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Sleep Apnea Patient Centered Outcomes Network (SAPCON): Part 1

Last year, Sleep Review Magazine published in an introductory story about the SAPCON project, which focuses on collecting input from patients with sleep apnea as a way to “democratize” research and gain valuable insights to promote more effective treatments. Just last month, Sleep Review published a follow-up story to discuss some of the preliminary findings, which you can read about here on pages 26-28.

The article, which was written by three leaders of the project, reported initial information gathered through the www.MyApnea.org forum (the location of the SAPCON project), where patients described, “significant gaps in the care and information they receive from sleep medicine professionals.” With this background material, they sought additional feedback from users of the website via an extensive list of interesting SAPCON surveys that inquired about what patients see as information gaps, what they are missing from their clinicians, and their suggestions for best practices. The article then goes on to list a set of challenges and potential solutions for a professional audience. In the following posts, we’ll discuss each of the challenges and the solutions offered as well as how our sleep center, Maimonides Sleep Arts & Sciences, Ltd might offer additional or different approaches.

First Challenge: They said I need a machine, that’s it?

The essence of this complaint is the failure of healthcare providers to fully educate patients so they have a clear understanding of what it means to be diagnosed with sleep apnea. Patients are often unable to digest information about apneas or hypopneas (and no mention is made here of UARS, RERAs, or flow limitations). The main insight is that patients often find the learning process overwhelming due to different learning abilities and preferences. Additionally, sleep doctors are not taking enough time to educate their patients, or they lack specific plans or information sheets to spell out the process for patients to follow over time.

What surprised me most about this challenge point was the absence of any mention of underlying cognitive impairment in these patients due to their OSA-induced sleep deprivation or fragmentation. This impairment reflects our default position in dealing with every patient with a sleep disorder, because we know we must use great precision to tailor our educational and coaching pathways to effectively engage them. What I learned about this process in the 1990s was quite a surprise, because I had always assumed talking with a patient before a sleep study (the traditional approach to care) would prove a successful model of care. It never occurred to me most patients actually forget sizeable chunks of information following these appointments, especially when I was working at an institution where the patients could not be tested for a month or longer following the appointment. Although my research on this process point fits into the category of “straw poll,” it nevertheless was provided to me by a slew of sleep technologists who confirmed with me that most patients were not remembering much from their initial intake encounter.

When we opened our sleep center in 2003, we immediately moved in the direction of “shoot first, ask questions later.” The model comprised an extensive on-line intake system, which after completion by a patient led to phone discussions with my staff or me to clarify how to proceed. Because of the uncertainty on how patients might respond to the uniqueness of the system, a strategically placed question at the end of the Sleep Medicine History component of the intake offered the patient a choice of starting in clinic versus starting in the lab. At the inception of our program, I was stunned that greater than 80% of our patients opted for the sleep lab. As of today, greater than 95% of patients choose the sleep lab over a clinic appointment to start their sleep treatment program.

As you can see below, the wording is geared toward encouraging patients to attempt the sleep lab first, yet provides enough mentions of clinic appointments so that a patient would feel comfortable requesting one. If uncertain, this issue can be addressed over the phone to determine how to proceed. Occasionally patients who want a sleep lab test are persuaded to instead start with clinic and vice versa.

Visits to Dr. Krakow’s sleep medical center include clinic appointments and sleep lab tests. Although you may schedule clinic visits as you need, Dr. Krakow advises starting in the lab. Sleep tests not only clarify the nature of sleep problems much faster, but they also speed up your treatment program. In some instances, a patient benefits by starting in the clinic. If you are unsure about how to schedule, our staff will help you decide. (The patient checks the box by one of these two options.)

     I would be comfortable following your recommendations for scheduling.

     I would prefer starting with a clinic appointment to discuss my sleep problem

This lab-oriented system, however, served a much greater objective in attacking the cognitive impairment head-on through picture-focused education the morning after the sleep study. We recognized “strike while the iron is hot” as an essential ingredient to enhancing patient education and motivation. Thus, we created the following system:

  • Upon completion of the sleep study (diagnostic or titration), the patient sits down with the sleep technologist that morning for anywhere from 15 to 60 minutes to review images on the computer showing breathing events, leg jerks, arousal activity and so on and to discuss the importance of treating sleep-disordered breathing. Of course, the sleep technologist cannot make a diagnosis, but these preliminary visual impressions have proven very memorable to our patients and, in turn, informative and motivating.
  • Each sleep study report is generally finalized within 24 hours of testing, and greater than 90% are done the same morning, shortly after the procedure is concluded.
  • Our Results Coordinator (RC), using HIPAA-compliant, encrypted emails, sends the final report with my interpretations and recommendations to the patient (some patients walk-in for the report or have it faxed or mailed to them).
  • That same day, the RC phones the patient to discuss results and answer certain questions. In many instances, patients are so motivated by the process, they choose to go forward with a titration test as their next step or to request immediate set-up with PAP therapy.
  • If or when a patient expresses concerns, confusion, resistance, or impairment or any other potential barrier, the case is turned over to the Clinical Manager (a licensed, registered sleep technologist), after which the patient will be scheduled for either a clinic appointment or a phone call with me to determine the next best steps.

We also recently published our Patient Process brochure, detailing in 16 pages and largely with graphics, the sequence of steps from “ABCs to ZZZs.” The pamphlet is especially relevant for those patients who need frequent reminders about the process they are undergoing and for those who just want a one-time overview of how things likely unfold. The brochure, which will soon be available on our website (www.sleeptreatment.com) for easier access, spends the first six pages with simple flow charts to show the progression through our sleep center operations. Next, two pages discuss the role of DME companies and how resupply of equipment occurs. The second half of the brochure describes how to assess whether or not you are gaining an optimal response to PAP therapy, the role of retitrations in the sleep lab to achieve optimal results, how to take advantage of various types of follow-up appointments, alternative OSA/UARS treatments, a brief bio on my work in sleep medicine and an extensive glossary of sleep medical terminology, described in lay words. From a convenience standpoint, when patients open the brochure the left-hand page shows a broad overview flow chart of several key sleep treatment pathways, and the right-hand page shows every direct phone number for any administrative, clinical, or laboratory service.

Undoubtedly, aspects of our system might lead to a patient falling through the cracks, which regrettably occurs in every medical clinic setting, be it traditional or non-traditional. Nonetheless, we are very proactive in reminding patients we are just a phone call or email away, and we have been operating a web-based “ticketing system” to address patient needs for non-urgent issues. Finally, in the past year we instituted a no-appointment, walk-in system to rapidly review objective data downloads and measure changes in outcomes (e.g. sleepiness, insomnia, and nocturia) in order to evaluate progress or lack thereof in various types of individuals who may need more regular contact with our staff.

Summing up, the SAPCON project is a fantastic concept, which has the potential to be a real game changer by discovering flaws in the current practice models of sleep medical care. Like any information gathering system, whether more broad-based like SAPCON or narrowly tailored like a targeted research protocol, the output developed from the efforts is greatly influenced by the initial input, namely, the relevancy of the questions will greatly impact the relevancy of the answers received. As we continue to explore the other Challenges posed in the Sleep Review article and the preliminary solutions, we will take the opportunity to attempt to predict whether or not they are asking all the right questions, an objective rarely achieved in this type of project or even a research protocol. And, we will continue our discussion on how our sleep center operations may tackle these problems in different ways. We trust some of our commentary will be informative for the SAPCON group and other sleep medical center professionals.

Last, to be clear and fair, the SAPCON authors and their team who have put this grand, highly commendable scheme into actual practice can only report so much information in a brief report such as the Sleep Review article; in this context, then, they deserve the benefit of doubt when a piece of information may not appear in their comments due to these gross space limitations. Thus, any point made in my posts that might be read as a criticism or an omission regarding their work has no such intent. Rather, I would hope these posts will be viewed as informative and speculative commentary.

In the next post, we will look at the Second Challenge: So I have sleep apnea? So what?

Second Opinions and the Rise of REPAP: Part II

We attempted our first submission of the REPAP paper with a leading sleep journal, which summarily rejected the work for many of the reasons described in the previous post. The reviewers emphasized methodological weaknesses as well what in our opinion appeared to be obvious confusion about how sleep centers currently address CPAP failure.

One of the first complaints described in the rejection letter was at odds with what most people think or know about the practice of sleep medicine: “The practice of mask changes, mode and pressure changes are the usual treatment for patients who re-present to sleep clinic and are willing to retry CPAP.” No doubt the reviewer did not carefully review our work, because we explained our sample comprised second opinion patients who failed CPAP at their original sleep centers, yet from these patients’ perspectives there was no additional support or suggestions regarding changes in mask, modes or pressures. And, in treating a fair number of CPAP failure patients outside New Mexico who made the effort to travel to Albuquerque for a second opinion, the same complaints were registered in the general form of “no other options were discussed,” or “no other equipment changes were recommended for pressure delivery modes or pressure settings.” Some reported they never underwent a single titration study in the sleep lab.

Another claim from the reviewers was as follows: “The select patient population willing to undergo multiple repeat titrations and obtain a second opinion at a special sleep clinic do not represent the bulk of CPAP failures in the community;” however, both points are indefensible as virtually no second opinion research exists in the scientific literature. For all we know many CPAP failure cases would be extremely motivated to obtain second opinions if offered the opportunity. Likewise, once these individuals were educated on the underlying flaws in the use of continuous positive airway pressure (CPAP), they might express considerable motivation to pursue a retitration to test out dual-pressure technology.

A different reviewer made a very interesting comment on the number of retitrations completed by patients who ultimate used PAP therapy: “Those who had multiple titrations had a greater proportion of CPAP users than those who had a single titration. It is unclear whether it was the persistence of the patient and/or the physician that generated the multiple titrations. Were the patients who underwent multiple titrations more likely to be patients who were dedicated to the treatment and persisted, which would make them more likely to be users than those who had one titration or was it that the single titration was adequate.”

The reviewer made valid points, because our study was not a randomized controlled, prospective design in which we investigated one group undergoing single retitrations compared to another group undergoing multiple retitrations to determine which group showed more PAP use and adherence. However, at the same time the reviewer seems to neglect that every patient entered the REPAP protocol with virtually the same baseline, that is, attempted CPAP and either rejected it immediately or ceased use at some point after completing setup and trying to adapt at home. Therefore, any patient in our sample who became a user was deemed to have reversed CPAP failure, and those who renewed use were significantly more likely to have undergone more than one retitration study. Again, it’s a valid statement we did not prove that multiple retitrations were a key aspect of reversing CPAP failure, but nonetheless, common sense tells us that just by bringing these patients back to the sleep lab to try out dual-pressure, auto-adjusting technology and then have them report the experience as more comfortable and positive than past trials withCPAP strongly hints at the potential value of this model of care.

The most remarkable comment in this initial rejection of our manuscript was as follows: “There was a missed opportunity to emphasize the importance of evaluating the presence of residual events with the data provided by CPAP software rather than dwell on retitration as a dose adjustment. Unlike medication adjustments, the success of the titration for the most part, is quite evident during the procedure hitting the mark of AHI <5. Therefore, I would take exception for characterizing the current method as “one and done”. It is ‘one and done’ because it can be.”

The one and done remark refers to our introduction in the manuscript highlighting how many sleep centers only complete one titration for the vast majority of patients and then claim optimal results have been achieved because the AHI < 5. However, there are many discrepancies in the reviewer’s comments because the AASM standard for any titration is RDI < 5, because the RDI metric is much more accurate in measuring residual breathing events. For these reasons, and contrary to the reviewer, we believe PAP therapy is exactly like an adjustment to a medication dosage, and we would go so far as to exclaim that the standard of care should be to retitrate OSA/UARS patients in the first few months or years of use, because their pressure settings frequently need adjustment upwards or downwards to improve individual clinical responses. The bold statement by the reviewer implying that “one and done” is a very successful model has little if any support in the scientific literature. Rather, one and done is actually a conventional wisdom followed by a huge proportion of sleep technologists and specialists, because they have chosen to follow outdated guidelines (AHI instead of RDI) and perhaps are intimidated by their relationships with insurance carriers (spending healthcare dollars on retitrations).

Naturally, in any review there are useful pointers on how to improve the manuscript, but I trust you can see from the above criticisms, the reviewers demonstrated either a lack of knowledge on our approach to care or simply rejected our ideas as lacking clinical relevance. No surprise, then, the editor and reviewers rejected the manuscript.

The second attempt on the manuscript was submitted to another well-respected and widely read (by sleep professionals) sleep medicine journal, and the progression of events culminating in another rejection were very illuminating, because we chose to appeal their decision, which revealed even more gaps in knowledge regarding how some sleep experts manage CPAP failure.

In this appeal response to this second rejection from the second journal we noted: “Technology to our way of thinking is the elephant in the room as prior research routinely ignores the pervasive subjective complaints and objective findings of expiratory pressure intolerance.” In another words, the reviewers all but ignored or rejected the idea that technology might play an instrumental role in overcoming CPAP failure by addressing a physiological side-effect of CPAP.

A particularly telling comment along these lines emerged from a reviewer declaring our manuscript had “too much detail.” We could only assume this complaint was directed at our detailed discussion on the mechanics of expiratory pressure intolerance arising when a CPAP titration attempts to eliminate RERAs (flow limitations), the discrete and more subtle breathing events observed in exclusively in UARS or partially in OSA. By providing this detail, we had hoped to persuade reviewers a rationale for the application of advanced PAP technology to directly address expiratory pressure intolerance and thus outline a scientific hypothesis to test by using ABPAP or ASV in CPAP failure cases.

The next complaint, a fair one to be sure, was whether or not the REPAP protocol would be cost-prohibitive. The specific comment from a reviewer though again proved more telling, “For example, given the current climate of insurances severely restricting repeat titration studies one begins to wonder if retitration is the best form of action.” To our way of thinking, this conflation of insurance carrier restrictions somehow determining the best care for our patients may be understandable, but it still seems inappropriate. That is, regardless of cost, it is the physician’s duty to determine and recommend the best forms of treatment for patients. How the patient proceeds with this knowledge depends on many factors of which cost and insurance reimbursement are certainly relevant. However, the context of our research paper frames this issue in a patient-centric manner. We reviewed charts on individuals who rejected or ceased use of CPAP once started, which by all current evidence is an extraordinarily expensive state of affairs due to the innumerable health and economic costs linked to untreated UARS/OSA. By offering this perspective, our paper noted the importance of reversing CPAP failure in 70% of patients undergoing second opinions, thereby bringing into play a new set of health and economic factors likely to far outweigh the cost of one or two “extra” retitrations. For example, two retitrations might cost an insurance carrier around $1500 to $2,000 in New Mexico, but a hospitalization for a heart attack or a motor vehicle accident could easily exceed $50,000 or even $100,000.

A reviewer then made several interesting points about the degree of follow-up in this cohort of patients prior to their seeking care at our sleep center, the critical role of follow-up to improve adherence, and then raised the question of whether or not education, not technology, was the more relevant factor in the how and why of our patients reversing CPAP failure.

On the first point, our manuscript detailed how CPAP failure patients complained about numerous gaps in their follow-up at previous sleep centers, including the specific lack of attention to the potential use of new masks or PAP modes. Several other complaints were lodged with the process that directly applied to or indirectly hinted at technology failure such as pressure intolerance, struggling to adapt, mask discomfort and leak, and no perceived benefits. Regarding the second point on follow-up in general, the reviewer made no mention of a role for retitrating the patient in the sleep lab as if technology could not improve outcomes. Finally, in raising the question on the impact of education, we could only assume the reviewer believes that expiratory pressure intolerance is merely a psychological symptom that goes away once someone uses the device long enough. This conventional wisdom is rife within the sleep medicine community and in our view demonstrates a blind spot regarding the objective physiological stressors patients must endure to eventually adapt to a PAP device. We responded to the reviewer: “We find it difficult to imagine how education/insight from clinicians explains how patients overcame their discomfort with the PAP device and how it would have eliminated their expiratory pressure intolerance.” Clearly, because we routinely see ABPAP or ASV eliminating this pressure intolerance, we have chosen the path to treat failing CPAP patients more aggressively with this model of care; and, despite our chart review research (retrospective design), our data generate a testable hypothesis: can advanced PAP therapy reverse CPAP failure?

Last, one reviewer had considerable difficulty understanding our entire approach to the sleep lab as exemplified by this quote: “Moreover, it’s not clear to me how the method of re-titration described in this paper was developed. For example, were patients first re-titrated with CPAP and were switched to BPAP or ASV due to EPI? It’s also not clear what is meant by subjective and objective EPI. If BPAP was in fact needed, why use an auto BPAP instead of manually titrating BPAP?”

Subsequently, we attempted to respond to this critique, but the manuscript was again rejected, which prompted us to write a second appeal, particularly in light of this seeming resistance to how PAP technology might be delivered in a novel way. In this second appeal, we chose to introduce our response by directly attacking this issue in the following way:

“As a preface to our detailed letter, we wish to underscore a key issue that surfaces in every critique we have received from the reviewers. The issue involves the concept of manually titrating auto-adjusting, dual-pressure PAP technology in the sleep lab environment. Each reviewer in both versions of the manuscript expressed confusion about this idea or appeared to not understand the concept.

“The concept is straightforward. In the sleep lab, an auto-adjusting device can be set to auto mode, but then the attending sleep technologist manipulates all pressure settings on ABPAP or ASV devices to produce what amounts to a better response than the auto-mode only. Still, the auto-mode is retained, because the device continues to self-adjust to provide a better airflow signal, but through the added information of the manual titration, the pressure settings are now constrained in a more effective manner. Unfortunately, it appears our reviewers, like many other sleep researchers and clinicians, seem to only be aware of the use of auto-adjusting devices used with HST, but even then the auto mode may have only been used to set a fixed CPAP pressure.

“Our paper is describing how fixed CPAP or BPAP pressures cause iatrogenic problems to the airflow curve, which can be resolved by manually titrating auto-adjusting, dual-pressure PAP in the sleep lab.   The patient is then prescribed pressure modes and pressures according to settings determined in the sleep lab, based on the sleep tech’s titration and the physician’s interpretation.

“Thus, our use of auto-adjusting technology reflects a novel way to approach titrations and has no relationship whatsoever to the current use of auto-adjusting technology in the HST environment. We are spelling out this point, because it is clear that reviewers do not understand or are confused about what we are doing in the lab. And, we believe this lack of understanding or clarity has led to an inaccurate and incomplete review of our work.”

This second appeal was again rejected, prompting us to seek out another journal,Respiratory Care, which earlier in the year had given us a favorable response to our paper on adherence and sub-threshold adherence to PAP therapy when using advanced PAP technology. The publication of that paper prompted us to direct our next submission of the REPAP study to the journal Respiratory Care

Second Opinions and the Rise of REPAP: Part I

In prior work on this site and elsewhere we have put forth the necessity to use sleep lab retitration protocols as a mainstay of practice to solve the problem of CPAP failure. In this post, we will delve into the history on the development of this concept, which has culminated most recently in the acceptance of our first peer-reviewed, research paper on the REPAP approach (REPAP stands for repeat, rescue, retitrations to reverse CPAP failure). Our paper will appear online in the next few months in the journal Respiratory Care, after more than ten years of effort to bring to fruition.1

Our story begins in 2005 in the third year of operations at our new private sleep center,Maimonides Sleep Arts & Sciences. Initially, we were treating all patients with CPAP, auto-CPAP, and a few patients with CFLEX. With careful analysis of the airflow curve in the sleep lab, we eventually recognized a specific objective finding (described below) to explain the inferior results generated by fixed CPAP pressures. Going forward, we only used bilevel devices in the vast majority of patients. During this timeframe, we were already receiving an influx of patients seeking second opinions, and nearly all of them were using or had previously failed CPAP; these patients in particular guided us in narrowing our focus to explore the advantages of bilevel. The linchpin of all this work was the objective finding that CPAP patients could not tolerate fixed pressures when breathing out; bilevel alleviated the problem, providing considerable relief of both discomfort and distress. What surprised us most about our insights in 2005 and thereafter was the rarity of any discussion on the topic in the scientific literature. Specifically, we found few recommendations or strategies on how patients should be directed to proceed when they fail CPAP and want a second opinion.

In fact, we could only find a few articles on the potential value in conducting retitrations in some patients, but it was rarely spelled out that these patients were seeking second opinions. To this day, we are uncertain whether or not other papers or guidelines cover the concept of second opinions in the field of sleep medicine for failing CPAP patients. When you consider this omission from the scientific literature, we believe it should cause concern and possibly apprehension about the workings of the field of sleep medicine. After all, is it not a standard of care in virtually every aspect of medicine, surgery or psychiatry to educate and inform patients on the value of seeking second opinions for a host of medical, surgical and psychiatric disorders? I daresay virtually every person reading this post has either personally experienced the need for a second opinion or knows of a friend or family member who required one, if not more of these encounters to solve assorted health problems.

Why then are there no obvious tracking systems, research articles, or formal policy statements about second opinions in the field of sleep medicine? I believe no immediate or satisfactory answers to this question are forthcoming other than our field is relatively young compared to many specialties. Nevertheless, dispensing with diplomacy for a moment, I also wonder whether this lacuna is more representative of a large blind spot among sleep experts, a phenomenon likely to occur when a group of medical professionals form consensus opinions and policies about specific diseases or health issues, which then become set in stone. From my vantage point as something of an outsider who left the academic-oriented university environment and who has offered a number of criticisms of the American Academy of Sleep Medicine (an organization largely comprised of professionals with continuing ties to academia), I remain disconcerted by the lack of attention to second opinions in the field of sleep medicine.

In 2007, with this framework in mind, we began to collect cases from our database of patients who had come to us specifically seeking a second opinion, nearly all of them were using CPAP. As our caseload grew, we re-examined the scientific literature as well as policies and procedures from the American Academy of Sleep Medicine (AASM). To our surprise, there was almost nothing to read on the topic of second opinions except a few researchers describing how they had successfully switched patients from CPAP to auto-CPAP or bilevel. From the AASM the only salient point in their published procedures was the suggestion to consider bilevel in patients with complaints of expiratory pressure intolerance, usually due to high CPAP pressures defined as > 15 cm H20.

In 2008, we started writing our first draft of a manuscript to submit for peer-review publication. Our main intent at the time was to publish data on how switching patients from CPAP to BPAP not only improved comfort but also improved use and adherence rates. At this same point, we were also moving on from bilevel to auto-adjusting bilevel (ABPAP) devices and soon thereafter the even more advanced auto-bilevel device known as adaptive servo-ventilation (ASV). Because of this transition in the types of modes applied at our center, we paused temporarily in our manuscript preparation, because we were seeing better results with ABPAP and ASV compared to fixed BPAP.

Another issue that appeared, one that took a few years to iron out, involved how to define CPAP failure. By 2010, we had already seen more than 1000 second opinion patients, but with greater scrutiny we realized many CPAP failure cases actually represented various stages of noncompliance, which encouraged us to developed an internal “CPAP failure timeline.” For example, obviously someone who completely rejected CPAP before ever trying it or perhaps trying it once in the sleep lab during a titration is different than a patient who filled a prescription for a device, took it home and attempted to use it for a few months or longer. Still more differentiation could be found among patients using CPAP irregularly for a long time with fair results versus those using regularly for a long time with poor results. Then, some patients reported great early results for several months and then a steady deterioration in sleep caused by other sleep problems or simply a decline in the response to PAP.

You can imagine many other permutations, but there was a larger problem embedded within our efforts to define CPAP failure, which we soon realized would make things more difficult in trying to publish a research paper. The problem, which we noted around 2011, was most other sleep experts, clinicians or researchers were not investigating CPAP failure in this much detail. Because so many sleep professionals by this time were entranced and obsessed in dealing with Medicare’s definition of CPAP adherence, the compliance concept of use > 4 hrs per night for 70% of nights permeated medical judgment and decision-making in the treatment of OSA/UARS patients.

Consider the most obvious example: a patient reports sleeping with CPAP six hours per night for 6 nights per week, which by the way is the standard we strive for in our patients. However, the patient reports persisting symptoms of insomnia and nocturia at night and sleepiness and fatigue during the daytime. Did you know that among a fair number of sleep professionals, the first approach to this patient might assume the co-occurrence of some other health problem, sleep-related or otherwise? To be sure, nowadays many sleep specialists would want to review a data download of the patient’s CPAP use, but viewing these data and interpreting the findings often yield cognitive dissonance because of the following: many data downloads do not properly record the discrete breathing events (flow limitations) of UARS; elevated leak values are frequently deemed in the “normal” range; many sleep staff ignore the presence of central apneas if only 1 or 2 centrals per hour are recorded; and finally, even today, the majority of sleep physicians do not even consider the potential value of a retitration study as an important component of the work-up to determine the cause of the persistent daytime and nighttime symptoms.

Thus, from our vantage point of trying to “sell” this research to sleep professionals who might be unwilling to define CPAP failure with greater precision, we knew our efforts would be wasted unless we could unequivocally convince reviewers of the absolute certainty our patients had failed CPAP.

To be clear, we think someone using CPAP regularly for many hours per night yet reporting poor outcomes is experiencing CPAP failure. This scenario does not mean we are not attentive to other possible causes of the problems, for example, two of the most common co-occurring issues observed in these types of poor responders would be depression or leg jerks. In various ways, we look for both subjective and objective evidence for these conditions in a large proportion of second opinion, failing patients, because our sleep center specializes in the treatment of mental health patients with sleep disorders. Nevertheless, while these problems emerge as a key factor in CPAP failure in a small proportion of cases, actual CPAP failure caused by none other than “CPAP Failure” is in fact the leading cause of…you guessed it…CPAP failure!

Sorry, just trying to emphasize a point that remains largely ignored in our field, namely CPAP does not really work as well as many sleep professionals profess, and perceptions that mislead sleep docs into thinking CPAP works well are often based on their lack of experience in trying out other modes of PAP therapy in exactly the kinds of patients who report obvious residual symptoms.

By 2013, we treated more than 2000 second opinion patients and spent the next several months sorting them into different categories of CPAP failure developed using our timeline of failure. During this exploration, we realized a majority of patients were currently attempting CPAP but with either poor results or constant struggles to adapt or both. Because these patients might be using the device—at any level of use—we sensed it might be too difficult to explain their failure problems to sleep experts reviewing our research manuscript. To solve this possible confound, we selected only patients with the most extreme or obvious forms of CPAP failure, which included patients who originally underwent a titration at another sleep center, during which CPAP was attempted, but then:

  • – Rejected and refused CPAP setup
  • – Completed setup, attempted CPAP, but then ceased use entirely

In our minds, there was no confusion about such patients designated as CPAP failure, yet we continued to polish our manuscript during the next three years in ways that informed us of new barriers we would face in trying to publish a paper on the REPAP protocol. Over that time, we predicted that two large obstacles would hamper our efforts, and these barriers related to how other experts and clinicians in the field of sleep medicine would view our aggressive attempts to titrate RERAs as well as our use of the sleep lab to manually titrate the auto-adjusting technology of ABPAP and ASV. Despite our small attempts to head these problems off at the pass, we would learn later once we completed our first attempt at a submission that reviewers could not grasp or simply rejected both ideas about treating RERAs and manually titrating ABPAP and ASV.

Although our foresight was vindicated in the long-run, in the near term we decided to directly attack these two obstacle with projects that would ultimately strengthen the REPAP manuscript, one a very in-depth study on the neglect of RERAs manifesting in theJournal of Clinical Sleep Medicine (JCSM) and the other a brief commentary explaining several factors that prevented past researchers from demonstrating the value of auto-adjusting PAP modes.

In the first effort, we examined seven years-worth (2006 to 2012) of original research papers in JCSM (219 that provided objective data on sleep breathing disorders) to determine whether or not other sleep researchers were holding up the AASM standard to score RERAs on the diagnostic or titration studies. (2) In the study, we showed how few published papers were adhering to these AASM recommendations as only 36 of 219 paper reported RERAs, and only 25 of 219 included the RERAs in the respiratory disturbance index (RDI). Moreover, another sign of high quality research is whether or not a paper acknowledges important omissions in a study design or in results to provide insight to improve future investigations; but, in the 179 papers that did not reports RERAs or RDI data, 157 made no mention of their neglect in the limitation sections.2

These proportions (< 20% use of RERAs or RDI; >85% failing to acknowledge the omission) were striking and indicated very weak endorsement of AASM recommendations described between 1999 and 2005. That RERAs were ignored by leading researchers in the field of sleep medicine, despite all the evidence compiled by the AASM indicating the essential need to treat RERAs, demonstrated the vast majority of sleep researchers publishing in JCSM were working at sub-standard levels of care in the diagnosis and treatment of OSA/UARS. The publication of our paper led to a commentary on the topic by Dr. Nancy Collop who in nutshell called out Medicare for not addressing this issue accurately and stated that regardless of what name is given to these more subtle breathing events, they need to be scored and titrated.3 Last, in a follow-up commentary in response to Dr. Collop and another researcher’s letter to the editor,4 we reiterated how failing to attend to RERAs in a titration sleep study would most likely lead to residual daytime symptoms in most sleep-disordered breathing patients.5

The second effort was also a commentary, and it specifically addressed the work of Powell et al in 2012, “A Pilot Study Assessing Adherence to Auto-Bilevel following a Poor Initial Encounter with CPAP,”6 which claimed ABPAP was no better than CPAP in attempting to improve adherence in patients doing poorly with CPAP. This paper represented a perfect opportunity for us to highlight the flaws in this type of research, which employed only the auto-mode of therapy instead of manually titrating the device in the sleep lab. In the same volume of JCSM that published their paper, the editor and colleagues, Quan et al, authored a commentary about the Powell et al’s paper, concluding that routine use of an ABPAP device was not indicated,7 yet Quan et al completely ignore the two primary flaws in the study design: 1) the lack of manual titration of ABPAP; and 2) the failure to address residual RERAs. The most telling quote from Quan et al indicated a strong aversion to technology solving CPAP adherence problems: “Finally, such negative device trials [auto-adjusting devices, etc.] suggest that any improvement in PAP adherence rates will more likely occur by addressing social and psychological obstacles to usage rather than newer technical innovations in PAP delivery or interface design.”7

In response, our commentary published a few months later, “Driving on ‘auto’: Hands-on is more effective than Hands-free,” we explain the flawed premises in both Powell et al and Quan et al works.8 We highlighted the inappropriate use of auto-mode without sleep technologist intervention as poor quality because it does not meet standards of AASM titration guidelines. Further, we explained how this approach fails to titrate out RERAs and prevent expiratory pressure intolerance. Last, we explained only through a manual titration overriding the auto mode can such approaches achieve successful outcomes.

With our background papers published in 2012, we returned to the drawing board to prepare our best effort at a new manuscript to describe the REPAP process, and the next three years proved highly instructive as we went through various rejections and appeals in two leading sleep medicine journals before landing a home for the manuscript in a respiratory journal in 2016.1 That story will follow in the next post.

 

References

 

  1. Krakow B, Ulibarri VA, McIver ND, Yonemoto C, Tidler A, Obando JJ, Foley-Shea, MR, Ornelas J, Dawson SC. 2016. Reversal of CPAP Failure with the REPAP Retitration Protocol. Resp Care (in press).
  2. Krakow B, Krakow J, Ulibarri V, McIver N. 2014 Commentary on the Frequency and Accuracy of “RERA” and “RDI” Terms in the Journal of Clinical Sleep Medicine 2006 to 2012. Feb 15;10(2):121-4.
  3. Collop, N. Breathing related arousals: call them what you want, but please count them. J.Clin.Sleep Med. 2-15-2014;10:125-126.
  4. Masi AM. The lumpers and splitters paradox. J Clin Sleep Med 2014;10:701.
  5. Krakow B, Ulibarri VA, McIver ND. 2014. A RERA by any other name…Journal of Clinical Sleep Medicine. Jun 15;10(6):703-4.
  6. Powell ED, Gay PC, Ojile JM, Litinski M, Malhotra A. A pilot study assessing adherence to auto-bilevel following a poor initial encounter with CPAP. J Clin Sleep Med 2012;8:43-7.
  7. Quan SF, Awad KM, Budhiraja R, Parthasarathy S. The quest to improve CPAP adherence–PAP potpourri is not the answer. J Clin Sleep Med 2012;8:49-50.
  8. Krakow B, Ulibarri VA, Sanchez JN, Kikta S, McIver N, Melendrez D. 2012. Journal of Clinical Sleep Medicine Driving on “auto”: hands-on is more effective than hands-free. 8(3):343-4

Sleep Onset Insomnia and Advanced PAP Therapy

In prior posts, we discussed how treatment of sleep onset insomnia with PAP therapy showed mixed results and delved into our research on the potential for greater improvements using advanced PAP devices (ABPAP and ASV) in these patients. With the very recent publication of our research paper, “A Novel Therapy for Chronic Sleep-Onset Insomnia: A Retrospective, Nonrandomized Controlled Study of Auto-Adjusting, Dual-Level, Positive Airway Pressure Technology,” we can now dig much deeper into our study methods and the precise details of the results to understand the clinical relevance of this hypothesis-generating study. This term for the study refers to its design not being at the highest level of evidence, which would have been a randomized controlled trial comparing ASV or ABPAP to a CPAP device as one example. Our nonrandomized design means the claims we offer are not proof ASV or ABPAP effectively treats sleep onset or early insomnia; instead, our findings indicate a need for more research on these ideas, because a hypothesis or theory was developed in our work to explain why advanced PAP devices might treat this problem when other traditional modes of PAP (e.g. CPAP) demonstrated mixed results.

In developing our research protocol, we started with the premise to isolate a group of patients with severe sleep onset insomnia (SOI) as opposed to a group with a mixture of equal degrees of early, middle and late insomnia. Thus, the chief insomnia complaint of eligible patients needed to be severe SOI, rated in two different ways. First, they needed to self-report sleep onset latency at bedtime greater than 60 minutes, and second on the Insomnia Severity Index rating system for question number one, they had to rate their difficulty in falling asleep as severe or very severe. By focusing only on these types of patients, we believed that whatever results we obtained would have more credibility because there would be no confusion about the type of insomnia we were attempting to treat with advanced PAP therapy.

Moreover, to solidify the perspective that these sleep onset insomnia patient were truly suffering from sleep onset problems, we asked them a series of questions that directly related to the most common symptoms seen in these types of patients. Here is a sample of a few of the behaviors indicative of sleep onset insomnia, and the percentages of patients who reported this issue:

  • – Racing thoughts keep me from sleeping (82%)
  • – Mind won’t turn off enough to fall asleep (72%)
  • – Clockwatching causes me frustration (67%)
  • – I clockwatch when trying to fall asleep (48%)

Of a possible 18 different indicators of insomnia in general and sleep onset insomnia in particular, each patient endorsed on average 9 of these maladaptive behaviors, and each patient averaged two or more psychiatric symptoms, conditions or disorders. All in all, our chart review collected 74 individuals with severe to very sleep onset insomnia whose profiles clearly established patterns consistent with the problem of early insomnia or SOI.

Other indications of severe global insomnia as well as severe sleep onset insomnia were demonstrated by their self-reported sleep patterns. They averaged less than 5 hours of total sleep per night despite remaining in bed on average for more than 8 hours, and they required more than 2 hours on average to fall asleep. They suffered from chronic insomnia for an average of more than 8 years, and 68% were using prescription sleeping pills, and 51% were using over-the-counter sleep aids. The sample included a mix of adult men and women, mostly White or Hispanic, average age 49 years-old, and mildly obese with an average BMI of 31 (roughly 25 to 30 pounds overweight).

Next, while all the patients were diagnosed with co-occurring OSA or UARS, we wanted to clarify why they were unable to tolerate standard CPAP therapy in order to provide the rationale demonstrating their need to attempt an advanced PAP therapy device. CPAP failure occurred in three phases of their treatment course:

Prescribed CPAP: 24 of the 74 patients initially used a CPAP device at home and failed primarily due to:

 

  • – Noncompliance (insufficient use)
  • – Subjective reports of difficulty breathing out (expiratory pressure intolerance,EPI)
  • – Poor outcomes defined as persisting insomnia, sleepiness or fatigue symptoms

 

Presleep/Desensitization: 48 of the 74 patients attempting CPAP in the sleep lab and prior to starting the actual titration failed CPAP during the desensitization trial primarily due to:

 

  • – Subjective reports of EPI
  • – Note: Actual instances of EPI equaled 65 due to patients failing on multiple devices (e.g. APAP, BPAP) before attempting advanced PAP

 

Titration: 69 of 74 patients titrated with CPAP, APAP, or BPAP in the sleep lab failed primarily due to:

 

  • – Needing variable pressure settings (auto-adjusting technology) to stabilize airflow signal
  • – Residual breathing events including central apneas
  • – Diagnosis of complex sleep apnea (residual central apneas meeting sufficient criteria)
  • – Note: Objective EPI equaled 83 instances, including failure on more than one PAP mode.

 

Within the 74 patients, the most striking difference was that some patients clearly were using their advanced PAP device more than others, which led to a dichotomy involving 56 patients who were using PAP on average more than 42 hours per week or greater than 6 hours per night (designated PAP Users) compared a Partial User group averaging less than 12 hours per week or less than 2 hours per night. Using this dichotomy, we compared how the severity of global insomnia and sleep onset insomnia changed in the two groups.

In the PAP User group, the Insomnia Severity Index total scores (ISI-TOT) dropped from 21.8 (consistent with severe global insomnia to 13.0 (consistent with less than moderate levels of insomnia severity). This change reflects what is known as a very large effect size, a statistical term that demonstrates the clinical relevance of a treatment response. In other words, a large effect size, or in this case a very large effect size usually coincides with a very large clinical change, which then is very noticeable to the patient. Small effects are usually less noticeable to patients while medium sized effects are noticeable but not as pronounced.

Remarkably, even the Partial User group demonstrated a large effect size with ISI-TOT scores dropping from 21.6 to 16.3. The changes between the two groups demonstrated statistical significance, which in this study is a way of declaring that the superior results in the PAP Users compared to the Partial Users was a very reliable finding, likely to be replicated if the research were repeated. However, to reiterate, the research is only a chart review and not a randomized controlled trial, the latter the highest form of evidence when attempting to prove the validity of a particular treatment.

The findings on the ISI-SOI single item score showed equally impressive results with the PAP User group demonstrating decreased ratings from midway between severe and very severe sleep onset difficulties to just under the moderate level of intensity. This change yielded a very large effect size double that observed in the Partial Users; yet even the latter group dropped their ratings from slightly more than severe to midway between moderate and severe. Again, both groups showed impressive improvements in sleep onset insomnia, but the PAP Users results were superior and statistically significant to the Partial Users.

An obvious question, one we could not answer in this study, was whether or not the two devices, ABPAP or ASV, were any different in their effects on SOI. The results were the same whether a patient used ABPAP (24 patients) or ASV (50 patients). And, regardless of the degree of use (PAP Users vs Partial Users), there were also no differences based on PAP mode. However, our findings on these points are not reliable given the numbers were relatively small when we divided up these patients by their status as Users vs Partial Users and by ABPAP vs ASV modes. A more sophisticated level of research design would be required to compare or contrast ABPAP and ASV effects.

One of the main clinical findings of the study was that many patients were using prescription sleeping pills or over-the-counter sleep aids, yet they were clearly failing these treatment approaches, and undoubtedly this failure explains at least part of their motivation to seek treatment at a sleep center. Moreover, their use of these medications combined with their strong endorsements of psychological factors as the primary cause of their sleep onset insomnia attests to the perspective that these individuals did not imagine a sleep breathing condition would prove to be an integral factor in their problems. The epitome of this mental framework was the ubiquitous problem of racing thoughts at bedtime. And, yet anecdotally, some patients reported a decrease in mental activation upon initiating and regularly use of advanced PAP therapy. These reports do not constitute evidence, but future studies must look carefully at whether or not racing thoughts are effectively decreased with advanced PAP. If so, such findings would strongly support a new theory on the underlying factors that cause racing thoughts as we have described previously, in which a psychological vantage point shifts to a physiological standpoint, albeit both could still play major roles in the development of sleep onset insomnia.

Along the same lines, there is no effort on our part to negate the potential role of medications or other forms of treatment for sleep onset difficulties such as sleep hygiene instructions or cognitive-behavioral therapy for insomnia (CBT-I). Rather, our work in this realm is about finding definitive or comprehensive treatment for various types of insomnia. We would be surprised if PAP therapy proves curative for a large proportion of patients with severe sleep onset difficulties, despite the provocative findings in our research. More commonly, sleep onset insomnia patients describe the problem of unfinished business when they hit the sack, which leads them to bring their work and worries into the bedroom and into bed.

If advanced PAP therapy ultimately proves a potent technique to decrease racing thoughts, then such information would be a game-changer in the treatment of insomnia. Nevertheless, it would still be likely such patients would benefit from other improvements in their coping skills to resist bringing unfinished business into the bedroom. These skills could be directly improved with sleep hygiene, CBT-I, and a host of psychotherapy methods. Finding comprehensive care for these patients is our primary goal, but we remain concerned that so many professionals in sleep medicine continue to overlook the potential relationships between OSA/UARS and chronic insomnia. We trust this new research will catalyze greater interest in more vigorous research protocols that use randomized controlled trials to learn how we can assist insomnia patients, and when relevant, how to treat that part of their insomnia properly addressed with advanced PAP therapy.

Complex Insomnia vs COMISA

Summarizing the final points from the last post, a term like COMISA is sufficient when talking about the larger picture in a public health discussion, but clinically we need terms to educate both physicians and patients. The term “comorbid insomnia” will be in use for a long time, because so many healthcare providers will continue to believe the main or obvious co-occurring condition is the dynamic partner in the co-morbidity. For sleep physicians, I would speculate the term “complex insomnia” will carry a certain cachet, because it was derived specifically from the construct of chronic insomnia patients who possessed no awareness of a breathing connection to their bouts of sleeplessness. In our long-term clinical research experience, these patients are astonished to learn a sleep breathing condition is a primary component of their problem, and our impression has been that millions of insomniacs suffer both disorders. For these reasons, I believe the complex insomnia term could engage patients and physicians to more readily accept the multi-factorial nature of their insomnia disorder, which in turn could increase motivation to address all facets.

Since 1995 to the present, we have come to recognize at least three categories of complex insomnia, and the remainder of this post addresses the clinical features and treatment nuances observed in these distinctive presentations.

The first type of complex insomnia (CI-Type A) reflects the original research we published in 2001, that is, patients with moderate to severe chronic insomnia do not believe a relationship exists between their psychologically-driven sleeplessness problem and sleep-disordered breathing.

The second type of complex insomnia (CI-Type B) involves patients who have awareness of sleep breathing symptoms yet still do not connect the two problems. The breathing symptoms reside in a different world of physical symptoms, and there is no reason to imagine they could affect the psychology of insomnia, a condition best described as a mental symptom.

The third and final type (CI-Type C) are those who report sleep breathing symptoms and either wonder or already believe a connection exists between the two conditions.

A fourth type that we do not designate in the complex insomnia framework are those OSA/UARS patients who also report insomnia symptoms, but they are already focused on their sleep breathing symptoms as the primary source of their sleep problems. Some of these individuals clearly perceive that the sleep-disordered breathing is causing or aggravating their insomnia. Others do not necessarily connect the dots, but they view the insomnia issue as relatively minor, not something to worry about or address, especially compared to their worries and desire to address OSA/UARS. These types of patients might be designated COMISA under the big umbrella, but they do not fit in the category of comorbid insomnia.

CI-Type A is the most problematic of three types of complex insomnia for both patients and physicians because neither person intuitively imagines this potential for a dual diagnosis. In contrast, our clinical and research teams are now so keen in evaluating these patients that for better or worse we share a “guilty until proven otherwise” mentality when they present to the sleep center complaining of chronic insomnia. For a typical board-certified pulmonary sleep doctor or for a primary care physician, our zeal would be viewed as heresy or fanaticism, maybe both, based on their beliefs that this high prevalence is improbable. Even though many sleep doctors have encountered these types of patients, it is equally true many sleep specialists do not possess a high index of suspicion for the OSA/UARS component in most insomnia patients. We know the latter point is clinically relevant, because we routinely meet chronic insomnia patients who at their first encounters at another sleep facility were informed a diagnostic sleep test would be a waste of time. Another subset among these Type A patients was tested with diagnostic PSG, but the results were reported as “no abnormalities” or “very mild and inconsequential sleep-disordered breathing.” Both kinds of patients, those tested and those not, upon entering into our system, are immediately recommended for overnight sleep testing, which with our aggressive scoring of flow limitation events (the discrete breathing event components of UARS) confirms the diagnosis of an underlying and comorbid case of OSA/UARS. Remarkably, some cases never tested demonstrated severe OSA with frequent oxygen desaturations. As you can imagine, such patients are perplexed if not dumbfounded by these objective results in comparison to their previous encounters.

Once diagnosed, the Type A complex insomnia patients tend to fall into their own two sub-divisions, succinctly described as those who embrace the results and those who reject the findings. In general, chronic insomniacs who are greatly surprised by the finding of a physiological component to the sleep fragmentation that underlies their insomnia more often than not are excited to hear this news, because it relieves a great deal of mental anguish about the nature of their unwanted and unpredictable sleeplessness. To hear that something physical is causing something mental is invariably a relief to any mental health patient, which by way of example explains why so many chronic depression patients at some point in their evaluations are tested for thyroid disease. While these receptive responders who embrace the full depth and breadth of the complex insomnia diagnosis are not jumping up and down begging for a PAP machine, the vast majority will attempt every conceivable conservative approach to care (e.g. nasal strips, nasal hygiene, nasal sprays, snore pillows, position therapy, weight loss), and a surprisingly high proportion of cases move forward rapidly with either a titration sleep study to initiate PAP therapy or seek consultation from a dentist for oral appliance therapy (OAT).

Adaptability to therapy, particularly regarding PAP or OAT, is the single greatest problem for these patients, because by definition their insomnia correlates with their higher than normal levels of sensitivity to external stimuli. When we think of insomniacs, it is easy to picture individuals who awaken from sleep to the slightest noise, so earplugs must be employed. Just so, these same individuals show more difficulty adapting to pressurized airflow and PAP masks.

Among the second subset, those who reject the OSA/UARS diagnosis or resist further consideration or treatment of the condition, it is not unusual to see a long gap where the patient is lost to follow-up for anywhere from one to five years. Based almost exclusively on the gradual deterioration of their sleep quality from untreated sleep-disordered breathing over this extended time period, the patient returns when a breaking point is reached. And, they almost always are willing to try PAP therapy.

From our experience, anyone expressing and demonstrating motivation to try out PAP has an excellent chance of learning to use it regularly. In our clinic, we routinely run numbers to evaluate 100 consecutive patients who fill a prescription to use PAP therapy, and the proportions always range between 86 to 92% of patients using the device at some level at follow-up several months later.

The Type B Complex Insomnia patients are naturally inclined to believe the theory connecting the two disorders if given the necessary education, and subsequently they are more likely to accept this diagnosis as something highly relevant to their care. Because they experience or suffer from the ill-effects of sleep breathing symptoms, it is not a great leap to explain how breathing events cause sleep fragmentation and thus fractured sleep cycles. Nonetheless, these patients do not start at the point of connecting the dots, so the Type B patients do manifest a spectrum of interest in how they rate the importance of the breathing disorder’s impact on their insomnia. Some patients have already heard of PAP therapy and want no part of it, no matter how effectively they are educated on the role PAP plays in reducing sleep fragmentation and thus insomnia awakenings at night. For these individuals, the best bet is to work on the conservative sleep-disordered breathing protocol of nasal strips, nasal hygiene, appropriate nasal sprays, positional therapy and possibly small and achievable efforts at weight loss.

In time, these individuals are likely to come around to the idea of more aggressive OSA/UARS treatment when confronted by at least three common and highly noticeable residual symptoms: nocturia, daytime fatigue or sleepiness, and aggravation of another medical condition such as hypertension, chronic pain, headaches, cardiac arrhythmias, or other heart conditions. In these scenarios, the patients may have used cognitive-behavioral therapy for insomnia, sleeping pills, or other advanced psychological therapies and attained substantive improvements in early, middle or late insomnia. Yet, if any of the listed medical conditions (or other conditions) persists in a patient who acknowledges no other explanation, then the pain, aggravation, concern, or suffering from the residual symptoms usually leads to a new motivation to problem-solve. At such a juncture, the patient shows an earnest desire to try PAP or OAT, and these patients return to the center, using the actual phrase, “I’m ready to treat my sleep apnea.”

The third group (Type C) already sees both the disorders as relevant and that both conditions need to be treated. Their main questions often revolve around whether one condition should be treated first, that is, a sequential approach, or whether both conditions should be treated simultaneously, that is, a concurrent approach. We typically favor concurrent therapy, and usually see faster and larger results by moving forward in this way.

There are a few notable exceptions. For example, we may encounter someone with very severe insomnia with all the facets of a strong psychological component including psychiatric disorders, excessive time monitoring behavior, very poor sleep hygiene and obvious psychophysiological conditioning, but this same individual has done their homework, read up on the role of OSA/UARS, and presents to the center with a narrowed vision to attack the sleep-disordered breathing exclusively. In these cases, the patient has been suffering a long time with inadequate treatments; the individual recalls no consistent or large improvements in insomnia while attempting psychotherapy, sleep hygiene instructions or even cognitive-behavioral therapy. From his or her perspective, it is time for something new, and the patient is eager to try PAP. Even though such individuals often benefit from the aforementioned psychological therapies and educational approaches, we have found it more reassuring to follow their lead and initiate PAP therapy as soon as feasible.

From the other side of the coin, there are a few patients who clearly understand the links between the two disorders, but they also express too much hesitancy and worry about PAP; they respond better by first learning both sleep hygiene instructions and cognitive-behavioral therapy, not to mention our more advanced approaches of cognitive-imagery techniques and sleep-related emotion focused therapy. Many of these therapies subsequently aid the patient in learning to use PAP therapy, while at the same time they are appreciating their active treatment of the insomnia problem.

The fourth category comprises those with obvious sleep breathing disorders and lesser insomnia symptoms. They clearly want sleep breathing treatments first and may never request any assistance on the problem of insomnia. The surprising aspect is howcommon this presentation manifests among treatment-seeking patients at sleep centers, but there is much less consistency in who wants or even needs treatment for both conditions. Thus, COMISA works as the umbrella term, but it does not key us in to the type of treatments to apply or how these patients might respond.

Comorbid Insomnia, Complex Insomnia, or COMISA? Selecting a term matters.

Sourced from Classic Sleep Care Blog

In the early 1990s I launched a large research project to measure the impact of imagery rehearsal therapy on chronic nightmare patients, while simultaneously training to increase my clinical experience in sleep disorders medicine and completing my board certification with the AASM. It is around this time we first suspected sleep apnea was more common among insomnia patients. The more I encountered OSA/UARS patients in clinic, the more I realized the “classic” presentation of OSA did not fit the majority of patients. Instead, patients often presented with many other sleep symptoms or different types of sleep disturbance complaints, and the picture often appeared as if the individual suffered from a current psychiatric condition that perhaps was the real or primary cause of the sleep disturbance. In other words, OSA/UARS was not the obvious chief complaint in patient’s mind.

For the next two decades, we published nearly thirty research papers in opposition to the idea that the psychiatric condition is the sole cause of sleep problems. We broached the topic in the reverse order by attempting to explain how sleep disorders should be more clearly understood and treated as primary conditions, co-occurring with mental health disorders. We declared that “sleep problems as a secondary feature of psychiatric conditions” reflected a flawed and outdated model. In a new perspective, we preached the expectation that treating an independent sleep disorder would not only improve sleep but might also improve mental health. The work listed above was one of the first research articles to demonstrate that treating nightmares (a sleep disorder functioning as an independent condition) led to decreases in both sleep complaints and mental health symptoms such as anxiety, depression and posttraumatic stress.

In the 1990s and 2000s Dr. Kenneth Lichstein was among the limited number of researchers exploring this relationship. In 1999 Dr. Lichstein published one of the first articles on occult sleep apnea in elderly patients, followed by a seminal commentary in 2006 on insomnia comorbidity with the provocative title: “Secondary insomnia: a myth dismissed”. Although this paper discussed all facets of comorbidity, not just the co-occurrence of insomnia and sleep apnea, the term “comorbid insomnia” came to mean insomnia manifesting in the context of another illness while retaining an independent character requiring specific insomnia treatments. Some of the common co-occurring conditions noted were: PTSD, anxiety, depression, cancer, pain syndromes, menopausal states, chronic fatigue, fibromyalgia, post-concussive syndrome, heart conditions, neurologic conditions and so on. The list may prove to be nearly limitless when we consider how vulnerable our sleep is to any sort of medical or psychological disturbance.

We applaud the use of the comorbid insomnia terminology, because it pushes more physicians and therapists to recognize the clinical relevance of aggressively treating insomnia; whereas, in the past, many healthcare providers focused solely on treating the co-occurring condition (e.g. pain, anxiety, menopausal symptoms) with the expectation the insomnia would dissipate. Or, they offered only simplistic therapeutic approaches such as prescription or over-the-counter sleep aids, instead of referring patients for comprehensive care at sleep medical centers. Sadly, the treatment of the primary condition first and/or the use of sleep aids is still one of the most widely used practice models in medical clinics around the world. Nonetheless, among health professionals now learning about comorbid insomnia, many are gaining sufficient education to recommend evidence-based, sleep-oriented treatment approaches to a growing number of patients.

With this background, we still believe some refinement is needed in terminology, which is why we view the term complex insomnia as a better fit for many of these patients instead of comorbid insomnia. We also believe the term COMISA should be considered as well. To begin this exploration of terms, we think a most relevant analysis would determine what is the most common co-occurring condition linked to insomnia. For example, arguments could easily be made for mental health as the single most frequent comorbid condition with chronic insomnia. Reading the DSM-5 nosology handbook that lists all psychiatric disorders strongly supports this point of view, because nearly all mental health conditions include sleep disorders as criteria for the diagnosis of the psychiatric condition itself.

A potentially large flaw in the argument in favor of mental health comorbidity, however, is the presumption that psychiatric factors must be the only cause of the insomnia. And, yet this last statement is confusing, because there can be no doubt that anxiety, depression or PTSD cause or aggravate insomnia through well-documented psychophysiological factors. You can imagine that someone with any type of mental health issue must at times show some difficulties coping with life stressors; therefore it would be no surprise for poor sleep to arise as well.

Given the crucial juncture in the timetable of a psychiatric patient’s insomnia, it does not seem likely some other factor, physical or mental, could be more common as the co-occurring condition. In other words, whichever came first, insomnia or the mental health condition (or perhaps both emerge at the same time), it stands to reason the two conditions are joined at the hip….

….unless, we were to discover these patients actually have a special vulnerability to a sleep-disordered breathing condition that only emerges covertly during the inception of the patient’s sleep problems. In this hypothetical and speculative model, we are proposing sleep breathing problems are already present in a large proportion of mental health patients. Or in a corollary to this speculation, unbeknownst to these patients, they already possess a nasal or oral airway anatomy susceptible to the development of sleep breathing problems.

Let’s analyze both examples.

 

  1. In the first example, the mental health patient has a known sleep-breathing symptom, such as snoring, that causes mild sleep fragmentation. Add in the factor of sleep fragmentation associated with virtually any mental health condition, and at first glance this double whammy of sleep fragmentation appears to be from two seemingly unrelated sources. However, in studies dating back to 1994, Canadian researchers Sériès F, Roy N, and Marc I. were able to demonstrate that sleep fragmentation itself worsens sleep breathing. That is, sleep breathing-induced sleep fragmentation worsens breathing, and any other sort of sleep fragmentation appears to worsen sleep breathing as well. This presumably occurs through changes in the central nervous system (CNS) that affect the natural respiratory drive of the individual. Simply stated, while awake, you breathe according to one part of the CNS, and while asleep you switch to another CNS area. Obviously, these two respiratory drive systems overlap to an extent, but it seems sleep fragmentation causes a problem in how these two systems interact. Specifically, arousals and awakenings during the night (sleep frag) trigger too much alternation between the two breathing drives (waking and sleeping). This theory, while not very well researched, remains the most commonly described hypothesis among sleep experts who theorize on how someone with insomnia might develop a sleep breathing disorder.
  2. And, to quickly summarize the second scenario, potential insomniacs suffering anatomic irregularities (e.g. deviated septum, enlarged tonsils, crowded airway, large tongue, etc.) are naturally vulnerable to the future development of a sleep breathing condition. If accurate, then this individual’s sleep breathing might worsen under stress-induced sleep fragmentation.

 

To encapsulate the above, if breathing system vulnerability underlies insomnia problems by the interrelationship of sleep interruptions (fragmentation) and breathing events (apneas, hypopneas, flow limitations), then a new rationale would view the physical or physiological dimension to insomnia as more prominent than the psychological factor. This idea is highly relevant to clinical care when we consider current research interestson how well CBT-I works among chronic insomnia patients with known OSA/UARS. The premise of such research alleges that despite the physical sleep fragmentation of OSA/UARS, patients who learn cognitive-behavioral instructions to cope with insomnia will report fewer episodes of unwanted sleeplessness regardless of the persistence of their sleep breathing events. However, the reverse of this paradigm must also be researched once we understand the full breadth and depth of these interactions. That is, if someone with chronic insomnia is treated with PAP therapy, how much would insomnia improve despite the lack of CBT-I to change their coping skills? In both instances, questions arise as to whether residual sleep breathing events still need to be treated in patients receiving only CBT-I and whether residual insomnia behaviors still need to be treated in patients receiving only PAP therapy.

Back to the terms, I trust you see the direction taken in this post indicates a larger role for sleep breathing than the actual mental health condition, and the parsimony of the hypothesis would be upheld if chronic insomnia in pain, cancer, or cardiac patients as three examples also manifested the same nexus between sleep fragmentation and sleep breathing events. While these theories certainly warrant more research to verify or disprove the priority of sleep-disordered breathing, the selected term would convey insomnia and sleep-disordered breathing as the relevant disorders joined at the hip. If so, the COMISA term appears the most salient of the three discussed, because it is the only one to convey both disorders as in CoMorbid Insomnia Sleep Apnea.

On the surface, COMISA seems reasonable, but my concern with the term is it would be used too broadly for all patients who suffer both conditions. Why would such an approach prove problematic? COMISA might be too vague if it only functions as an umbrella term without actually conveying specific clinical relevance to a particular case. For example, although identifying a medical or psychological condition accurately with clear-cut terminology is an essential aspect of healthcare, the presentation of the disorder also plays a key part in how medical professionals recognize or treat the problem. In contrast to what is conveyed by COMISA (i.e. both conditions are present), comorbid or complex insomnia often present in varying ways based on patient perspectives, and these presentations factor a great deal in how medical professionals understand and treat a condition. In my opinion, a more incisive terminology is needed when we are dealing with insomnia patients who literally have no idea that a breathing disturbance is part of their disorder. Instead, the typical insomnia patient is more apt to report on insomnia symptoms with psychological words as in “stressed out, racing thoughts, overwhelmed,” while almost no attention would be given to breathing, let alone connecting breathing symptoms to the insomnia.

For the above reasons, when most chronic insomnia patients use the term insomnia directly or use substitute terms (e.g. horrible sleep) to describe their condition and thus appear overly focused on insomnia, I believe a better term would attend to the patient’s perspective. Thus, I favor using the word “insomnia” in the selected terminology, because most chronic insomniacs are not in a position to readily accept their condition as something caused or aggravated by a sleep breathing disorder. Instead, their mindset is more apt to believe they will require pills or psychological therapies. In the next post, I will return to our original term – “complex insomnia” – to argue why it is still the preferred way to communicate in describing these types of patients.