United States Court of Appeals for Veterans Claims

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Vet. App. No. 16-1515

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JOSEPH HARVEY, JR.,

Appellant,

ROBERT A MCDONALD,

Secretary of Veterans Affairs,

Appellee.

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BRIEF FOR APPELLANT

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David Anaise, MD, JD

Benham & Anaise, LLC

1001 W. San Martin Dr.

Tucson AZ 85704

(520) 219-7321

STATEMENT OF THE ISSUES

Whether the Board’s decision to deny Appellant compensation for sleep apnea and tinnitus was clearly erroneous and, therefore, must be reversed or remanded.

We argue:

I. The Board erred when it stated that there is a lack of medical nexus for sleep apnea.

II. The rules require that the Board relies on medical opinion and may not substitute its own medical judgment for independent medical evidence.

III. The Board mischaracterized the treatise provided.

IV. Obstructive Sleep Apnea (OSA) is not limited to obese veterans.

V. The Board erred in stating “while this article supports a correlation between mental health disorders and sleep apnea (and other sleep disorders), it does not support a causal relationship, or, specifically, a finding that psychiatric disorders cause sleep apnea.” [R. at 26]

VI. The Board erred in denying service connection for tinnitus.

STATEMENT OF THE CASE

The veteran, who is the Appellant in this case, had active service from June 1988 to June 1992. This matter came before the Board of Veterans’ Appeals (BVA or Board) from February 2009, February 2013, and April 2013 rating decisions by the above Department of Veterans Affairs (VA) Regional Office (RO) in St. Petersburg, Florida.

The BVA decision of January 14, 2016 [R. at 2-45] states:

1) Regarding the claim for service connection for PTSD [R. at 7]:

“In a February 2009 rating decision, service connection was granted for depressive disorder. The Board found that the medical evidence of record indicates that the Veteran’s psychiatric symptoms cannot be differentiated between the service-connected depressive disorder and non-service-connected PTSD. VA treatment notes indicate he has been variously diagnosed with both PTSD and depression, and that the same or similar symptoms - such as depressed mood, panic, social isolation, and anxiety - have been attributed to both diagnoses.”

The Board found that the criteria for a 70 percent disability rating for depressive disorder had been met for the entire initial rating period on appeal. [R. at 36].

2) Regarding a claim for service connection for Nerve Damage to the Bilateral Upper and Lower Extremities [R. at 21]:

“Resolving reasonable doubt in the Veteran’s favor, the Board finds that service connection for a medically unexplained chronic multisymptom illness manifested by pain and numbness of the bilateral upper and lower extremities as a result of exposure to environmental hazards during Gulf War service, claimed as nerve damage, is warranted.”

The claim for a medically unexplained chronic multisystem illness was reopened and granted. [R. at 44].

3) Regarding a claim for service connection for sleep apnea [R. at 23]:

“…the Board does not find that the evidence sufficiently supports recurrent symptomatology of sleep apnea since service, so as to warrant a finding of a nexus between the current sleep apnea and active service.”

4) Regarding a claim for service connection for tinnitus the Board stated [R. at 10]:

“Although in-service acoustic trauma and possible exposure to toxins were conceded in light of the Veteran’s combat service in Saudi Arabia, service treatment records did not show any symptoms, reports, findings, diagnosis, or treatment for hearing loss, tinnitus, or headaches.”

SUMMARY OF THE ARGUMENTS

We argue:

VII. The Board erred when it stated that there is a lack of medical nexus for sleep apnea.

VIII. The rules require that the Board relies on medical opinion and may not substitute its own medical judgment for independent medical evidence.

IX. The Board mischaracterized the treatise provided.

X. Obstructive Sleep Apnea (OSA) is not limited to obese veterans.

XI. The Board erred in stating “while this article supports a correlation between mental health disorders and sleep apnea (and other sleep disorders), it does not support a causal relationship, or, specifically, a finding that psychiatric disorders cause sleep apnea.” [R. at 26]

XII. The Board erred in denying service connection for tinnitus.

ARGUMENTS

I. The Board erred when it stated that there is a lack of medical nexus for sleep apnea.

The Board decision in this case, dated January 14, 2016, states [R. at 26]:

“…in this case, there have been no favorable medical opinions supporting a medical nexus between the Veteran’s service-connected psychiatric disability and his current sleep apnea.”

In addition to being a lawyer, I am also a board certified surgeon (transplantation surgery).[1] In the appeal brief provided in this case, on December 8, 2014, I opined that there is a medical nexus for sleep apnea; that it is more likely than not that the veteran’s OSA is secondary to his service-connected PTSD. The brief clearly identified me as an M.D., J.D. [R. at 89]. The Board, in recent cases, has recognized that I am a physician and has attributed the medical opinions correctly. [2]

II. The rules require that the Board relies on medical opinion and may not substitute its own medical judgment for independent medical evidence.

We provided our appeal brief on December 8, 2014. [R. at 82]. A Statement of the Case was provided on March 6, 2015, denying the veteran’s claim for service connection for sleep apnea, relying on an expert opinion[3] made on April 4, 2013. [R. at 404]. It is clear that the expert was never given the opportunity to review the appeal brief and the enclosed medical treatise.

The rules require that the Board relies on medical opinion and may not substitute its own medical judgment for independent medical evidence. There is no evidence in the record that the Board provided our medical treatise to an expert asking for a comment on the assertions we have made. Thus, the determination by the BVA that the scientific information we provided in out brief is incorrect is contrary to law:

In Colvin v. Derwinski, 1 Vet. App. 171(1991), this Court held that the Board may not substitute its own medical judgment for independent medical evidence. See also Cosman v. Principi, 3 Vet. App. 503, 506 (1992); Hatlestad v. Derwinski, 3 Vet. App. 213, 217 (1992) (Hatlestad II); Budnik v. Derwinski,3 Vet. App. 185, 187 (1992); Quarles v. Derwinski, 3 Vet. App. 129, 139 (1992); Tobin v. Derwinski, 2 Vet. App. 34, 39 (1991). While the Board is not required to accept the medical authority supporting a claim, it must provide its reasons for rejecting such evidence and, more importantly, must provide a medical basis other than its own unsubstantiated conclusions to support its ultimate decision. Colvin,1 Vet. App. at 175; see also Simon v. Derwinski, 2 Vet. App. 621, 622 (1992); Hatlestad v. Derwinski, 1 Vet. App. 164, 169 (1991) (HatlestadI); Gilbert,1 Vet. App. at 57; Murphy v. Derwinski, 1 Vet. App. 78, 81 (1990).

III. The Board mischaracterized the treatise provided.

The Board stated [R. at 26 (emphasis added)]:

“The Board also acknowledges the article submitted by the Veteran in December 2014 entitled “Sleep Disorders and Associated Medical Comorbidities in Active Duty Military Personnel.” That article states that recent evidence suggests the increased incident of sleep disturbances (including sleep apnea) in redeployed military personnel is potentially related to PTSD, depression, anxiety, or TBI. The article cites to a particular study that evaluated polysomnographic data in 69 redeployed soldiers with PTSD, TBI, and other mental health disorders in which a diagnosis of obstructive sleep apnea was made in 76.8% of the participants. The Board finds that while this article supports a correlation between mental health disorders and sleep apnea (and other sleep disorders), it does not support a causal relationship, or, specifically, a finding that psychiatric disorders cause sleep apnea.”

The treatise attached to the appeal brief addresses sleep disturbances, including insomnia. It does provide a unique and detailed review of obstructive sleep apnea (OSA) in veterans deployed in recent wars [R. at 102-103 (emphasis added)]:

“This is the first study to systematically describe primary sleep disorders and associated comorbidities in a large cohort of military personnel referred with sleep complaints in accordance with standardized diagnostic criteria. OSA was the most frequent diagnosis in 51.2%, consistent with previous reports of primary sleep disorders at civilian sleep centers…Notably, our results more closely reflect a recent report describing the prevalence of sleep disorders in North American police officers, where 40.4% screened positive for a sleep disorder with OSA and insomnia as the most common diagnoses…The percentages of military personnel
with PTSD (13.2%) and mTBI (12.8%) are similar to previous reports, whereas a larger percentage of those in our study had depression (22.6%) and anxiety (16.8%).”

This high incidence of OSA in these veterans (and 76.8% in a subgroup noted by the Board [R. at 26]) is much higher than the incidence of OSA in the civilian population, which is only 7%.[4] Thus, the article clearly supports the argument that sleep apnea is more prevalent in veterans suffering from PTSD and mood disorder.

IV. Obstructive Sleep Apnea (OSA) is not limited to obese veterans.

The SOC of March 6, 2015 states that only obesity can cause OSA [R. at 404]:

“The examiner provided the following rationale: ‘Per medical literature review, obstructive sleep apnea is not caused by a mental condition. The major cause of obstructive sleep apnea is weight gain. The Veteran entered the service weighing 155 lbs. in 1988. By 26 May 1992 the Veteran’s weight was 175 lbs. On 4 March 2013, the Veteran’s weight was 255 lbs.’”

The treatise provided states that “Seven hundred sixty-one PSGs and corresponding medical records were reviewed and adjudicated for a primary sleep disorder…the group was 35.5 (8.6) y with a BMI of 29.8.” [R. at 100]. While not at an ideal weight, the veterans in this study were not obese. In addition to obesity there are at least ten medical conditions that cause sleep apnea including: upper airway disease like rhinitis, sinusitis, GERD and asthma; tinnitus; PTSD; mood disorder; pain; and the use of narcotics. Obesity may aggravate sleep apnea, but the law requires that if there are two causes of an additional disability, one service-connected and the other non-service-connected, the service-connected disability prevails.[5]

The Board demands that Appellant not only show that sleep apnea has a much higher incidence in veterans suffering from PTSD and mood disorder, than in veterans not suffering from PTSD, but that Appellant also explain the precise mechanism by which PTSD causes sleep apnea. Interestingly, the Board did not require of the VA expert to explain how obesity causes sleep apnea. The mistaken belief is that obesity causes fat deposits which obstruct the upper airway. 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. Sleep apnea always occurs during sleep, and thus, could not be entirely mechanical.

A growing body of evidence suggests that disturbed sleep is more likely to be a core feature of PTSD rather than just a secondary symptom. Hypoxia, sympathetic discharge from respiratory disturbances, dysfunctional REM sleep, and abnormal REM mechanism have been proposed as a mechanism for sleep apnea in PTSD patients.[6]

Kobayashi[7] et al. conducted a meta-analytic review of 20 polysomnographic studies comparing sleep in people with and without PTSD. Results[8] showed that PTSD patients had more stage 1 sleep, less slow wave sleep, and greater rapid-eye-movement density compared to people without PTSD.

A recent study[9] showed that treatment of OSA with CPAP is associated with a decrease in the number of nightmares and daytime sleepiness in PTSD patients. This study also showed a positive correlation of REM sleep percentage with the number of nightmares. This supports the hypothesis that dysfunctional REM sleep mechanism may be involved in the pathogenesis of PTSD. A recent study[10] reported that REM AHI and interrupted sleep at night were independent predictors of nightmares in OSA patients, and CPAP therapy results in significant improvement in nightmare occurrence. Apparently when a patient spends more time in REM the likelihood of having nightmares becomes higher. REM suppression with prazosin, an α-1 inhibitor, showed improvement in combat-related PTSD nightmares and sleep quality in active-duty soldiers in a recent trial. This may indicate that suppressing the “dysfunctional REM” in PTSD patients may have helped reduce symptoms.

OSA patients were shown to maintain their upper airway patency in wakefulness via a compensatory, augmented EMG activity of their airway dilator muscles, during wakefulness [and non-rapid eye movement (NREM) sleep]. 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.

In the treatise provided Mysliwiec et al[11] reported [R. at 100, emphasis added]:

“Military personnel with mild and moderate-to-severe OSA had an elevated AHI and desaturation profile corresponding with their severity of disease with notable sleep architectural changes including an elevated Al, decreased SE, and decreased N3 and REM sleep.”