This past week, in one of our ongoing insomnia research projects, I encountered a patient who reported he was receiving enormous benefits from the use of a PAP therapy device. He has been on PAP for nearly two months and is delighted with the marked changes in his sleep fragmentation and as a result the near elimination of his insomnia. But, recently, he reported a small increase in daytime sleepiness. The fascinating thing about this complaint is he had reported minimal sleepiness when he entered the study. His main complaints were insomnia and daytime fatigue, but suddenly he was reporting sleepiness despite his overwhelmingly positive remarks about using PAP therapy.
What’s going on? Why would someone who reports no sleepiness, a cardinal symptom of OSA/UARS, suddenly develop sleepiness after treating the sleep breathing problems with PAP therapy?
We have seen this story play out many times in two decades of work with trauma survivors who suffer from posttraumatic stress symptoms or full-blown PTSD, a condition within the specific diagnostic class known as anxiety disorders. While most insomniacs do not suffer from PTSD, the vast majority of chronic insomnia patients suffer from anxiety. In the case of more severe insomnia or more severe PTSD, the anxiety may develop into a chronic state described as hypervigilance, which refers to the predisposition to be on high alert much more than considered normal.
If you were in a car accident, or suffered a sexual assault, or soldiered in a combat zone, the experiences of traumatic exposure make you highly vulnerable to a belief such events could recur. If the car crash occurred on the interstate, then the next time you found yourself driving on that interstate or possibly any interstate, your antennae will be raised to measure the risks or threats of another accident while you are driving. It is almost impossible in the early going after such traumatic events, not to see your level of alertness rise and remain elevated while driving at high speeds. One might argue these reactions are healthy and in fact may help you prevent a subsequent accident.
But what if a rape occurred in a woman’s own bedroom? Will the hypervigilance be a welcome addition to her night time ritual in preparing for sleep? Yes, if her home environment continues to be unsafe and persistent insecurity reigns. But if future threats have been diminished through appropriate safeguards (e.g. security system, new locks, better lighting), then we anticipate hypervigilance would subside. If not, this hyper alert state eventually leads to chronic insomnia. The increased level of alertness may prove initially helpful, as it could have encouraged even greater resource planning to adopt new strategies (e.g. watchdog, handgun, deadbolt locks); but, again with the new strategies in place, the goal would be to gain comfort and relaxation to enable falling asleep in the bedroom. All these steps may be for naught because when hypervigilance persists, insomnia persists.
A similar scenario occurs for the combat veteran even after leaving the war zone. Loud noises, car backfires, or other specific cues reminding the individual of the combat area may trigger hypervigilance despite a distance of 10,000 miles between “here” and the site of traumatic exposure. Again, if the hypervigilance is triggered too much during the daytime, chances are high it will persist into the night, resulting in chronic insomnia.
All these cases epitomize the related phenomenon of an anxiety process that obliterates one’s natural sleepiness. The sequence is straightforward: suffer a stressful life event, develop hypervigilance as a reactive safeguard that might prevent a repeat of a similar event, which ultimately leads to a state of chronic anxiety and eventually sleeplessness. Even on the smallest of scales, insomnia almost always starts with some type of stressful experience in virtually any one who has ever suffered insomnia.
Depending upon an individual’s unique personality traits and coping styles, the stressful episode could be remarkably benign in its degree of threat, but if the individual perceives things as more threatening, it could be enough to trigger the same cycle, leading to hypervigilance, anxiety, and insomnia. People who for example show a tendency to make a mountain out of a molehill will repeatedly encounter the problem of insomnia, because they have never learned how to adequately face and resolve their natural reaction to worry first and ask questions later.
To come full circle, then, it should be clear that if you suffer from anxiety or hypervigilance, you cannot easily experience “sleepiness on demand” when you hit the sack. Therefore, a major therapeutic approach to any patient with insomnia is to directly target the anxiety symptoms so that sleepiness can emerge. For this reason alone, sleeping pills or tranquilizers (anxiolytics) are very appealing therapies for insomnia, because they usually have a pharmacological structure that alleviates anxiety in addition to creating artificial sleepiness to foster sleep onset.
As you may know if you have read my book Sound Sleep, Sound Mind, I do not favor sedatives of any sort as a first-line treatment for chronic insomnia, because I believe the vast majority of insomnia patients can learn to recruit their natural sleepiness with a fairly short period of education and coaching. However, the issue of anxiety often remains among insomniacs even after they have learned to recruit sleepiness at bedtime or in the middle of the night after an awakening. This residual anxiety may cause other daytime symptoms even if the patient has learned to side-step it at bedtime or during the night. Treatment of anxiety may require medications, more psychotherapy, or advanced techniques such as emotion-focused therapy or other somatic-oriented therapies.
We have been monitoring this daytime anxiety component among insomnia patients who treat their sleep-disordered breathing, particularly those who use PAP therapy. Our impression and theory involves an attempt to understand the process of how sleeping better by eliminating the sleep fragmentation of sleep apnea would lead someone to experience less daytime anxiety. If in fact this point is valid, then the second half of our theory is to understand how the decrease in anxiety during the daytime creates a new opportunity for the emergence of daytime sleepiness. While this sleepiness was probably always present in the insomnia patient due to his or her underlying loss of actual sleep time, we suspect the decrease in anxiety, which was previously blocking the sleepiness, now unmasks these drowsy feelings.
In a nutshell, it is at least somewhat normal to experience mild daytime sleepiness; albeit it does not mean you necessarily need to nap or need to drink caffeinated beverages to function. There may be multiple factors and circumstances in any individual that contribute to sleepiness without designating this sleepiness as abnormal let alone a clinical problem. Yet, at intake or baseline, a hypervigilant patient often reports Epworth Sleepiness Scores of zero, which is arguably explained by anxiety levels masking any feelings of sleepiness.
When such patients use PAP therapy, there may be several steps or sequences of events in a process that leads to the unmasking of sleepiness. Clearly, the worst case scenario would be a PAP device working poorly or delivering ineffective pressures, so the individual ends up with worst sleep quality than before starting with PAP. This scenario, thank goodness, is quite rare. Even wrong pressures unless dramatically too low or too high provide some boost in sleep quality even if only mildly so and usually reduce sleepiness if modestly.
The more likely scenarios in accord with our theory relate to the potential effects of PAP therapy on anxiety. First, raising someone’s sleep quality is known to benefit one’s mood. Just by sleeping better, a person may feel better during the day, leading to some noticeable decreases in anxiety. This straightforward explanation is the most plausible one in that you can account for the changes by looking at measurable symptoms during the day while someone is awake. We suspect such individuals might show decreasing anxiety scores and concomitant increases in sleepiness scores as confirmation of the theory. As anxiety lessens, its masking effect lessens and daytime sleepiness emerges.
A more nuanced theory suggests sleep apnea itself is a direct cause of anxiety, because virtually anything that disrupts breathing (e.g. asthma, bronchitis, common cold, COPD) easily causes or aggravates anxiety symptoms. Think about what it feels like to not breathe well, and you know anxiety would enter the picture quite rapidly. Among PAP users, especially in the early adaptation periods, a fair proportion of patients notice problems with pressure levels, either too low or too high. Try to imagine what it would feel like to put a mask on your face to breath, but it does not feel like you are getting enough air into your lungs because the pressures are too low. Naturally, you would rapidly become quite anxious. And, conversely, if the pressures were too high such that you could not naturally maintain a proper breathing rhythm due to the adverse impact of the excess airflow, again anxiety would rapidly emerge. It is therefore a reasonable assumption to imagine that during the night when you suffer from OSA/UARS, you are also suffering pervasive and unrelenting breathing irregularities that could easily lead to the feeling of anxiety all night long. Thus, successful treatment with PAP therapy or another sleep breathing treatment, by logic, would eliminate the feelings associated with breathing irregularities when your breathing becomes more regular and normal.
Another prime example of this phenomenon would be those middle of the night awakenings accompanied by anxiety. Many awakenings at night are of no consequences when the individual rolls over and returns rapidly to sleep. But in these circumstances, we could almost guarantee that the individual did not really awaken fully to a level of high alertness. In other words, when they aroused, they remained very sleepy, which permitted the rapid return to sleep.
But what about the awakenings that seem to occur with rapid ascension to high alertness, a mini-hypervigilant state, if you will. In these instances, almost invariably caused by a breathing-related disruption of sleep, the sympathetic nervous was activated, leading to higher blood pressure and heart rate. Occurring in tandem with or because of these autonomic nervous system changes anxiety enters the picture; the individual may never fully understand how he or she suddenly awakened and felt wide awake, but it would not be uncommon for such a patient to report a feeling of discomfort or frank anxiety in trying to return to sleep with the PAP device, because at that moment in time and space there is insufficient comfort or relaxed feelings to settle into the flow of pressurized air.
Surprisingly, not much research has been conducted on the relationship between OSA and anxiety. Two of the most interesting works were authored by Dr. April Shapiro and are listed below. On the one hand, a review of research in this area showed apneic awakenings were associated with anxiety, similar to what we theorized above, but in contrast, the research also suggested that higher sleepiness scores were associated with higher anxiety scores, the opposite of what we described above. Regardless, a lot more investigations are necessary to tease apart these relationships.
Shapiro AL, Culp S, Azulay Chertok IR. OSA symptoms associated with and predictive of anxiety in middle-aged men: secondary analysis of NHANES data. Arch Psychiatr Nurs. 2014 Jun;28(3):200-5. doi: 10.1016/j.apnu.2014.02.002. Epub 2014 Feb 27.
Shapiro AL. Anxiety in middle-aged men with obstructive sleep apnea: state of the science. J Am Assoc Nurse Pract. 2014 Dec;26(12):689-95. doi: 10.1002/2327-6924.12118. Epub 2014 Mar 31.