ptsd Sleep Apnea Filing secondary to a SC Disability!

[Buck52]

This maybe helpful to some of you  wanting to File a secondary claim from a SC DISABILITY THAT YOU MAY HAVE  FOR A SLEEP APNEA CLAIM.

Even though this case is an old one   some of you may want to read up on this case that are thinking about filing a Claim of Sleep Apnea secondary to a SC disability that you may have.

you can get pull up these CFR'S That you need to read up on and do what you need to do for your claim..and submit your evidence accordingly.

 

Please read this   it sure could help you with your claim.

 

Citation Nr: 0102100 Decision Date: 01/25/01 Archive Date: 01/31/01 DOCKET NO. 99-22 315 ) DATE On appeal from the Department of Veterans Affairs Regional Office in St. Louis, Missouri THE ISSUE Entitlement to service connection for sleep apnea as secondary to service-connected post-traumatic stress disorder (PTSD). REPRESENTATION Appellant represented by: Disabled American Veterans ATTORNEY FOR THE BOARD Richard A. Cohn, Associate Counsel INTRODUCTION The veteran served on active duty from April 1970 to December 1971. This matter comes before the Board of Veterans' Appeals (Board) on appeal from an August 1999 rating decision of the Department of Veterans Affairs (VA) Regional Office in St. Louis, Missouri (RO) which denied service connection for sleep apnea as secondary to service-connected PTSD. FINDINGS OF FACT 1. The record includes all evidence necessary for the equitable disposition of this appeal. 2. There is competent medical evidence linking current sleep apnea to the veteran's service-connected PTSD. CONCLUSION OF LAW The veteran's sleep apnea was aggravated by his service- connected PTSD. Veterans Claims Assistance Act of 2000, Pub. L. No. 106-475, 114 Stat. 2096 (2000); 38 U.S.C.A. § 5107, 38 C.F.R. § 3.310(a) (2000). REASONS AND BASES FOR FINDINGS AND CONCLUSION The veteran attributes sleep apnea to his service-connected PTSD. The veteran does not contend that he incurred or aggravated sleep apnea during service and there is no evidence of sleep apnea or other sleep disorder in the veteran's service medical records SMRs. Procedurally, this appeal is developed fully and ready for Board adjudication. The RO has verified the veteran's period of service; there is no issue as to the substantial completeness of the veteran's application for VA benefits; the veteran has undergone VA examination pursuant to the application; the RO has requested and associated with the claims file all available service and postservice medical records pertinent to this appeal; VA is unaware of other unrequested records pertinent to this appeal, and; the evidence is sufficient to permit the Board to proceed with appellate review. See Veterans Claims Assistance Act of 2000, Pub. L. No. 106-475, 114 Stat. 2096, (2000). A veteran may be entitled to service connection for a disability under either a direct or secondary analysis. Direct service connection is warranted for disability resulting from disease or injury incurred or aggravated in service. 38 U.S.C.A. §§ 1110, 1131 (West 1991); 38 C.F.R. § 3.303 (2000). Secondary service connection is warranted both for a disability caused by a service-connected disorder and for a disability aggravated by a service-connected disorder. 38 C.F.R. § 3.310(a) (2000). In the latter case, compensation is limited to the extent to which the service- connected disorder increased the severity of the secondary disorder. Allen v. Brown, 7 Vet. App. 439, 448 (1995); Jones (Wayne) v. Brown, 7 Vet. App. 134, 136-37 (1994). A service- connected secondary disorder becomes part of the original disorder. 38 C.F.R. § 3.310(a). The veteran is a decorated former Army combat soldier whose PTSD has been service-connected since July 1995. SMRs include no evidence of a sleep disorder in service and the veteran claims none. VA medical records confirm that the veteran underwent sleep studies in February and October 1998 from which he was diagnosed with sleep apnea. A VA psychiatric progress note from February 1999 briefly reviewed the studies' findings and applicable research and concluded that PTSD and its treatment "in all probability has aggravated the obstructive sleep apnea." The note further states that "it is certainly as likely as not that this veteran's sleep apnea is directly related to his PTSD." The VA physician who examined the veteran in July 1999 identified two likely causes of his sleep apnea: enlarged tonsillar tissue and obesity. The physician found no etiological connection between PTSD and enlarged tonsillar tissue. However, he acknowledged that "an argument could be made" linking the veteran's obesity with PTSD although the veteran's medical records did not include another medical opinion to that effect. In the Board's judgment the record presents adequate evidence upon which to base a finding that the veteran's PTSD aggravated his sleep apnea. The opinion expressed in the February 1999 progress note is neither ambiguous nor equivocal on that point. The July 1999 examination report is more tentative -- finding only a medical possibility of attenuated causality under a different rationale. Nevertheless, the July 1999 opinion does not refute the February 1999 opinion, and it is well established that VA itself may not refute expert medical conclusions in the record with its own unsubstantiated medical conclusions. Colvin v. Derwinski, 1 Vet. App. 171, 175. (1991). Therefore, absent medical evidence actually denying a causal linkage between PTSD and sleep apnea in this case, the Board reads the two opinions together as providing, at minimum, evidentiary equipoise which must be resolved in the veteran's favor. See 38 U.S.C.A. § 5107(b). Accordingly, the Board is constrained to find that service connection for sleep apnea is warranted here under a secondary analysis. See 38 C.F.R. § 3.310. ORDER Service connection for sleep apnea is granted secondary to service-connected PTSD.   WARREN W. RICE, JR.

[silverdollar22]

Thanks Buck,

                        Yea I think it may be a tough road but what isn't?  I have had a good experience with my PCP doing nexius for me so if my MH doc won't help me maybe my PCP doc will talk with him!  I'm just going to try to get as much info and reasons together and present it to him and see how that goes.  If he is going to be a but head about it well, he's the one that has to deal with me in the long run every session if you know what i mean!!!! LOL   

[Andyman73]

8 hours ago, Jerry Harris said:

What is a fully developed claim and c&p exam? Also does anyone know of a correlation between SA and heart disease, high blood pressure, diabetes and cholesterol? Could they be related and has anyone used this connection.

Jerry!!! My brother in Arms!!! Yes and yes and yes  and yet again, once more, yes!

Because SA does not allow the body to reach REM sleep, or it limits the amount of REM sleep you get, the body can not go into full restoration and healing mode, which happens during REM sleep. All of those things you mentioned are some of the side effects of SA.  The first 2 because the body isn't fully relaxing and is under constant stress during SA effected sleep.

And the second 2 also, but more long term, like over a period of years, but also memory loss and depression as well.  And if you have PTSD, that compounds the SA issue.

I don't know the science behind it, but these and more are known side effects of SA.

FDC, fully developed claim, is where you send in all your evidence and the RO can decide your claim without a C&P(compensation and pension) exam.

Hope this helps you.

Semper Fi

Andy

[Jerry Harris]

My last sleep study was 2009. I still use same auto cpap and purchase my own masks. Do you think they will require a new study? I was first diagnosed in 1994 had a UPPP also. This will be first time applying for comp.

[silverdollar22]

Yes, more than likely knowing the va.  Did you get your equipment through the VA?  If so, you can get new equipment from them for free while your doing your new sleep study. Wish you the best!!  Being your first rodeo hang on tight for a long ride and remember to get all your information and documents in a row before you file a claim.  This will make their job easier and hopefully will result in a positive outcome for you!!!  Remember to be informed and this is the best place to do that!!! 

[Andyman73]

You would want a new sleep study anyway, since it's been that long since your last one.  I have one coming up in June for re-evaluation from my private provider.

Semper Fi

[syne7]

Here are some snippets from my SA IMO, in case anyone wants to a see sample of what's out there.  I'd appreciate any thoughts or opinions on the content as well:

Sleep apnea secondary to service-connected asthma
I opine that the veteran's sleep apnea is more likely than not secondary to his service ­connected asthma. Several studies have confirmed that asthmatic patients are more prone to develop OSAS symptoms than are members of the general population. The common asthmatic features that promote OSAS symptoms are nasal obstruction, a decrease in pharyngeal cross sectional area, and an increase in upper airway collapsibility.i The August 2007 National Asthma Education and Prevention Program Expe1i Panel Report 3 (EPR3) recommends that clinicians evaluate symptoms that suggest OSAS in unstable, poorly controlled asthmatic patients. Patients with OSAS have an increased vagal tone during sleep as a consequence of paiiial or complete airway obstruction occurring during apneas. The mechanics of this potent vagal stimulation are similar to those of the Muller maneuver, which consists of an inspiratory effo1i against a closed glottis. Increased vagal tone occurring during apnea episodes could be a trigger for nocturnal asthma attacks in sleep apnea patients. ii In fact, several studies have shown that increased vagal tone stimulates the muscarinic receptors located in the central airways leading to bronchoconstriction and causing nocturnal asthma. Furthermore, suppression of the increased vagal tone by inhaled anticholinergic drugs leads to improvement in forced expiratory flow, reduction in early morning falls in peak expiratory flow, and protection against nocturnal astluna symptoms. iii Another factor in the neural reflex mechanism involves the neural receptors at the glottic inlets and in the laryngeal region; these receptors have powerful reflex bronchoconstrictive activity. Nadal et al showed that mechanical irritation of the laryngeal mucosa increased total lung resistance distal to the larynx.

Sleep apnea secondary to chronic pain from service-connected ankle ankyloses
I opine that it is more likely than not that the veteran's sleep apnea is secondary to his chronic pain syndrome due to his left ankle injury. Clu·onic pain and disrupted sleep are commonly associated, and they share a clear cause-and-effect relationship. A bidirectional relationship exists between pain and sleep disturba11ces. Pain fragments sleep continuity, impairs sleep quality, and disrupts normal sleep architecture. Reciprocally, poor quality or insufficient quality of sleep may decrease the pain tlu·eshold, impair recovery from injuries, or further exacerbate the pain response. Painful stimuli produce micro-arousals which disrupt sleep continuity and alter normal sleep. Chronic pain is associated with increased high frequency EEG activity and a decrease in slow frequency EEG activity. Furthermore, chronic pain is associated with the appearance of alpha waves superimposed on slower EEG frequencies, or "alpha-delta" sleep. In short, pain produces a state of shallow sleep while disrupting restorative slow-wave sleep. An estimated 28 million Americans have sleep complaints due to chronic pain syndromes. Among patients with chronic pain, more than 50% experience sleep disturbances. Some repotis show that as many as 70% - 88% of patients with chronic pain repoti sleep trouble. Sleep disturbance shows an independent and linear correlation with pain severity, even after controlling for health measures and sleep habits. Sleep complaints portend worse outcomes among those with chronic pain.

Dr. Vincent Mysliwiec, et al, reported in Sleep Disorders and Assodated Medical Comorbidities in Active Duty Military Personnel [Exhibit 4]:

"Military personnel with the diagnosis of pain syndromes were more likely to have insomnia. Poor sleep is a recognized symptom in individuals who have medical disorders associated with pain. Previous studies using both questionnaires and PS Gs have reported patients with pain have difficulties initiating and maintaining sleep, supporting the association of pain syndromes with insomnia.v In the study's cohoti, 24.7% were identified as taking medications for pain."

Sleep apnea secondary to service-connected diabetes mellitus type 2
I opine that the veteran's sleep apnea is more likely than not secondary to the veteran's service-connected diabetes mellitus type 2.
There is a high prevalence of OSA in people with Type 2 Diabetes and abnormal glucose metabolism, which may in part be explained by obesity. Conversely, people with OSA have a high prevalence of Type 2 Diabetes and related metabolic disorders. There is a link between OSA and daytime somnolence. Sleep-disordered breathing (SDB) has been associated with insulin resistance and glucose intolerance, and is frequently found in people with Type 2 Diabetes. SDB not only causes poor sleep quality and daytime sleepiness, but has clinical consequences, including hypertension and increased risk of cardiovascular disease. The International Diabetes Federation (IDF) Taskforce on Epidemiology and Prevention convened a Working Group in February 2007 to review the subject_Yi OSA based on overnightpolysomnography has been noted in up to 9% of women and 24% of men.

Cross-sectional surveys show that obesity (particularly central obesity) is the strongest risk factor for OSA; male gender, age and ethnicity also contribute. Some studies have suggested that Hispanic and African-American populations may be at greater risk than Europids. Over 80% of patients with moderate to severe OSA go undiagnosed. There has long been a recognized association between Type 2 Diabetes and OSA, and there is emerging evidence that this relationship is likely to be at least partially independent of adiposity. Cross-sectional estimates from clinic populations and population studies suggest that up to 40% of patients with OSA will have diabetes. Polysomnography-dejined OSA and Type 2 Diabetes: A study of French men referred for assessment of sleep showed those with OSA (AHI 10) were significantly more likely to have impaired glucose tolerance (IGT) and diabetes than were those without OSA. The Sleep Heart Health Study showed a significant association between oxygen desaturation during sleep and elevated fasting and 2-h plasma glucose concentrations during an oral glucose tolerance test (OGTT). The severity of the OSA was also associated with the degree of insulin resistance after adjustment for obesity. The Wisconsin Sleep Study (n = 1387) showed a significant cross-sectional association between OSA and Type 2 Diabetes for all degrees of OSA.

Among those with diabetes, sleep duration and quality have been shown to be significant predictors ofHbAlc. Some studies of the effect of CPAP treatment for OSA on carbohydrate metabolism have shown improvements in insulin sensitivity, glycaemic control and HbAlc. There are a number of proposed causal pathways linking OSA with Type 2 diabetes.  There is evidence that the physiologic stress imposed by intermittent hypoxia and/or sleep fragmentation may be involved in the pathogenesis of insulin resistance via one or more of the following biological mechanisms:

1)    Sympathetic nervous system activation - the sympathetic nervous system plays a central role in the regulation of glucose and fat metabolism. OSA has been shown to increase sympathetic activity not only during sleep, but also when subjects are awake. Sympathetic activation is thought to be predominantly a result of nocturnal hypoxia. However, the repeated arousal from sleep that follows each obstructive breathing event is likely to exacerbate this effect.
2)    Direct effects of hypoxia - the temporal alliance between oxyhaemoglobin desa­turation and arousal from sleep in OSA poses the challenge of segregating their independent pathophysiologic effects. Recent work in normal human subjects, however, has shown that sleep disruption and intermittent hypoxia can each decrease insulin sensitivity and worsen glucose tolerance. Furthermore, animal data show that intermittent hypoxia during waking hours (i.e. not accompanied by arousals or other sleep disturbances) leads to a reduction in insulin sensitivity.
3)    Hypothalamic-pituitary-adrenal (HP A) dysfunction - hypoxia and sleep fragmentationmay lead to activation of the HPA axis and excessive and/or an abnormal pattern of elevation of cortisol levels with the potential for negative consequences on insulin sensitivity and insulin secretion.
4)    Systemic inflammation.

OSA patients have been shown to have higher levels of inflammatory markers as well as showing increased monocyte and lymphocyte activation with evidence that these changes are independent of adiposity. These effects are thought to be largely due to the effects of intermittent hypoxia, but sympathetic activation probably also plays a role.

A recent study examined selective suppression of slow-wave sleep (a phase of sleep thought to be the most restorative stage) in healthy young adults, without affecting sleep duration or causing hypoxia. The intervention markedly reduced insulin sensitivity and led to an impairment of glucose tolerance.

 

Seems like fairly substantive rationale, in my uneducated opinion.

Thoughts?

 

Edited May 13, 2016 by syne7
Typo corrections