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In the prior post on the Respiratory Threat Matrix Model, we delved into many facets of this theory, which you can read about here. In this post, we will focus on a few key points about this theory especially is it relates to the concept of threat.

Not being able to breath or suffering through a temporary episode of struggling to breathe is a mind-boggling event like very few other experiences in one’s life. Instantaneously, the potential for the loss of your life can overwhelm your consciousness inducing a state of panic and abject fear. There is no way to overestimate how emotionally painful and physically frightening you would feel in the instant you might believe you cannot re-establish your breathing. As described in the earlier posts on racing thoughts and ruminations, these events are arguably the most terrifying experiences you might suffer, because you actually feel or believe you are about to die.

Most people probably know what these episodes feel like, because most people experience rare episodes of choking on something while eating, or swallowing too much water while swimming, or getting the wind knocked out playing sports. Another common one is roughhousing as kids and ending up on the bottom of the pile. Any of these episodes and more could lead to the sensation of being unable to breathe properly. Therefore, virtually everyone knows how horrific the sensation feels while awake.

In sleep-disordered breathing, you could argue we have the advantage of being asleep at the time, so perhaps the traumatizing nature of the experience is much less severe. That theory is a reasonable one, but I wonder if an opposing point of view is more valid. That is, because you are asleep and do not gain much awareness or memory of these events (except for the occasional waking with the feeling of choking, gasping, or frank apneas), perhaps you are in such a highly vulnerable state on an unconscious level that the experience may prove more traumatizing to you than if you were awake. While awake the semblance of control is real; while asleep you would feel no sense of control.

In my opinion, one of the reasons OSA/UARS patients awaken most mornings feeling awful may not simply be due to the chronic sleep fragmentation and subsequent nonrestorative sleep caused by sleep breathing events. In addition, the individual suffering through hundreds of these events each night is literally, not figuratively, being assaulted minute after minute with episodes of apneas, mini-suffocations, or other feelings of constrained breathing. In other words, the main issue regarding threat is not just a diminution of the volume of each breath. It is the all-out assault on your respiratory system’s primary function to breathe in and breathe out. The sleeper arising in the morning has been attacked nonstop in most cases throughout the night, during which he or she was defenseless against the assaults.

Imagine suffering the same experiences of sleep-disordered breathing events but now in the hypothetical circumstances of being awake. In fact, individuals with severe lung diseases such as asthma or emphysema periodically encounter circumstances in which they cannot draw in a full breath; and, in extreme cases, these patients must be hospitalized and sometimes intubated with mechanical ventilation because the respiratory system has become severely compromised. Yet, even these diseases might pale in comparison to the theoretical scenario of your actually suffering sleep breathing events while awake. In such a circumstance, you would be constantly fighting through airway collapse, at whatever severity level, every single minute of your waking experience, hour after hour. It would prove impossible to function, let alone accomplish anything of value or meaning in your daily existence. Your entire life would be consumed with efforts to breathe, just as if you were walking around all day long with a wet washcloth draped over your nose and mouth through which it would be impossible to inhale or exhale a full breath.

It is useful to consider sleep breathing events in this light, because you will more accurately comprehend how problematic these sleep breathing episodes must be for any OSA/UARS patient in general as well as for those individuals who are the topic of this discussion, namely, insomniacs. Indeed, this theoretical concept may also help other people understand the disease from which their friends and family members suffer. Just consider the look on someone else’s face when you would say: “Each night when I sleep, my breathing is so disrupted from these attacks that were you to see me suffering in this same way while awake, you would presume I were some sort of respiratory cripple.”

Ironically, however, the human body adapts in ways that typically do not manifest outwardly regarding this respiratory compromise unless one suffers the most severe forms of OSA, where the bed partner watches first-hand these frequent ghastly episodes of choking or stoppage of breath. It is unclear whether or not this adaptation is related to the fact that a human suffers these events during the “luxury” of sleeping, that is lying down, and not while trying to function. However, internally, the individual suffers in this horrific way to some degree in virtually all cases of sleep-disordered breathing, because disturbed and restricted breathing is too threatening of an experience not to induce some reaction to attempt to overcome the problem. And, the feeling of distress is a highly effective and common way to achieve vigilance; and, in the case of more prolonged or intense breathing events, this severity of distress may be a factor in why or how one awakens from any particular episode.

All these points persuade me the actual intensity and frequency of breathing attacks occurring during sleeping hours must play a critical if not primary role in the development of the insomnia condition, the most obvious manifestation of which would be the racing thoughts and ruminations that emerge within the individual in the attempt to prevent sleep from happening. If sleep is prevented, then sleep breathing events are prevented.

Furthermore, I cannot help but wonder whether the problem goes deeper. What happens to a person’s psyche when he or she is constantly attacked in this life-threatening physical way during sleep by an unknown assailant? What perspective on life does the insomniac bring into waking hours after so many hours of these assaults? How likely is the night time threat going to carry over into the person’s waking hours as a sense of doom and gloom as he or she would always know on a subconscious level that in so many hours hence, the attacks will begin again without respite and without any predictive knowledge of the severity of the assaults? This latter point is one I have used to explain to night owls how their subconscious thoughts and feelings may promote later and later bedtimes. Why not delay your entry into the bedroom and into bed if only terror awaits you?

These questions are not merely speculative. I believe these theories raise relevant clinical questions germane to most insomniacs. Again, as in the starting point of this discussion on racing thoughts, I remain persuaded this inability to turn off one’s mind is frequently related to the threat of the unsuspected breathing events. But, in digging deeper, we need to ask whether or not sleep-disordered breathing by its mechanisms plays a substantial role in the development of anxiety in a large proportion of insomniacs. The clinical relevance of this theory is enormous, because for at least 100 years if not longer the theory would be the reverse: anxiety symptoms arise due to mental issues and over time anxious patients show irregularities in their waking breathing patterns. Here, we hypothesize the reverse, wherein irregular sleep breathing patterns habituate individuals to unknowingly lose confidence in their respiratory system. Over time, acutely and chronically, the unpleasant and disturbing feelings associated with this pathophysiological breathing pattern leads to anxiety, not the other way around.

If this theory is accurate, it will cause a radical paradigm shift in how mental health patients are treated in general and insomnia patients in particular. The conventional model of therapy for many of these conditions revolves around “abnormal brain chemistry.” Drugs then must be the answer. And, with the bombardment of advertisements in all sorts of media on the psychotropic/sedative medication approach, this conventional wisdom leads a huge proportion of patients to believe drugs must either be the best option or perhaps the only option. And it follows that among patients currently on medications yet reporting sub-optimal responses, often their most immediate question arising out of their continued misery is: “well, what drug do I try next?” not “what other treatment options should I consider?”

To learn more, insomniacs and mental health patients must receive more frequent evaluations for OSA/UARS and subsequently more evidence-based therapies such as PAP, OAT or site-specific ENT surgeries. When large cohorts of these patients are routinely treated in primary care clinics or mental health facilities as if sleep-disordered breathing were of the utmost importance, then and only then will we discover the true impact of these breathing events on the individual’s sleep, mood, and personality. Regrettably, with the current and ongoing disruptions to the healthcare systems and the expanding denigration of the field of sleep medicine, particularly sleep centers and labs, we are many years away from gathering this essential data.

However, regardless of the absence of treatment data in large sample, we are beginning to see some interesting information emerge about the treatment of insomnia in patients with untreated OSA/UARS. Thought it might seem surprising, given the so-called potency of this respiratory threat, it is of considerable clinical interest that cognitive-behavioral therapy for insomnia (CBT-I) still may prove effective in treating insomnia even when the patient suffers from co-occurring sleep-disordered breathing. Unfortunately, the small number of studies covering this topic has shown mixed results, so the jury may be out, but anecdotally many insomnia treatment experts report they have treated numerous patients with co-morbid OSA/UARS, wittingly or unwittingly, and have observed marked decreases in insomnia severity. This perspective is very good news in light of how many insomnia patients will go undiagnosed in the years ahead with their unsuspected OSA/UARS.

Nevertheless, this research area is ripe for vigorous attention, because we now recognize that a huge proportion of these patients are presenting to sleep centers; and, they are presenting with both complaints regardless of whether they emphasize the sleeplessness or the sleep breathing symptoms. Several recent research studies and review articles (1-13) are examining this comorbidity, and eventually clarity should be forthcoming on how the threat of sleep breathing events impacts the insomnia condition in the conventional circumstances in which only non-breathing interventions treat the sleeplessness, such as sedatives or CBT-I. Would the untreated sleep breathing events still impact the quality of sleep, prolonged awakenings or daytime fatigue and sleepiness? Or, would enhanced sleep consolidation that often follows the use of stimulus control and sleep restriction therapy (standard CBT-I tools) lead to deeper sleep, fewer awakenings and improvement in daytime energy levels? Furthermore, would this improved sleep consolidation create more stable sleep architecture, which in turn might diminish sleep breathing events? We published a few papers more than a decade ago raising some of these questions (14-16).

Other symptoms as research variables will also prove informative in how these patients respond to either single or combined treatment programs. Looking at the residual OSA/UARS symptoms in patients receiving only CBT-I or sedatives, we will learn a great deal from patients’ changes or lack thereof for nocturia, morning headaches, fatigue, and hypertension. All four conditions, with the possible exception of fatigue, have fairly clear-cut mechanisms to explain the symptoms. Nocturia is caused by the SDB-induced expansion of blood flow into the right atrium and subsequent release of the body’s natural diuretic, atrial natriuretic peptide. Morning headache is thought to arise when excess CO2 in the blood from untreated OSA causes a dilation of blood flow in the cerebral arteries. Hypertension seems to result from damaged to the inner lining of blood vessels, rapidly fluctuating levels of oxygenation, and the elimination of the normal “dipping” or lowering of the blood pressure during the sleep period. If patients were only treated with CBT-I, we might expect some of these physiological symptoms to persist because the sleep breathing events were not eliminated?

Last, fatigue is a more mysterious symptom, one that circles us back to the whole discussion of threat, because threat in general is a very draining experience for anyone to suffer through. As mentioned above, vigilance or hypervigilance is a natural result of suffering too many threats, real or imagined. If a person experienced the respiratory threat while asleep, there is no obvious way to measure its impact or to even gauge how it might have affected daytime energy levels. Of course, it would not be surprising to observe that nonrestorative sleep was the major cause of fatigue in patients who otherwise do not seem to develop sleepiness. And, there are many such OSA/UARS patients who present without sleepiness and only with fatigue. On the other hand, we have always surmised that the combination of anxiety plus sleepiness leads to the feeling of fatigue by somehow obliterating the sensation of sleepiness. If so, then parsimoniously, the respiratory threat matrix model may help us understand more than just the racing thoughts of insomniacs; it may shed light on why so many insomniacs are more likely to report the symptom of fatigue.

 

References

  1. Lack L, Sweetman A. Diagnosis and Treatment of Insomnia Comorbid with Obstructive Sleep Apnea. Sleep Med Clin. 2016 Sep;11(3):379-88. doi: 10.1016/j.jsmc.2016.05.006. Epub 2016 Jul 21.
  2. Sweetman AM, Lack LC, Catcheside PG, Antic NA, Chai-Coetzer CL, Smith SS, Douglas JA, McEvoy RD. Developing a successful treatment for co-morbid insomnia and sleep apnoea. Sleep Med Rev. 2016 May 6. pii: S1087-0792(16)30010-7. doi: 10.1016/j.smrv.2016.04.004. [Epub ahead of print] Review.
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