Summarizing the final points from the last post, a term like COMISA is sufficient when talking about the larger picture in a public health discussion, but clinically we need terms to educate both physicians and patients. The term “comorbid insomnia” will be in use for a long time, because so many healthcare providers will continue to believe the main or obvious co-occurring condition is the dynamic partner in the co-morbidity. For sleep physicians, I would speculate the term “complex insomnia” will carry a certain cachet, because it was derived specifically from the construct of chronic insomnia patients who possessed no awareness of a breathing connection to their bouts of sleeplessness. In our long-term clinical research experience, these patients are astonished to learn a sleep breathing condition is a primary component of their problem, and our impression has been that millions of insomniacs suffer both disorders. For these reasons, I believe the complex insomnia term could engage patients and physicians to more readily accept the multi-factorial nature of their insomnia disorder, which in turn could increase motivation to address all facets.
Since 1995 to the present, we have come to recognize at least three categories of complex insomnia, and the remainder of this post addresses the clinical features and treatment nuances observed in these distinctive presentations.
The first type of complex insomnia (CI-Type A) reflects the original research we published in 2001, that is, patients with moderate to severe chronic insomnia do not believe a relationship exists between their psychologically-driven sleeplessness problem and sleep-disordered breathing.
The second type of complex insomnia (CI-Type B) involves patients who have awareness of sleep breathing symptoms yet still do not connect the two problems. The breathing symptoms reside in a different world of physical symptoms, and there is no reason to imagine they could affect the psychology of insomnia, a condition best described as a mental symptom.
The third and final type (CI-Type C) are those who report sleep breathing symptoms and either wonder or already believe a connection exists between the two conditions.
A fourth type that we do not designate in the complex insomnia framework are those OSA/UARS patients who also report insomnia symptoms, but they are already focused on their sleep breathing symptoms as the primary source of their sleep problems. Some of these individuals clearly perceive that the sleep-disordered breathing is causing or aggravating their insomnia. Others do not necessarily connect the dots, but they view the insomnia issue as relatively minor, not something to worry about or address, especially compared to their worries and desire to address OSA/UARS. These types of patients might be designated COMISA under the big umbrella, but they do not fit in the category of comorbid insomnia.
CI-Type A is the most problematic of three types of complex insomnia for both patients and physicians because neither person intuitively imagines this potential for a dual diagnosis. In contrast, our clinical and research teams are now so keen in evaluating these patients that for better or worse we share a “guilty until proven otherwise” mentality when they present to the sleep center complaining of chronic insomnia. For a typical board-certified pulmonary sleep doctor or for a primary care physician, our zeal would be viewed as heresy or fanaticism, maybe both, based on their beliefs that this high prevalence is improbable. Even though many sleep doctors have encountered these types of patients, it is equally true many sleep specialists do not possess a high index of suspicion for the OSA/UARS component in most insomnia patients. We know the latter point is clinically relevant, because we routinely meet chronic insomnia patients who at their first encounters at another sleep facility were informed a diagnostic sleep test would be a waste of time. Another subset among these Type A patients was tested with diagnostic PSG, but the results were reported as “no abnormalities” or “very mild and inconsequential sleep-disordered breathing.” Both kinds of patients, those tested and those not, upon entering into our system, are immediately recommended for overnight sleep testing, which with our aggressive scoring of flow limitation events (the discrete breathing event components of UARS) confirms the diagnosis of an underlying and comorbid case of OSA/UARS. Remarkably, some cases never tested demonstrated severe OSA with frequent oxygen desaturations. As you can imagine, such patients are perplexed if not dumbfounded by these objective results in comparison to their previous encounters.
Once diagnosed, the Type A complex insomnia patients tend to fall into their own two sub-divisions, succinctly described as those who embrace the results and those who reject the findings. In general, chronic insomniacs who are greatly surprised by the finding of a physiological component to the sleep fragmentation that underlies their insomnia more often than not are excited to hear this news, because it relieves a great deal of mental anguish about the nature of their unwanted and unpredictable sleeplessness. To hear that something physical is causing something mental is invariably a relief to any mental health patient, which by way of example explains why so many chronic depression patients at some point in their evaluations are tested for thyroid disease. While these receptive responders who embrace the full depth and breadth of the complex insomnia diagnosis are not jumping up and down begging for a PAP machine, the vast majority will attempt every conceivable conservative approach to care (e.g. nasal strips, nasal hygiene, nasal sprays, snore pillows, position therapy, weight loss), and a surprisingly high proportion of cases move forward rapidly with either a titration sleep study to initiate PAP therapy or seek consultation from a dentist for oral appliance therapy (OAT).
Adaptability to therapy, particularly regarding PAP or OAT, is the single greatest problem for these patients, because by definition their insomnia correlates with their higher than normal levels of sensitivity to external stimuli. When we think of insomniacs, it is easy to picture individuals who awaken from sleep to the slightest noise, so earplugs must be employed. Just so, these same individuals show more difficulty adapting to pressurized airflow and PAP masks.
Among the second subset, those who reject the OSA/UARS diagnosis or resist further consideration or treatment of the condition, it is not unusual to see a long gap where the patient is lost to follow-up for anywhere from one to five years. Based almost exclusively on the gradual deterioration of their sleep quality from untreated sleep-disordered breathing over this extended time period, the patient returns when a breaking point is reached. And, they almost always are willing to try PAP therapy.
From our experience, anyone expressing and demonstrating motivation to try out PAP has an excellent chance of learning to use it regularly. In our clinic, we routinely run numbers to evaluate 100 consecutive patients who fill a prescription to use PAP therapy, and the proportions always range between 86 to 92% of patients using the device at some level at follow-up several months later.
The Type B Complex Insomnia patients are naturally inclined to believe the theory connecting the two disorders if given the necessary education, and subsequently they are more likely to accept this diagnosis as something highly relevant to their care. Because they experience or suffer from the ill-effects of sleep breathing symptoms, it is not a great leap to explain how breathing events cause sleep fragmentation and thus fractured sleep cycles. Nonetheless, these patients do not start at the point of connecting the dots, so the Type B patients do manifest a spectrum of interest in how they rate the importance of the breathing disorder’s impact on their insomnia. Some patients have already heard of PAP therapy and want no part of it, no matter how effectively they are educated on the role PAP plays in reducing sleep fragmentation and thus insomnia awakenings at night. For these individuals, the best bet is to work on the conservative sleep-disordered breathing protocol of nasal strips, nasal hygiene, appropriate nasal sprays, positional therapy and possibly small and achievable efforts at weight loss.
In time, these individuals are likely to come around to the idea of more aggressive OSA/UARS treatment when confronted by at least three common and highly noticeable residual symptoms: nocturia, daytime fatigue or sleepiness, and aggravation of another medical condition such as hypertension, chronic pain, headaches, cardiac arrhythmias, or other heart conditions. In these scenarios, the patients may have used cognitive-behavioral therapy for insomnia, sleeping pills, or other advanced psychological therapies and attained substantive improvements in early, middle or late insomnia. Yet, if any of the listed medical conditions (or other conditions) persists in a patient who acknowledges no other explanation, then the pain, aggravation, concern, or suffering from the residual symptoms usually leads to a new motivation to problem-solve. At such a juncture, the patient shows an earnest desire to try PAP or OAT, and these patients return to the center, using the actual phrase, “I’m ready to treat my sleep apnea.”
The third group (Type C) already sees both the disorders as relevant and that both conditions need to be treated. Their main questions often revolve around whether one condition should be treated first, that is, a sequential approach, or whether both conditions should be treated simultaneously, that is, a concurrent approach. We typically favor concurrent therapy, and usually see faster and larger results by moving forward in this way.
There are a few notable exceptions. For example, we may encounter someone with very severe insomnia with all the facets of a strong psychological component including psychiatric disorders, excessive time monitoring behavior, very poor sleep hygiene and obvious psychophysiological conditioning, but this same individual has done their homework, read up on the role of OSA/UARS, and presents to the center with a narrowed vision to attack the sleep-disordered breathing exclusively. In these cases, the patient has been suffering a long time with inadequate treatments; the individual recalls no consistent or large improvements in insomnia while attempting psychotherapy, sleep hygiene instructions or even cognitive-behavioral therapy. From his or her perspective, it is time for something new, and the patient is eager to try PAP. Even though such individuals often benefit from the aforementioned psychological therapies and educational approaches, we have found it more reassuring to follow their lead and initiate PAP therapy as soon as feasible.
From the other side of the coin, there are a few patients who clearly understand the links between the two disorders, but they also express too much hesitancy and worry about PAP; they respond better by first learning both sleep hygiene instructions and cognitive-behavioral therapy, not to mention our more advanced approaches of cognitive-imagery techniques and sleep-related emotion focused therapy. Many of these therapies subsequently aid the patient in learning to use PAP therapy, while at the same time they are appreciating their active treatment of the insomnia problem.
The fourth category comprises those with obvious sleep breathing disorders and lesser insomnia symptoms. They clearly want sleep breathing treatments first and may never request any assistance on the problem of insomnia. The surprising aspect is how common this presentation manifests among treatment-seeking patients at sleep centers, but there is much less consistency in who wants or even needs treatment for both conditions. Thus, COMISA works as the umbrella term, but it does not key us in to the type of treatments to apply or how these patients might respond.