Citation Nr: 21013635 Decision Date: 04/05/21 Archive Date: 03/10/21 DOCKET NO. 15-12 720 DATE: April 5, 2021 ORDER Service connection for peripheral neuropathy, to include as due to herbicide agent exposure, for substitution purposes is denied. FINDING OF FACT The preponderance of the evidence is against a finding that the Veteran’s peripheral neuropathy is the result of his active service, to include as due to conceded exposure to herbicide agents. CONCLUSION OF LAW The criteria for service connection for peripheral neuropathy, to include as due to herbicide agent exposure, for substitution purposes have not been met. 38 U.S.C. §§ 1101, 1110, 1112, 1113, 1116, 1137, 5103, 5103a, 5107; 38 C.F.R. §§ 3.102, 3.103, 3.303, 3.307, 3.309. REASONS AND BASES FOR FINDING AND CONCLUSION The Veteran served on active duty in the United States Army from August 1966 to August 1969. He died in March 2018 and his surviving spouse has been substituted as the Appellant. This matter was previously before the Board in March 2019 at which time it was remanded for further evidentiary development. Substantial compliance with the remand requests having been accomplished, the Board may proceed to consider the claim. See Stegall v. West, 11 Vet. App. 268 (1998). The Board has limited the discussion below to the relevant evidence required to support its finding of fact and conclusion of law, as well as to the specific contentions regarding the case as raised directly by the Veteran and those reasonably raised by the record. See Scott v. McDonald, 789 F.3d 1375, 1381 (Fed. Cir. 2015); Robinson v. Peake, 21 Vet. App. 545, 552 (2008). Service Connection Generally, in order to prove service connection, there must be competent, credible evidence of (1) a current disability, (2) in-service incurrence or aggravation of an injury or disease, and (3) a nexus, or link, between the current disability and the in-service disease or injury. See, e.g., Davidson v. Shinseki, 581 F.3d 1313 (Fed. Cir. 2009); Pond v. West, 12 Vet. App. 341 (1999). This means that the facts establish that a particular injury or disease resulting in disability was incurred coincident with service in the Armed Forces, or if preexisting such service, was aggravated therein. 38 U.S.C. § 1110; 38 C.F.R. § 3.303(a). Service connection may be granted for any disease diagnosed after discharge, when all the evidence, including that pertinent to service, establishes that the disease was incurred in service. 38 C.F.R. § 3.303(d). Furthermore, if a veteran was exposed to herbicide agents (e.g., Agent Orange) during active service, presumptive service connection is warranted for certain specified diseases. 38 C.F.R. §§ 3.307, 3.309. Exposure to herbicide agents has been conceded based on the Veteran’s confirmed service in the Republic of Vietnam (Vietnam). 38 U.S.C. § 1116A. The specified diseases for which presumptive service connection due to exposure is warranted include early-onset peripheral neuropathy if manifest to a degree of 10 percent or more within a year of last exposure. 38 C.F.R. §§ 3.307(a)(6), 3.309(e). Notwithstanding the foregoing presumption provisions, a claimant is not precluded from establishing service connection for a disability due to exposure to herbicide agents with proof of direct causation. Combee v. Brown, 34 F.3d 1039, 1042 (Fed. Cir. 1994); Ramey v. Brown, 9 Vet. App. 40, 44 (1996), aff’d sub nom, Ramey v. Gober, 120 F.3d 1239 (Fed. Cir. 1997), cert. denied, 118 S. Ct. 1171 (1998). VA is responsible for determining whether the evidence supports the claim or is in relative equipoise, with the Veteran prevailing in either event, or whether a preponderance of the evidence is against the claim, in which case the claim is denied. 38 U.S.C. § 5107; Gilbert v. Derwinski, 1 Vet. App. 49 (1990). Turning to the evidence of record, the Veteran’s service treatment records (STRs) do not contain any complaints, symptoms, treatment, or diagnosis of peripheral neuropathy or a similar condition. His July 1969 separation examination was negative for any relevant symptomology and an evaluation of the upper and lower extremities was normal. The Veteran denied any pertinent symptoms on a report of medical history. Post-service, the Veteran underwent a February 1987 VA evaluation for possible exposure to toxic chemicals, nearly two decades after service. At that time, he reported direct and repeated exposure to herbicide agents. An evaluation of his bilateral extremities was normal and there were no reports of peripheral neuropathy symptoms or neuropathic complaints. Indeed, the first report of neuropathic symptoms occurred in October 2010, over four decades after service. The Veteran described dull, aching numbness in both arms, tingling up into his shoulders, and stabbing pains in the lower arms and back of his hands for two months following administration of a flu shot. While there was tingling and numbness in his forearms, wrists, and hands, there was no involvement in the legs or feet. Sensory and reflex examinations of the bilateral upper and lower extremities were completely normal. The clinician suspected Guillain-Barre syndrome and oral steroids were prescribed. Following the complaints of arm numbness since the flu shot, an x-ray of the cervical spine was conducted in December 2010. It revealed degenerative disc disease (DDD) involving the cervical spine with mild neural foraminal narrowing at the C5-C6 level. The examining clinician stated that given his symptoms, the Veteran might have peripheral neuropathy associated with flu vaccines. A March 2012 VA treatment record reflected a report of tingling and numbness in the Veteran’s arms and previous symptoms in his legs. He also stated that his hands felt swollen. The clinician diagnosed possible peripheral neuropathy and possible carpal tunnel syndrome (CTS). It was also noted that the Veteran was borderline diabetic. Subsequently, CTS and idiopathic peripheral neuropathy were added as current problems in his VA medical record. An undated private treatment record, which the Board identifies as occurring on or around April 2012 in light of the Veteran’s noted age at the time (i.e., 65 years, 9 months) demonstrated an abnormal electrodiagnostic evaluation. All sensory nerve conduction studies revealed borderline to mildly prolonged latencies, reduced amplitudes, and mildly prolonged durations. Motor nerve conduction studies revealed normal distal motor latencies, borderline to normal amplitudes, normal conduction velocities, and mildly prolonged latencies more than expected for height with several notable waves indicative of prior reinnervation. Needle electromyography (EMG) screening of select muscles in the more symptomatic left upper limb was within normal limits with no evidence of abnormal spontaneous activity, normal motor unit waveforms with some chronic appearing larger motor units noted, and normal recruitment patterns. The examiner noted that the Veteran reported a history significant for prior Agent Orange exposure and clinically diagnosed Guillain-Barre syndrome approximately 18 months previously after receiving the H1N1 vaccination that required a protracted course of outpatient oral steroids. The examiner stated that the pattern of abnormalities seen on the electrodiagnostic study could be related to any of the reported conditions including remote toxic neuropathy and residual evidence of prior acute inflammatory demyelinating polyneuropathy (AIDP) with mild axonal involvement (Guillain-Barre). A September 2012 EMG/nerve conduction study (NCS) demonstrated peripheral neuropathy. The clinician’s conclusion was “peripheral polyneuropathy – sensory greater than motor, mixed demyelinating and axonal, symmetric.” It was explained to the Veteran that this was evidence of a disease involving the peripheral nerves, more severe for the sensation and feeling function of the nerves than the motor control over the muscles, involving both sides, and showing evidence of disruption of the myelin sheaths that also involved the major nerve fiber (axon). The clinician considered that this sort of nerve damage could result from Agent Orange exposure or from the previous Guillain-Barre experience following the flu vaccinations. Other possible causes included diabetes mellitus, alcohol abuse, pernicious anemia, lead or arsenic poisoning, other drugs such as chemotherapy agents, porphyria, and other causes. Medication management was suggested to treat the Veteran’s symptoms. An October 2012 private treatment record reflected the Veteran’s complaints of numbness, heaviness, tenderness, burning, and a swollen sensation in his bilateral lower extremities radiating from thighs to feet. The clinician suspected that peripheral neuropathy could be due to his pre-diabetic state or could be due to lumbar radiculopathy. Lumbar imaging demonstrated DDD with facet joint narrowing. A sensory examination reflected a slight reduction in pinprick and vibration sense. A reflex evaluation demonstrated that deep tendon reflexes were absent in the upper extremities and reduced in the lower extremities. A motor examination revealed no abnormal spontaneous movement, normal tone, no atrophy or fasciculations, no drift in the extremities, normal direct muscle testing, and normal fine motor movements. The Veteran sought emergency care for numbness in his left arm and facial muscles in July 2013. A transient ischemic attack (TIA) was suspected, given his past history of a remote TIA. In August 2013 and October 2013 VA treatment records, peripheral neuropathy since Agent Orange exposure was noted, due to the Veteran’s report. The Veteran submitted a statement in June 2014 describing exposure to Agent Orange from helicopters with spray tanks on a weekly basis. He stated that his skin and clothes were wet with the sprayed substance. In October 2014, clinicians stated that the Veteran was a borderline diabetic but wondered if his condition had worsened because he reported that pain in his hands and feet was worse. A neurology consultation was obtained in July 2015. The Veteran reported numbness, tingling, and burning with sharp, shooting pains in his hands and feet starting 5 to 10 years previously. The symptoms began on an intermittent basis at first, mostly at night, slowly progressing into sharp, shooting pains and a burning sensation. The symptoms were in the upper extremities initially and later in his feet. Prescribed medications had helped to decrease the sharp pains and burning but numbness continued on a constant basis for the past two to three years. Both upper and lower extremities were equally affected. The Veteran denied back pain, neck pain, or radicular pain. The clinician noted that a prior EMG was indicative of peripheral neuropathy and x-rays showed multilevel mild-to-moderate disc changes from C3 to C7. The clinician’s impression was mild peripheral neuropathy, probably a small fiber disease. An EMG/NCS was conducted which revealed residual evidence of peripheral neuropathy with electrical improvement as compared to the 2012 EMG/NCS. The clinician noted that such conventional testing would not detect whether a small fiber neuropathy was clinically present. An August 2016 VA treatment record noted a current diagnosis of idiopathic progressive neuropathy. A September 2016 neurology consultation stated that the Veteran’s peripheral neuropathy was probably related to small fiber disease. October 2016 imaging demonstrated mild degenerative changes in the Veteran’s lumbar spine. In a December 2016 record, the Veteran noted that when he took the H1N1 vaccine he was allergic and had swelling and pain in his hands and forearms. He stated that he took oral steroids for a year thereafter due to Guillain-Barre syndrome. He described his Agent Orange exposure and wondered whether the vaccine reacted with the prior Agent Orange exposure and caused changes in his hips and legs. After repeated reports of chronic low back pain, an x-ray was conducted which revealed mild multilevel disc space narrowing and endplate spurring with facet hypertrophy in the lower lumbar spine. May 2017 and November 2017 VA treatment records noted neuropathy from Agent Orange. A CT scan was conducted in November 2017 which demonstrated multilevel degenerative disease of the cervical spine with varying degrees of stenosis. Numbness of unknown etiology in the right side of the Veteran’s head was reported in November 2017. VA neurology consultations in January 2018 and February 2018 noted peripheral neuropathy related to small fiber disease. Clinicians stated that his peripheral neuropathy appeared to be under fairly good control. A VA medical opinion was obtained in October 2019. The clinician determined that it was less likely than not that the Veteran’s peripheral neuropathy was caused or aggravated by service or by Agent Orange exposure. In support, she stated that his neuropathy symptoms emerged around 2010, 41 years after discharge. Toxic neuropathy from Agent Orange is present within a year of exposure to Agent Orange. The Veteran’s STRs and medical records were silent regarding neuropathy symptoms until 2010. He was also clinically diagnosed with Guillain-Barre syndrome in 2010 with symptoms of bilateral upper extremity weakness, pain, and pins/needles. The 2012 EMG showed a polyneuropathy. The Veteran reported bilateral lower extremity neuropathy symptoms in 2012, noting symptoms had been present for about one year prior. The neurologist suspected he had lumbar radiculopathy. Lumbar imaging demonstrated DDD with facet joint narrowing. Cervical spine imaging in 2015 noted DDD. Both conditions have the potential to cause neuropathy (radiculopathy). The Veteran’s medical record revealed that he started experiencing symptoms of bilateral upper extremity and lower extremity peripheral neuropathy in 2010 (when he was diagnosed with Guillain-Barre syndrome) and in 2011 for lower extremity symptoms (due to suspected lumbar radiculopathy). His repeat EMG in 2015 showed an improvement from the 2012 EMG which would be consistent with Guillain-Barre. The EMG at the time noted that EMGs cannot evaluate for small fiber neuropathy. Small fiber neuropathy would be diabetes mellitus neuropathy, but the Veteran had no diagnosis of diabetes mellitus and was not treated for hyperglycemia, meaning that diabetes mellitus neuropathy was not a valid diagnosis. As such, the clinician concluded that the Veteran’s bilateral lower extremity neuropathy was at least as likely as not related to lumbar DDD and his bilateral upper extremity neuropathy was at least as likely as not related to his cervical DDD. Service connection for peripheral neuropathy, to include as due to herbicide agent exposure, for substitution purposes, is denied. As noted above, the Veteran has conceded exposure to herbicide agents in service. However, there is no indication that peripheral neuropathy manifested to a degree of 10 percent or more within a year of exposure. Indeed, in this case, there is no indication the Veteran has any neurological manifestations for over four decades after service. As such, service connection on a presumptive basis is not warranted. 38 C.F.R. §§ 3.307, 3.309. As presumptive service connection based on herbicide agent exposure is not available, the evidence must demonstrate proof of direct causation. There were multiple speculations throughout the medical record regarding the Veteran’s symptomology. Clinicians noted the Veteran’s report of peripheral neuropathy due to Agent Orange exposure and the April 2012 and September 2012 private clinicians stated that his symptoms could be related to his remote toxic exposure or Guillain-Barre syndrome. However, there is no medical opinion of record concluding that the Veteran’s peripheral neuropathy was the result of his remote herbicide agent exposure. The private clinicians’ statements that his symptoms “could be” related to herbicide agent exposure, without any supporting rationale, are too speculative to support a finding of service connection. See McLendon v. Nicholson, 20 Vet. App. 79, 85 (2006) (stating that speculative medical opinion as to causation cannot establish medical nexus to service); see also Polovick v. Shinseki, 23 Vet. App. 48, 187 (2009) (holding physician’s statement that veteran’s brain tumor “may well be” connected to Agent Orange exposure was speculative); Bloom v. West, 12 Vet. App. 185, 187 (1999) (noting that the use of the term “could,” without additional rationale or supporting data, is speculative); Tirpak v. Derwinski, 2 Vet. App. 609, 611 (1992) (holding that medical opinions are speculative and of little or no probative value when a physician makes equivocal findings such as “the veteran’s death may or may not have been averted”). Further, the Veteran’s and Appellant’s belief that peripheral neuropathy was the result of herbicide agent exposure does not constitute competent evidence. The Veteran was competent to describe what he experienced in service and the onset of his symptomology. However, he and the Appellant have not been shown to have the requisite medical knowledge and training to provide an opinion regarding the etiology of a complex medical condition. As such, their beliefs on etiology carry no probative weight. (Continued on the next page)   In contrast, the Board attaches significant probative value to the VA opinion as it is well-reasoned, detailed, consistent with other evidence of record, and included consideration of the Veteran’s pertinent medical history. See Prejean v. West, 13 Vet. App. 444, 448-9 (2000). The VA clinician discussed the Veteran’s progression of symptoms, noting that the fluctuation in severity of symptomology was consistent with the successful treatment for Guillain-Barre syndrome and that the onset of upper and lower extremity symptoms was consistent with radiological findings of degenerative changes in the cervical and lumbar spine. Further, she identified the most likely causative factors for his peripheral neuropathy symptoms, namely cervical and lumbar DDD demonstrated on imaging. The clinician also addressed the other speculated causes of the Veteran’s symptoms. She determined that his symptomology was not due to diabetes mellitus neuropathy/small fiber neuropathy as he was not diagnosed with diabetes and concluded that it was not due herbicide agent exposure as such toxic exposures resulted in peripheral neuropathy within a year of exposure and not many decades after exposure, such as in the Veteran’s case. Based on the foregoing, the Board finds that service connection for peripheral neuropathy on a direct basis is not warranted. Accordingly, the preponderance of the evidence is against a finding that service connection for peripheral neuropathy, including as due to herbicide agent exposure, is warranted; therefore, the benefit of the doubt rule is not for application. Shereen M. Marcus Veterans Law Judge Board of Veterans’ Appeals Attorney for the Board Rachel E. Jensen, Associate Counsel The Board’s decision in this case is binding only with respect to the instant matter decided. This decision is not precedential and does not establish VA policies or interpretations of general applicability. 38 C.F.R. § 20.1303.