How does OSA cause PTSD?

I was reading your article in the Sleep Review on the connection between obstructive sleep apnea (OSA) and PTSD. How does OSA cause PTSD? 

A theory that OSA causes posttraumatic stress disorder (PTSD) would fit with a scenario in which an individual with poorly treated or undiagnosed OSA suffered from excessive sleepiness that caused a car accident. As motor vehicle crashes are a leading cause of PTSD, this scenario assigns OSA the status of a contributing factor to the development of posttraumatic stress symptoms and ultimately PTSD. Notwithstanding, it is prudent to note many children, adolescents, and adults experience traumatic incidents or other stressful life events that may or may not result in chronic PTSD. While an acute stress response is quite common following such events, the overwhelming majority of individuals exposed to trauma do not develop PTSD.

Another way in which OSA could influence PTSD development would be through a sleep fragmentation model. If someone experiences a traumatic event, but he or she already suffered from undiagnosed and untreated sleep-disordered breathing, it is conceivable their lack of high quality slumber adversely influences the recovery process following the incident. If a person were sleepy, tired, or exhausted from poor sleep, how well would he or she muster the resources needed to effectively go through the post-trauma healing process in mind and body? To be able to heal from a traumatic event, the individual usually needs to remember what occurred, transition through some intense emotional responses about what occurred, and then come out the other end not only feeling whole again but also gaining a sense of growth or an insight of self-discovery from this tumultuous process.

What is so very interesting about this 3-step process that engages and challenges one’s memory, emotional coping skills, and capacity for self-discovery is that a long train of research has suggested REM sleep appears to incubate a similar process while asleep. As such, researchers are actively examining whether or not specific objective markers in REM sleep are associated with risks for PTSD. Two researchers, Thomas Mellman and Wilfred Pigeon, conducted a few studies showing that highly fragmented REM sleep in the early post-trauma period appears strongly associated with greater risk for PTSD compared to someone who went through the same type of trauma, but whose REM sleep remained well-consolidated.(1;2)

In these studies on car accident survivors, the research showed that patients with shorter duration of discrete REM sleep periods were more likely to develop PTSD one to two months after the accident compared to those patients who had longer or normal periods of REM duration. They were even able to demonstrate that PTSD symptom severity inversely correlated with the duration of these REM sleep periods, which is a truly remarkable finding because it associates an objective marker on a sleep study with the patient’s subjective report of PTSD symptoms.(2) On a similar note, Insana et al showed a lifetime diagnosis of PTSD correlated with some degree of REM sleep fragmentation.(3) In other words, this research points to a specific objective finding—fractured REM sleep or shorter segments of REM were associated with the diagnosis of PTSD.

At our center, we have speculated that one major cause of this REM fragmentation is OSA, a disease process known not only to fracture or inhibit REM sleep in many patients, but also most patients show their very worst or most severe breathing events and oxygen desaturations in REM sleep. Many in sleep medicine have wondered whether the level of breathing severity in REM might lead the human organism to trigger an exit from REM sleep to prevent this worsening of the disease during any night of sleep. As you may recall, when a successful titration is conducted in the sleep lab on the first night of PAP use, it is common for REM to come roaring back in action.

Taken together, we could now speculate on another pathway through which OSA could influence the development of PTSD through these effects on REM. If REM is fractured or diminished by OSA, then the REM processing capacity described above is no longer available to this type of patient after the traumatic event. Thus, all those effects that naturally occur in REM including memory entrainment, emotional processing, and learning may no longer unfold in a normal way. Investigators from the field of dream research have designated this REM function as the “therapist-in-residence” while you sleep without which greater risks for PTSD may arise. If this theory is proven correct, the fracturing impact of OSA on REM may prove critical to how a patient’s recovery from PTSD may be thwarted by undiagnosed sleep breathing disorders. Or, the reverse may be true, that is, treatment of PTSD with PAP therapy in patients with comorbid sleep-disorder breathing might improve or otherwise expedite PTSD treatment, a finding recently demonstrated by Gold et al’s study in which PTSD patients received both evidence-based psychological therapies and PAP therapy.(4)

From a mental health perspective, it is surprising how sparsely the psychological literature reports on definitive risk factors about who will develop chronic PTSD following traumatic exposure. It seems virtually any one might have a potential to develop PTSD after a traumatic event, but predicting PTSD status soon after the trauma has proven quite difficult. It is of further interest to the sleep field that specific sleep factors may provide a critical window into our understanding of this problem. Years ago, it was noted that individuals who developed nightmare problems after a trauma were at higher risk for PTSD, and if the nightmares lasted as little as one month or up to three months, chances for PTSD were much higher than if the nightmares abated within the first few weeks. Many additional sleep factors may prove important in this context.

Recently, I completed a talk in Berkeley for the International Association for the Study of Dreams (available as an audio file later this summer on their website entitled, “Nightmare Triad Syndrome.” In this talk, I delve into some history about our investigations on the treatment of nightmares that led us to the odd finding that most chronic nightmare patients seeking treatment frequently suffer co-morbid insomnia and sleep apnea or upper airway resistance syndrome. And, I mention the work of one researcher who has shown a reduction in nightmares in OSA patients following the use of CPAP,(5) a finding we often see at our sleep center as well. If this pans out, then perhaps OSA will prove to be an even greater causal factor in PTSD and nightmares, thus creating a pivotal role for PAP therapy in the treatment of some PTSD patients.


1. Mellman TA, Bustamante V, Fins AI, Pigeon WR, Nolan B. REM sleep and the early development of posttraumatic stress disorder. Am J Psychiatry 2002;159(10):1696-1701.
2. Mellman TA, Pigeon WR, Nowell PD, Nolan B. Relationships between REM sleep findings and PTSD symptoms during the early aftermath of trauma. J Trauma Stress 2007;20(5):893-901.
3. Insana SP, Kolko DJ, Germain A. Early-life trauma is associated with rapid eye movement sleep fragmentation among military veterans. Biol Psychol 2012;89(3):570-579.
4. Amin, M., Thomesen, C, Gold, M. S., Parisi, J., and Gold, A. R. The effect of nasal continuous positive airway pressure on Veterans' posttraumatic stress disorder symptoms: a randomized, pilot study. Annual SLEEP Meeting. June, 2014. Conference proceeding.
5. BaHammam AS, Al-Shimemeri SA, Salama RI, Sharif MM. Clinical and polysomnographic characteristics and response to continuous positive airway pressure therapy in obstructive sleep apnea patients with nightmares. Sleep Med 2013;14(2):149-154.

Barry Krakow MD


Dr Krakow’s 27 years of sleep research have focused on the complex relationship between physiological and psychological sleep disorders. Dr Krakow currently operates private sleep medical center, Maimonides Sleep Arts & Sciences, Ltd., and serves as Classic SleepCare’s paid Medical Director.

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