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 and sleep apnea. In addition to being a psychologist with expertise in PTSD and other mental health conditions like depression and anxiety, 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 is a specialty doctor for sleep apnea secondary to PTSD (and/or other service connected mental health concerns). He 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. If you would also like a sleep apnea DBQ completed in addition to the nexus letter Dr. Finnerty will also complete a DBQ for an additional fee.
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
How do you prove your sleep apnea is secondary to your PTSD (or another service connected mental health condition like depression or anxiety)?
With an evidence-based nexus letter of course.
Sample nexus letter statements/ research related to sleep apnea secondary to PTSD Dr. Finnerty may use:
Curious about some of the research articles Dr. Finnerty tends to cite for sleep apnea secondary to PTSD? There are lots of studies out there. Here is the type of rationale Dr. Finnerty tends to use in his nexus letters for sleep apnea secondary to PTSD:
There is ample evidence of multiple risk factors which show an association with sleep apnea– one of these factors— at least as likely as not on par with the others or with stronger association than the others is PTSD; we also know the direction of the relationship as by definition PTSD is caused by trauma and PTSD is not caused by sleep apnea. These associated factors (ex: weight gain) can significantly contribute to the development of sleep apnea and/or substantially aggravate sleep apnea. There is scientific evidence that PTSD can also at least as likely as not cause sleep apnea through multiple pathways. Some C&P examiners perform a cursory review of data related to sleep apnea using resources such as UpToDate; UpToDate does not reflect an adequate literature review related to the evidence associated with sleep apnea being secondary to PTSD. It is not peer-reviewed research literature, it is geared toward giving a basic overview of the characteristics of sleep apnea to non-experts, and it does not address the growing body of primary source journal articles that are specifically related to sleep apnea secondary to PTSD. Citing sources such as UpToDate– or no sources at all– is a sure sign that the C&P examiner lacks relevant expertise in the subject matter.
Some C&P examiners attempt to describe what sleep apnea is characterized by as if this is what it is ultimately caused by, however this confuses the signs and symptoms of the sleep apnea process (or things that aggravate it) for sleep apnea’s cause; this is an error. Factors such as sleeping position, weight gain, dentition, and pharyngeal anatomy are symptoms of or may worsen the symptoms of the sleep apnea process but do not necessarily reflect the ultimate cause of sleep apnea.
PTSD at least as likely as not has a profound impact on the development and subsequent substantial aggravation of sleep apnea in many Veterans. 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. The supporting research is outlined 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
- 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 Jan;38(1):155-65
- Koob (1999) Corticotropin-releasing factor, norepinephrine, and stress; Biol Psychiatry Nov 1;46(9):1167-80
- Block, et. al. (2009) Psychosocial stress and change in weight among US adults; Jul 15;170(2):181-92
- Lettieri, et. al. (2016) OSA Syndrome and Posttraumatic Stress Disorder: Clinical Outcomes and Impact of Positive Airway Pressure Therapy; Chest 149(2):483-490
- El-Solh, et al. (2017) The effect of continuous positive airway pressure on post-traumatic stress disorder symptoms in veterans with post-traumatic stress disorder and obstructive sleep apnea: a prospective study. Sleep Med ;33: 145-150
- Lechat et. al. (2021) Co-morbid insomnia and obstructive sleep apnoea is associated with all-cause mortality; European Respiratory Journal, DOI: 10.1183/13993003.01958-2021
- Chang WH, Wu HC, Lan CC, Wu YK, Yang MC (2021) The Worsening of Positional Mild Obstructive Sleep Apnea over Time Is Associated with an Increase in Body Weight: Impact on Blood Pressure and Autonomic Nervous System. Respiration. 2021;100(11):1060-1069.
- Pevernagie DA, Gnidovec-Strazisar B, Grote L, Heinzer R, McNicholas WT, Penzel T, Randerath W, Schiza S, Verbraecken J, Arnardottir ES. On the rise and fall of the apnea-hypopnea index: A historical review and critical appraisal. J Sleep Res. 2020 Aug;29(4):e13066. doi: 10.1111/jsr.13066. Epub 2020 May 14. PMID: 32406974.
Additional citations related to impairment- especially in regards to CPAP use and cognitive impairment (the citations are in the text and I’ll add links at some point):
Sleep apnea leads to functional impairment and CPAP can help with this functional impairment, however, it is a misconception that CPAP/ PAP therapy is expected to resolve all impairments for an individual with sleep apnea; this is not consistent with the scientific evidence. Some relevant information from the scientific literature includes (but is not limited to):
OSA “impairs quality of life for numerous patients and leads to various OSA complications.” The authors noted that “the role of serotonin (5-HT) in many physiological processes, studies on its connection with the circadian system, and relationship to changes in sleep architecture are insufficient to assess the interaction of this neurotransmitter with nocturnal hypoxia,” but they did find that treatment with PAP therapy did lead to an increase in serotonin levels in individuals with sleep apnea [Madaeva IM, Berdina ON, Kurashova NA, Semenova NV, Ukhinov EB, Belskikh AV, Kolesnikova LI. Sleep Apnea and Serum Serotonin Level Pre- and Post-PAP Therapy: A Preliminary Study. Neurol Ther. 2021 Dec;10(2):1095-1102. doi: 10.1007/s40120-021-00290-z. Epub 2021 Oct 20].
We know that sleep apnea leads to “an increase in occupational accidents due to reduced vigilance and attention” in individuals with sleep apnea. “Such involvements were related to excessive daytime sleepiness and neurocognitive function impairments” [see Rabelo Guimarães Mde L, Hermont AP. Sleep apnea and occupational accidents: Are oral appliances the solution? Indian J Occup Environ Med. 2014 May;18(2):39-47]. We know that “cognitive impairments are commonly seen in patients with an OSA diagnosis” [see Wang G, Goebel JR, Li C, Hallman HG, Gilford TM, Li W. Therapeutic effects of CPAP on cognitive impairments associated with OSA. J Neurol. 2020 Oct;267(10):2823-2828. doi: 10.1007/s00415-019-09381-2. Epub 2019 May 20. PMID: 31111204]. “One of the major consequences of OSAS is an impact on neurocognitive functioning. Several studies have shown that OSAS has an adverse effect on inductive and deductive reasoning, attention, vigilance, learning, and memory” [see Lal C, Strange C, Bachman D. Neurocognitive impairment in obstructive sleep apnea. Chest. 2012 Jun;141(6):1601-1610].
Jackson, et. al. (2018) treated 110 patients with OSA with CPAP for three months and compared them to individuals in the community without OSA. “Compared to the community sample, participants with OSA were significantly sleepier, had impaired mood and quality of life, and showed decrements in neuropsychological function, specifically psychomotor function, working memory and vigilance. Some neuropsychological and mood outcomes were normalized with CPAP, but significant decrements persisted in most outcomes even in those participants with adequate device usage.” The authors found that “Patients with mild to moderate OSA have significant neurobehavioral morbidity. During “gold standard” treatment, normal function was not achieved, even with adequate device usage. CPAP efficacy for improving sleepiness and neuropsychological function in this milder end of the OSA spectrum may be poor, which may affect CPAP adherence. These findings suggest that there may be neurological changes related to OSA that do not respond to CPAP treatment. [see Jackson ML, McEvoy RD, Banks S, Barnes M. Neurobehavioral Impairment and CPAP Treatment Response in Mild-Moderate Obstructive Sleep Apneas. J Clin Sleep Med. 2018 Jan 15;14(1):47-56].
Jiang, et, al. (2021) completed a metanalysis of multiple studies and found that sleep apnea is associated with “high risks of cognitive impairment, including Alzheimer’s disease” and that CPAP only offers “partial” improvement in the cognitive problems caused by sleep apnea [see Jiang X, Wang Z, Hu N, Yang Y, Xiong R, Fu Z. Cognition effectiveness of continuous positive airway pressure treatment in obstructive sleep apnea syndrome patients with cognitive impairment: a meta-analysis. Exp Brain Res. 2021 Dec;239(12):3537-3552].
Kielb, et. al. (2012) also note that OSA is “associated with a number of adverse health consequences, and a growing literature focuses on its cognitive correlates.” They note that “multiple studies indicate” that individuals with OSA “show impairment in attention, memory, and executive function.” While CPAP was the “most effective and widely used treatment” for sleep apnea, the studies of CPAP use showed that “in general, no consistent effect of CPAP use on cognitive performance was evident.” The authors noted also that “several prior reviews of the literature suggested that OSAS patients exhibit significant impairment on neuropsychological tests.” They reviewed evidence that OSA patients are “are at increased risk for motor vehicle accidents.” The reviewed multiple studies with mixed results and design. While some research shows some potential cognitive improvement with CPAP use, they noted that “in fact, several studies have reported that CPAP treatment has no effect on cognitive performance.” The authors concluded that “cognitive deficits have long been observed in OSAS patients, and although findings in this domain remain inconsistent, evidence exists for deficits in intellectual function, memory, attention, and executive function in OSAS.” Due to the mixed results of treatment studies, which may be due to variability in inclusion and exclusion criteria, study design, and duration of treatment, it is not possible to make definitive conclusions regarding the impact of CPAP treatment on cognition in OSAS. Although CPAP is a well-established, effective treatment for OSAS, it does not definitively reduce the host of cognitive deficits observed among OSAS patients. Daytime somnolence can particularly impact attention and executive functioning, including slower reaction time. Intermittent hypoxemia also can impact the performance on cognitive tests and is associated with declines in motor and processing speed, spatial abilities, mental flexibility and attention. “Some researchers argue that intermitted hypoxemia, together with sleep fragmentation, leads to prefrontal cortical degeneration, which could explain the impairment in executive function observed in patients” with OSA. Sleep fragmentation itself may be “an important mechanistic factor in the development of cognitive impairment” in sleep apnea. “For example, the number of arousals from sleep is a strong predictor of memory impairment in OSAS.” Sleep fragmentation has been associated with poorer cognitive performance and reduction in neurogenesis. “Another potential mechanism that may contribute to cognitive impairment in OSAS is disruption in circadian rhythms. Researchers have reported an association between disturbed circadian rhythms (as measured by actigraphy) and severity of cognitive impairment” [see Kielb SA, Ancoli-Israel S, Rebok GW, Spira AP. Cognition in obstructive sleep apnea-hypopnea syndrome (OSAS): current clinical knowledge and the impact of treatment. Neuromolecular Med. 2012 Sep;14(3):180-93. doi: 10.1007/s12017-012-8182-1. Epub 2012 May 9].
Alcohol use can substantialy aggravate sleep apnea
The “medical literature” actually demonstrates that alcohol use can make sleep apnea worse. For example, a recent meta-analysis on the topic reviewed 1,266 studies and concluded “alcohol consumption is associated with worsening severity of snoring, altered sleep architecture, AHI, as well as lowest oxygen saturation among patients susceptible to snoring and obstructive sleep apnea” [see Burgos-Sanchez C, Jones NN, Avillion M, Gibson SJ, Patel JA, Neighbors J, Zaghi S, Camacho M. Impact of Alcohol Consumption on Snoring and Sleep Apnea: A Systematic Review and Meta-analysis. Otolaryngol Head Neck Surg. 2020 Dec;163(6):1078-1086]. The American Academy of Sleep Medicine (an organization I am a member of), has practice guidelines related to sleep apnea. The American Academy of Sleep Medicine’s practice guidelines related to obstructive sleep apnea include, as a standard of care in the field, that there be “patient education” on the impact of “alcohol avoidance” on sleep apnea. The “avoidance of alcohol” is also included as one of the “behavioral strategies” in managing sleep apnea [for the practice guidelines see Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine (2009), Epstein LJ; Kristo D; Strollo PJ; Friedman N; Malhotra A; Patil SP; Ramar K; Rogers R; Schwab RJ; Weaver EM; Weinstein MD. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009;5(3):263–276].
Suggested YouTube Videos:
- You can watch me (Dr. Finnerty) discuss sleep apnea secondary to PTSD claims on YouTube (though I assure you I’m not a YouTube star)
- If you’re curious you can watch an athletic and muscular Shaquille O’Neal go through the process and talk about his diagnosed sleep apnea
Psychological Interventions are used to treat sleep apnea:
PSA: The VA & other organizations have psychologists who can help with your sleep apnea treatment – Nexus Letters from a Psychologist (learn more here: http://nexusletters.com/2022/03/15/psa-the-va-other-organizations-have-psychologists-who-can-help-with-your-sleep-apnea-treatment/
Should the VA consider a psychologist’s opinion in relation to sleep apnea and psychological disorders?
Administrative bodies like the VA get to decide who the expert is. Whether someone is considered to be an expert on a particular topic isn’t just established by their professional licensure alone. For example, just because someone is a physician assistant doesn’t mean they are an expert on all medical and psychological questions under the sun. The credentials, education, training and experience for each professional should be considered on a case-by-case basis for the specific question being asked. Professionals offering opinions on sleep apnea secondary to PTSD should be familiar with both sleep apnea and PTSD (not just sleep apnea or PTSD). Likewise, the VA has the ability to consider whether the opinions from a specific professional are credible, consistent with the evidence and reflect competent medical evidence for the purposes of a VA disability claim. Per the VA:
Competent medical evidence means evidence provided by a person who is qualified through education, training, or experience to offer medical diagnoses, statements, or opinions. Competent medical evidence may also mean statements conveying sound medical principles found in medical treatises. It would also include statements contained in authoritative writings such as medical and scientific articles and research reports or analyses.
Public Comments on the VA’s Proposed Changes to the Sleep Apnea rating:
- Dr. Finnerty’s blog post: Potential changes to How the VA rates mental disorders, sleep apnea, tinnitus, etc.
- Dr. Finnerty’s public comments provided to the VA related to the sleep apnea proposed changes