Sleep Apena denied

[Berta]

This is from a poster on my profile-

"JaeNobe said:

I was denied OSA claim secondary to Depression and Chronic Pain. I have an IMO from David Anise connecting it to my service related injuries and depression, Sleep Dr. put I my C-Pap was a necessity.  I have a c-pap. Even, submitted the NIH Sleep Disorder study.   I do not have my letter stating why the denied it Im pretty sure its because of the VA's PA that half way did my C&P (5 mins) said that she believed it wasnt.  It was I want to appeal but not sure what the best ave is to do so. Do I hire a lawyer (if so, who do you recommend)? Do I use DAV, VSO. I've seen someone say ask them to send to BVA.  I'm at a complete lost as to what my next step should be. "

 

[Berta]

Here is another award PTSD aggrevating Sleep Apnea:

In part:

"In this regard, the Veteran is service-connected for PTSD. He has a current diagnosis of obstructive sleep apnea. The Veteran does not assert that his obstructive sleep apnea is caused by PTSD. Rather, in his May 2013 substantive appeal he asserted that his obstructive sleep apnea is aggravated by PTSD. The Veteran has submitted medical opinions from private physicians indicating that PTSD aggravates obstructive sleep apnea. A March 2015 letter from a private physician stated that the Veteran was diagnosed with obstructive sleep apnea in 1995 and has used a continuous positive airway pressure (CPAP) system since that diagnosis. The physician noted other comorbidities including hypertension and hyperlipidemia. Additionally, the physician opined that it is at least as likely as not that the Veteran's obstructive sleep apnea is secondary to his service-connected PTSD and that PTSD aggravates the obstructive sleep apnea. In a May 2015 letter, a psychologist opined that it was at least as likely as not that the Veteran's obstructive sleep apnea is aggravated by his PTSD. The psychologist stated that the opinion was based upon medical and behavioral health literature showing that 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. He stated that the functional syndromes overlap the signs and symptoms of PTSD. The March 2015 and May 2015 medical opinions were based on knowledge and consideration of the Veteran's pertinent medical history as well as treatment of the Veteran for sleep apnea and PTSD and were adequately supported by sufficient rationale. See Guerrieri v. Brown, 4 Vet. App. 467, 470-71 (1993); Owens v. Brown, 7 Vet. App. 429, 433 (1995); Nieves-Rodriguez v. Peake, 22 Vet. App. 295, 304 (2008) There is thus a current diagnosis of obstructive sleep apnea, which the medical evidence of record shows is aggravated by the Veteran's service-connected PTSD. VA examinations in August 2012 and February 2014 provided negative nexus opinions. However, these VA medical opinions are not as thorough as the May 2015 private opinion. The evidence for and against the claim is at least in equipoise. Accordingly, service connection for obstructive sleep apnea is granted as secondary to service-connected PTSD.

ORDER Entitlement to service connection for obstructive sleep apnea, as secondary to service-connected PTSD, is granted. ____________________________________________ P. M. DILORENZO Veterans Law Judge, Board of Veterans' Appeals

https://www.va.gov/vetapp16/Files6/1648003.txt

BVA decisions are not evidence because they pertain only to the claimant. However, they provide a lot of information as to why a claim is granted by the BVA and why the BVA has to deny a claim.

[JaeNobe]

 Pretty long IMEO .... but I tried to post majority of it. 

 

 

INDEPENDENT MEDICAL EXPERT OPINION                                     January 21, 2019

To:       Veterans Administration ) Re:       

File#: 

 

 

As my attached curriculum vitae indicates [Exhibit 1], I am a surgeon with almost thirty years of medical experience. I was Clinical Associate Professor of Surgery and Attending

Surgeon in Transplantation at SUNY at Stony Brook. I served as President of the New York Transplantation Society and as Assistant Editor of Transplantation Proceedings. I hold three

patents. I have authored three book chapters and 106 research papers published in peer reviewed medical journals.

 

Opinions

 

The following opinions are all to a reasonable degree of medical certainty at least at the "more likely than not" (more than 50 percent) level.

 

I do not have a vested interest in the assignment of this patient's medical diagnostic codes as I am an expert and paid a flat fee prior to the writing of any of my reports. My opinions are based on the judicious application of the medical principles / my training / experience.

 

This report conforms to the federal guidelines on expert testimony as they apply to medical data/facts, reliable principles/methods (see my attached C.V. and book references), and the application of medical principles/methods to the facts/data and is therefore not in any way speculative.

 

After reviewing the veteran's c-file and the pertinent recent medical literature, I opine that it is more likel y than not that the veteran's sleep apnea is caused by and/or aggravated by his service-connected conditions of depressive disorder and chronic pain syndrome related to his service-connected injuries.

Sleep apnea diagnosis

 

A sleep medicine consult dated July 20, 2006 reports [Exhibit 2]:

 

"The supervising practitioner of record for this patient care encounter is Dr. xxxxxx

HISTORY OF PRESENTING ILLNESS

Patient is a 26 y/o veteran who is being evaluated in sleep clinic for excessive day time sleepiness. He typically retires at about 10 pm .Falls asleep in about 20 mins. He does not c/o restless leg activity while going to sleep. His sleep is not interrupted by nocturnal awakenings. He wakes up at 4:30 am. On awakening patient feels /does not feel refreshed. He has a dry mouth but no head ache on waking up. He has nocturnal reflux episodes. He does not report any symptoms s/o narcolepsy of cataplexy, hypogogic hallucinations or on rare occasions he has experienced sleep paralysis. He does not report any parasornnias.

Epworth Sleepiness scale 10 Depression Score...

Assessment:

Patient appears to have Obstructive Sleep Apnea with an Epworth Score of 10 indicating mild excessive day time sleepiness."

 

Sleep apnea diagnosis

A sleep medicine consult dated July 20, 2006 reports [Exhibit 2]:

"The supervising practitioner of record for this patient care encounter is Dr. Sxxxxxx.

HISTORY OF PRESENTING ILLNESS

Patient is a 26 y/o veteran who is being evaluated in sleep clinic for excessive day time sleepiness. He typically retires at about 10 pm .Falls asleep in about 20 mins. He does not c/o restless leg activity while going to sleep. His sleep is not interrupted by nocturnal awakenings. He wakes up at 4:30 am. On awakening patient feels /does not feel refreshed. He has a dry mouth but no head ache on waking up. He has nocturnal reflux episodes. He does not report any symptoms s/o narcolepsy of cataplexy, hypogogic hallucinations or on rare occasions he has experienced sleep paralysis. He does not report any parasornnias.

Epworth Sleepiness scale 10 Depression Score...

Assessment:

Patient appears to have Obstructive Sleep Apnea with an Epworth Score of 10 indicating mild excessive day time sleepiness."

A medical record dated February 23, 2007 shows [Exhibit 3]:

"The supervising practitioner of record for this patient care encounter is Dr. Sxxxxx.

Referred for: Patient is a 26 year old veteran referred with Obstructive sleep apnea who is seen for follow up. CPAP machine is set at a pressure of 8 H20 .Checked against a manometer and delivers the set pressure."

What is sleep apnea?

For VA rating purposes, the veteran needs to show that he suffers from sleep apnea; whether of the obstructive type, central type or mixed type

Obstructive sleep apnea (OSA) (ICD-9-CM 327.23) is the most common form of sleep apnea and is caused by an airway blockage that occurs when the soft tissue in the back of the throat narrows or closes during sleep. The brain then senses the inability to breathe and briefly arouses the person to begin breathing again. True obstructive sleep apnea occurs when tissues block the upper airway (e.g. large adenoids, deviated septum).

Central sleep apnea (ICD -9-CM 327.27) occurs when the brain does not send proper signals to the muscles that control breathing which results in the person awakening with shortness of breath.

 Complex or mixed sleep apnea is a combination of both obstructive and central sleep apnea.

As mentioned earlier, pure obstructive sleep apnea involves abnormalities of the upper airway such as enlarged tonsils, large tongue or blocked nasal passages. Interestingly , in all these cases there is no mechanical blockage to the airway during wakefulness; obstruction occurs only during sleep. Thus, it is clear that in obstructive sleep apnea cases, the brain is also involved. The brain does not send proper signals to the muscles that control breathing during sleep.

Referring to the illustrations below one can clearly see that abnormalities of the upper air way (pure obstructive) and laxity of the airway muscles (central) result in exactly the same outcome, i.e. obstructive apnea. Thus, all sleep apnea cases are in fact mixed sleep apnea. I have yet to encounter a single case, however, that was not diagnosed as obstructive sleep apnea. Obstructive sleep apnea has become the term of art for all sleep apnea. For rating purposes, the rating table does not distinguish between obstructive, central and mixed sleep apnea.

OSA patients were show.    to maintain their upper airway patency in wakefulness via a compensatory, augmented electromyography (EMG) activity of their airway dilator muscles, during wakefulness [and non-rapid eye movement (NREM) sleep]. Remarkably, sleep apnea patients experience little or no problems with their breathing or airway patency while awake. In fact, the great majority of people with sleep apnea possess ventilatory control systems that are capable of precise regulation of their alveolar ventilation and arterial blood gases with extremely small variations from the norm. Electrical activity from medullary inspiratory neurons, and EMG activity of diaphragm and abductor muscles of the upper airway in healthy humans show reductions in amplitude upon the transition from awake to NREM sleep, usually accompanied by a mild to moderate hypoventilation and two- to fivefold increases in upper airway resistance.

A fast and highly variable breathing frequency is a hallmark of rapid eye movement (REM) sleep in mammals. An excitatory drive to breathe is common in REM, with increased diaphragmatic EMG activity and increased activity in many medullary respiratory neurons above those levels observed in NREM sleep or quiet wakefulness. In REM sleep, there are both tonic excitatory inputs and phasic inhibitory inputs in the brain respiratory centers that account for irregularities in breathing pattern, as well as the loss of excitation , which contributes to hypotonia of the muscles of the upper airway. This results in collapse of the airway leading to sleep apnea.

 

Tongue & Throat

There are two basic mechanisms for obstructive sleep apnea. The first is static narrowing of the airways due to swelling of structures that block the airway. Some examples are septal deviation of the nose, or accumulation of fat in the retro pharynx noted in certain types of obesity. The second, and more frequent reason for sleep apnea, are dynamic processes that involve the muscle tone, mostly of the tongue due to hypotonia of the genioglossus muscle.

Jordan et al.i published a study: Airway Dilator Muscle Activity and Lung Volume During Stable Breathing in Obstructive Sleep Apnea:

" Obstructive sleep apnea (OSA) is a common disorder, characterized by repetitive upper airway collapse during sleep. Upper airway collapse in OSA is thought to occur at sleep onset because of the reduction of activity of several upper airway dilator muscles, which then do not hold the anatomically vulnerable airway open.

The severity of OSA varies throughout the night and between sleep stages. Generally, obstructive respiratory events are more common and longer in REM than NREM sleep."

The picture above demonstrates how the tongue plays a major role in airway obstruction, especially if one breathes through the mouth rather than the nose. When the tongue muscle (the genioglossus) tone is deactivated or relaxed , the tongue will slip backwards and obstruct the airway. Jordan et al. have shown that when patients with OSA spontaneously overcome their tendency for airway collapse and have stable breathing during sleep, the genioglossus muscle is more active than during disordered breathing events:

"Electrical activation of the genioglossus muscle or hypoglossal nerve is known to dilate the retroglossal airway and reduce the pharyngeal critical closing pressure in humans. 

Thus, it would appear lik .ly that the increased genioglossus muscle activity is playing a causal role in contributing to the sleep stage and time of night differences in the severity of OSA...

Prior research has shown that the genioglossus is activated by chemoreceptor stimulation and by reflex activation in response to negative pressure. There is also evidence to suggest that the genioglossus receives an independent stimulation during wakefulness which is lost at sleep onset and is known as the 'wakefulness stimulus'

 

Sleep Stage Effects

The "normal" sleep-onset latency is approximately 10 minutes. The "normal" sleep stage distribution is 5% stage I; 50% stage II; 15-25% stage III, slow wave or deep sleep (SWS); and 20-25% stage REM.

The activity of the genioglossus has previously been reported to be higher during SWS than stage II sleep. The high arousal threshold that occurs during deeper stage II can allow large genioglossus muscle activity to develop, stabilizing the airway such that sleep can continue and SWS can develop.

Respiratory events are often worse during REM than NREM sleep. Jorden et al. found that the tonic (expiratory) activity of the genioglossus was reduced during respiratory events in REM compared to stage II sleep. This reduction in tonic genioglossus activity may contribute to the predisposition to airway collapse that occurs in REM because airway collapse typically occurs at the end of expiration. During REM sleep, further suppression of the tonic component of the genioglossus activity was observed, potentially contributing to the increased severity of OSA in REM sleep.

Sleep apnea secondary to Veteran's service-connected mood disorder

It is my professional opinion that Veteran's sleep apnea is more likely than not caused by and/or aggravated by his service-connected psychiatric condition (depressive disorder). Sleep apnea in military personnel has now reached an epidemic proportion. A studyii from the Defense Medical Surveillance System (DMSS) reported the incidence of OSA and associated attrition from service in active component military members from 1 January 2004 through 31 May 2016. The study identified 223,731 incident cases of OSA with an overall incidence rate of 139.2 per 10,000 person-years, between 2004 and 2015. Rates increased more than 3-fold between 2004 and 2015. In 2015, 48.1% of all incident cases of OSA were diagnosed in the last year of service.

Sharafkhanel et al. in the study Association of psychiatric disorders and sleep apnea in a large cohort iii' reviewed the Veterans Health Administration data from 1998 to 2001 and identified patient records indicating sleep apnea and various psychiatric conditions. Out of 4,060,504 unique cases, 118,105 were identified as having sleep apnea (estimated prevalence of 2.91%). Psychiatric comorbid diagnoses in the sleep apnea group included depression (21.8%), anxiety (16.7%), posttraumatic stress disorder (11.9%), psychosis (5.1%), and bipolar disorders (3.3%). Compared with patients not diagnosed with sleep apnea, a significantly greater prevalence (P < .0001) was fou)!d for mood disorders, anxiety, posttraumatic stress disorder, psychosis, and dementia in patients with sleep apnea. The study concluded that sleep apnea is associated with a higher prevalence of psychiatric comorbid conditions in Veterans Health Administration beneficiaries.

Scientists at the Madigan Army Medical Center have recently studied the incidence of sleep apnea in military personnel.iv Mysliwiec et alv studied the associations between sleep disorders and service-related diagnoses of depression and posttraumatic stress disorder (PTSD). They evaluated 110 active duty soldiers referred to the sleep disorders clinic within 18 months of deployment. These soldiers were young ( average age 33.6 years) and not obese. Overall, 62.7% met diagnostic criteria for obstructive sleep apnea (OSA) and 63.6% for insomnia. 38.2% had comorbid insomnia and OSA. The incidence of PTSD, TBI and mood disorder reached.

 

"In this study, we report that medical and psychologic comorbidities are frequent in military personnel referred for sleep disturbances, with 70% having at least one of the following: depression, mild TBI, pain, or PTSD, and almost one-half (47.3%) reporting two or more diagnoses . . . Patients with comorbid insomnia and OSA had the highest rates of depression, mild TBI, PTSD, and two or more diagnoses."

Hattori et al. in the study Risk factors for obstructive sleep apnea syndrome screening in mood disorder patientvs \

 

" ... conducted polysornnography for patients who satisfied the following criteria: (i) diagnosis of according to the Mini-International Neuropsychiatric Interview (MINI); (ii) a score of > or =10 on the Hamilton Rating Scale for Depression (HAM-D); (iii) fulfillment of either (a) or (b) below: (a) at least one of the following: severe snoring, witnessed apnea during sleep, excessive daytime sleepiness; (b) at least one of the following plus an oxygen desaturation index of 4% > or =5 times/h by pulse oximeter: mild snoring, sleep disturbance , headache, high blood pressure. The patients with apnea hypopnea index > or =5 were diagnosed with OSAS...

 

The authors studied 32 mood disorder patients suffering from major depressive disorder or bipolar disorder, 59.4% had OSAS. The diagnosis rate with our criteria was significantly higher than the previousl y reported incidence of OSAS in patients with depression. There was n, o s ignificant difference among diagnosis rates as to individual risk factors or the number of risk factors. A multiple regression test showed no significant association between apnea-hypopnea index and other clinical factors including depression severity."

 

The basis of sleep apnea in mood disorders is most likel y due to aberration of the Rapid Eye Movement stage (REM).

 

OSA patients were shown to maintain their upper airway patency in wakefulness via a compensatory, augmented EMG activity of their airway dilator muscles, which extended an earlier report of more frequently occurring genioglossus EMG activity during wakefulness [and non-rapid eye movement (NREM) sleep] in OSA patients . Remarkably, sleep apnea patients experience little or no problems with their breathing or airway patency while awake. In fact, the great majority of people with sleep apnea possess ventilatory control systems that are capable of 

statistical significance when compared to control group. The study reports (emphasis added) [Exhibit 4]:

"In this study, we report that medical and psychologic comorbidities are frequent in military personnel referred for sleep disturbances, with 70% having at least one of the following: depression, mild TBI, pain, or PTSD, and almost one-half (47.3%) reporting two or more diagnoses . . . Patients with comorbid insomnia and OSA had the highest rates of depression, mild TBI, PTSD, and two or more diagnoses."

Hattori et al. in the study Risk factors for obstructive sleep apnea syndrome screening in mood disorder patientvs \

" ... conducted polysornnography for patients who satisfied the following criteria: (i) diagnosis of according to the Mini-International Neuropsychiatric Interview (MINI); (ii) a score of > or =10 on the Hamilton Rating Scale for Depression (HAM-D); (iii) fulfillment of either (a) or (b) below: (a) at least one of the following: severe snoring, witnessed apnea during sleep, excessive daytime sleepiness; (b) at least one of the following plus an oxygen desaturation index of 4% > or =5 times/h by pulse oximeter: mild snoring, sleep disturbance , headache, high blood pressure. The patients with apnea hypopnea index > or =5 were diagnosed with OSAS..

The authors studied 32 mood disorder patients suffering from major depressive disorder or bipolar disorder, 59.4% had OSAS. The diagnosis rate with our criteria was significantly higher than the previousl y reported incidence of OSAS in patients with depression. There was n, o s ignificant difference among diagnosis rates as to individual risk factors or the number of risk factors. A multiple regression test showed no significant association between apnea-hypopnea index and other clinical factors including depression severity."

 

The basis of sleep apnea in mood disorders is most likel y due to aberration of the Rapid Eye Movement stage (REM).

 

OSA patients were shown to maintain their upper airway patency in wakefulness via a compensatory, augmented EMG activity of their airway dilator muscles, which extended an earlier report of more frequently occurring genioglossus EMG activity during wakefulness [and non-rapid eye movement (NREM) sleep] in OSA patients . Remarkably, sleep apnea patients experience little or no problems with their breathing or airway patency while awake. In fact, the great majority of people with sleep apnea possess ventilatory control systems that are capable of precise regulation of their alveolar ventilation and arterial blood gases with extremely small variations from the norm.

Electrical activity from medullary inspiratory neurons, EMG activity of diaphragm and abductor muscles of the upper airway in healthy humans and/or in cats, show reductions in amplitude upon the transition from awake to NREM sleep, usually accompanied by a mild to moderate hypoventilation (+2 to 8 mmHg Pac02) and two- to fivefold increases in upper airway resistance. Sleep induces consistently greater proportional reductions in the EMG activity in the upper airway versus chest wall pump muscles.

A fast and highly variable breathing frequency is a hallmark of rapid eye movement (REM) sleep in mammals. An excitatory drive to breathe is common in REM, with increased diaphragmatic EMG activity and increased activity in many medullary respiratory neurons above those levels observed in NREM sleep or quiet wakefulness. In REM sleep, there are both tonic excitatory inputs and phasic inhibitory inputs in the brain respiratory centers that account for irregularities in breathing pattern, as well as the loss of excitation, which contributes to hypotonia of the muscles of the upper airway. This results in collapse of the airway leading to sleep apnea. ··

 

Wang et al reported in the study The Neurobiological Mechanisms and Treatments of REM Sleep Disturbances in Depressionvii:

"Sleep electroencephalograms have shown characteristic changes in depression such as reductions in non-rapid eye movement sleep production, disruptions of sleep continuity and disinhibition of rapid eye movement (REM) sleep. REM sleep alterations include a decrease in REM sleep latency , an increase in REM sleep duration and REM sleep density with respect to depressive episodes. Emotional brain processing dependent on the normal sleep-wake regulation seems to be failed in depression, which also promotes the development of clinical depression. Also, REM sleep alterations have been considered as biomarkers of depression. The disturbances of norepinephrine and serotonin systems may contribute to REM sleep abnormalities in depression. Lastly, this review also discusses the effects of different antidepressants on REM sleep disturbances in depression."

 

Yang et al in Sleep State Instabilities in Major Depressive Disorder : Detection and Quantification with Electrocardi?gram-based Cardiopulmonary Coupling Analysivsi i i   reported:

"Our findings of decreased stable sleep and increased unstable sleep and REM/wakeful states in depressed individuals are consistent with well-known features of altered EEG sleep structures in major depression, namely an increase in sleep state fragmentation, a reduction in slow wave sleep, and an increase in REM pressure (Armitage, 1995; Germain, Nofzinger, Kupter, & Buysse, 2004; Jindal, et al., 2002; Thase, Fasiczka, Berman, Simons, & Reynolds, 1998)."

 

Sleep apnea secondary to Veteran's chronic pain related to service-connected injuries

It is my professional opinion that it is more likely than not that the veteran's sleep apnea is secondary to and/or is aggravated by his chronic pain syndrome related to his service­ connected injuries. Scientists at the Madigan Army Medical Center have recently examined the incidence of sleep apnea in military personnel. They observed that sleep disturbances are increasing in frequency and are commonly diagnosed during deployment and when military personnel return from deployment (redeployment) [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 PSGs have reported patients with pain have difficulties initiating and maintaining sleep, supporting the association of pain synd_rqmes with insomnia.  In the study's cohort, 24.7% were identified as taking medications for pain."

 

Insomnia and sleep apnea overlap

Luysterix et al. reported:

 

" . .. Insomnia can be defined as a symptom comprising sleep-specific complaints-such as difficulty falling asleep, difficulty staying asleep, early awakenings, or unrefreshing or nonrestorative sleep-or as a disorder denoting sleep and waking symptoms ... Typically, insomnia is defined by subtype based on frequency, duration, and etiology. The following qualitative insomnia diagnostic criteria have been suggested: sleep-onset latency or wake after sleep onset greater than 30 minutes, occurring at least 3 times per week, and with duration of at least 6 months.x ... OSA_i _patients presenting with insomnia complaints has been examined in several studies)x. 1 xii xiii Lichstein and colleaguesxiv found that 29% of older adults with insomnia recruited for a research study (n = 80) had polysomnography­ diagnosed OSA (AHI > 15)... Among 394... women with chronic insomnia complaints

without major psychiatric or medical disorders, 67% (n = 264) had an AHI of at least 5

[signifying at least mild OSA] based on either home monitoring or polysomnographyx_v  ,,

Mysliwiec et axlv i reports in the study Sleep Disorders in US Military Personnel : A High Rate of Comorbid Insomnia and Obstructive Sleep Apnea [Exhibit 4] :

"Sleep disturbances are reported in almost one-third of military personnel who have deployed in support of Overseas Contingency Operations (OCO), resulting in approximate y 600,000 military personnel and veterans with clinically relevant sleep conditions.xvii US Department of Defense medical data report a marked increase in the incident diagnoses of insomnia and obstructive sleep apnea (OSA) across all servicesx.v iii

x xi     From 2001 to 2009, the diagnostic rates for insomnia and OSA increased by 19 and

5.8 times, respectively ...

Considering insomnia and OSA as separate disorders, 62.7% subjects met PSG criteria for OSA and 63.6% clinical criteria for insomnia. However, if comorbid insomnia and OSA is classified as a distinct disorder, it was the most common diagnosis in 38.2% of subjects...

Our finding that comorbid insomnia and OSA ("complex insomnia") was a frequent diagnosis in military personnel with combat exposures is consistent with previously reported civilian studies of patients who had traumatic experiencexs.x xx i xx ii ... "

 

A brief description of the sleep cycle is needed to fully understand the relationship between pain and sleep disorder. The dynamic, cyclic process of sleep is divided into non-rapid­ eye-movement (NREM) sleep, traditionally stages 1-4 with the deepest stages 3-4 referred to as slow-wave-sleep (SWS) or N3, and rapid-eye-movement (REM) sleexpx_ iii      SWS predominates

during the first third of the night, whereas REM sleep predominates during the last half of the night. Each NREM to REM sleep cycle lasts about 80-110 minutes, and over the course of the night these cycles are repeated three to six times.

 

Pain causes sleep apnea in a similar manner as PTSD causes sleep apnea; namely by dysregulation of REM sleep. Moldofsky reported in Sleep and pain (Sleep Med Rev. 2001 Oct; 5(5):385-396) that painful disorders interfere with sleep.

 

Migraine and cluster headaches are related to REM sleep, whereas headache is associated with snoring and sleep apnea. The management of the sleep disorder ameliorates both morning headache and migraine. Noxious stimuli administered into muscles during slow-wave sleep (SWS) result in decreases in delta and sigma but an increase in alpha and beta EEG frequencies during sleep. Noise stimuli that disrupt SWS result in unrefreshing sleep, diffuse musculoskeletal pain, tenderness, and fatigue in normal healthy subjects.

 

Such symptoms accompany alpha EEG sleep patterns that often occur in patients with fibromyalgia. The alpha EEG patterns include phasic and tonic alpha EEG sleep as well as periodic K alpha EEG sleep or frequent periodic cyclical alternating pattern. Moreover, alpha EEG sleep, as well as sleep-related breathing disorder and periodic limb movement disorder, occur in some patients with fibromyalgia, rheumatoid arthritis and osteoarthritis. Depression and not alpha EEG sleep are features of somatoform pain disorder. Disturbances in sleep, pain, behavior and psychological distress influence return to work in workers who have suffered a soft tissue injury , e.g. low back pain. Patients with irritable bowel disorder have disturbed sleep and have increased REM sleep.  In conclusion, there is a reciprocal relationship between sleep quality and pain.

B.urstrom et al  xxiv reported  :

" Sleep and pain interact in a bidirectional manner. Complaints of sleep disturbance are ubiquitous among patients with chronic pain disorders, and conversely, patients with persistent insomnia symptoms commonly report suffering from chronic pain chronic pain...chronic pain conditions and sleep disturbances are intertwined through comorbidities , which together cause detrimental psychologicaland physical consequences ...

About 50% of people with persistent insomnia disorder report suffering from chronic pain, and conversely, the same percentage of people with chronic pain meet criteria for

persistent insomnia disordexrx_v    Complaints of sleep disturbance are ubiquitous among

patients  with chronic pain disorders (67-88%?xv i_      Besides the direct impact of pain and its comorbidities on sleep, some widely used pain medications, such as opioids, may exert direct negative effects on sleep profilesX,w ii X,w iii  x_xi

 

Osteoarthritis [OAJ

 

OA is among the top 10 causes of disability worldwide, and in older adults in the USA, lower extremity OA is the leading cause of mobility impairmenxtxx_ The primary symptom of OA is pain, and sleep disturbances are also common. In a large cohort (n=613) of older patients 'Suffering from moderate OA of the hip or knee, 70% reported

poor slee=p _  i    Regression analyses revealed that greater arthritis severity, depressed

mood and restless legs syndrome (which was found in 25% of the patients) were

 

 

 

 

 

                                                                 

independent correlates of poor sleep. Interestingly , treatment of OA with arthroplasty or opioid analgesics, have been shown to improve not only pain, but also subjective and objective measures of sleexpxx ixi xx iii .

. . . [Leigh et al.] studied an OA population (OA of the hip or knee, or both). In this sample

of OA patients, Leigh et axlx_ x vi     found a significant increase ofNl  (23.6±6.9 vs 15.2±3.9

%), and decrease ofN2 (47.7±8.2 vs 54.4±7.8 %) as compared to HC [healthy controls]. There were no sleep continuity differences between the groups, but it is important to note that both groups had low SE [sleep efficiency] (OA: 81.5±7.9 %; HC: 80.4±7.7 %), and high WASO [wakefulness after sleep onset] (OA: 102.8±38.2 min; HC: 85.3±37.0 min), indicating fragmented sleep...

 

Pathophysiologic mechanisms underlying the connection between sleep and pain

 

Etiologically, the bidirectional relationship between persistent pain and poor sleep. .. include central neuroimmune activation , disturbed neurotransmitter balance, and neuroendocrine axis aberrations .. .Imbalances in central pro- and anti-inflammatory

 

Cytokines have been detected across several human chronic pain populationxsxxv , and these cytokines, especially IL-IP [interleukin] and TNF-a [tumor necrosis factor], have also been found to play a .role in the physiological regulation of sleep, and sleep homeostasixsxxv i.

Levels of IL-1P and TNF-a vary with the sleep-wake cycle, and in animal experimental models, administration of IL-1p and TNF-a increase NREM sleep in a dose- and time­ dependent manner. IL-1 p typically causes sleep fragmentation, high doses actually suppress both REM and NREM sleep, and sleep deprivation has been shown to increase IL-Ip mRNA in the brainxxxvii_

 

Nadeemxxxv iii   et al reported that Obstructive sleep apnea and chronic musculoskeletal pain both affect Sleep architecture

 

There were 393 subjects: 200 cases (obstructive sleep apnea and chronic musculoskeletal pain) and 193 controls (obstructive sleep apnea alone). There was significant difference in total sleep time (274.5 ± 62.5 vs. 302.2 ± 60.1 min, p = 0.0001), sleep efficiency

(73.54 ± 15.8 vs. 78.76 ± 14.3%, p = 0.0003), and REM sleep onset (148.18 ± 80.5 vs.

124.8 ± 70.9 min, p = 0.006). Subgroup analysis within the obstructive sleep apnea with chronic musculoskeletal pain group revealed that subjects had better total sleep time and sleep efficiency if they were on REM sleep affecting medications (suppressants and stimulants). Those on REM sleep suppressants slept 25.7 min longer and had 6.4% more efficient sleep than those not on REM suppressants (p = 0.0034 and p = 0.0037).

He concluded that Patients with obstructive sleep apnea and chronic musculoskeletal pain sleep not only significantly less but also with inferior sleep quality. Their REM sleep is also less in duration and its onset is delayed. Despite low TST and SE, these patients may not exhibit sleepiness."

Aytekinxxxi     et al reported:

" ... In many studies, a positive correlation has been found between sleep disorders and chronic pain... Between 50% and 89% of chronic pain patients complain of poor sleep

pain, fibromyalgia, and rheumatoid pain are the most frequent conditions that lead to chronic pain. Pain is also a relatively frequent complaint of patients suffering from restless leg syndrome (RLS), which manifests as periodic limb movements during sleep (PLMS). ..and/or feeling unrefreshed  upon awakeningx  ¹     Back pain, temporomandibular myofascia

In this study, the prevalence of CWP [chronic widespread musculoskeletal pain] in patients with obstructive sleep apnea was 55.4%...

He concluded that Pain and sleep influence each other in many ways, and the relationship between them seems to be bidirectionaxl li_ Multiple biological and psychological factors may initiate and maintain paixnli i  . . .

Okurxa iiil    et al reported:

" In comparison to normal subjects , sleep duration was shorter in CWP [chronic widespread musculoskeletal pain] patients (-71 min; p<0.01); sleep efficiency was significantly lower in C\YP and insomnia patients (-10.1% and -11.1%, respectively; p<0.05). CWP and PLMS [periodic limb movements during sleep] patients lost one non­ rapid eye movement (REM) to REM sleep cycle (p<0.04). An intermediate level of PLM was observed during the sleep of CWP patients in comparison to normal subjects (8.8/h vs. 2.0/h) and PLMS patients (33/h). Regular use of non-narcotic analgesics did not seem to interfere with sleep variables."

Conclusion

After reviewing all of the veteran's medical and military records, it is my expert medical opinion that it is more likely than not (50% or more) that the veteran's sleep apnea is caused by and/or aggravated by his service-connected conditions of depressive disorder and chronic pain syndrome related to his service-connected injuries. While each of these conditions solely is sufficient to cause OSA, clearly a combination of these disabilities will cause OSA.

[Berta]

"The submitted statement from Dr. XXXXX opined that yourmedications associated with the treatment of your service connected depressivedisorder assisted in causing your obstructive sleep apnea.

The evidence shows no medication treatment for any mental health condition prior to or at the time of your diagnosis of obstructive sleep apnea. "

I am stuck on that statement from your decision and have not found the meds mentioned in the IMO.

Is that a true statement from the VA?

If it is a false VA statement, what meds were you on prior to the SA diagnosis?

The IMo doc said:

"After reviewing the veteran's c-file and the pertinent recent medical literature, I opine that it is more likel y than not that the veter...etc"

The C file is not the medical record file- he did refer to a few entries in the medical records but did he have the entire VA medical records to show your medication profiles?

 

 

 

[Berta]

There certainly are awards at the BVA similar to your claim- here is one of them based on Dr Anaise's IMO:

http://www.danaise.com/bva-approves-osa-due-to-ptsd-based-on-dr-anaises-imo/

In this next claim, the BVA made a very good legal point:

 

"In support of his claim, the Veteran has submitted various studies, including a study by the National Institute of Health (NIH) which shows some evidence of correlation between sleep disordered breathing and depression. He has also submitted an opinion from a private physician which states that, after reviewing the Veteran's military and civilian psychiatric records and sleep studies, it is as likely as not that the Veteran's major depressive disorder is causally related to his obstructive sleep apnea. That opinion is supported by citation to the NIH study, as well as a second study conducted at Stanford University between 1994 and 1999. In July 2014 the Veteran was afforded a VA examination in connection with his claim which opined against a medical nexus between his sleep apnea and depression. However, the Board notes that this examination report is inadequate as it stated that there is no clear evidence in the medical literature showing major depression causes sleep apnea. However, it does not address the studies provided by the Veteran or cited by the private physician, let alone provide a reason for rejecting those medical studies. Therefore, the Board finds this opinion to have no probative value. Thus, the only probative medical opinion of record weighs in favor of the Veteran's claim. Consequently, the Board finds that the evidence is at the very least in relative equipoise as to whether the Veteran's sleep apnea is the result of or proximately due to his service-connected major depressive disorder. Therefore, affording benefit of the doubt in favor of the Veteran, the Board finds that service connection is warranted for obstructive sleep apnea as secondary to major depressive disorder. 38 U.S.C.A. § 5107 (West 2014); 38 C.F.R. §§ 3.102, 3.310 (2015). ORDER Service connection for obstructive sleep apnea is granted, as secondary to service-connected major depressive disorder.

https://www.va.gov/vetapp16/Files3/1624350.txt

Can you post the C & P exam results?(Cover C ile #, name prior to scanning it)

If it contains this type of statement_

. "However, the Board notes that this examination report is inadequate as it stated that there is no clear evidence in the medical literature showing major depression causes sleep apnea. However, it does not address the studies provided by the Veteran or cited by the private physician, let alone provide a reason for rejecting those medical studies."

It can be appealed on that basis if the examiner stated something to that affect.

BVA decision are not evidence -however it is quite obvious ,with the above BVA decisions,  that the medical literature you have, within the IMO,should be sufficient for an award.

You could ask for a reconsideration, using any BVA decision ,like the one above, to bolster that. And cite Allen V... Brown:

"A disability may also be found service connected on a secondary basis by demonstrating that the disability is either (1) proximately due to or the result of an already service-connected disease or injury or (2) aggravated by an already service-connected disease or injury. See Allen v. Brown, 7 Vet. App. 439, 448 (1995); 38 C.F.R. § 3.310 (2015)."

The above vet https://www.va.gov/vetapp16/Files3/1624350.txt

did not even have an IMO.

If their entry about the lack of medications is correct,maybe Dr Anaise should write an addendum.

Did your IMO doctor have a copy of the C & P exam?

It helps considerably when a IMO/IME doctor has the VA's negative opinion, and then can argue against it effectively.

 

Edited June 25, 2019 by Berta
added more

[JaeNobe]

1 hour ago, Berta said:

"The submitted statement from Dr. XXXXX opined that yourmedications associated with the treatment of your service connected depressivedisorder assisted in causing your obstructive sleep apnea.

The evidence shows no medication treatment for any mental health condition prior to or at the time of your diagnosis of obstructive sleep apnea. "

I am stuck on that statement from your decision and have not found the meds mentioned in the IMO.

Is that a true statement from the VA?

If it is a false VA statement, what meds were you on prior to the SA diagnosis?

The IMo doc said:

"After reviewing the veteran's c-file and the pertinent recent medical literature, I opine that it is more likel y than not that the veter...etc"

The C file is not the medical record file- he did refer to a few entries in the medical records but did he have the entire VA medical records to show your medication profiles?

 

 

 

I was stuck on that statement as well. 

I have been on pain meds since I was in and first hurt my back until now 20 years later. 

Yes, I sent him my medication records as well. 

[JaeNobe]

47 minutes ago, Berta said:

 

If their entry about the lack of medications is correct,maybe Dr Anaise should write an addendum.

Did your IMO doctor have a copy of the C & P exam?

It helps considerably when a IMO/IME doctor has the VA's negative opinion, and then can argue against it effectively.

 

No I had the IMEO done first then went to the C&P Exam. 

 

I will post the C&P in a few minutes....