Dr. Todd Finnerty enjoys working on claims looking at whether your sleep apnea is secondary to your PTSD. Dr. Finnerty has a special interest in sleep. In addition to being a psychologist with expertise in PTSD, Dr. Finnerty is also a member of the American Academy of Sleep Medicine and the Society of Behavioral Sleep Medicine. On a personal note, Dr. Finnerty also has sleep apnea and knows firsthand the difficulties with adjusting to wearing a mask with PAP therapy (ex: CPAP, APAP, BiPAP, etc.).
Dr. Finnerty typically can write nexus letters for sleep apnea secondary to PTSD based on a records review only (with no exam needed); it doesn’t matter where you are physically located. Dr. Finnerty will review your records and address any relevant medical evidence and personal statements related to this. He will cite relevant scientific research and relate it to your medical evidence. He will also cite relevant past VBA decisions which relied upon this scientific research.
Oftentimes denials of sleep apnea secondary to PTSD claims are more based on a scientific debate rather than a Veteran’s own medical evidence. The Veteran’s burden of proof in a VA disability claim is not 100% scientific certainty (not that such a thing even exists). The VA has already found sleep apnea to be secondary to PTSD for countless Veterans and it is arbitrary and capricious for the VA to say that the science says one thing for one Veteran but something else for a different Veteran.
Have you been denied sleep apnea secondary to PTSD before or are you looking to connect sleep apnea and PTSD now? Reach out to Dr. Finnerty and Get a Free Consultation
Research related to sleep apnea secondary to PTSD
Curious about some of the research articles I tend to cite for sleep apnea secondary to PTSD? There are lots of studies out there. I’ve summarized just a small selection of them below:
The incidence of insomnia and obstructive sleep apnea (OSA) in service members is increasing. “Between 2005 and 2019, incidence rates of OSA and insomnia increased from 11 to 333 and 6 to 272 (per 10,000), respectively.” The incidence rates have “markedly increased” since 2005 [see Moore, et. al. (2021), Incidence of Insomnia and Obstructive Sleep Apnea in Active Duty United States Military Service Members. Sleep, doi: 10.1093/sleep/zsab024]. However, the evidence for service connection is not based on incidence rates alone. Significant associated factors that reflect both a causal relationship and substantial aggravation have been identified in the research literature. There is scientific evidence supporting a link between psychiatric disorders (ex: PTSD) and sleep apnea. The research literature establishes that PTSD is commonly associated with sleep apnea and that there is an arousal-based mechanism initiated by PTSD that promotes the development of sleep apnea in trauma survivors. Sharafkhaneh, et. Al. (2005), in the article Association of Psychiatric Disorders and Sleep Apnea in a Large Cohort (SLEEP, Vol. 28, No. 11, 2005) found that sleep apnea is associated with a higher prevalence of psychiatric comorbid conditions in Veterans Health Administration beneficiaries, including PTSD. Compared with patients not diagnosed with sleep apnea, a significantly greater prevalence (P < .0001) was found for posttraumatic stress disorder in patients with sleep apnea. The research supports the presence of a significant connection between PTSD and sleep apnea, including an arousal-based mechanism initiated by PTSD that promotes the development of sleep apnea in trauma survivors: This is supported by the article Krakow, B., Melendrez, D., Warner, T.D. et al. To Breathe, Perchance to Sleep: Sleep-Disordered Breathing and Chronic Insomnia Among Trauma Survivors. Sleep Breath 6, 189–202 (2002): Emerging evidence invites a broader comorbidity perspective, based on recent findings that post-traumatic sleep disturbance frequently manifests with the combination of insomnia and a higher-than-expected prevalence of sleep-disordered breathing (SDB). In this model of complex sleep disturbance, the underlying sleep pathophysiology interacts with PTSD and related psychiatric distress; and this relationship appears very important as demonstrated by improvement in insomnia, nightmares, and post-traumatic stress with successful SDB treatment, independent of psychiatric interventions. Continuous positive airway pressure treatment in PTSD patients with SDB reduced electroencephalographic arousals and sleep fragmentation, which are usually attributed to central nervous system or psychophysiological processes. Related findings and clinical experience suggest that other types of chronic insomnia may also be related to SDB. We hypothesize that an arousal-based mechanism, perhaps initiated by post-traumatic stress and/or chronic insomnia, may promote the development of SDB in a trauma survivor and perhaps other patients with chronic insomnia. We discuss potential neurohormonal pathways and neuroanatomatical sites that may be involved in this proposed interaction between insomnia and SDB. These neurobiological processes are further reviewed by Kelly, et. al. (2016) in the article Understanding Recent Insights in Sleep and Posttraumatic Stress Disorder from a Research Domain Criteria (RDoC) Framework (Curr Sleep Medicine Rep, 2016, 2:223–232). They note that PTSD is associated with sleep disturbances, including insomnia, nightmares, REM abnormalities and “sleep-disordered breathing” such as in sleep apnea. They note that “recent studies have expanded our knowledge of the neurobiology of trauma and sleep. In addition, intervention research has provided valuable information about how sleep treatments affect PTSD symptoms and how PTSD treatments affect sleep symptoms.” Chronic activation of stress hormones (hypothalamo-pituitary adrenal axis activity) caused by PTSD is known to lead to a neural sensitization leading to upper airway dysfunction such as sleep apnea. [see van Liempt, et. al. (2013) Sympathetic activity and hypothalamo-pituitary-adrenal axis activity during sleep in post-traumatic stress disorder: A study assessing polysomnography with simultaneous blood sampling. Psychoneuroendocrinology, 38(1), 155-165; and Kritikou, et. al. (2016) Sleep apnoea and the hypothalamic-pituitary-adrenal axis in men and women: effects of continuous positive airway pressure. European Respiratory Journal, 47(2):531-540.] Colvonen, et. al. (2015) [see Obstructive Sleep Apnea and Posttraumatic Stress Disorder among OEF/OIF/OND Veterans; Journal of Clinical Sleep Medicine 11(5):513-518] found that “PTSD symptom severity increased the risk of screening positive for OSA.” The authors concluded that “veterans with PTSD screen as high risk for OSA at much higher rates…” Zhang, et. al. (2017) [see Prevalence of obstructive sleep apnea in patients with posttraumatic stress disorder and its impact on adherence to continuous positive airway pressure therapy: a meta analysis; Sleep Medicine, 36:125-132] performed a metal-analysis and concluded the OSA is commonly seen in patients with PTSD. They noted that “patients with PTSD and OSA demonstrated significantly lower adherence to CPAP therapy.” There is ample evidence that treating OSA improves PTSD symptoms. In Orr, et. al. (2017) Treatment of OSA with CPAP is Associated with Improvement in PTSD Symptoms Among Veterans; J Clin Sleep Med, 13(1):57-63, the authors describe “a growing body of research has suggested a link between obstructive sleep apnea and PTSD” and “prevalence estimations for OSA in PTSD patients range from 52% to 69%, with some as high as 95%.” They note “treatment of OSA with PAP therapy is associated with improvement in PTSD symptoms.” They note one factor is that “treatment of OSA with CPAP appears to reduce the frequency of nightmares in PTSD patients.” The authors concluded that sleep apnea treatment “should be considered an important component of PTSD treatment for those with concurrent OSA.” Psychiatric concerns in general have been noted to be associated with sleep apnea. Rezaeitalab, et. al. (2014) [see The correlation of anxiety and depression with obstructive sleep apnea syndrome, Journal of Research in Medical Sciences, Mar; 19(3): 205–210] studied individuals with obstructive sleep apnea. They found that “53.9% of the individuals had some degree of anxiety, while 46.1% demonstrated depressive symptoms. In terms of OSAS severity, this study showed that OSAS severity was associated with the frequency of anxiety, choking, and sleepiness (P : 0.001). According to polysomnographic results, we found that the majority of patients suffering from anxiety and choking (66.7% and 71.4%, respectively) had severe OSAS.” Jehan, et. al. (2017) [see Depression, Obstructive Sleep Apnea and Psychosocial Health, Sleep Med Disord, 1(3): 12] note that “there is a co-linear relationship between” obstructive sleep apnea and depression.” Patients with OSA have impaired health and their psychosocial health and daily performance also decrease. They note “because disturbed sleep can cause poor concentration, mood problems, anxiety, and MDD, these factors are also the part of poor daytime performance.” Some postulate that weight gain may be a primary cause of sleep apnea, however it is interesting to note that treating sleep apnea with CPAP often actually leads to more weight gain, not less weight gain [see de Milo and Genta (2016), Continuous Positive Airway Pressure and Weight Gain: Do We Know the Mechanisms? American Journal of Respiratory and Critical Care, 194(7): 915].
A classic but outdated view of OSA is that it is only structural, caused by obstruction of the upper airways and is predominantly found in overweight individuals. However, it would be an error to suggest that Veterans’ weight gain occurs in a vacuum. Factors associated with psychiatric disturbance/PTSD likely significantly contribute to obesity. The scientific literature links psychiatric disturbance to decreased activity and emotional eating which can lead to weight gain. While weight gain potentially contributing to sleep apnea could also likely be due to psychiatric disturbance, it would be an error to rely on opinions that sleep apnea was simply due to being overweight. This is not consistent with the current state of the scientific literature. In fact, neither being overweight nor the presence of structural abnormalities fully explains the presence of sleep apnea in a substantial number of cases. Being overweight is not sufficient to explain the existence of sleep apnea in many individuals. Simply suggesting that OSA was due to being overweight would reflect an overly simplistic and mechanistic view of sleep and obstructive sleep apnea which does not reflect the current state of the science. It would overlook the sleep regulating functions of the brain and the impact of psychiatric disturbance on the sleep regulating functions of the brain, including arousal-based mechanisms associated with sleep apnea. In fact, the scientific literature tells us that “a substantial portion” of patients with obstructive sleep apnea are “not obese” (Gray et. al. 2017). The authors of a 2017 study note that “a substantial proportion of OSA patients are not obese. Non-obese patients with OSA are a challenging group to treat with existing therapies… Our data also indicate that a key nonanatomical contributor to OSA pathogenesis, a low threshold for arousal, is likely to be particularly important in the pathogenesis of OSA in non-obese patients with OSA. A greater propensity for awakening in nonobese patients with OSA may also be a physiological factor contributing, at least in part, to poor CPAP tolerance in these patients. These findings have important implications for the treatment of OSA in nonobese individuals.” (Gray, et. al., 2017). In addition, “arousal” plays a significant role in sleep apnea [see Gray, et. al. (2017) Obstructive Sleep Apnea without Obesity Is Common and Difficult to Treat: Evidence for a Distinct Pathophysiological Phenotype; Journal of Clinical Sleep Medicine, 13(1): 81-88]. PTSD is linked to sleep apnea directly, but it is also linked more indirectly through weight gain, which is also associated with sleep apnea. PTSD negatively impacts motivation (ex: reducing activity) and can lead to overeating. PTSD increases the risk for obesity, which in turn further increases the risk for obstructive sleep apnea. Veterans’ weight gain often occurs in the context of PTSD. Subthreshold and threshold post-traumatic stress disorder (PTSD) are associated with binge eating symptoms in both men and women based on: Braun J, El-Gabalawy R, Sommer JL, Pietrzak RH, Mitchell K, Mota N. Trauma exposure, DSM-5 posttraumatic stress, and binge eating symptoms: results from a nationally representative sample. The Journal of Clinical Psychiatry. 2019;80(6):19m12813. Hoerster, et. al. (2015) noted in “PTSD and depression symptoms are associated with binge eating among US Iraq and Afghanistan veterans” [see Eating Behaviors; Volume 17, April 2015, Pages 115-118] that “PTSD and depression are common conditions among Iraq/Afghanistan Veterans. In the present study, PTSD and depression symptoms were associated with meeting binge eating screening criteria, identifying a possible pathway by which psychiatric conditions lead to disproportionate burden of overweight and obesity in this Veteran cohort.” Doerflinger & Masheb (2018), in the research article “PTSD is associated with emotional eating among veterans seeking treatment for overweight/obesity” [see Eating Behaviors, Volume 31, December 2018, Pages 8-11] presented findings that “suggest that emotional eating is common among veterans reporting PTSD symptoms, and that any degree of PTSD symptom severity is associated with more frequent emotional eating.”
The scientific literature supports a direct connection between sleep apnea and arousal associated with psychiatric disturbance, including PTSD. In addition, past VBA decisions have supported this interpretation. The scientific evidence supports findings that the evidence for sleep apnea being secondary to his PTSD is at least in equipoise. Multiple recent VBA decisions have been decided favorably based on this scientific literature, including, but not limited to: Citation Nr: 19133904 (Docket NO. 18-05 0350 5/1/2019; Citation Nr: 19164013 (Docket NO. 15-12 470) 8/19/19; Citation Nr: 19136285 (Docket NO. 18-01 222) 5/10/19; Citation Nr: 20011070 (Docket NO. 19-05 577) 2/10/2020; Citation Nr: 19155477 (Docket NO. 18-28 822) 7/18/19; Citation Nr: 19107744 (Docket NO. 16-51 926) 2/1/19; Citation Nr: 19103608 (Docket NO. 17-05 487) 1/15/19; Citation Nr. 19144930 (Docket NO. 17-49 916) 6/11/19; Citation Nr: 19141163 (DOCKET NO. 18-18 750A) 5/29/19; Citation Nr: 19110858 (Docket NO 16-53 449), 2/12/19). This is not an exhaustive list. This interpretation of the scientific literature should be utilized in favor of Veterans as it would be arbitrary and capricious for the VA to treat the science differently for one Veteran over another and say the science says one thing for one Veteran but says the opposite for another Veteran.
Veterans’ burden of proof on VA disability claims is at least as likely as not. The VA’s process is intended to be Veteran-friendly and does not require without-a-doubt-definitive proof of causation or the non-existent reality of “100% scientific certainty” (science does not speak in certainties- only probabilities).
Pharyngeal anatomy explains only a minimal portion of the variability in measures like the Apnea-Hypopnea Index (AHI). We know it is not just an anatomical disease when surgery to alter anatomy is of minimal benefit to a large number of individuals with OSA. Individuals with OSA often likely have hyperarousal concerns– a low threshold for arousal– which is an underlying mechanism of obstructive sleep apnea. Individuals have difficulty activating the muscles and stabilizing breathing in a normal fashion. PTSD can lead to this hyperarousal.
Other interesting research article links for that deep dive to help you fall asleep:
- Sforza E, Addati G, Cirignotta F, Lugaresi E. Natural evolution of sleep apnoea syndrome: a five year longitudinal study. Eur Respir J. 1994;7:1765–1770.
- Berry & Gleason (1997) Respiratory arousal from sleep: mechanisms and significance; Sleep 20(8):654-75.
- Edwards, et. al. (2014) Clinical predictors of the respiratory arousal threshold in patients with obstructive sleep apnea; Am J Respir Crit Care Med 2014 Dec 1;190(11):1293-300
- Malhotra, et. al. (2020) Endotypes and phenotypes in obstructive sleep apnea; Curr Opin Pulm Med 2020 Nov;26(6):609-614