One of the most problematic and regrettable perspectives today in healthcare is the overall neglect or mismanagement of sleep complaints and related sleep disorders among mental health patients suffering suicidal ideation and behaviors. Not only are sleep disorders routinely ignored in these dire circumstances, but worse they are routinely misdiagnosed, under-treated or incorrectly treated. At the sleep conference, several of these points were highlighted, both during presentations of data about suicidal patients and by the failure to provide more penetrating analyses of the same data.
As the best example of the latter phenomenon, several poster presentations as well as lectures given at the symposium consistently described biased recruitment strategies to exclude OSA/UARS patients from protocols examining insomnia or suicidal behavior or both. You might be puzzled on the rationale to exclude sleep-disordered breathing patients, especially if you imagine as I do that SDB is a regularly occurring feature of patients suffering from suicidal ideation and behavior. Why then exclude these patients?
To understand this research approach, we need to delve a bit deeply into the topic of research design wherein researchers in general attempt to narrow the focus on the patients they study, that is, by limiting specific characteristics of the patients under investigation. For example, if you want to understand how insomnia operates in depression, you would pick a sample of patients with insomnia and depression, but you would avoid patients who also reported serious heart disease or chronic pain disorders. These two conditions could have so much influence on insomnia or depression such that you would not know at the end of the study whether or not they affected your results.
As a related example, if you were studying cognitive-behavioral therapy for insomnia (CBT-I) in depressed insomniacs, conceivably heart disease or pain conditions would affect how well or how poorly some patients responded. Of course, you could also choose to study CBT-I in a group of rheumatoid arthritis patients (chronic pain) who reported both insomnia and depression. Such a study would be valuable, but it would narrowly apply to RA patients with depression and how their insomnia responds to CBT-I.
With regards to OSA/UARS, in any of the above examples had you not excluded patients with sleep breathing problems, you would then need to account for this additional sleep disruption factor. Because the patho-physiological effects of sleep-disordered breathing lead to chronic sleep fragmentation, it would then appear to make perfect sense to choose patients without OSA/UARS. Otherwise, you might not know how to interpret the results of your study since either insomnia or SDB could be causing the sleep fragmentation.
Most researchers think in these ways to increase precision and thus keep their eyes on just a few elements. For example, to reiterate, to investigate the precise connections between depression and insomnia, you would prefer to select patients who reported just these two conditions and not much of anything else, assuming you could find such people. You would probably choose to exclude cardiac patients or chronic pain patients or those with poorly treated respiratory conditions like asthma and COPD. And, you would exclude people who had recently suffered the loss of a loved one. You can see how the list of exclusions might be never-ending. Yet, while there are many variables you would try to exclude to maintain your narrow focus, you probably would need to permit depressed patients currently using medications or those previously attempting to treat their depression. These variables are common characteristics among cohorts of depressed patients, so you might lose too many of them for your study if such recruitment criteria were too narrow.
In sum, if you include patients with too many characteristics reflecting too many different disease conditions, your treatment might not work as you expected or if it did work, you might not be so certain as to why. What if a pain patient in your research is using opiate medication for pain? Sometimes opiates improve insomnia. Ultimately, research is designed so the information can be translated, so to speak, into real-world clinical medicine. This process refers to a concept called generalizability, which is itself a bit confusing, so I will explain in a little more detail, which will then circle us back to why some people choose to eliminate OSA/UARS patients from their research.
Since most sleep patients actually suffer from lots of different ailments, in some ways it would seem odd to keep narrowing down the focus of the sample studied in your research. The narrower things get, the more you are losing generalizability. That is, your results would not reflect what happens in everyday life, because it would be peculiar to imagine you could find people who only suffer from depression and insomnia and not be suffering from several other conditions. On the other hand, if you do work with a narrow group of patients who report predominantly problems of depression and insomnia, then your results would show that treating insomnia with CBT-I works in depressed patients. This finding, though narrow, starts the process of generalizability, because you know at minimum CBT-I resolved insomnia in your sample of depressed patients. It’s best then to think of generalizability along a spectrum of usefulness. A narrow sample focus provides a narrower yet still valid generalizability, whereas a broader sample focus provides greater overall generalizability.
In current research studies on sleep complaints in suicidal patients, we are in the earlier phases of research development where the narrow focus paradigm predominates. Therefore, with this point in mind, it would make sense to eliminate OSA/UARS patients from the mix. But, there is a problem here, which some of you might quickly notice when you hear the elimination criteria would be an AHI > 10 or 15.
Think about it: if you wanted to eliminate all OSA/UARS patients from interfering in your study design, then why not pick the standard in the field for the past 30 or more years, namely, AHI > 5? Why pick an AHI that means you are only excluding moderate to severe OSA, but not excluding mild OSA? What would be the rationale for doing so? The obvious argument would likely be the more pronounced the sleep-disordered breathing the more pronounced the underlying sleep disruption. In other words, to examine a treatment for insomnia in suicidal patients, why include the confound of a more noticeable SDB-induced sleep fragmentation. Now, if we accept this principle, then why include any degree of sleep fragmentation caused by SDB? Why not exclude the mild cases of OSA as well? Or, is their sleep fragmentation so mild, it would not affect the study?
The answer to this riddle will not surprise you if you are a regular reader of this blog. The real reason they had to raise the level of AHI for the exclusion criteria is simple—the astronomical prevalence rate of OSA, including mild OSA, among insomnia patients. Thus, had they kept the standard AHI of 5 events/hr, they would not have been able to capture enough patients to conduct the research in the first place. In a way, this change in recruitment strategies is a “hat tip” to the small cadre of research groups around the globe who are actively studying the connections between SDB and chronic insomnia. As other types of insomnia research groups are exposed to the works of this vanguard of scientists, the traditional researchers have begun to realize they must look more closely at the OSA connections. In doing so, they are now confronted with the emerging paradigm that SDB is all too frequent to be ignored among insomniacs.
Overall, this new paradigm leaves many of these research groups in a quandary because they may not have the skill, expertise or motivation to appreciate and treat OSA or UARS in their insomnia patients. They may be “stuck” so to speak in wanting to continue to research through a narrow lens by imagining the prevalence of OSA is not so common. Of course, they can really only do so by claiming that it’s really moderate to severe SDB that’s the big deal, and then they are giving themselves permission to keep mild OSA (AHI < 15) in the mix.
Can we find further problems in these research studies should they choose to discount the role of OSA/UARS? I believe we can, and the way to understand the problem is to consider two of the main perspectives provided by researchers who study sleep and suicide. First, we have the theory of hyperarousal, which in general refers to the increase in EEG brain activity during sleep, which lessens the depth of sleep. In mental health, we also talk about hyperarousal while awake, referring to someone such as a PTSD patient who is hypervigilant, or in lay terms always on edge. The second theory refers to the sequencing or timeline in how we view the longitudinal relationship between specific sleep symptoms or disorders and the final outcomes of suicidal thinking, behavior and ultimately death. Both of these aspects overlap, so our continued discussion will attempt to weave things together.
The ultimate in hyperarousal during sleep would be a disorder that constantly fragments sleep, causing either brief or lengthy arousals from a few seconds to much longer periods of wakefulness. The ironic history on sleep fragmentation research is the out and out failure of so many investigators of insomnia to repeatedly declare that hyperarousal observed regularly in such patients has no obvious cause, other than to declare “insomnia is a hyperarousal disorder.” This statement is much less useful compared to a declaration like “cars driven through red lights spend more time in junkyards.” In both instances, something is being fractured, your sleep or your car, but the first statement (about sleep) provides no cause for the break, while for the car you can at least suspect that driving through red lights must lead to more crashes that total cars, landing them in junkyards.
Insomnia research for decades has attempted to drive home the point that the cause of sleeplessness is the sleep fragmentation due to hyperarousal, yet without providing a clear mechanism through which the brain becomes aroused. Indeed, the most common explanation is “the brain of an insomniac is hyperaroused” and probably genetically predisposed to be so. The irony of course is that OSA/UARS are leading precursors to and causes of hyperarousal. The argument is not that OSA/UARS needs to be understood as the only cause of hyperarousal among chronic insomniacs, because these individuals may also suffer from a predisposition of some sort, but the fact that so much recent research shows high rates of sleep-disordered breathing among insomniacs should be raising a very large red flag about the incomplete state of affairs observed in most insomnia research.
If OSA/UARS are major contributing or causal influences on the excessive arousal activity in the brains of chronic insomniacs, and treatment of these conditions leads to clear-cut decreases in hyperarousal, aren’t we obligated to wonder just how much SDB is operating in these patients? Why continue to espouse the belief that hyperarousal is simply innate to insomnia when you can easily observe and document (with the correct respiratory sensors in the hands of a competent sleep technologist, interpreted by a competent sleep specialist) this connection between SDB and EEG arousal? Again, as described in earlier posts, we are moving closer and closer into the realms of potential medical malpractice. It is not reasonable to keep prescribing hypnotic medications to insomnia patients to tamp down their hyperarousal for more than a decade without ever considering the possibility the hyperarousal has a cause other than genetics. It is a requirement of standard of care paradigms to ask the question: why don’t these drugs work or why don’t they work very well? Moreover, it is an ethical requirement of a physician or a prescribing psychologist to be curious enough to wonder if something is being missed in the differential diagnosis (the list of conditions or diseases we suspect might be causing the problem at hand).
Perhaps the greatest barrier to accurate and timely recognition of the presence of OSA/UARS in a suicidal patient with sleep complaints is the nearly ubiquitous example where these patients present with symptoms of insomnia or nightmares or both. Because insomnia and nightmares are so vexing to the patient and often described with desperation and other emotional distress, it would be surprising for a psychologist and even a sleep physician to not be swayed into thinking that insomnia and nightmares are the primary sleep conditions to be evaluated, diagnosed and treated. Unfortunately, what we have seen for more than two decades is that either or both insomnia or nightmares are more often than not a flare in the sky signaling the presence of a sleep breathing disorder as a potentially much larger threat to mental and physical health. This sleep breathing disorder resides, figuratively, in a place hidden from the eyes of the patient and the provider, thus leading to its relative invisibility and delayed identification unless someone interprets more comprehensively the meaning of the flare above.
Still another confound is the link between insomnia and hyperarousal as well as nightmares and hyperarousal. Both links have been written about for decades and have led researchers and clinicians to reasonably make the assumption nightmares and insomnia are the source of excessive arousal activity. Our point is nightmares or insomnia could also be considered downstream effects. Evidence for this perspective is mounting, because research continues to show OSA/UARS treatment decreases both insomnia and nightmares. In this paradigm, we would then look at the sleep breathing disorder as the source of the hyperarousal activity, which somehow caused insomnia and nightmares or somehow catalyzed a part of the brain’s systems to increase vulnerability to develop the problems of insomnia and nightmares. Either way, the net effect is logical: if SDB treatment decreases insomnia and nightmares along with their related hyperarousal activity, then we would no longer link the hyperarousal directly to these usual suspects despite their being the more obvious sleep disorders in plain sight. Instead, we would need to declare the primary culprit as sleep-disordered breathing, the ultimate upstream activity that all along the way was leading to hyperarousal.
However, we could also trace things further back in the sequence to investigate the brain itself and ask the question of whether or not something in the brain of the suicidal patient adversely alters the way the person breathes night or day and whether such a finding could lead to the eventual development of OSA/UARS. In some ways, this theory is even more appealing, because there is no apparent logic that supports the idea most suicidal patients with insomnia and nightmares should have sleep-disordered breathing. Whereas, if you could discover something “wrong” in the brains of suicidal patients, it would make intuitive sense to believe brain dysfunction was the ultimate starting point of the problem, that is, the ultimate upstream factor. Next, the research would need to confirm whether or not this brain problem/change/condition in fact can be shown to alter nocturnal respiration and lead to sleep-disordered breathing.
In looking back over this post (multiple times) I can see how it feels circuitous. Though not necessarily intended, I wish to point out that a lot of ideas in research come about through circuitous pathways. Some may imagine there is a more logical stream of ideas that neatly package themselves together in linear fashion and then proceed step by step to inevitable outcomes. As far I have observed in research, the pathways are often choppy, misdirected, and lacking any obvious destiny to a final set of definitive observations.
Again, here we are 45 years after Guilleminault and colleagues reported in 1973 the first cases of insomnia linked to sleep apnea. And, yet in the present research environment that investigates conditions such as we have been discussing suicidal ideation and behavior and completed suicide there remains tremendous resistance if not outright ignorance on the rather obvious problem of chronic sleep fragmentation induced by OSA/UARS in these fragile patients. Instead, these deeply suffering individuals are repeatedly informed the problem is in their minds, their neurotransmitters, their genetic predisposition, or perhaps their sensitivity to environmental or psychological stressors, without ever once hearing about the possibility that their rotten, degraded, no-good sleep is the perfect substrate that feeds the fire for all these other contributors to their disheartening and demoralizing anti-life perspective and attitudes.
It cannot go without saying what a dramatic turn of events may arise AFTER A GOOD NIGHT’S SLEEP!
Yet this pearl of wisdom continues to be relegated to a footnote in the patient’s care, if that, due to all the biases described above. Where does that leave us in our efforts to help these patients?
Not in a very good place in my estimation as both clinicians and researchers demonstrate only a fair degree of motivation to want to engage this way with their patients or samples of patients for studies. This silo effect has been repeatedly described and has proven pervasive in numerous fields of medicine, wherein a subspecialty of any type can develop its own brand of tunnel vision, after which new information is nearly impossible to disseminate within the confines of the subspecialty itself.
Imagine right now that every family member with a suicidal patient read this blog and then proceeded to contact a primary healthcare provider, mental health or medical, demanding their loved one undergo sleep testing. Sadly, far greater than 50% of the doctors or therapists would imagine only that the family member was grasping at straws and the other smaller half might imagine the idea was interesting but would have no conceivable way to take action; or, they would believe there was nothing they could do about this new information.
So, again what would happen? The answer is nothing in most cases. This last point highlights the frustration of so many patients and their family members who ultimately must confront these narrow perspectives so routinely expressed by many healthcare professionals. Internet access and unlimited availability to growing knowledge bases will have some impact on these processes and may speed up the translation of scientific evidence into actual clinical practice.
In the meantime, many individuals continue to suffer and continue to engage in suicidal ideation and behavior, and some successfully kill themselves. Yet, there is no way to declare that had the true nature of their sleep disorders been correctly diagnosed, they somehow would have been spared these tragic endings. There is a great deal of complexity to suicidal behaviors and suicide, so the jury is out on the extent to which sleep fragmentation triggered by undetected OSA/UARS aggravates these mental health problems. Nonetheless, we already know that treating insomnia and nightmares, each one independently, appears to decrease suicidal ideation and behavior. Therefore, it certainly seems reasonable to hypothesize that OSA/UARS is an active component of these processes and merits much greater attention in research circles.
With the above in mind, here’s my modest proposal. Let’s collect the top 100 mental health researchers of suicide in the world along with the top 100 government grant administrators or related officials who oversee the distribution of funding for suicide research. Next we place them in various sleep laboratories around the globe, hook them up to EEG monitors and then proceed to keep them awake for days on end. At most, there are permitted to experience two hours of sleep, but overall whenever they sleep it must be highly fragmented through the use of artificial techniques, such subtle sound waves to kick them out of deep sleep. Then, over the course of days we would observe their psychological status and video tape their rapid decline in mood, culminating in some instances in depression and suicidal ideation and possibly self-harming behaviors. Finally, we would ask each of these research subjects when he or she would like to be permitted to sleep normally again, which would be affirmed by all of the individuals sooner or later.
Once they recovered from their sleep fragmentation/deprivation, they would be asked to watch the videos of their behavior. Then, they would be asked whether or not they have a new perspective on the value of healthy restorative slumber? Finally, they would be shown the videotape sections where they began to demonstrate suicidal ideation or behavior, as applicable. Afterwards, they would go through a series of didactics to learn about the role of sleep-disordered breathing and how it causes the sleep fragmentation/deprivation they had been exposed to in extreme fashion to mimic what suicidal patients might be experiencing chronically year after year.
Would some of these professionals get it? Would the light bulb go off in their heads? Again, sadly, probably not a lot, but for sure some what finally understand. Indeed, a lot occurs when any individual actually experiences the problem of SDB first hand. That alone would be enough to “wake up” the individual from the slumber that had prevented him or her from understanding how badly poor sleep had affected mental health and mood.
Though the experiment above might be a game-changer, we’re more likely to see the change through the methodical development of research studies proving these points. On an individual basis we might see some new trends emerge soon. But overall, unfortunately, I must say I won’t be holding my breath regarding rapid changes in policies and guidelines to help suicidal patients.
Sourced from Classic Sleep Care – Sleep & Psychiatry Symposium – A recap of detailed lectures
One of the most interesting sessions I attended in Baltimore delved into the impact of sleep disorders in mental health patients. As I’ve repeated, ad nauseum, how we specialize in mental health patients with sleep disorders, this topic naturally piqued my curiosity, and it did not disappoint.
Three main speakers covered specific topics often including case report information, and a fourth served as a discussant; this final speaker also brought up hypothetical cases to review to integrate the material from the earlier speakers.
The three speakers gave very thoughtful and detailed lectures, all of which pointed to the imperative to closely examine the nature of the sleep disorders in various psychiatric patients. The first presentation was entitled, “Common Psychiatric Conditions in Adults who Present with Sleep Problems.” This talk presented by Dr. Sam Fleishman set the table by clarifying the need to realize that sleep symptoms—all manner of sleep symptoms—can often be manifestations of underlying sleep disorders. He focused on insomnia, sleep apnea, restless legs, leg jerks, and circadian rhythm conditions.
Among the many important insights offered in his talk, three stood out for me. First, there is a growing recognition that circadian rhythm abnormalities may not just be associated with mental health problems, but also these schedule irregularities may be causing or aggravating these conditions. Second, the hopelessness that often arises from chronic insomnia may itself be a risk factor or otherwise contributes to suicidal ideation. Third, more attention needs to be given to residual insomnia especially in the context of failed antidepressant therapy when treating depressed patients with sleep complaints. In other words, is insomnia a co-morbid condition or still something secondary to depression? The verdict seems clear on the co-morbidity angle, but it remains uncertain how many practitioners in mental health fields recognize this distinction and how much it impacts therapeutic decision-making.
The second talk, by Dr. Ann Ivanenko, entitled “Common Psychiatric Conditions in Children and Adolescents who Present with Sleep Problems” made key points for these age groups that aligned with the first talk on adults. In addition, there is increasing recognition of the prevalence of other sleep disorders in patients with ADD/ADHD such as RLS/PLMD and sleep-disordered breathing. There was a brief mention of the problem of racing thoughts in children as a classic manifestation of insomnia, but I was expecting some commentary on assessment of enlarged tonsils in this age group, because such patients often suffer OSA/UARS. If you were not aware, many children report a decrease in racing thoughts following the T & A procedure.
The third talk, “The Impact of Psychological Issues in Parents on Management of Sleep Problems in Infants and Mothers” was presented by Dr. Reut Gruber, but unfortunately I was called out of the workshop to deal with a sleep center problem back in NM. As you can imagine, this talk would have covered the gross sleep deprivation experiences parents must struggle with when attempting to resolve insomnia and other sleep disorders in their young children.
Last, Dr. Merrill Wise, presented as a Discussant in his talk, “Navigating Through Sleep Clinic When It Seems Like Psychiatry Clinic” and spent most of his time on interesting patient case histories to highlight many of the points brought up by the earlier speakers. In so doing, he delved into an adolescent case of delayed sleep phase syndrome and an adult case where the patient had difficulties adapting to PAP therapy. In the former case, he discussed how something as simple as bright light therapy, timed for effective intervention, might be a valuable tool to employ in adolescents who commonly report this delayed schedule problem. In the adult case, he pointed to many of the behavioral interventions, such as mask habituation strategies (e.g. learning to wear it in front of a TV to overcome and distract from its sensations), and cognitive-behavioral therapy for insomnia wherein the PAP user may have to abide by the strategy to not try to go to sleep with PAP when not sleepy. In sum, the points were made repeatedly in this last talk as well as throughout the symposium that just because a sleep patient looks more like a mental health patient, we still owe it to these individuals to aggressively treat their sleep problems, often as co-morbid conditions, with a reasonable expectation their mental health symptoms will decrease in severity.
I concurred with virtually all the points made at the symposium and expressed my gratitude for the fine talks and discussion between the members of the panel. However, I expressed a need to consider making these points in a stronger and more assertive fashion. In particular, I brought up several points in the Q & A discussion afterwards, and later reiterated several facets of how we operate our sleep center in the management of mental health patients with sleep disorders. In this blog post, I will now elaborate in more detail on the various “bullet points” I offered at the end of the symposium, and my hope is that more mental health providers and sleep medicine professionals will heed this call for more aggressive strategies in dealing with sleep problems in psychiatric patients.
Here are the bullet points, after which I will elaborate:
- Spotting the sub-optimal responses to psychiatric treatment is a huge red flag for undetected sleep disorders.
- Ironically, the psychiatric community is currently blessed with its own diagnostic manual, the DSM-V, in which resides a compendium on sleep disorders, the likes of which puts many professional sleep publications to shame.
- The co-morbidity angle is where it’s at and should always be at the top of the list of the differential diagnosis in sorting out sleep complaints in mental health patients.
- Signs and symptoms of nonrestorative sleep may prove to be an even larger signal telegraphing the necessity to suspect undetected sleep disorders in patients with psychiatric disorders.
- Contrary to the conventional wisdom, and no surprise to readers of this blog, CPAP is not only a poor starting therapy for OSA in psychiatric patients, but also CPAP itself often proves to be a traumatizing stimuli that disrupts and delays actual use of PAP therapy for months or years.
- Last, using advanced PAP therapy modes (ABPAP, ASV) as well as repeat trips to the sleep lab for desensitization experiences (PAP-NAP) or retitrations (REPAP) are the foundational keys to enhancing adaptation and increasing hours of use (along with adherence) in challenging mental health patients with OSA or UARS.
Sub-optimal responses. This construct, or more simply, the way in which patients report less than stellar results to their treatment will one day be viewed as the most glaring error made by the professional psychiatry and psychology communities, because it prevented them from recognizing how frequent and how much these undetected and untreated sleep disorders were ravaging the mental health of their patients.
Throughout all of medicine, a sub-optimal response almost invariably triggers further exploration of additional contributing factors to someone’s poor health. When a diabetic is not responding to medications, we evaluate the timing and dosage of meds. If the meds check out, we go back to the basics of diet and exercise. When things are persistently subpar, we look for other contributing factors such as whether the diabetes represents a more complex problem, needing not just one or two medications, but maybe 3 medications and possibly insulin. And, in some cases, it becomes imperative for an obese patient to commit to losing at least 10% of their excess weight.
This same phenomenon occurs in a much more narrowed scheme among numerous psychiatric patients, particularly those suffering from depression. There may be a discussion of adding psychotherapy, prescribing regular exercise, and of course adjusting and revising medications. But, dealing with the sleep disturbances falls to the bottom of the list of things to reevaluate or newly explore. Yet, the sub-optimal results routinely look just like an undiagnosed and untreated case of insomnia or OSA/UARS or both. The patient says the depression is somewhat better, but they still feel tired or fatigued throughout the day. Sleep is a little better, but there are still far too many awakenings during the night and not much pep in the morning upon awakening. Small or not so small clues also could be noted if the patient reports persistent nocturia, a symptom rarely discussed between psychiatric patients and their mental health providers. Another issue would be hypertension creeping up slightly or concerns about cardiac arrhythmias. These two symptoms could easily be explained away by a psychiatrist or psychologist as stress-related, if they do not know how these common medical conditions connect to OSA/UARS. To repeat, the report of a sub-optimal response to psychiatric treatment should be an automatic, “do not pass GO, do not collect $200…go straight to the sleep center!”
DSM-V Sleep Disorders Section. The fields of psychiatry and psychology are now very fortunate because their main guiding manual for diagnosing patients was re-written just a few years back to focus on the critical importance of looking at sleep disorders as independent conditions affecting psychiatric disorders instead of the older and conventional way of relegating the sleep disturbance to secondary status as if the mental disorder was the sole cause of the sleep complaint. This traditional view has been extremely problematic because it meant and still proposes that the vast majority of mental health patients must traverse tortuous pathways to eventually have a healthcare provider of assorted stripes recognize an ongoing and undetected independent sleep disorder is playing a much larger role in the clinical picture. Sadly, most mental health providers continue to misdiagnose their patients in this way, that is focus on the mental issues and avoid the sleep complaints. Yet, now they have this wonderfully concise and accurate section in the DSM-V. If they would read and study this material, it would advance their practice skills enormously, and it would lead to much more accurate and timely diagnoses of sleep disorders in their patients.
Concepts of Co-Morbidity. This issue reprises the one above by seeking to eliminate the old terminology of “sleep disturbances due to a mental illness,” which had been in use for arguably a century or more, starting well before the use of the DSM manuals. The great value that arises from the use of the “co-morbidity” construct is that ultimately it will change the way both sleep and psychiatry are practiced. As I alluded to in other posts and which I discussed with several colleagues at the conference, the field of sleep medicine should prepare itself for the inexorable slicing up into various niches.
If we look just at the fields of psychiatry and psychology we can make several predictions that to my way of thinking are virtually inevitable. First, training to become a psychiatrist or psychologist is going to change sooner than later, where these professionals will likely be required to complete six to twelve months of sleep medicine training. Some might argue that we already have programs called “sleep fellowships” similar to other types of fellowships for medical subspecialties. But, I do not see such an approach maintaining itself long term for mental health providers. Because their work and training directly involves care of patients, millions of whom are actively suffering from sleep disorders, it is common sense to start training these healthcare providers in the trenches where they work, not separately in some other sleep-oriented facility.
Moreover, this problem is so widespread, we could be talking about 80 to 90% of mental health patients, because when you just glance at the DSM-V, you notice virtually every disorder listed includes a sleep disorder factor, which Dr. Lieberman noted in his talk. And, making matters more acute, psychiatric hospitals in particular will need to insert sleep testing equipment into their facilities, because so many inpatients also suffer from these undetected and untreated conditions, which most likely are delaying patients from receiving optimal care in the hospital and quite possibly prolonging their hospitalization. I would anticipate most psychiatric hospitals will need to employ a sleep specialist at their facilities, and once this process embeds itself, a short time later, all the psychiatric residents or fellows (the next levels of training after medical school) will clamor for education from the sleep specialist.
While the above will create major disruptions to current care in mental health, I believe such processes are inevitable given the obvious improvement in outcomes that will follow. Currently, just among public awareness, tons of people are describing their experiences through social media and mainstream media on how life-changing their sleep treatments have been. Chief among these treatments are PAP therapy. Therefore, the earliest disruption we will see could be family members demanding that their loved ones be permitted to bring their PAP devices with them during their psychiatric hospitalizations.
Nonrestorative sleep. This factor has also been crucial in understanding the sleep problems in psychiatric patients. The concept was brought up several times during the symposium. A singular point I brought up was the imperative to appreciate that this particular complaint almost always is sufficient to qualify a patient for a sleep study or most certainly a comprehensive sleep medicine review of symptoms and complaints.
However, my concern remains that most people linked to mental health professional facilities and institutions imagine that feelings of fatigue or daytime lethargy or not feeling rested in the morning (all three can be signs of nonrestorative sleep) are simply signs of depression or some other psychiatric co-occurring symptom or disorder. I am in no way suggesting these mental health factors would not contribute to these feelings; I am urging my colleagues to realize that sleep disorders are in the equation as well. And, for years, we have often used the single question: “is your sleep refreshing or unrefreshing?” to rapidly assess a patient’s probability for an objectively diagnosable sleep disorder. In our clinical experience, the “unrefreshing” answer is linked to diagnosable and treatable sleep disorders in well over 90% of cases. I trust mental health professionals will find the same to be true once they push to evaluate these patients with comprehensive or diagnostic sleep tools.
CPAP Traumatization. This problem remains my greatest concern of all because of the many patients who suffer from the consensus opinion that nearly anyone can adapt to CPAP if they just try hard enough. What a joke!? If more than half the patients who try CPAP are quitting in the first few weeks or months, among which are many who reject CPAP after just one night in the lab or just one night at home, I do not see how it is reasonable to make the assumption there is something “wrong” with all these patients. Logic dictates it would be just the opposite—there must be something wrong with CPAP!
There is something wrong with CPAP, and it centers around two key features of this technology. The first and most obvious is that CPAP, even auto-CPAP provides exactly the same pressure on inspiration and on expiration at any given moment in time and space. In other words, even if the CPAP is auto-adjusting, breath by breath you get the same pressure breathing in or out. You may turn on your back or enter into REM sleep, but once the CPAP device (if in auto mode) adjusts, the pressure is fixed on inhalation and exhalation. This constraining feature of CPAP sets the stage for expiratory pressure intolerance, because the human body in responding to PAP in general needs higher pressures when breathing in, but lower pressures when breathing out. Expiratory pressure intolerance occurs because it is unnatural to breathe out again such high pressures. This finding was established in 1992 in a study first demonstrating that bilevel settings were different anywhere from 2.5 to 7.5 units higher on inspiration as on expiration, and yet still established normal breathing on both limbs of respiration.
So, CPAP is wrong because the pressure is too rigidly delivered, and it’s wrong again because it cannot adjust sufficiently during expiration. Even with the use of expiratory pressure relief (EPR) systems, we do not find an adequate or consistent response, because EPR is more or less a mini-bilevel response. Thus, we move nearly all our patients onto auto-adjusting dual pressure devices, such as ABPAP and ASV.
Advanced PAP and Revisiting the Sleep Lab
On this blog, you have seen many past references to our use of advanced PAP devices and the need to return patients to the sleep lab where we can fine tune their experiences with these sophisticated technological devices. The key driver in this approach derives from auto-adjusting algorithms in the ABPAP and ASV devices, which on the one hand provide much greater sensitivity to necessary changes in the pressures for the individual (e.g. when changing sleep positions, entering REM sleep), but on the other hand are not consistently effective in managing the common residual problem of flow limitation or RERAs in the attempt to fully normalize the airflow signal.
This problem fits into the OSA equation under the general question: “How do we diagnose and how do we treat upper airway resistance syndrome (UARS)?” UARS has been a controversial diagnosis for many years, and the greatest of all ironies from our perspective is that this variant of OSA appears to be especially common in mental health patients. A further barrier to care in treating UARS is that it almost always requires higher pressure settings to attain a fully normalized airflow signal. In other words, mental health patients often need much higher pressure than might other patients with less UARS activity in their sleep breathing disorder, yet because of the nearly ubiquitous problem of anxiety among psychiatric patients, we often observe they cannot tolerate the higher pressures.
If you look at the two slides below, you can understand the general nature of this problem. When you suffer from a fully collapsed airway, an apnea, it takes very little pressurized air to re-open your airway, if just a little bit. This treatment is not like inflating a balloon, where you need lots of pressure in the very beginning to start inflating. Just a little pressure converts the apnea to a hypopnea. Then, adding just a little more air pressure converts the hypopnea to the flow limitation event. Finally, the highest pressures are needed to bring the airway fully open. The pictures with my hands are offered as a figurative example of how the airway transitions from apnea to hypopnea to flow limitation and finally fully open and normal airway.
This understanding of the treatment of OSA/UARS with PAP led us nearly a decade ago to use these devices in mental health patients and with that our publication of several research papers describing these processes and their advantages over CPAP in this patient population.
Sourced from Classic Sleep Care – Sleep & Psychiatry Symposium – A recap of detailed lectures
Sourced from Classic Sleep Care – Sleep Center Models of Care (part II) – Newer models of care and natural conclusions
There were many exciting developments to write about from this year’s annual SLEEPconference in Baltimore. In the weeks and months ahead, I will discuss several SLEEPtopics that directly or indirectly relate to the problems inherent in the traditional model of sleep care and the potential benefits from transitioning to the experiential paradigm. There will be other topics covered as well. For these reasons, I will continue with the current series on newer models of care and attempt to arrive at its natural conclusion, because it is increasingly obvious more and more sleep centers and sleep specialists must move in the direction defined by our innovative paradigm. As sleep medicine evolves, it must experiment with and deploy more expedient methods to effectively help patients, and the experiential model stands to become one of the more engaging and comprehensive approaches to address several deficits currently affecting our field.
In Part I, we traversed patient entry through our sleep center’s intake system all the way to the completion of diagnostic testing in the sleep lab. Obviously for some patients, the use of the HST model could apply, but to reiterate our specialization in mental health patients with sleep disorders currently persuades us to stick with in-lab testing for these vulnerable folks, albeit we have no doubt advances in HST monitoring, for example more accurate assessment of UARS and the addition of testing for PLMD, will expand the use of this technology.
Once the Results Coordinator (RC) completes the discussion with the patient, greater than 90% of individuals proceed to the next night in the sleep lab for the titration study. As noted in Part I, due to the intensive training we provide our sleep technologists, often through hands-on, experiential peer-to-peer mentoring in the sleep lab, the patient would next find himself or herself at the most important phase of the process. This first experience with PAP is truly the most clinically relevant and personally informative aspect of our entire model. Even for second opinion patients who had already failed CPAP, this first attempt at retitrations with advanced PAP provides the chance to be brought over the threshold and through a doorway into a far different and tremendously more satisfying experience than previously encountered. You might imagine this viewpoint places a lot of pressure (no pun intended) on the sleep technologists. Not really, because the truth is we could not imagine any other approach, as anywhere from 75 to 95% of patients wake up the next morning reporting their sleep was clearly better than sleeping without PAP. For the second opinion patients, the proportion of cases asserting a positive response to PAP also remains very high, but in these instances the comparison is now between advanced PAP and their prior failing experiences with CPAP.
“Sleeping better” the morning after is one of the most valuable prognostic indicators for future success and a key element in achieving or maintaining momentum for subsequent steps. Most patients are eager to get started with a PAP device. Some are so eager or so greatly in need of the treatment, we will occasionally equip them with a loaner device in the short-term. On average, however, patients are faced with a wide spectrum of follow-up initiatives through their efforts with the DME company they select or as is often the case in the “competitive bidding” era, the DME selected by their insurer.
In many instances how well the DME operates is determined by the relationships between the DME and the insurance company. The DME must send paperwork to the insurer to get a coverage determination on the patient’s PAP device and related supplies. This process can be simple and straightforward with a fair number of private insurers. On the other hand, when dealing with Medicare patients as well as some private insurers, the paperwork can often drag out for weeks on end before the patient acquires the device. The DME is certainly not going to invest in the new device until the insurer has granted coverage. In all these cases the paperwork must be provided by the sleep medical center, but things again can get bog down when every “I” is not dotted and every “T” is not crossed. When dealing with more advanced devices such as BPAP, ABPAP, and ASV, the delays may be even longer if the DME company is not familiar with various ways in which a patient can fail CPAP and thus qualify for a better device.
Our results coordinator (RC) has her hands full in attempting to manage these prescriptions, because there are often minor wrinkles to be ironed out, and the communication snafus often do not promote expeditious management in the process. As you might also imagine, there is frequently a lot of bickering where one organization insists documents were faxed but the other organization can find no record of the alleged fax. Another snafu that surfaces much more frequently than you would expect is that DMEs sometimes have difficulty track down the patients even though the PAP machine is ready to be delivered. As I’ve indicated previously, the DME link is one of the more problematic areas of sleep medicine care, which is why I have so much more trust in Classic SleepCare as they only deal in sleep apnea related equipment, and they are heavily invested in a strong, patient-centric infrastructure. Otherwise, par for the course are the frequent back and forth exchanges with DMEs trying to get all the paperwork completed and the patient finally setup with the device.
Usually, in our model, the morning after discussion with the sleep tech combined with the RC discussion typically held the next day are sufficient for 80% or more of patients to move forward. The other 20% require additional services, clinic appointments, new testing, discussions, or just ordinary delays due to the human condition such as intercurrent illnesses, finances, and family matters. The beauty of this system is that from start (completion of intake) to finish (initiating PAP) most patients have their PAP machine at home and ready to use within one month. Obviously for the other 20%, the delays could be additional weeks or months and in rare cases a year or more when dealing with a patient who is not even close to committing to long-term PAP use.
The next phase of our model and arguably the most difficult from the patient’s perspective is the protracted adaptation process that affects so many individuals. Here again, we are fortunate in the implementation of advanced PAP therapy, because so many of our patients don’t just declare “better sleep” during the lab night, they also receive their device a couple weeks later and report sleeping better very early in the process. Nonetheless, the trials and tribulations of dealing with mask leaks, mouth breathing, nasal congestion, pressure adjustments, mask fitting, skin irritation, aerophagia and host of other nuisances absolutely become deal-breakers in many patients who are not rapidly attended to. As you probably know, these issues are virtually all allegedly dealt with in the domain of the DME companies, but among our local suppliers we find several weaknesses in the delivery of this care. I don’t want to belabor this point, but I must insist on the well-known facts that sleep technologists spend typically 2000 hours per year in direct patient management and have learned to deal with virtually all these hassle factors with precise steps and adjustments. Unfortunately, many DMEs today still only employ respiratory therapists who have never worked a night in a sleep lab. I believe this problem remains one of the major obstacles to higher quality of care in the DME environment.
In our system, multiple pathways are available for patients to interact with our center. The three most direct pathways include emailing with our staff, phoning in to our staff, and creating a troubleshooting ticket on our website. Our troubleshooting system also has several distinctions, for example a patient might ticket an equipment issue, a prescription needed, a complaint, or a request for a certain type of appointment. The messaging system also permits the patient to describe the ticket as urgent or solvable in 1 to 2 days or within a week.
Several backup systems include the 24 hour telephone line in the sleep lab, which means someone can call and leave a message any time, and the call will almost always be returned within 4 hours if it wasn’t answered at the time of the call. The most difficult patients receive my cell phone in the early weeks of their care, so they can text with me or occasionally talk through obstacles. Many of these 5 to 10-minute talks help patients regain their momentum, but more importantly, all these pathways are designed to look for very specific targets to address. The question that always arises for nearly all patients is whether the solution requires hands-on at our center or the DME or both, telephone instructions, adjustments in medications prescribed by me, or solving insurance snafus as they relate to patients obtaining the right supplies.
Where we have seen the most valuable services are in the one-on-one sleep technologist encounters that we call Patient or PAP Management appointments (PMA), which we bill through the CPT code 94660. These appointments are directly supervised by me, but only about 25% require my intervention during the actual appointment; whereas, certain insurer policies require sleep tech/doctor combination appointments to provide the face-to-face encounters. Although I can be very helpful in the tech/doctor appointments in solving more intricate issues such as when to consider a retitration, how to adjust leg jerk medications, and when to more aggressively treat complex nasal congestion issues, we know our patients absolutely adore our sleep techs and love the time they get to spend working through very specific mask issues as well as the accompanying mouth breathing, chinstrap, mouth taping, and aerophagia complaints. Although these appointments cannot resolve every nuisance factor, it is very clear such efforts build patient confidence in ways that pay off in the home environment.
In this follow-up phase of care, we have multiple players involved in staffing assignments. We use a main follow-up coordinator, and we use a web-based Detailed Tracking system, where every daytime encounter, be it phone, email, in-person clinic or PMA, walk-ins, or text messages gets tracked by time and content. Depending upon the immediate resolution versus the necessity for future follow-up, staff will enter a tracking date for future correspondence or communication with the patient. For example, a patient starts leg jerk medication, and we want to know the response 2 to 4 weeks later; or a patient tries a new chinstrap for mouth breathing, and we want to know the response a week later; or, the patient has been struggling with several factors and knows a retitration is necessary but wants to be contacted for scheduling two months later.
Every daytime staff person, including myself, receptionist, new patient coordinator, results coordinator and various day time techs who may be working on clinic or research activities lend a hand to follow the Detailed Tracking system. To be clear, each day, a new set of tracked patients shows up on the date previously inserted during the last entry in the system. There may be as few as 3 established patients emerging or as many as 20 established patients showing up on the tracking system on any given day. In the course of a week, there are usually 30 to 70 patient follow-ups noted. Most of these follow-ups are not urgent, but this system has populated them into our awareness list, so we know to make contact within the next few days or next few weeks. As you might imagine again, there are frequent delays when we are unable to make the contact with the patient or the patient is less interested in returning our calls or emails.
Summing up, many patients receive maximal care in the early going, and the result is a very happy sleeper who is responding well to PAP and is already in the stages of what we call fine-tuning. However, a proportion of cases are those with the greatest sensitivities and therefore the most complaints. These patients will always require more time and care and for whom we devised protocols such as the PAP-NAP and REPAP. Suffice to say, as you know from past blogs, returning difficult or problematic patients to the lab is often the most cost-effective way to get them over the hump.
The questions going forward revolve around whether or not this experiential or mixed-model of care is better than the traditional model. Obviously, a true test of superiority would require a large sample of patients treated at numerous centers, for example hypothetically 1000 patients at each of 20 centers, where 10 centers practice traditionally and 10 practice experientially. Such an exercise or experiment is not likely to occur anytime soon for the simple reason that so many medical professionals are wedded to the traditional model. One would need to find special funding from an organization that could provide millions of dollars to rigorously test the differences in the models.
Thus, as with many things in medicine we are left with some degree of frustration, because so much of what we have described resonates well with common sense, yet surely there are cracks in this new model, and traditionally-oriented practitioners might find may ways to poke holes in the argument of “test first, and answer questions later.”
In my opinion, I think it is fair and right to say that the jury is out with no definitive verdict in sight regarding our innovative model, because of the lack of evidence described above. But, anecdotally, I will point to our interesting experiences with second opinion patients. All of them as far as we can tell come to us from traditional models of care where the patient is first seen by the medical professional and then proceeds through testing. As mentioned at the outset of the series in Part I, we have observed a tremendous amount of knowledge apparently not effectively transferred to these patients via their travels through the traditional care model. Take the problem of trips to the bathroom at night (nocturia) as a prime example of how this information should be incorporated into a traditional model and how we use it in our experiential model.
We cannot speak to the omission in the traditional model as we would have presumed it would be standard of care to discuss nocturia with potential OSA/UARS patients. In our model, this issue is front in center in four different ways. First, the nocturia questions on our intake are listed under a survey titled, “Sleep-Disordered Breathing-30” where we ask 30 questions about various symptoms. Among some of the most relevant are issues about cognitive impairment, dry mouth upon awakening and morning headaches. Nocturia is the only two-part question, and it is the very last questions on the SDB-30. It reads: “The need to use the bathroom to urinate at night,” to which the patient is asked to rate frequency, “Never, Sometimes, Often, or Always” and the intensity, “None, Mild, Moderate, or Severe.” Next, they respond with a number for the last part, “On average, how many times do you wake up at night to use the bathroom to urinate?” Notice the questions are neutral by not asking the patients whether the nocturia itself awakened them. It simply asks for the data on this symptom. As most patients are somewhat curious, we purposely put this symptom at the end, hoping to pique their interest in “why is there a question about trips to the bathroom on this sleep breathing symptoms survey?”
Second, when the new patient care coordinator or myself is talking with the patient by phone prior to or during sleep study scheduling, we always look at this question to note whether it is a relevant topic for the patient and particularly so if the patient indicates any degree of reluctance about moving forward. The action usually starts with a question like, “do you know about the connection between sleep apnea and trips to the bathroom?” Most patients want to hear more, so in some instances, the conversation delves immediately into the details, or we simply show them a video.
Then, the third occurrence arises at the sleep study, where again depending upon patient reluctance or motivation, the sleep technologist will return to this symptom and ask if the patient has watched the video or start again, by asking “do you know about the connection between sleep apnea and trips to the bathroom?” Again, when the patient has now heard for the third time nocturia might improve with treatment of OSA/UARS, we notice these patients are on the verge of remembering the connection.
The last bit of knowledge transfer occurs after I have completed the final interpretation and recommendations of the sleep study report. When the RC discusses these findings and action steps with the patient, the question and information may again arise if we feel a patient is lacking motivation.
We are not suggesting that every single patient receives all these instructions, but we are saying that we are very much on the lookout for individuals who suffer from the combination of nocturia and poor motivation about treating OSA/UARS in general or using PAP. And, I think it is fair to say that we dispense a lot of knowledge upstream (no pun intended) before it would have been delivered in a traditional care model, because the new patient intake coordinator spots the relevant patient and sends the educational video. Thus, before the patient would ever step into our environment, regardless of whatever might constitute the first step in our center, he or she would have learned about one of the most crucial motivating pieces of knowledge you can use in the education of a sleep apnea patient. Then downstream in their interactions with the sleep technologist and the Results Coordinator, the information is reinforced. And, in the truly treatment-resistant patient, a fifth encounter occurs either when I also call the patient following the sleep study or I meet with the patient in clinic and ask them to watch the 5 minute video at that time if they had not done so already.
In my personal and professional experience, this model of care appears highly effective because it meets the criteria of “personally-tailored medical practice,” which should be the basis of any “patient-centric model.” Indeed, when a physician or other healthcare professional finds a symptom highly relevant to the patient’s desire to seek treatment and the ensuing explanation reveals how the disease causes the symptom, then a patient will usually act on new knowledge if he or she believes the therapy would resolve the problem.
Of course, in the traditional model of care, one could easily discuss nocturia, show the video and described the benefits, but our concern is with an approach that lacks an experiential connection to nocturia. In other words, how easily does the patient use all this speculation to connect the dots? In our model, they have undergone the sleep study first, confirmed the diagnosis or reconfirmed the diagnosis in the 2nd opinion patient, thus eliminating a lot of speculation. Staff to patient: “As we have shown on the computer, you have a sleep disorder called sleep apnea, known to cause nocturia; if you treat sleep apnea, nocturia would decrease. How would you like to proceed?” The above questions can be asked by the sleep technologist, the Results Coordinator or myself at any point, and at every juncture the patient already knows OSA/UARS is the decisive factor to be reckoned with.
In the future, we will look back on several flaws in the traditional medical model of care. Robots no less will lead the way in some fashion by a capability for gathering a great deal of subjective and objective data that will permit more instantaneous evaluation and treatment. Such models of care would be the ultimate mixture, combining traditional and experiential approaches and will likely prove far superior because of a capacity for more rapid, accurate results and more rapid, effective interventions.
Sourced from Classic Sleep Care – Sleep Center Models of Care (part II) – Newer models of care and natural conclusions
Sourced from Classic Sleep Care- Sleep Center Models of Care – advantageous or outdated?
In the field of sleep medicine, there are various models of care delivery that generally divide up into traditional medical versus non-traditional. The traditional model is based on a principle of initiating care with a doctor-patient encounter in which the individual seeking care enters the clinical environment to meet with a medical professional such as a physician, nurse practitioner, physician’s assistant or registered nurse. There are several premises that underlie this model, some of which are advantageous and others of which are outdated.
The main beliefs about the traditional model of care include:
- -Patients must start with a discussion and education session with a medical professional as an essential launching point.
- -This initial type encounter greatly increases the chances the patient would follow through on taking action, because of the rapport established with the provider or from a change in motivation post-education or both.
- -Patient’s presenting knowledge or understanding about sleep issues is so limited, no other way forward seems feasible.
- -Conventional wisdom has forged a general consensus around these ideas and encourages most medical systems, sleep medicine or otherwise, to follow the same plan.
Obviously, in the Age of the Internet, virtually all the beliefs listed above could be accommodated through different or non-traditional systems. However, the doctor-patient interaction (or other medical professional) would remain a crucial ingredient of any system (at least until the robots take over the planet), albeit the timing of such encounters may vary. As a prime example of a transformative step to accommodate rapid acquisition about the patient’s health information, a system can be employed on-line to gather data by patients completing various surveys with click and point technology, but more on this point later.
The most frequently employed non-traditional model of sleep care harkens back to the laboratory-centered approach where in earliest days of sleep medicine many patients were referred to the lab for testing after having been evaluated by their primary physicians who was typically not a sleep-oriented physician. Of course, this approach appears more stream-lined and worked in many situations, particularly rural environments during the very beginning eras in sleep medicine in the 1970s and 1980s. However, for a variety of reasons, this approach was frowned upon largely because of the perception and reality that a sleep doctor never interacted with the patient, which might have led to a lower quality of care. Over the next few decades, several institutions banded together to attempt to eradicate this model of care, which was largely successful.
However in many locations, particularly more rural settings, a part-time medical director relationship served to permit these laboratory-based models to remain in place. It should be noted many of these lab-oriented centers were also in the business of selling DME equipment (i.e. PAP devices and supplies); and, therefore because of their intimate contact with patients in the lab and afterwards in managing PAP, some centers demonstrated very high rates of PAP compliance, arguably much higher than centers focused on the traditional medical model. In the context of these turf wars, a unique company like Classic Sleepcare emerged and recognized the highly relevant window of opportunity for selling only sleep-related DME (again, PAP and supplies), thus providing a superior service from which many traditional sleep medical centers now benefit.
Regardless of which side of the debate you find yourself on, it is very clear both models of care have pros and cons, and to be sure no model is perfect in light of the miserable rates of non-compliance still rife within the innumerable sleep apnea cohorts seeking treatment all across the globe. The question that arises is whether there is knowledge to be gained from both these models to inform an innovative pathway, one that extracts the best from both enterprises.
To some extent, we have formed a mixed model derived from the standard traditional and the lab-based centers, and our center has been practicing this approach for more than a decade and a half. Our results are very good to excellent to outstanding for different types of patients, but certainly we have not attained anything close to perfection. Nonetheless, our model is unconventional (while still following all insurance rules and AASM policies), and I would like to describe key features, so others may investigate whether similar approaches are worth testing out at their own centers.
First and foremost, we do not believe a patient sitting down with a doctor or another degree-holding sleep medicine professional is a necessary starting point for the vast majority of sleep apnea patients. In fact, we have been persuaded for 25 years that this standard model has several pitfalls that may lead to just as much harm as benefit. The harms we are referring to are not that sleep doctors or mid-level professionals cannot do a decent to outstanding job in educating and communicating with their patients on the essentials of diagnosis and treatment of sleep apnea. Rather, the problem is this sort of attempt to connect with patients is based on several faulty premises on the nature and style of the how and why patients seek care for sleep apnea.
As discussed previously, patients who are treatment-seeking and straightforward (a surprisingly rare occurrence at most sleep centers) would absolutely do fine in this traditional model, although nowadays this model is often a waste of their time and resources, because 90% or greater could easily and happily start in the sleep lab with a split night study before ever meeting with a physician. Or, they could reasonably start with the HST/APAP model and see the doctor or even the sleep technologist at first follow-up. And, the same could be said for the HST/OAT model as well. Check out this link from HST America, a company offering home sleep testing services and sleep apnea education.
More commonly, most sleep apnea patients report numerous complexities or co-morbidities to their cases, not the least of which are several mental and physical symptoms or disorders for which they are also attempting to treat or in many cases not attempting to treat. Infrequently would a patient enter a sleep center environment anticipating that many or most of their other ills would improve by fixing their sleep problems. All these points, then, immediately suggest education would be a high priority before the patient sets foot in the lab. However, this premise turns out, we believe, to be faulty, because it assumes sleep apnea patients would retain this knowledge. Take an example where you are persuaded you developed the perfect system that educates sleep apnea patients extremely well at whatever level of educational background, and your system guaranteed the patient would retain 90% or greater of the information. If so, I would support the traditional model of care. But, I’m not convinced this outcome is occurring at the majority of sleep centers. And, though undoubtedly there are some centers better than others, we routinely meet with second opinion patients where they report never having been instructed at any point in their care on the following factors:
- -Three types of breathing events including apneas, hypopneas and RERAs.
- -Clinical relevance of RERAs and why they must be aggressively treated in most patients.
- -How sleep apnea causes nocturia and how it can be reversed with PAP therapy.
- -The huge array of mask styles and the value of each one (nasal pillows, nasal masks, and full face masks) as an all options on the table approach.
- -Intricate distinctions between mouth leak, mouth breathing, and jaw dropping (without mouth breathing) and the role of chinstraps or mouth taping in problem-solving.
- -Interference from chronic rhinitis, especially nonallergic rhinitis, and the treatment steps to overcome these problems.
- -Why and how fixed pressurized airflow is a major obstacle to regular use of CPAP and how advanced technology is readily available to solve the problem.
- -Relationships between sleep apnea and chronic insomnia and how treatment of the former frequently decreases or cures the latter.
- -Relationships between sleep apnea and chronic nightmares and how treatment of the former frequently decreases or cures the latter.
- -Relationships between sleep apnea and parasomnias and how treatment of the former frequently decreases or cures the latter.
- -Special impact of RLS and PLMD leg movement symptoms and disorders on overall sleep fragmentation and their adverse influences on PAP users.
Irrespective of when a sleep patient might have been counseled on these items, be it before testing or after starting PAP, we repeatedly encounter cases where most or none of this information has been dispensed to the patient, a void in the field of sleep medicine for which we can offer no explanation. Then again, I trust the above list (which I daresay remains incomplete) would overwhelm most sleep patients at their intake unless they bring a special kind of perspective to the encounter. This last point brings us to the heart of the problem with sleep apnea patients in general.
Sleep apnea patients experience the problem of sleep apnea while they are sleeping. Thus, on the most basic cognitive level it could be argued they don’t experience sleep apnea at all. Which means any instruction or knowledge you provide to a sleep apnea patient will be viewed as either an abstraction or speculation or both. No matter how much you might attempt to drill this information into the patient’s mind, it just cannot be fully understood or comprehended in ways that carry forward in high retention fashion. Instead, whatever information is given generally fades away and in some cases might scare the patient enough to steer them away from proceeding with testing. Not as an aside, keep in mind that the sleep fragmentation these patients suffer from undoubtedly affects their memory, concentration and attention, which further compromises the capacity to retain even the most important clinical information about their potential sleep apnea diagnosis.
Compared to the traditional approach, our mixed-model is based on an experiential paradigm. We believe sleep apnea patients need to experience things first-hand in the sleep lab to more rapidly digest the likely diagnosis of OSA or UARS; and, such experiences are retained more fully and more accurately. Consider that when anyone undergoes a test, he or she is vigilant to the experience, because it is an extremely personal one. Someone else, a medical professional, is paying very close attention to something about the way your mind or body or both are operating. The patient believes that some important and hopefully useful information will be forthcoming from the test, and when the individual receives this information there is no abstraction or speculation. In the case of sleep testing, patients place their trust in the sleep technologist who provides them with all manner of information, knowledge, and assurance about the experience they are undergoing, often with repeated interactions requiring sleep tech assistance throughout the night. The patient is being cared for by a professional who is helping them through a somewhat stressful and sometimes difficult experience. By the end of the night, a degree of rapport has been established far greater than can be established when a doctor and patient talk abstractly about sleep apnea. Finally, in the morning, we have developed standardized verbiage on how our sleep techs use the computer to review with the patient the key parts of the PSG findings.
By the end of the experience, patients not only have established the sense of successfully completing an important health test, but also when they can be shown the test “results” immediately (technically, the standardized impressions) the proverbial light bulb switches on in their heads and a huge “aha” or “wow” ensues. Such encounters lead someone to “feel” the importance of the experience and thus emotional connectivity is generated that will almost invariably either cause them to remember the information very well or said another way, prevent them from forgetting they stop breathing at night.
These differences between a traditional versus an experiential model are not minor distinctions. To paraphrase a Sufi adage, “speech may very well be the annihilation of experience, because speech clearly is not the experience.” Talking about things is not even close to experiencing things. And, while it is true many of the knowledge points listed above must eventually be addressed for the majority of OSA or UARS patients, the dispensing of this information works best on a readiness timeline. Once the patient has gained experience and thus a more direct perception of the sleep problem, this initial context or foundation now permits a more rapid introduction of more knowledge into the patient’s mind.
As the best example, how would a patient relate to learning about PAP masks and tubes as well as pressurized air immediately after viewing the computer impressions of the sleep apnea? The answer should be obvious compared to sitting in an office and hearing about an abstract discussion regarding, “…and once we diagnose you with sleep apnea, then we can fit you with this mask and pump air into your throat to keep it open.” By way of analogy, do you remember going into the classroom to listen to an instructor explain the mechanics of how bicycles operate before you set foot on the pedals? Worse, do you recall someone talking to you about how to pedal the bike, how to stay balanced and how not to fall before you got on the bike? Or, did you just get on the bike with someone helping you a bit? The latter approach of course is experiential and is the universally tried and true one.
What happens next in our mixed-model approach? To backup for a moment, recall we mentioned the possibility of the on-line intake system. Our on-line system called WebIntake, which is designed to eliminate paper, pencil, and clipboard in the medical center’s reception area, not only collects valuable and pertinent health history to be incorporated into the patient’s first sleep study or first clinical encounter, but also provides us with so much information that 98% of the time we can guide patients to start taking certain instructional or therapeutic steps from the outset as well as guide them in how we think they should start in our system, for example, doctor’s clinic appointment, sleep tech appointment, night in the lab appointment, daytime PAP-NAP, or with an administrator for complex billing or insurance issues. We have used the on-line intake system for more than 15 years, and some years ago I presented our model in a Meet the Professor session at the annual SLEEP conference. One highlight from the session was the enthusiastic response we received for this online system as an innovative way to gather intake data. My understanding is that many other medical clinics, including sleep clinics, are beginning to adopt such systems.
The second step for many patients is to experience PAP therapy in the sleep lab with the sleep study known as the titration procedure in which pressures are titrated to open the airway and decrease breathing events. Here, the patient enters into a more experiential situation whether they undergo the full titration or the PAP-NAP. The titration experience is the single most important encounter for a great many OSA/UARS patients, easily the vast majority, because it can so easily make or break the patient’s motivation to move forward. A positive experience with PAP guided by the trusting hands of a compassionate sleep tech greatly influences patients capacity to endure the inevitable hassles that always arise in the first few days, weeks, or months after initiating PAP at home.
In contrast, a bad experience in the lab, leading to a poor response to PAP, in the hands of an under performing sleep tech will often prove sufficient to provoke outright PAP rejection. In such cases, the patient will not even consider a prescription for use of PAP at home, and either ignores the OSA/UARS diagnosis, begins exploration for another evidence-based approach such as OAT or possibly surgery, or simply searches the Internet for conservative tools such as nasal dilator strips, special pillows, supine-position prevention devices and numerous nasal hygiene regimens. Some are persuaded by their physicians, unsurprisingly, to enter a weight loss program, which sounds reasonable, but it is based on the faulty premise that weight loss eliminates OSA or UARS. Weight loss decreases the severity of these conditions but rarely cures it. Most importantly, it is much more difficult to lose weight than it is to learn how to use a PAP device—assuming you can get the right PAP device for you.
Thus, of all the components of an experiential model of care, the sleep technologist is the single most important player in the PAP process and must be trained in ways to accommodate a wide variety of patient types. This statement is important to consider in the context of the traditional model of care. Many standard sleep medical centers severely restrict interactions between sleep technologists and patients. More importantly, many centers severely limit patient access to advanced PAP therapy modes, which often can turn a patient’s negative experience in the lab into a very positive one.
Of course, there is so much more to be said about the role of the sleep technologist, but we have delved into that arena in many previous posts, most recently in discussing their capacity to use advanced PAP modes by manually titrating them or in effect over-riding their auto-adjusting mode for portions of the night. Now, we will turn our attention to the additional infrastructure that supports our mixed-model or experiential paradigm.
Once I complete the review of a sleep study, I then finalize the Interpretation and Recommendation sections of medical report. In this process, I am reviewing all the pertinent historical aspects of the patient’s care to date. As the most relevant examples, we have Special Updates to detail any patient changes in six main categories: Insomnia; RLS/PLMD; Nightmares; Parasomnias; Narcolepsy/Hypersomnia; and Cardiac Health. And, there are distinct categories for two other areas of health: Medication Adjustments and Nasal/Oral Airway Health. Every time a patient undergoes a sleep study, all these areas are updated as key factors playing crucial roles in whether or not a patient can respond well to PAP specifically; or in other instances, how these factors affect other sleep disorders or other aspects of general sleep health.
When all this information is finalized, the chart and report are turned over to the Results Coordinator (RC), where we employ some of our most experienced staff who typically work at the position for more than one year and some of whom have gone on to become sleep technologists. The very first steps taken by the RC are to email the patient the final report of the sleep study and set up a discussion time to review the details by phone and answer questions. These discussions go extraordinarily well for at least three reasons: (1) I complete my reading of studies 95% of the time the morning after, which means we are almost always contacting the patient in the morning or afternoon following the night of the sleep study (or Monday for weekend studies); (2) the patients have already engaged in discussion with the sleep tech regarding some of the standardized impressions as well as having viewed pertinent tracings on the computer to gain a foretaste of what to expect in the results discussion; and (3) the RC has completed these discussions with thousands of patients, and the RC and I are effectively in constant contact throughout the day to clarify any issues or questions that must be fielded by the doctor.
The beauty of this system and its inherent expediency is that the knowledge transfer that begins with a patient intake and culminates in the diagnostic phase of care delivery has been streamlined to the point that the overwhelming majority of patients embrace this information wholeheartedly and elect, as noted above, to proceed with the second sleep study to test PAP therapy. Admittedly, the system does not work well for everyone, particularly older patients who are more comfortable with the standard doctor-patient relationships. One way I have accommodated this need is to make phone contact with such patients a fairly routine affair. Even though I receive no reimbursement for these conversations, most of our patients appreciate receiving a doctor call, and conversations typically last between 5 and 15 minutes, after which most patients regain motivation or simply feel better educated or clearer about what lies ahead.
Taken together, what we have found up to this point in the patient’s pathway is that most are retaining the knowledge transfer. We also perceive we have sparked some degree of curiosity in our patients, which then leads them toward further exploration on their own. For any of our patients up to this point (i.e., completion of diagnostic testing), and always directly after a diagnostic test, on our website we provide ourPatient Process Brochure.
Finally, in wrapping up the discussion on this diagnostic phase, there will always be exceptions to the rule. We are mindful of specific patient types who may not be able to move forward with PAP, or who need RLS/PLMD treatment first, or who might need coaching on insomnia issues before even considering PAP. Over the years, the truly remarkable statistic for our center is that even among these types of cohorts, we still observe many patients who actually are better served by trying PAP initially and receiving a very pleasant surprise on how much better they immediately feel. As I am sure you can see where I am going with this point, let me briefly state that this experience is then the ultimate aspect in the experiential paradigm. The patient walks in the door ‘indoctrinated” to all sorts of ideas and speculations about sleep, but once a PAP experience generates the experience of higher quality slumber, the patient’s perspective is transformed instantaneously to recognize a pivotal if not primary component of his or her sleep disorder. This point reflects the ultimate in patient education, because the individual “knows” first-hand the experience of sleeping better.
In the next components, we’ll delve deeper into the infrastructure that has successfully linked our daytime and nighttime staffs to enhance the education and treatment successes of our patients.
Sourced from Classic Sleep Care- Sleep Center Models of Care – advantageous or outdated?
Sourced from Classic Sleep Care- A new approach to treating restless leg syndrome and periodic leg movement disorder
Last year, I noticed a worsening of my restless leg syndrome (RLS) and my periodic limb movement disorder (PLMD) symptoms. For years, I only suffered from restless legs, and maintaining my serum ferritin levels above 50 with occasional iron supplements always solved the issue. Then, I suffered a decline in the quality of my sleep and visited my own lab here in New Mexico, where we discovered scattered independent leg movements, known as PLMD. Before taking the leap to test the standard, established evidence-based drugs, I pursued two other pathways. First, I bumped up my iron levels closer to 100 as one scientific publication suggested this step might further decrease RLS/PLMD symptoms. The second approach was to bump up my Vitamin D supplements as two recent publications have suggested a connection between RLS/PLMD and low levels. Neither of these efforts made any difference in the quality of my sleep.
Before asking my primary physician to prescribe a standard medication (e.g. Mirapex, Requip, Neurontin), I elected to investigate alternative medicine literature for anything newly researched. I’ve scoured these resources frequently over the past several years hoping to find something for those patients unwilling or uninterested in attempting prescription drugs. As you probably know, you can find tons of advertisements and almost no research on alternative medicine products; and as RLS/PLMD are so common you will see lots of “endorsements” for allegedly successful remedies. Indeed, I know a fair number of patients who have tried several alternative medicine approaches, but rarely do we see documented decreases of leg jerks in the sleep lab. Moreover, rarely do patients inform us of great benefits.
In my search near the end of 2017 I found this research on L-Tyrosine and RLS. A summary of this research proposal reads as follows:
Tyrosine is a non-essential amino acid that is the precursor of the neurotransmitter, dopamine. Tyrosine is converted into Levodihydrophenylalanine (L-Dopa) and L-Dopa is subsequently and avidly converted into dopamine. It is well known that dopamine deficiency leads to the manifestations of restless legs syndrome (RLS). Studies have shown dopamine agonists and L-dopa to be effective in controlling symptoms. No studies to date have been done to determine the role of Tyrosine in RLS. This open-label pilot study aims to determine the efficacy and tolerability of tyrosine in RLS, as current agents have limitations in treating RLS in addition to adding another possible agent to the investigators arsenal of treating RLS that may be more cost efficient. In this pilot study, the dose of Tyrosine will be escalated from 750 mg once daily by mouth (PO) up to 3000 mg once daily PO, as tolerated, in increments of 750 mg every week in patients who meet the inclusion criteria for RLS. Patients’ symptoms will be monitored on a weekly basis for six weeks.
The most remarkable finding on the website is the absence of any published results. The protocol was arranged by an organization named Seton Healthcare Family in Austin, Texas. I have attempted to contact this organization to find out whether the study was ever conducted and whether any results are available. To date, I have spoken with a sleep doctor in this organization who had no knowledge of the research, but he speculated there might be a neurology group involved in the work. He indicated if he found out some new information, he would contact me.
In the protocol, you will notice they mention open-label trial, which means there is no control group. In particular, there is no placebo used in this kind of study. Instead, all patients enrolled received the same protocol of 750 mg/daily of L-Tyrosine for one week followed by weekly increases to 1500 mg, then 2250 mg, and then 3000 mg. The last dosage of 3000 mg would be in use by the patients from the 4th through the 6th week, at which point the experiment would conclude.
The study was designed to assess RLS treatment without mention of PLMD. Nonetheless, those with RLS usually suffer from PLMD, and whatever works for RLS often works for PLMD as well. Many of the original drugs for these conditions are related to the pharmacology of the neurotransmitter dopamine, and the original agent (Sinemet) was a combination of two drugs called carbidopa/levodopa. For more than a decade, the drugs Mirapex (pramipexole) and Requip (ropinirole) have been mainstays in the fields of sleep, psychiatry, and even primary care for the treatment of RLS/PLMD.
With this backdrop, and as noted in the protocol, L-Tyrosine might be expected to work by enhancing availability of the precursors to dopamine and thus produce more dopamine. Not being a pharmacology expert, let me just say this explanation seems the most practical and coincides with the one offered in the protocol, but this theory does not preclude the possibility of other explanations for how Tyrosine might treatment leg movements or perhaps promote better sleep quality. In fact, if you explore the alternative medicine endorsements just using internet searches you will find a great deal of paradoxical information attesting that L-Tyrosine is beneficial for completely different purposes. For example, some use it for RLS/PLMD or for sleeping better, whereas others report using it in the daytime as a stimulant to decrease sleepiness and increase concentration. Others report L-Tyrosine has mood-altering properties such that it might decrease anxiety and depression. This bewildering array of effects might suggest it is a very powerful supplement, but it also might indicate contradictory evidence suggesting it doesn’t really work for anything.
Not knowing any way to judge the accuracy of these testimonials while holding a high level of suspicion for things that are advertised – but not thoroughly backed up by research, I elected to take the plunge and try L-Tyrosine for my objectively diagnosed, untreated independent leg jerks. Let me reiterate that my motivation for starting the supplement was generated by worsening of the quality of my sleep, which consistently led to degrees of daytime sleepiness and fatigue I had not experienced in years. Periodically, I have suffered minor bouts of sleepiness that often responded to changes in my masks or slight changes in my ASVAuto pressure settings. Or, in some cases, a cup of hot cocoa or green tea was sufficient to address the problem. But, the sleepiness I was now experiencing as much as two or three days in the week was sufficient to induce napping during the daytime. This degree of daytime hypersomnolence had been relatively rare for more than a decade.
The first night I selected the low dosage of L-Tyrosine 500 mg, and I can honestly report the very next morning I knew I had slept better with more dreaming that night and feeling more refreshed that morning. Given my scientific bent, I proceeded to alternate a few nights with 500 mg of L-Tyrosine and then a few nights without for about two weeks. At the end of this initial experiment, I was persuaded the benefits were positive and very noticeable. So, I went to every night use of 500 mg for the next two months, and among all the findings the most noticeable were two things. First and foremost, during the daytime, the sleepiness and napping behavior were virtually eliminated. However, the second and somewhat odd finding was the excruciating sense of deeper and more prolonged sleep inertia in the morning. There were episodes where I would awaken in the morning and would need to remain in bed for almost an hour, probably going in and out of various stages of sleep including REM as I recall dream activity. In this first phase of use, I noticed if I got out of bed ‘too early,’ I felt the need to walk more slowly, and if I had work at the computer, my typing speed was slower and clumsier. Still, the remainder of the day brought an overall level of productivity much higher in comparison to when I was suffering from the napping behavior and fighting drowsiness.
Early this year, having used the 500 mg dosage for about 2 months, I noticed a drop off in the effects and elected to increase the dosage to 1000 mg. I immediately noticed the same levels of improvement, that is decreased napping behavior and fighting off drowsiness, both of which lasted another two months, then I noticed another drop off. In March, the dosage was increased to 1500 mg and since then I have also used 2000 mg occasionally. However, recently, I was persuaded that the effects of the larger dosages were not necessarily any better than the 1000 mg, so for the past couple weeks I only use two 500 mg pills near bedtime.
Just like many of the prescription pills advertised for RLS/PLMD, there is no sedating effect of L-Tryosine at bedtime. Using the supplement at bedtime, 30 minutes before bedtime or even 2 hours before bedtime has had no impact on when I feel sleepy prior to lights out. And, since my RLS has remained under good control with iron supplements, my theory is that L-Tyrosine is treating my PLMD only. However, given the discussion of sleep inertia in the morning, I have experimented with taking the supplements more than 30 minutes before bedtime. I do think this timing issue has some impact on the duration and depth of the sleep inertia, but I have yet to sort out a perfect system to decrease these sensations. Then again, at this point, I am not overly concerned as it is clear some portion of this inertia represents actual sleep time, almost always with my ASVAuto PAP in place, so presumably high-quality sleep. On a few occasions without the PAP, my sense is this additional slumber remains at higher quality, probably due to the ‘momentum’ effect of having used PAP for several hours before this short non-PAP period.
Regarding some of our other like-minded individuals, you may know that many patients throughout virtually all healthcare systems show strong reluctance to the use of medications and instead frequently pursue alternative medicine pathways. I was intricately involved in several alternative medicine methods and institutions for almost a decade before entering medical school, so I am very aware of how so many people look for non-allopathic or natural remedies. At our center, we see many such folks who absolutely refuse to consider prescription pharmaceuticals. I believe that some of this reluctance comes from a proportion of RLS/PLMD patients who do not believe their legs are moving during the night. In some ways, this perspective is similar to people who do not believe they suffer from any breathing events at night and therefore question the need to attempt PAP therapy. Leg jerks of course are more difficult to define as an independent disorder until breathing has been normalized with PAP therapy or some other modality. So, in the clinical setting we might be at a disadvantage with some patients who were previously reluctant to use PAP, yet now must consider adding a medication to treat their leg jerks to optimize results. In most of these cases, patients are not gaining a superlative response to PAP, largely due to the untreated PLMD. Some will have tried prescription medications and suffered numerous side-effects. Others completely reject the notion of using prescription drugs.
Some anecdotal evidence has emerged from these types of patients. Among such individuals whom informed about L-Tyrosine use, we are aware of roughly 10 patients who attempted or are attempting regular use of the supplement. For a couple patients, there was no benefit, but the remainder reported similar improvements as described myself. A common report is “I am definitely sleeping deeper.” As we retain a certain cautionary approach to this atypical recommendation for these patients, we present them with the following information inserted into their most recent sleep study reports and discuss the ideas before they make their decision to start the supplement:
Regarding leg jerks, because the patient has tried other prescription medications and may no longer be interested in pursuing such treatments, the patient may wish to consider L-Tyrosine supplements, starting at 500 mg at bedtime and increasing over several weeks to the 1000 to 1500 mg range. There is no authoritative research on the use of this supplement, but there are several references to it in the alternative medicine community, and we know of a few patients who are reporting benefits from its use. Unfortunately, information on any side-effects related to L-Tyrosine are not well established, so any patients using the supplement must use their own judgment in initiating this medication and is advised to monitor for any other changes in mental or physical health. Two side-effects that may be relevant include: (1) patients with thyroid disease may need to check their thyroid function tests when using Tyrosine; and (2) some people report increased sleep inertia when awakening in the morning. Speculatively, as Tyrosine is a precursor to dopamine, the question might arise whether this amino acid supplement would produce side-effects similar to Mirapex or Requip, both dopamine agonists, including unexpected compulsive behaviors, potentially related to shopping, gambling and sexual activity. If the supplement is effective in decreasing RLS/PLMD symptoms, we anticipate the patient would note a deeper and more consolidated sleep when used in combination with PAP therapy.
Of course, the fact that L-Tyrosine is a supplement means the chances of finding high quality research that designates the frequency of side-effects would be very low. There is also the question of tolerance or eventual diminishing returns from the supplement just like any other drug. Again, it may be difficult to find research on these topics.
In summing up, we certainly can’t declare that L-Tyrosine is safe or that it provides benefits, but it appears at this point to be a supplement that might indeed provide benefits and potentially may have an excellent safety profile. When would we find out the definitive answers to these questions? Arguably ‘never’ might be the right answer because who would choose to fund this research? I already approached one of the leading manufactures of OTC vitamins, minerals and supplements, and they politely declined, indicating they would not fund a 3rd-party researcher. From a business perspective, however, we can see their rationale, because anyone who conducts the research and proves L-Tyrosine works well in RLS/PLMD has just opened a new revenue stream for every other company that makes the supplement. A quick internet glance suggests no less than 10 major manufacturers are making L-Tyrosine currently.
Therefore, the only alternative in an alternative medicine perspective is the trial and error approach, otherwise known as the “N of 1” experiment in which you experiment on yourself. That’s the approach I have taken for myself and going forward there are two more steps I am hoping to pursue later this year. First, I want to go back into the sleep lab after maintaining a stable dose of L-Tyrosine for a several months to determine whether there is a decrease in the frequency of independent leg jerks. Second, I want to taper off or discontinue L-Tyrosine and then try one of the dopaminergic medications such as Mirapex or Requip to see whether or not the response is identical to what I have achieved with the supplement. These steps would provide me with a lot more confidence in trying to understand how L-Tyrosine might be working and whether or not it is truly working.
In the meantime, caveat emptor remains in play, but so many people refuse to attempt prescription medications for RLS/PLMD, perhaps L-Tyrosine would be something a person would try on a temporary basis to determine if relief would be forthcoming. If so, the patient would then be convinced that the leg jerks clearly need to be treated, and from that point going forward the patient will at minimum recognize that RLS/PLMD is something they need to get a leg up on in their treatment of all their sleep disorders.