of Pathophysiology on Treatment of OSA/Hypopnea Syndrome
  • Positive Pressure Management of SDB in Special Populations+
  • Physiology of Intermittent Hypoxia*
  • Endothelial Dysfunction, Vascular Disease & SDB
  • Obesity & Clinical Implications for the Pulmonary, Critical Care & Sleep Physician
  • Comprehensive Update on Polysomnography: Interactive State of the Art Review & Case Discussion*
  • Functional Modeling of the Pediatric Upper Airway
  • Hypoxic Pulmonary Hypertension: A Half Century of Discovery
  • Sleep in Chronic Lung Disease: Challenges of Sleeping & Breathing
  • Susceptibility to Cardiovascular Consequences of OSA
  • Understanding & Identifying Non-Adherence to Better Treat Asthma, COPD and OSA
  • What the CTSA Consortium Can Do For You
  • Comparative Effectiveness Research: Why Now?
  • Quantitative Thoracic Imaging: The Past, the Present & the Future


*Postgraduate course

Sleep Spindles May Phasically Increase the Tonus Of the Upper Airway Dilator Muscles


John Zimmerman, Ph.D., DABSM, RPSGT; Madhukar Kaloji, M.D. FCCP; Michael Buxton, Ed.D.; Susan Jiannine, Rabindra Mohabir; Mark Hopkins, RPSGT and Laurel Kulm, RPSGT


We propose that the upper airway dilator muscles, especially the genioglossus muscle, receive tonic stimulation during wakefulness when alpha or beta activity is present in the EEG.  It has long been known that the upper airway tonic dilator muscle activity decreases during sleep onset.  However, we hypothesize that some phasic stimulation of the upper airway muscles does occur during sleep and that this phasic stimulation occurs during the time when sleep spindle are present in the EEG tracings.  We note the closeness and partial overlapping of the frequency ranges between alpha activity (8-13 Hz) and sleep spindles (11-16 Hz).  We also note that past experiments have shown that biofeedback or neurofeedback training of a wakefulness brainwave called the sensorimotor rhythm increases the number of sleep spindles in the sleep EEG.  Extrapolating from this data we propose that sensorimotor rhythm neurofeedback training during the day may reduce the severity of upper airway obstructions (apneas) or partial obstructions (hypopneas) occurring during the sleep period.


Sleep spindles are phasic, short bursts of brain wave activity that used to be defined in the Rechtschaffen and Kales Manual1 as 12 to 14 Hz bursts of activity lasting at least ½ second in duration and typically about a second or two.  A new 2007 definition of a sleep spindle was defined as a slightly broader range of frequencies in The AASM Manual for the Scoring of Sleep and Associated Events Rules, Terminology and Technical Specifications.  The new sleep spindle definition now used states that a sleep spindle is “A train of distinct waves with frequency 11-16 Hz (most commonly 12-14 Hz) with a duration of >0.5 seconds, usually maximal in amplitude using central derivations.” 2 Both sleep spindles and K-complexes are distinct brain waves that define the presence of Stage N2 sleep.  They are both present during stage N3 sleep as well but are usually absent during stage N1 sleep and REM sleep.


Surprisingly, no one has yet noticed the relationship between the frequent occurrence of sleep spindles in the EEG and the typical, usual absence (with two exceptions noted below) of obstructive sleep apnea/hypopnea in the respiratory channels of a polysomnogram (PSG).  More importantly, to the best of our knowledge, with the exception of only one paper no one has noticed that when sleep spindles are absent or sparse in the sleep EEG that obstructive sleep apnea/hypopnea is present.  One 1997 paper by Sembrano, Barthien, Wallace, and Lamm describes the results of a polysomnogram on a 23-year-old woman with mitochondrial encephalomyopathy with neurogenic muscle weakness, ataxia, and retinitis pigmentosa.  They stated, “An overnight polysomnogram (PSG) showed apnea, EEG slowing, and a paucity of sleep spindles” 3 but did not generalize their findings beyond this specific case.

We are presenting what we call the sleep spindle upper airway phasic EMG stimulation hypothesis.  We specifically propose that sleep spindles phasically increase the tonus of the dilator muscles of the upper airway.  As a consequence we propose that the more frequently sleep spindles occur, the more often the upper airway dilator muscles are phasically stimulated to increase their tone.  The more often the upper airway is phasically stimulated during the sleep spindle duration, the less likely the person is to have upper airway near-total collapse causing obstructive sleep apnea or upper airway partial collapse causing obstructive sleep hypopnea.  Two exceptions to this rule for obstructive sleep apnea/hypopnea and one exception regarding central sleep apnea/hypopnea will be noted later.



The elements of empirical evidence indirectly supporting this sleep spindle hypothesis are as follows:

1)      Obstructive sleep apnea/hypopneas and their resulting oxygen desaturations most often occur during transitions from wakefulness to Stage N1 sleep, when sleep spindles are absent.

2)      Obstructive sleep apnea/hypopnea often worsens during periods of REM sleep when again sleep spindles are largely absent and the muscle tonus of the upper airway decreases even further owing to the non-reciprocal tonic motor inhibition of muscle tone throughout the body.  In fact the sudden disappearance of both sleep spindles and K-complexes in the EEG is an indication that REM sleep is about to begin or has in fact begun.  When actual rapid eye movements occur in the presence of a slightly lower amplitude EEG signal (lower than that seen during stage N1 sleep), a relatively more uniform amplitude EEG pattern (more uniform less variable EEG amplitude than that present during stage N1 sleep EEG), a low tonic chin electromyogram (EMG) signal, then REM sleep is unequivocally present.

3)      Within the same night when a patient with obstructive sleep apnea/hypopnea has alternating periods of normal breathing and obstructive sleep apnea/hypopnea it is clear that during normal breathing and while oxygen saturation levels are the highest and the most stable that sleep spindles occur frequently in the EEG.  Conversely, during the same night when obstructive sleep apnea/hypopneas and their resulting oxygen desaturations are present, then during that time period sleep spindles are usually absent or sparse.


This is a hypothesis that is clearly open to experimental testing by simultaneously recording the EMG of some of the muscles of the upper airway; say the genioglossus muscle, while recording a regular PSG with the sleep EEG and breathing patterns.  If this hypothesis is correct, there should be a recordable phasic increase in the genioglossus EMG each time a sleep spindle occurs.  Furthermore, we would predict a tonic increase in genioglossus EMG during periods of time of alpha (8-13 Hz) or beta activity in the EEG as well, i.e. while the patient is awake.


The alpha rhythm and sleep spindles share some similarities.  The alpha rhythm has an AASM-defined frequency of 8-13 Hz, whereas the sleep spindle frequency range is 11-16 Hz.2 These frequency ranges somewhat overlap in the 11 to 13 Hz range.  Because of the overlap in frequencies sometimes long duration sleep spindles are difficult to distinguish from alpha activity if topographic data is not available.  Alpha activity is concentrated in the occipital and parietal areas.  Sleep spindles are most well developed over the central areas of the brain such as at the C3 and C4 electrode locations.  Both the alpha rhythm and sleep spindles depend upon recursive thalamocortical feedback networks4,5.  We hypothesize that alpha activity tonically stimulates the upper airway dilator muscles over a period of seconds, to minutes to as long as hours in duration during EEG arousals and during wakefulness.  Sleep spindles stimulate the upper airway dilator muscles in a shorter durations (0.5 to 3 second time intervals) phasic manner.


Thus this hypothesis explains why the alpha activity of an EEG arousal following an apnea or hypopnea is usually associated with increased amplitude air flow signals as it predicts higher tonic airway dilator muscle activity during alpha or beta activity.  This alpha-induced tonic stimulation of the upper airway dilator muscles thus eliminates the upper airway near total obstruction (apnea) or partial upper airway collapse (hypopnea).  Conversely when both tonic alpha or beta activity is absent and phasic sleep spindle activity is also absent as is the case during the EEG slowing phase of sleep onset during the wake-to-stage N1 sleep transition, this allows upper airway collapse to occur.  Thus we are postulating that in the presence of either a stage N1 EEG or a stage REM EEG pattern, when sleep spindles are absent, and when the EEG consists primarily of only low amplitude, mixed frequency EEG patterns that this allows obstructive sleep apneas or hypopneas to occur.


Normally, at the beginning of the night, perhaps the reason why stage N1 sleep is so short is that it is to the advantage of a sleeping person to quickly pass through the vulnerable stage N1 sleep stage, when sleep spindles are absent.  It is best, from a respiratory standpoint, to enter stage N2 sleep quickly so that the airway-dilating attributes of sleep spindles can phasically stimulate the muscles of the upper airway to prevent the occurrence of obstructive sleep apnea/hypopnea.  In fact someone suggested at an APSS conference several years ago that if a patient could get out of stage N1 sleep and quickly into stage N2 sleep, using a sedative hypnotic, that this might help to reduce the severity of or perhaps even alleviate obstructive sleep apnea/hypopnea6.


Two exceptions to the protective effects of sleep spindles upon obstructive sleep apnea/hypopnea have been noted.  Specifically, obstructive sleep apnea/hypopnea may occur even while sleep spindles are present under two conditions: 1) When the apneas or hypopneas are extremely long and 2) when the apneas and hypopneas are extremely frequent as is the case with patients who have very severe obstructive sleep apnea/hypopnea with an apnea/hypopnea indexes of 30 or more apneas or hypopneas per hour of sleep.


The first exception occurs when a hypopnea (or rarely an apnea) is extremely prolonged that is over 60 seconds in duration and sometimes an event that is three minutes or longer measured from start to finish.  Usually such super-long duration events often occur during REM sleep but if they happen to occur during stage 2 sleep, then the patient may be asleep long enough to shift the brain wave patterns from a low voltage mixed frequency EEG pattern (Stage N1 sleep) into spindle sleep (Stage N2 sleep).  The same reasoning explains why a patient on CPAP therapy, who had not had many sleep spindles while untreated and while breathing just plain room air does have frequent sleep spindles while being treated with CPAP.  It is simply because the patient is able to sleep long enough to shift the brain wave patterns from stage N1, without sleep spindles, to stage N2, with sleep spindles.


The other exception occurs when the apneas or hypopneas occur extremely frequently once every other minute or so.  This would represent an apnea/hypopnea index of 30 apneas or hypopneas per hour of sleep when an event occurs about every other minute while asleep.  When a respiratory disturbance begins with about every fourth 30-second epoch, then the EEG arousals become so frequent and sleep continuity becomes so disrupted with literally hundreds of EEG arousals per night that a significant amount of sleep deprivation occurs.  This naturally builds up a great deal of sleep pressure.  This may cause the patient to enter Stage N2 sleep much more quickly than a person with a more mild degree of sleep-disordered breathing, less sleep disruption, and a more typical amount of sleep pressure.  Such severe OSAH patients, with an AHI of 30 or more, sometimes do show sleep spindles during apneas or hypopneas simply because they are so extremely sleepy.


Neither one of these exceptions, though, that is extremely prolonged events or extremely frequent events should distract from the hypothesis that sleep spindles may under more usually encountered circumstances phasically stimulate the muscles of the upper airway and usually (but not always capable) prevent the occurrence of sleep apnea or sleep hypopnea (except when the events are extremely prolonged or frequent).  In such extreme cases of sleep disordered breathing tonic stimulation of the muscles of the upper airway, such as occurs when alpha or beta activity is present in the EEG, may be necessary to keep the upper airway patent rather than just phasic stimulation as afforded by sleep spindles.


Another major exception to this theory occurs with central, mixed, or complex sleep apnea.  Sleep spindles are frequently present during periods of central sleep apnea/hypopnea such as in patients with idiopathic central sleep apnea or complex sleep apnea brought about by initial therapy with continuous positive airway pressure (CPAP).  This is because the pathophysiological mechanisms underlying the development of central sleep apnea/hypopnea are different than for obstructive sleep apnea/hypopnea.  In central apnea there appears to be an increased hysterisis of the feedback control loop between the pCO2 set point of the waking state, say 45 mm Hg and the higher pCO2 set point of the sleeping stage, say 49 mm Hg.


At the transition from wakefulness to sleep minute ventilation decreases, causing the PCO2 level to increase.  Thus at sleep onset the pCO2 level may be at the waking value stimulatory of respiration say at 45 mm Hg but if it remains at 45 mm Hg at sleep onset and is below the sleep pCO2 set point to breathe, say at 49 mm Hg, then a central apnea/hypopnea may develop because the hypercapneic drive is already satisfied.  The patient will simply not breathe until the pCO2 level builds up to the sleep set point value of, say 49 mm Hg, and then breathing will resume with no deep gasp or large breath.  Sleep spindles may still readily be observed during repetitive periods of central sleep apnea/hypopnea and may still be phasically stimulating the muscles of the upper airway but to no avail since the hypercapneic drive has been blunted by the transition from wakefulness to stage N1 sleep and the changing pCO2 set point to breathe.


Thomas, Daly, and Weiss provided evidence that blunting of the hypercapneic drive leads to central sleep apnea by adding tiny amounts of CO2 to a CPAP mask to a patient experiencing complex sleep apnea and repetitive central sleep apnea/hypopnea episodes7.  Upon adding just 0.5 to 1.5% of carbon dioxide to the CPAP circuit thus increasing TcCO2 from 46.3 to 49.3 mm Hg, the central apneas/hypopneas disappeared.


We further hypothesize that complex sleep apnea may be an iatrogenic problem caused by inadvertent lowering of the pCO2 via dozens of liters per minute of fresh air blowing off the CO2 that otherwise might be inhaled by a sleeping patient with their nose partially sunk into a pillow or covered with a sheet or blanket.  The added pCO2 resulting from re-breathing one’s exhaled carbon dioxide with the patient’s nose adjacent to a pillow could stimulate the hypercapneic drive just enough to prevent the occurrence of central apneas or central hypopneas (shallow, in-phase breathing with no snoring).  In addition, during initial CPAP therapy if the average oxygen saturation level increases say from somewhere in the 80s on room air to somewhere in the 90s while on CPAP this would blunt the hypoxic drive as well thus also leading to central apneas/hypopneas.  Lastly, inflating the lungs more than usual with 30 to 60 or more liters per minute of pressurized air entering the upper airway is likely to stimulate the muscle spindle receptors of the intercostal muscles thus stimulating the Hering-Breuer reflex, which is also likely to cause a central apnea/hypopnea.


There is, in the biofeedback literature, a brain wave type called the sensorimotor rhythm or sensory-motor rhythm (SMR).  In humans, the SMR has a frequency of 9-13 Hz8.  This frequency is similar to the new definition of the sleep spindle frequency of 11-16 Hz.  Back in the early 1970s M.B. Sterman showed that SMR biofeedback training could reduce the occurrence of epilepsy and seizure activity9,10.  Given the similarities between the sleep spindle frequency (11-16 Hz) and the SMR frequency (9-13 Hz) it should be no surprise that biofeedback or neurofeedback training of the SMR during several days resulted in an increase in spindle-burst sleep (stage N2) at night.  Thus it appears that neurofeedback training in the waking state of the SMR rhythm at least somewhat generalized to the sleeping state thus increasing the number of sleep spindles at night11.  Given the proposed protective effect of sleep spindles through purported phasic stimulation of the muscles of the upper airway, such neurofeedback training to increase the amount of sensorimotor rhythm could possibly be a novel treatment for obstructive sleep apnea/hypopnea.


We would welcome any experimental verification of this sleep spindle-upper-airway EMG-stimulation hypothesis.  An animal model is one method to experimentally prove or disprove this hypothesis by artificially increasing or decreasing the number of sleep spindles, say with benzodiazepine class of drugs, and to then correlate the increase in benzodiazepine-induced sleep spindles with increased phasic stimulation of the muscle tone of the upper airway muscles.




  1. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects, 1968; US Department of Health, Education, and Welfare Public Health Service – NIH/NIND.
  2. Iber C, Ancoli-Israel S, Chesson A, and Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events Rules, Terminology and Technical Specifications, 2007; 1st ed: Westchester, Illinois: American Academy of Sleep Medicine.
  3. 3. Sembrano E, Barthlen, GM, Wallace S. and Lamm C. Polysomnographic findings in a patient with the mitochondrial encephalomyopathy NARP.  Neurology, 1997 Dec; 49(6): 1714-7.
  4. Lindsley, DB. Foci of activity of the alpha rhythm in the human electro-encephalogram. J Exp Psych, 1938; Vol 23(2):159-71.
  5. Velasco, M and Lindsley, DB. Role of orbital cortex in regulation of thalamocortical electrical activity. Science, 1965; 149(690):1375-7.
  6. Presentation of someone at an APSS conference suggesting using a sedative-hypnotic to help get a patient out of stage N1 sleep quickly and into stage N2 sleep as a way of treating obstructive sleep apnea/hypopnea.
  7. Thomas, R.J., Daly, Robert W. and Weiss, J. W. Low-concentration carbon dioxide is an effective adjunct to positive airway pressure in the treatment of refractory mixed central and obstructive sleep-disordered breathing.  Sleep, 2005; Vol 28, No. 1: 69-77.
  8. Kropotov, J. Quantitative EEG, event-related potentials and neurotherapy, 2008; Academic Press, 542 pages.
  9. Sterman, M.B. and Friar, L. Suppression of seizures in epileptic following sensorimotor EEG feedback training.  Electroenceph. Clin. Neurophysiol, 1972; 33:89-95.
  10. Sterman, M.B., Macdonald, L.R., and Stone, R.K. Biofeedback training of the sensorimotor EEG rhythm in man: Effects on epilepsy, Epilepsia, 1974; 15:395-417.
  11. Sterman, M.B., Howe, R.D. and Macdonald, L.R. Facilitation of spindle-burst sleep by conditioning of electroencephalographic activity while awake.  Science, 1970; 167:1146-1148.


Please address all correspondence to Madhukar Kaloji, M.D., F.C.C.P. and John Zimmerman, Ph.D. at 1020 Independence Blvd. Suite 205, Virginia Beach, Virginia 23455.


www.sleepscholar.com  May 11, 2011

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Why CMS Approved Home Sleep Testing for CPAP Coverage

Alejandro D. Chediak, M.D.
President, American Academy of Sleep Medicine
On December 14, 2007 the Centers for Medicare & Medicaid Services (CMS) released its proposed decision for modification of National Coverage Determination (NCD) policy 240.41 pertaining to coverage of continuous positive airway pressure therapy (CPAP) for adult obstructive sleep apnea (OSA). The proposed modification allows for an initial 12 week period of CPAP coverage when OSA is diagnosed using both a clinical evaluation and performed in the sleep laboratory (PSG) or a clinical evaluation and unattended testing (HST) using a Type II, III or IV device. CPAP would be subsequently covered for those diagnosed with OSA who benefit from CPAP during the 12-week trial. CMS further intends to modify the criteria for a positive sleep study by removing the requirement for a minimum two hours of continuous recorded sleep (the 2-hour rule) and remove the current requirements that an individual have moderate to severe OSA and that surgery is a likely alternative to CPAP. Finally, CMS will expand Medicare coverage for CPAP for beneficiaries with a clinical diagnosis of OSA without either PSG or HST only when provided in the context of a clinical study that meets specific standards. A clinical study seeking Medicare coverage for CPAP pursuant to Coverage with Evidence Development must necessarily address specific questions as stipulated in the NCD.
Modifying the 2-hour rule as proposed is likely to be perceived favorably by all vested parties. However, allowing unattended HST to diagnose OSA has the potential to fundamentally change sleep healthcare delivery, economics and outcomes in ways that are difficult to confidently predict.
The debate over the use of HST to establish the diagnosis of OSA began long before the 2007 CMS review of NCD policy 240.4. In fact, unattended HST has been reviewed by CMS since 1989 with subsequent reviews in 1995, 2001 and 2005. The most recent prior challenge to NCD 240.4 occurred in 2004 and culminated in April of 2005 with CMS opining that “…there is not sufficient evidence to conclude that unattended portable multi-channel sleep study testing is reasonable and necessary in the diagnosis of OSA for CPAP therapy, and these tests will remain non-covered for this purpose.” I was initially surprised by the CMS decision to include unattended HST in NCD 240.4, particularly without expert oversight of HST and a mandate for a well-defined comprehensive sleep evaluation. After thoughtful reflection on the proposed changes and the CMS coverage determination policy process, I intend to offer my personal insight on the proposed modifications of NCD 240.4 and on the message that CMS is sending to the sleep community. An appreciation of the events leading up to the 2007 decision is helpful in understanding the rationale behind the CMS decision. Therefore, I will begin with a brief historical overview.
In January 2007 Dr. David R. Nielsen, Executive Vice President and Chief Executive Officer of the American Academy of Otolaryngology-Head and Neck Surgery requested that CMS revise NCD 240.4. Among the challenges to the 2005 NCD policy included the notion that the diagnosis of OSA is restricted by requirement for PSG, a test described as expensive and not widely available. Further, Dr. Nielsen argued that HST was a validated, less costly alternative to PSG and that even less expensive paradigms for diagnosis and treatment were currently being explored and that HST was an important first step in promoting and working toward these alternatives.
The American Academy of Sleep Medicine (AASM) response to CMS by then-President Dr. Michael Silber included an appraisal of the literature on the availability of PSG across the United States, a survey of PSG and sleep specialist wait times in AASM accredited facilities and a review of the clinical and economic data on HST after the 2004 challenge to NCD 240.4. The AASM April 10, 2007 letter to CMS Director of Coverage and Analysis Group, Dr. Steve Phurrough, methodically established the factual basis for the following AASM positions:
  • The most recent data indicate that PSG is widely available in the United States.
  • There is no evidence to suggest that a change in the NCD policy for HST will have a significant effect on patient access.
  • Published studies up to 2004 have not provided evidence in support of HST for the diagnosis of OSA.
  • Subsequent to 2004, two studies provide some evidence in support of HST when used in highly selected cases and managed intensively in academic sleep centers.
  • Available data do not indicate that HST is more cost effective than PSG, especially taking into account technical failures, as well as false negative and false positive results.
  • Wide spread use of HST by physicians lacking training and/or experience in sleep disorders will likely result in adverse patient outcomes.
  • There is credible evidence that patients managed for OSA at AASM accredited sleep centers have better outcomes.
  • If HST is demonstrated in the future to be of utility in the management of some patients suspected of having OSA, it will be necessary that such procedures be restricted to use in accredited sleep centers in order to ensure optimal patient care.
CMS used several sources of evidence in its decision to modify NCD 240.4. In addition to receiving commentary from professional societies, industry and individuals, CMS prepared for the decision by commissioning an external technology assessment from the Agency for Healthcare Research and Quality (AHRQ) to review published clinical evidence on the use of HST in the diagnosis of OSA,2 reviewed relevant published evidence based guidelines since 2003 and held a Medical Coverage Advisory Committee (MedCAC) meeting on September 12, 2007. Collectively, the evidence largely aimed to answer three fundamental questions regarding OSA and CPAP coverage. Firstly, CMS inquired if there is sufficient evidence to determine that diagnostic strategies other that facility based PSG accurately identify patients with OSA who will benefit from CPAP treatment. Secondly, they questioned the notion that at least two hours of continuous recorded sleep is necessary for the accurate diagnosis of OSA. Thirdly, CMS queried if a diagnosis of OSA by clinical criteria alone is sufficient for the use of CPAP.
The AASM testimony that I delivered to the MedCAC panel largely mirrored the April 10, 2007 AASM letter to CMS. Other professional societies providing testimony included the American Academy of Otolaryngology-Head and Neck Surgery (in favor of HST), American Association of Respiratory Care (spoke to the 2-hour rule), the American College of Chest Physicians (ACCP), and the American Thoracic Society (ATS). While there was variance in the degree of conviction, in general the AASM, ACCP and ATS testified against the indiscriminate use of HST. AASM member Dr. David Kuhlmann testified as a private individual and was supportive the AASM position. The sleep device and healthcare delivery industry representatives such as Ion Healthcare, Apria Healthcare, Freudman Healthcare Consulting, Advanced Brain Monitoring, SNAP Laboratories, and others countered with their opinion that HST identified sleep-related breathing events similarly to PSG and that outcomes of patients diagnosed with OSA and treated with CPAP based on HST derived data was not worse than that when the diagnosis was based on data derived by PSG. The notion that PSG is the gold standard for diagnosing OSA was challenged along the lines that information derived from PSG (AHI, arousals, sleep and desaturation variables) correlate only weakly with symptom severity, response to CPAP therapy, utilization of CPAP and prognosis. Among the industry consultants and/or executives testifying in support of HST were AASM members Dr. Mark Goetting and AASM Past Presidents Drs. William Dement and Philip Westbrook. In essence, the MedCAC panel members were exposed to widely divergent opinions regarding the value of PSG and HST in the diagnosis of OSA and as a predictor of outcomes after treatment with CPAP. The panel expressed moderate to high confidence on the evidence used to determine if clinical evaluation and PSG can accurately diagnose OSA, moderate confidence on the evidence for clinical evaluation and HST and less confidence on the evidence for clinical evaluation alone. In regards to the accuracy of strategies used to diagnose OSA, the MedCAC panel expressed strong moderate to high confidence for a clinical evaluation combined with PSG, strong to moderate confidence for a clinical evaluation with a Type II HST, moderate confidence for a clinical evaluation with a Type III HST and less than moderate confidence for both a clinical evaluation with a Type IV HST and a clinical evaluation alone. Considering the value of a clinical evaluation alone or combined with either PSG or HST to predict CPAP use, the panel expressed moderately high confidence when combined with PSG, moderate confidence when combined with HST and low confidence in a clinical evaluation alone. Finally, the panel expressed low to moderate confidence that a trial of CPAP without prior PSG or HST would not produce clinically meaningful harm.
Considering that in general the MedCAC panel and AHRQ technology assessment review expressed greater diagnostic confidence in PSG than in HST (particularly in Type IV HST devices), what prompted CMS to allow HST in the diagnostic paradigm for CPAP coverage determination? Simply stated, CMS approached the 2007 decision on NCD 240.4 in a manner fundamentally distinct from earlier reviews. In contrast to the 2005 CMS decision where diagnostic accuracy was the primary determinant of CPAP coverage, in 2007 CMS deemphasized diagnostic accuracy in lieu of strategies more apt to predict favorable outcomes for treatment of OSA with CPAP. Since the available evidence does not confidently establish that indices derived from either PSG or HST can be used to reliably predict treatment outcomes in OSA patients treated with CPAP, neither could be specifically excluded from the coverage determination policy. The relative value of treatment outcome over diagnostic accuracy as the primary determinant of CPAP coverage is consistent with the CMS proposal to link long-term coverage for CPAP to demonstrable benefit after a 12-week trial of CPAP. Finally, the language of the proposed decision suggests that CMS is seeking evidence to add benefit from CPAP among the reasonable and necessary prerequisites to a diagnosis of OSA for CPAP coverage determination purposes.
CMS has not excluded PSG as reasonable and necessary for the diagnosis of OSA and makes no provision on the mechanism of CPAP titration. The proposed modification of NCD 240.4 does not specifically address management strategies after a failed home CPAP trial in patients diagnosed with OSA by clinical evaluation and HST. In this regard, PSG remains necessary in the diagnosis and management of OSA. However, in mandating benefit from CPAP as reasonable and necessary for continued coverage of therapy, is CMS encouraging the medical community in general and sleep medicine in particular towards a chronic care approach to OSA? Many patients with OSA have coexisting sleep disorders such as insomnia and residual sleepiness despite appropriate CPAP therapy, conditions that increase the likelihood of a CPAP trial failure if the combined sleep disorder is not simultaneously addressed.3 Postgraduate medical education in disciplines other than a dedicated sleep medicine fellowship affords little opportunity to gain proficiency at managing sleep disorders including complicated OSA. Physicians lacking experience in sleep medicine and unaccustomed to the nuances of modern positive pressure devices and interfaces are not likely to provide the longitudinal care mandated by NCD 240.4. This provision of the proposed decision can serve to raise the value of sleep specialists working in AASM accredited sleep facilities whom, by virtue of specialty training, experience and facility infrastructure, are best equipped to provide chronic care for patients with OSA. The past decade has seen explosive growth in our field. If sleep medicine is to continue its unprecedented growth we need be prepared to develop and embrace disease management paradigms with greater focus on chronic care and less emphasis on facility based testing.
Recognizing the potential for gains in healthcare outcomes and economics afforded by chronic care management paradigms,4,5 in January 2007 I proposed a meeting of AASM leadership with aims to enhance our understanding of chronic care models, consider the feasibility of chronic care models in sleep practices and to define the role of the AASM in developing chronic care models specific to sleep medicine. The meeting, scheduled to coincide with the April 2008 meeting of the AASM Board of Directors, fortuitously falls shortly after the final CMS decision on NCD 240.4 allowing AASM leadership to focus the discussion in light of the final ruling. I am optimistic that this conference will serve as a catalyst to promote sleep healthcare strategies that emphasize chronic care of our patients.
This editorial purposely avoids comment on inconsistencies and inaccuracies apparent in the proposed decision by CMS. A number of critical omissions including the failure of CMS to define terms crucial for coverage determination such as “clinical evaluation” and “benefit from CPAP” are similarly excluded as the official AASM response to the proposed modification of NCD 240.4 will elucidate on these and other salient issues. In sharing my experience and perspective it is hoped that this editorial helps prepare the individual sleep specialist and the field of sleep medicine for the challenges ahead.

J Clin Sleep Med. 2008 February 15; 4(1): 16–18.

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Obstructive hypopnea and gastroesophageal reflux as factors associated with residual obstructive sleep apnea syndrome


Department of Paediatrics, Gastroenterology and Allergology, Medical University of Bialystok, Waszyngtona Street 17, 15-274 Bialystok, Poland.



The mechanism of persisting obstructive sleep apnea (OSA) after adenotonsillectomy is not fully explained. The purpose of this study was to evaluate factors associated with residual OSA. The primary outcome measures were metabolic tests and polysomnographic respiratory indices in children with residual disease compared with children who were diagnosed with OSA but were untreated. Secondary outcome measures were acid gastroesophageal reflux indices recorded parallel to the sleep study.


In the one-year study consecutive series of patients with sleep disordered breathing hospitalized in a tertiary pediatric center were evaluated. Following the study protocol a sleep interview, physical examination, metabolic blood tests (serum leptin and the homeostasis model assessment index for insulin resistance, HOMA-IR) and an overnight polysomnography with pH-metry recording were performed. Children diagnosed with OSA were analyzed in two groups: I – residual OSA (after surgery), II – non-residual OSA (newly diagnosed). Logistic regression analysis was applied to obtain significant risk factors for prediction of OSA.


Fifty-seven children (mean age±SE, 6.9±0.5 years; 66.7% boys) met the inclusion criteria and were enrolled in the study as residual (n=19) or non-residual OSA (n=38). The groups differed significantly in mean oxygen saturation, SpO(2) (94.3% vs. 96.2%; p=0.018 respectively), in the Apnea Hypopnea Index, (20.6/h vs. 9.1/h; p<0.03), the number of respiratory arousals with desaturation (2.2/h vs. 0.8/h; p<0.03); mean intraluminal esophageal pH (5.36 vs. 5.86; p=0.007) and the Reflux Index (9.61% vs. 4.35%; p=0.003). The groups did not differ in total sleep time, tonsil size, BMI z-score and blood metabolic indices. Logistic regression analysis showed that residual OSA was significantly predicted by two polygraphic findings: the obstructive hypopnea index (OR 1.15; 95% CI 1.02-1.28; p=0.014) and by the Reflux Index (OR 1.01; 95% CI 1.00-1.34; p=0.042).


1. Obstructive hypopneas, rather than obstructive apneas, persist after adenotonsillar surgery resulting in residual OSA. 2. Children with residual OSA are at higher risk of acid gastroesophageal reflux and should be evaluated for gastroesophageal reflux disease.

Int J Pediatr Otorhinolaryngol. 2011 Mar 3.

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A systematic review of the efficacy of oral appliance design in the management of obstructive sleep apnoea


Discipline of Dental Public Health.


Oral appliances (OAs) are increasingly advocated as a treatment option for obstructive sleep apnoea (OSA). However, it is unclear how their different design features influence treatment efficacy. The aim of this research was to systematically review the evidence on the efficacy of different OAs on polysomnographic indices of OSA. A MeSH and text word search were developed for Medline, Embase, Cinahl, and the Cochrane library. The initial search identified 1475 references, of which 116 related to studies comparing OAs with control appliances. Among those, 14 were randomized controlled trials (RCTs), which formed the basis of this review. The type of OA investigated in these trials was mandibular advancement devices (MADs), which were compared with either inactive appliances (six studies) or other types of MADs with different design features. Compared with inactive appliances, all MADs improved polysomnographic indices, suggesting that mandibular advancement is a crucial design feature of OA therapy for OSA. The evidence shows that there is no one MAD design that most effectively improves polysomnographic indices, but that efficacy depends on a number of factors including severity of OSA, materials and method of fabrication, type of MAD (monobloc/twin block), and the degree of protrusion (sagittal and vertical). These findings highlight the absence of a universal definition of treatment success. Future trials of MAD designs need to be assessed according to agreed success criteria in order to guide clinical practice as to which design of OAs may be the most effective in the treatment of OSA.

Eur J Orthod. 2011 Jan 13.

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Subjective efficacy of oral appliance design features in the management of obstructive sleep apnea: a systematic review


Discipline of Dental Public Health, Faculty of Dentistry, University of Hong Kong, Hong Kong SAR.



The purpose of this study was to review available evidence on the efficacy of various oral appliances on subjectively perceived symptoms of obstructive sleep apnea syndrome.


A search of 4 databases was carried out. Articles were initially selected based on their titles or abstracts. Full articles were then retrieved and further scrutinized according to predetermined criteria. Reference lists of selected articles were searched for any missed publications. The finally selected articles were methodologically evaluated.


Of an initial 1475 references, 14 studies were randomized controlled trials, which formed the basis of this review. Mandibular advancement devices (MADs) were compared with either inactive appliances (6 studies) or MADs with different design features (8 studies). In comparison with inactive appliances, the majority of studies showed improved subjective outcomes with MADs, suggesting that mandibular advancement is a crucial design feature of oral appliance therapy for obstructive sleep apnea syndrome.


There is no 1 MAD design that most effectively influences subjectively perceived treatment efficacy, but efficacy depends on many factors including materials and method used for fabrication, type of MAD (monoblock or Twin-block), and the degree of protrusion (sagittal and vertical). This review highlights the absence of universally agreed subjective assessment tools and health-related quality of life outcomes in the literature today. Future trials of MAD designs need to assess subjective efficacy with agreed standardized tools and health-related quality of life measures to guide clinical practicitioners about which design might be most effective in the treatment of obstructive sleep apnea syndrome with oral appliances.

Am J Orthod Dentofacial Orthop. 2010 Nov;138(5):559-76.

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Maternal snoring during pregnancy is associated with enhanced fetal erythropoiesis – a preliminary study


Pediatric Sleep Center, Dana Children’s Hospital, Tel Aviv Souraski Medical Center, Tel Aviv University, Israel.



Snoring is common among pregnant women and early reports suggest that it may bear a risk to the fetus. Increased fetal erythropoiesis manifested by elevated circulating nucleated red blood cells (nRBCs) has been found in complicated pregnancies involving fetal hypoxia. Both erythropoietin (EPO) and interleukin-6 (IL-6) mediate elevation of circulating nRBCs. The intermittent hypoxia and systemic inflammation elicited by sleep-disordered breathing (SDB) could affect fetal erythropoiesis during pregnancy. We hypothesized that maternal snoring will result in increased levels of fetal circulating nRBCs via increased concentrations of EPO, IL-6, or both.


Women of singleton uncomplicated full-term pregnancies were recruited during labor and completed a designated questionnaire. Umbilical cord blood was collected immediately after birth and analyzed for nRBCs, plasma EPO and plasma IL-6 concentrations. Newborn data were retrieved from medical records.


One hundred and twenty-two women were recruited. Thirty-nine percent of women reported habitual snoring during pregnancy. Cord blood levels of circulating nRBCs, EPO and IL-6 were significantly elevated in habitual snorers compared with non-snorers (p=0.03, 0.005 and 0.01; respectively). No differences in maternal characteristics or newborn crude outcomes were found.


Maternal snoring during pregnancy is associated with enhanced fetal erythropoiesis manifested by increased cord blood levels of nRBCs, EPO and IL-6. This provides preliminary evidence that maternal snoring is associated with subtle alterations in markers of fetal well being.

Sleep Med. 2011 May;12(5):518-22.


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