NEUROFIBROMATOSIS

MICHAEL A. PAPPAS · 2026 · Case ID: 26005087

GRANTED

Summary

The veteran, who served in the U.S. Air Force from September 1968 to September 1972, appeals the denial of service connection for neurofibromatosis and ptosis. The veteran contended that both conditions were related to service, including exposure to Agent Orange, or were aggravated by service. The Board found that the veteran's neurofibromatosis pre-existed service, but the VA failed to rebut the presumption of aggravation, as service treatment records showed the condition underwent an increase in severity during service, including tumor growth and surgical excisions. A private medical opinion provided a detailed rationale, linking the accelerated progression of neurofibromatosis to herbicide exposure, concluding it was at least as likely as not aggravated beyond its natural progression. The Board found this opinion probative and the VA did not meet its burden to rebut aggravation, thus granting service connection for neurofibromatosis. For ptosis, the Board found it pre-existed service, as noted on entrance examination, but was aggravated during service. Service treatment records showed treatment for ptosis, including surgery, and the Board found it was as likely as not that the pre-existing condition worsened during service. While a VA examiner opined the aggravation was due to natural progression, a private physician concluded the ptosis was aggravated by the service-aggravated neurofibromatosis, a multifactorial process consistent with the Veteran's documented history. The Board found the private opinion probative and the VA failed to rebut aggravation, granting service connection for ptosis.

Rationale

Pre-existing condition noted on entrance examination.; Presumption of soundness rebutted by clear and unmistakable evidence of pre-existing condition.; Presumption of aggravation triggered by increase in severity during service.; VA failed to rebut aggravation by clear and unmistakable evidence.; Probative private medical opinion found aggravation beyond natural progression due to herbicide exposure.

Service Branch

AIR FORCE

Special Benefit

NO SPECIAL BENEFIT

Docket No.

16-47 290

Full Decision Text

Citation Nr: 26005087
Decision Date: 04/30/26 Archive Date: 04/30/26

DOCKET NO. 16-47 290
DATE: April 30, 2026

ISSUES

1. Entitlement to service connection for a neurofibromatosis disability.

2. Entitlement to service connection for a ptosis disability.

ORDER

Entitlement to service connection for a neurofibromatosis disability based on aggravation is granted, subject to the laws and regulations governing the payment of monetary benefits.

Entitlement to service connection for a ptosis disability based on aggravation is granted, subject to the laws and regulations governing the payment of monetary benefits.

FINDINGS OF FACT

1. It is not shown by clear and unmistakable evidence that the Veteran's preexisting neurofibromatosis disability was not aggravated by service.

2. Resolving reasonable doubt in the Veteran's favor, it is at least as likely as not that the Veteran's ptosis was aggravated by his service-connected neurofibromatosis.

CONCLUSIONS OF LAW

1. The criteria for entitlement to service connection for a neurofibromatosis disability have been met. 38 U.S.C. §§ 1110, 1111, 5107; 38 C.F.R. §§ 3.102, 3.303, 3.304, 3.306.

2. The criteria for service connection for a ptosis disability have been met. 38 U.S.C. §§ 1110, 1131, 5107; 38 C.F.R. §§ 3.102, 3.303, 3.304, 3.306, 3.310.

REASONS AND BASES FOR FINDINGS AND CONCLUSIONS

The Veteran served in the US Air Force from September 1968 to September 1972. This matter comes before the Board of Veterans' Appeals (Board) as a result of a May 2013 rating decision of the VA Regional Office, Indianapolis, Indiana.

The Veteran was afforded a Video Conference Board Hearing in April 2017, July 2022 and September 2025 before the undersigned Veterans Law Judge, and a transcript has been associated with the record.

By way of background, this case was previously before the Board in December

2018, October 2020, January 2023 and July 2024. In the December 2018 decision, the Board, in pertinent part, remanded the Veteran's claims of entitlement to service connection for neurofibromatosis and ptosis for further development the purpose of obtaining VA examinations and medical opinions.

In the October 2020 decision, the Board denied the Veteran's claims. In October 2021, the Veteran appealed that denial to the U.S. Court of Appeals for Veterans Claims (the Court or CAVC). In an October 2021 Order, the Court granted the parties' Joint Motion for Remand (JMR) to vacate the October 2020 Board decision and remanded the case to the Board for compliance with the JMR. See October 13, 2021, CAVC Order.

In the JMR, the parties agreed the Board erred under Quinn v. Wilkie, 31 Vet. App. 284 (2019), when it failed to provide the Veteran, an additional hearing as requested by the Veteran (through his counsel) in July 2020 correspondence-for the purpose of providing additional testimonial evidence following the Board's December 2018 remand. As mentioned above, the Veteran was afforded an additional hearing with the undersigned VLJ July 1, 2022.

In January 2023, the Board denied the Veteran's claims. The Veteran appealed the January 2023 decision to the United States Court of Appeals for Veterans Claims (CAVC or Court). In March 2024, the CAVC issued a Joint Motion for Remand (JMR), which vacated and remanded the January 2023 Board decision. See March 19, 2024, CAVC Order. The March 2024 Joint Motion for Remand (JMR) found that the Board did not provide an adequate statement of reasons addressing the Veteran's theory of entitlement, that his neurofibromatosis and ptosis disabilities are related to active-duty service, to include exposure to Agent Orange.

In July 2024, the matter was remanded for a medical opinion to address whether the Veteran's his neurofibromatosis and ptosis disabilities was incurred in, caused by or is otherwise attributable to his active-duty service, to include the Veteran's conceded exposure to herbicides, including Agent Orange.

The Board notes that multiple medical opinions were afforded to the Veteran on remand. Therefore, the Board finds there has
CAVC Order. The March 2024 Joint Motion for Remand (JMR) found that the Board did not provide an adequate statement of reasons addressing the Veteran's theory of entitlement, that his neurofibromatosis and ptosis disabilities are related to active-duty service, to include exposure to Agent Orange.

The Board notes that multiple medical opinions were afforded to the Veteran on remand. Therefore, the Board finds there has been substantial compliance with the Board's July 2024 remand. See Stegall v. West, 11 Vet. App. 268 (1998).

In a March 2025, Supplemental Statement of the Case (SSOC), the Veteran's service connection claim for neurofibromatosis and ptosis remained denied. The Board also notes that in November 2025, following the Veteran's April 2025 SSOC and September 2025 Board hearing, the Veteran submitted a private opinion in support of his claim, with waiver of AOJ consideration in the first instance. See November 26, 2025, Post Hearing Memorandum. 38 C.F.R. § 20.1305. Therefore, the Board will consider this private medical opinion in this adjudication.

The matter has been returned to the Board for adjudication. This appeal has been advanced on the Board's docket pursuant to 38 C.F.R. § 20.902 (c).

Service Connection

Service connection may be granted for a disability resulting from disease or injury incurred in or aggravated by service. 38U.S.C.§1131; 38 C.F.R.§3.303 (a). Service connection requires: (1) the existence of a present disability; (2) in-service incurrence or aggravation of a disease or injury; and (3) a causal relationship between the present disability and the disease or injury incurred or aggravated during service. Shedden v. Principi, 381 F.3d 1163, 1167 (Fed. Cir. 2004); see also Caluza v. Brown, 7 Vet. App. 498 (1995).

In addition, service connection may be established on a secondary basis. Establishing service connection on a secondary basis requires evidence sufficient to show (1) that a current disability exists and (2) that the current disability was either (a) caused by or (b) aggravated by a service-connected disability. 38 C.F.R. § 3.310(a)-(b). Secondary causation exists when, but for the service-connected disability, the non-service-connected was caused by a service-connected disability either in a direct, etiological way or via multiple steps in a causal chain. Spicer v. McDonough, 61 F.4th 1360, 1365 (Fed. Cir. 2023).

Secondary aggravation exists when the non-service-connected disability not caused by a service-connected disability would be less severe were it not for a service-connected disability. Id. at 1364. For example, secondary aggravation may be established where the natural progression of the non-service-connected disability could have been arrested or improved but for the service-connected disability. Id.

In addition to the laws and regulations outlined above, a veteran is presumed to be in sound condition upon entrance into service, except for defects, infirmities or disorders noted when examined, accepted, and enrolled for service, or where evidence or medical judgment is such as to warrant a finding that the disease or injury existed before acceptance and enrollment. 38U.S.C.§1111. Only such conditions as are recorded in examination reports are to be considered as noted. 38 C.F.R.§3.304 (b).

Pursuant to 38U.S.C.§1111, and 38 C.F.R.§3.304, to rebut the presumption of soundness on entry into service, VA must show by clear and unmistakable evidence both that the disease or injury existed prior to service and that the disease or injury was not aggravated by service. See Wagner v. Principi, 370 F.3d 1089 (Fed. Cir. 2004); VAOPGCPREC 3-03 (July 16, 2003).

VA is not precluded from determining that the presumption of soundness is rebutted, even if there is conflicting evidence. See Kent v. Principi, 389 F.3d 1380, 1383 (Fed. Cir. 2004) ("The clear and unmistakable evidentiary standard . . . does
presumption of soundness on entry into service, VA must show by clear and unmistakable evidence both that the disease or injury existed prior to service and that the disease or injury was not aggravated by service. See Wagner v. Principi, 370 F.3d 1089 (Fed. Cir. 2004); VAOPGCPREC 3-03 (July 16, 2003).

A determination that a condition had its onset prior to service may be supported by contemporaneous evidence or recorded history in the record which provides a sufficient factual predicate to support a medical opinion (Miller v. West, 11 Vet. App. 345, 348 (1998)), or a later medical opinion based on statements made by a veteran about the pre-service history of the condition (Harris v. West, 203 F.3d 1347 (Fed. Cir. 2000)).

Cases in which the condition is noted on entrance are, however, governed by the presumption of aggravation contained in 38 U.S.C. § 1153 (as opposed to that applicable under 38 U.S.C. § 1111 where the complained of condition was not noted on entrance into service).

Accordingly, if a disorder was not "noted" upon entering service but it believed to have pre-existed, the law requires that the VA show clear and unmistakable evidence that the disability pre-existed service, and that the preexisting disability was NOT aggravated by service in order to overcome the presumption of soundness. Therefore, simply finding no evidence of aggravation by service is not sufficient.

This statute provides that a pre-existing injury or disease will be considered to have been aggravated by active service where there is an increase in disability during such service, unless clear and unmistakable evidence shows that the increase in disability is due to the natural progress of the disease. 38 U.S.C. § 1153 (2012); 38 C.F.R. § 3.306 (2018).

Aggravation may not be conceded where the disability underwent no increase in severity during service on the basis of all the evidence of record pertaining to the manifestations of the disability prior to, during, and subsequent to service. 38 U.S.C. § 1153 (2012); 38 C.F.R. §§ 3.304, 3.306(b) (2018).

A pre-existing disease or injury will be presumed to have been aggravated by service only if the evidence shows that the underlying disability underwent an increase in severity; the occurrence of symptoms, in the absence of an increase in the underlying severity, does not constitute aggravation of the disability. See Davis v. Principi, 276 F.3d 1341, 1345 (Fed. Cir. 2002); 38 C.F.R. § 3.306 (a) (2018).

Aggravation is characterized by an increase in the severity of a disability during service, and a finding of aggravation is not appropriate in cases where the evidence specifically shows that the increase is due to the natural progress of the disease. Furthermore, temporary or intermittent flare-ups of a pre-existing disease during service are not sufficient to be considered aggravation of the disease unless the underlying condition, as contrasted to symptoms, worsens. See Jensen v. Brown, 4 Vet. App. 304, 306-07 (1993); Hunt v. Derwinski, 1 Vet. App. 292 (1991).

Agent Orange

VA has established a presumption of herbicide exposure applicable to veterans who served in Republic of Vietnam during the Vietnam War, and a presumption of service connection applicable to veterans who are either presumed to have been exposed to herbicide agents, or who are shown to have been actually exposed to herbicide agents during service. A veteran who, during active military, naval, or air service, served in the Republic of Vietnam during the period beginning on January 9, 1962, and ending on May 7, 1975, shall be presumed to have been exposed during such service to an herbicide agent, unless there is affirmative evidence to establish that the veteran was not exposed to any such agent during that service. 38 C.F.R. § 3.307 (a)(6)(iii).

In order for service connection to be established by presumption, there must be an herbicide-presumptive disease and there must be evidence to substantiate actual exposure to an herbicide agent. The following diseases are deemed associated with
to herbicide agents during service. A veteran who, during active military, naval, or air service, served in the Republic of Vietnam during the period beginning on January 9, 1962, and ending on May 7, 1975, shall be presumed to have been exposed during such service to an herbicide agent, unless there is affirmative evidence to establish that the veteran was not exposed to any such agent during that service. 38 C.F.R. § 3.307 (a)(6)(iii).

In order for service connection to be established by presumption, there must be an herbicide-presumptive disease and there must be evidence to substantiate actual exposure to an herbicide agent. The following diseases are deemed associated with herbicide exposure, under VA law: The presumptive diseases shall be service connected if a veteran was exposed to an herbicide agent during active military, naval, or air service, if the requirements of 38 C.F.R. § 3.307 (a)(6) are met, even though there is no record of such disease during service, provided further that the rebuttable presumption provisions of 38 C.F.R. § 3.307 (d) are also satisfied. See 38 C.F.R. § 3.309 (e).

The following diseases are deemed associated with herbicide exposure under VA law: AL amyloidosis, Chloracne or other acneform disease consistent with chloracne, Type 2 diabetes (also known as Type II diabetes mellitus or adult-onset diabetes), Hodgkin's disease, Ischemic heart disease (including, but not limited to, acute, subacute, and old myocardial infarction; atherosclerotic cardiovascular disease including coronary artery disease (including coronary spasm) and coronary bypass surgery; and stable, unstable and Prinzmetal's angina), all chronic B-cell leukemias (including, but not limited to, hairy-cell leukemia and chronic lymphocytic leukemia), Multiple myeloma, Non-Hodgkin's lymphoma, Parkinson's disease, early onset peripheral neuropathy, Porphyria cutanea tarda, Prostate cancer, Respiratory cancers (cancer of the lung, bronchus, larynx, or trachea), and Soft-tissue sarcoma (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma). 38 C.F.R. § 3.309 (c).

A disease associated with exposure to certain herbicide agents listed in § 3.309 will be considered to have been incurred in or aggravated by service even though there is no evidence of such disease during the period of service, provided that such disease shall have become manifest to a degree of 10 percent or more at any time after service, except that chloracne or other acneform disease consistent with chloracne, porphyria cutanea tarda, and acute and subacute peripheral neuropathy shall have become manifest to a degree of 10 percent or more within a year after the last date on which the veteran was exposed to an herbicide agent during active military, naval, or air service. 38 C.F.R. § 3.307 (a).

The Veteran's personnel records confirm that he had service in the Republic of Vietnam during the applicable time period; accordingly, his exposure to herbicides is conceded. See Military Personnel Records re: Cam Ranh Bay Airbase, Vietnam (PACAF) from September 18, 1968, to February 20, 1970, as a medical specialist. See also, August 15, 2024, Toxic Exposure Risk Activity (TERA) Memorandum re: Herbicide Agent.

However, ptosis and neurofibromatosis are not among the diseases for which the Secretary has determined that presumptive service connection is warranted based on herbicide exposure. See 38 C.F.R. § 3.309 (e) (2016).

Notwithstanding, the Federal Circuit has held that when a claimed disorder is not warranted on a presumptive basis, direct service connection may nevertheless be established by evidence demonstrating that the disease was in fact "incurred" during service. See Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994).

VA is required to give due consideration to all pertinent medical and lay evidence in evaluating a claim for disability benefits. 38 U.S.C. § 1154 (a). Lay evidence can be competent and sufficient to establish a diagnosis of a condition when (1) a layperson is competent to identify the medical condition, (2) the layperson is reporting a contemporaneous medical diagnosis, or (3) lay testimony describing symptoms at the time supports a later diagnosis by a medical professional. Jandreau v. Nicholson, 492 F.
by evidence demonstrating that the disease was in fact "incurred" during service. See Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994).

Lay evidence cannot be determined to be not credible merely because it is unaccompanied by contemporaneous medical evidence. Buchanan v. Nicholson, 451 F.3d 1331, 1336-37 (Fed. Cir. 2006). However, the lack of contemporaneous medical evidence can be considered and weighed against a Veteran's lay statements. Id. Further, a negative inference may be drawn from the absence of complaints or treatment for an extended period. Maxson v. West, 12 Vet. App. 453, 459 (1999), aff'd sub nom. Maxson v. Gober, 230 F.3d 1330, 1333 (Fed. Cir. 2000).

After the evidence is assembled, it is the Board's responsibility to evaluate the entire record. See 38 U.S.C. § 7104 (a) (2012). When there is an approximate balance of evidence regarding the merits of an issue material to the determination of the matter, the benefit of the doubt in resolving each such issue shall be given to the claimant. 38 U.S.C. § 5107; 38 C.F.R. § 3.102 (reasonable doubt to be resolved in veteran's favor); Gilbert v. Derwinski, 1 Vet. App. 49 (1990); Lynch v. McDonough, 21 F.4th 776 (Fed. Cir. 2021) (the benefit-of-the-doubt rule applies if the competing evidence is in approximate balance).

Definitions

Neurofibromatosis is defined as a congenital condition transmitted as an autosomal-dominant trait characterized by numerous neurofibromas of the nerves and skin, cafe-au-lait spots on the skin, and developmental anomalies of the muscles, bones and viscera. See Mosby's Medical Dictionary 1228 (11th ed. 2022).

Ptosis is defined as abnormal condition of one or both upper eyelids in which the eyelid droops because of a congenital or acquired weakness of the levator muscle or paralysis of the third cranial nerve. See Mosby's Medical Dictionary 1497 (11th ed. 2022).

The Board notes that it has reviewed all the evidence in the record relevant to the period on review. This includes the Veteran's STR's, VA treatment records and VA examinations of record, i.e., May 2013 VA examination and Medical Opinions; August 2013 Addendum Medical Opinion; August 2016 Skin Conditions examination; December 2019, Skin Condition examination and Medical Opinion; and Private Medical Opinions, received in October 2022 and November 2025 and April 2025 VA medical opinions.

Although the Board has an obligation to provide adequate reasons and bases supporting its decision, there is no requirement that the Board discuss every piece of evidence in the record. Hence, the Board will summarize the relevant evidence, as deemed appropriate, and the Board's analysis will focus on what the evidence shows, or fails to show, as to the claims. See Gonzalez v. West, 218 F.3d 1378, 1380-81 (Fed. Cir. 2000).

Entitlement to service connection for a neurofibromatosis disability.

The Veteran has contended that his current neurofibromatosis disability stems from his active-duty military service, including Agent Orange. The Veteran also contends that he was not aware that he had this disability until service. See July 2013 Notice of Disagreement (NOD); April 2017 Board Hearing transcript, pgs. 11-12; August 2017 Sworn Affidavit; see also, July 2022, Board Hearing transcript re: Agent Orange theory raised by the Veteran's counsel, pgs. 5-6. In the alternative, the Veteran has asserted that his neurofibromatosis disability was aggravated by service, to include his presumed exposure to herbicides.

The Veteran's diagnosed neurofibromat
contended that his current neurofibromatosis disability stems from his active-duty military service, including Agent Orange. The Veteran also contends that he was not aware that he had this disability until service. See July 2013 Notice of Disagreement (NOD); April 2017 Board Hearing transcript, pgs. 11-12; August 2017 Sworn Affidavit; see also, July 2022, Board Hearing transcript re: Agent Orange theory raised by the Veteran's counsel, pgs. 5-6. In the alternative, the Veteran has asserted that his neurofibromatosis disability was aggravated by service, to include his presumed exposure to herbicides.

The Veteran's diagnosed neurofibromatosis was not noted on entry. See March 1968 Entrance examination. If a disorder was not "noted" upon entering service but it believed to have pre-existed, the law requires that the VA show clear and unmistakable evidence that the disability preexisted service, and that the preexisting disability was NOT aggravated by service in order to overcome the presumption of soundness.

The Board notes that the probative and persuasive evidence establishes that the Veteran's current neurofibromatosis clearly and unmistakably existed prior to service.

In a December 2019 Skin Conditions examination an examiner opined that the Veteran's neurofibromatosis clearly and unmistakably existed before service. The examiner reasoned, in pertinent part, that like all people who have neurofibromatosis, the Veteran had the makings of it from before birth (congenital). The examiner explained that the manifestations of this medical condition are variable in terms of age of visible onset of signs and symptoms, and the signs and symptoms themselves can be variable, to include skin, neurologic, and other systems of the body. Additionally, the Veteran already had the eyelid lesion that was later diagnosed as neurofibromatosis. See December 2019 VA Skin Conditions examination.

Therefore, the Board concludes that the presumption of soundness is rebutted. See 38 U.S.C. § 1111 (West 2012); 38 C.F.R. § 3.304 (b).

Next, the Board must then determine whether the Veteran's pre-existing disability underwent an increase in severity during his period of active military service, thereby triggering the presumption of aggravation. See Maxson v. West, 12 Vet. App. 453 (1999) (the presumption of aggravation is generally triggered by evidence that a pre-existing disability has undergone an increase in severity in service); see also Sondel v. West, 13 Vet. App. 213 (1999).

The Board notes that service treatment records show that the Veteran was diagnosed with neurofibroma while on active duty. Further, the Veteran had a neurofibroma extracted from his right upper lid during service. See March 1970 and October 1971 Service Treatment Records.

The Veteran's Separation examination showed several small neurofibromas scattered over his trunk. See June 1972, Separation examination.

Based on these facts, the Board finds that it is as likely as likely that the Veteran pre-existing neurofibromatosis disability underwent an increase in severity during service. See Maxson v. West, 12 Vet. App. 453 (1999) (the presumption of aggravation is generally triggered by evidence that a pre-existing disability has undergone an increase in severity in service); see also Sondel v. West, 13 Vet. App. 213 (1999).

The Board finds that the presumption of aggravation has been triggered in this case.

Because of this finding, the VA has the burden to rebut by clear and unmistakable proof that there has been no increase in the severity of the preexisting condition or that any increase was the result of natural progression.

With regards to whether the Veteran's pre-existing neurofibromatosis was aggravated beyond its natural progression, the December 2019 examiner referenced above reported that so far as aggravation is concerned, although the Veteran had some lesions removed on active duty, "this was consistent with the natural history of the disease. Nothing about being in the military made his neurofibromatosis worse or better. The disease progresses and manifests itself without outside influence, such as being in the military. So far as his neck condition/surgery, there is nothing about his service that would have caused or aggravated his [neurofibromatosis] and led to these problems."

The examiner concluded that "neurofibromatosis type 1, also known as Von Recklinghausen's disease, is a neurodermal dysplasia. The pathological alterations behind it begin in the embryonic period." The examiner references medical literature: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491339. See December 201
natural history of the disease. Nothing about being in the military made his neurofibromatosis worse or better. The disease progresses and manifests itself without outside influence, such as being in the military. So far as his neck condition/surgery, there is nothing about his service that would have caused or aggravated his [neurofibromatosis] and led to these problems."

In November 2025, the Veteran (through counsel), submitted a private opinion in support of his claim. The private opinion was authored by a licensed physician who indicated review of the Veteran's claims file, to include service treatment records, post-service treatment records, VA examinations and medical opinions of record.

After reviewing the pertinent evidence of record, the physician determined that the Veteran's pre-existing neurofibromatosis was aggravated by service, to include his presumed exposure to herbicides, beyond the normal progression.

The physician reasoned that although neurofibromatosis is a genetic disorder, the progression documented in the Veteran's service treatment records including repeated tumor growth, surgical excisions, pleural and mediastinal involvement, and early-onset ocular and spinal manifestations demonstrates a pattern of unusually accelerated disease activity during and after his period of herbicide exposure.

The physician stated that scientific literature indicates that dioxin-based herbicides can cause neurological toxicity, glial injury, and central nervous system damage, which may biologically worsen the growth behavior of neurofibromas or amplify signaling pathways associated with tumor proliferation.

The physician reasoned that, given that neurofibromatosis is highly sensitive to alterations in neural and glial cellular environments, it is medically reasonable to conclude that brain and nerve tissue damage associated with Agent Orange exposure could have aggravated the underlying disease process, resulting in the extensive, multi-system progression recorded throughout his service and post-service medical history. Hence, the examiner determined that it is at least as likely as not that the Veteran's neurofibromatosis was aggravated beyond its natural progression by his in-service herbicide exposure.

The physician supported this reasoning with the following discussion of Neurofibromatosis: "Neurofibromatosis type 1 (NFl) is a dominantly inherited tumor-predisposing condition characterized by cutaneous neurofibromas, plexiform neurofibromas, and increased risk of malignant peripheral nerve sheath tumors, among other systemic manifestations. Although NFl is a germline disorder, it is well established that additional environmental, cellular, and microenvironmental factors can influence the tempo and severity of N Fl -related tumor growth. In the context [the Veteran] whose service treatment records document early onset of rapidly recurring neurofibromas, involvement of multiple organ systems, and unusually accelerated tumor behavior requiring repeated surgical interventions, it is medically reasonable to consider whether herbicide exposure specifically dioxin (TCDD), the toxic component of Agent Orange may have aggravated the underlying disease process. Among environmental toxicants, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent activator of the aryl hydrocarbon receptor (AhR) transcriptional axis and is extensively characterized for its epigenetic, developmental, immunologic, and carcinogenic effects. Mechanistic plausibility for aggravation of NFl-related neurofibromatosis by TCDD exposure emerges from converging lines of evidence that (i) TCDD can modulate NFl transcription via AhR-mediated promoter effects; (ii) TODD induces inflammatory and stromal changes that can dysregulate the tumor microenvironment in ways that enhance NFl-associated tumorigenesis; and (iii) TODD exposure is linked to increased risk of sarcomas, soft-tissue neoplasms, and oxidative/inflammatory injury, all of which may amplify N Fl -driven pathways." The physician stated that the following synthesis incorporates these mechanisms to establish a coherent model of aggravation, consistent with [the Veteran's] documented pattern of disease acceleration during and after his herbicide-exposed service.

The physician further explained that a "central component of aggravation plausibility is the demonstration that TCDD can influence NFl promoter accessibility and transcription through AhR signaling. Mechanistic work shows that TCDD exposure alters promoter accessibility at multiple genomic loci, including the NFl regulatory region, in an AhR-dependent manner (Wu & Whitlock, 1992). This provides a biologically credible pathway through which dioxin exposure could
, and oxidative/inflammatory injury, all of which may amplify N Fl -driven pathways." The physician stated that the following synthesis incorporates these mechanisms to establish a coherent model of aggravation, consistent with [the Veteran's] documented pattern of disease acceleration during and after his herbicide-exposed service.

The physician further explained that a "central component of aggravation plausibility is the demonstration that TCDD can influence NFl promoter accessibility and transcription through AhR signaling. Mechanistic work shows that TCDD exposure alters promoter accessibility at multiple genomic loci, including the NFl regulatory region, in an AhR-dependent manner (Wu & Whitlock, 1992). This provides a biologically credible pathway through which dioxin exposure could dysregulate NFl gene expression in Schwan n-cell derived tissues or their microenvironment, potentially exacerbating the proliferative behavior of N Fl -deficient cells. The AhR is a ligand-activated transcription factor known to regulate broad gene networks associated with cellular growth control, metabolic homeostasis, and xenobiotic response (Loertscher et al., 2001; Carreira et al., 2015; Puga, 2010). Because NFl is tightly coupled to Ras-MAPK and growth-factor signaling, even modest shifts in transcriptional regulation can, in theory, alter the phenotype of NFl-deficient Schwann cells or their supporting stromal cells."

Addressing the Veteran's individual circumstances, the physician stated that "in the context of [the Veteran's] medical history marked by unusually frequent recurrence of neurofibromas, need for repeated excisions, and later involvement of the spine and mediastinum the ability of TODD to modulate NFl regulatory circuits offers a plausible mechanism by which herbicide exposure may have worsened an already established genetic condition. N Fl -related tumor biology is profoundly shaped by developmental context, microenvironmental cues, and long-lasting changes in gene expression. Multiple studies demonstrate that developmental or early-life exposure to TODD produces persistent gene-expression changes lasting into adulthood and affecting organs such as cardiac and renal tissue (Aragon et al., 2007; Gannes et al., 2021). Such durable transcriptional reprogramming highlights the ability of TODD to produce long-term epigenetic and microenvironmental alterations, which in NFl biology could translate to enhanced Schwann-cell proliferation, abnormal EOM remodeling, or increased susceptibility to tumor formation. For individuals with underlying NFl, persistent TODD-induced changes in gene expression may shift the balance toward greater tumor burden or more aggressive lesion behavior. Evidence from developmental toxicology further shows that TODD exposure alters cellular differentiation, growth-factor signaling, and extracellular matrix pathways (Aragon et al., 2007; Gannes et al., 2021; Oarreira et al., 2015; Puga, 2010), all of which intersect with known drivers of neurofibroma formation. These mechanisms map closely onto [the Veteran's] clinical picture, including the appearance of neurofibromas in multiple anatomical regions during service and the progression to plexiform spinal involvement later in life patterns consistent with environmental aggravation of his genetic tumor predisposition. Taken together, the mechanistic, immunologic, mitochondrial, and microenvironmental pathways described in the literature provide a coherent and scientifically grounded explanation for how herbicide exposure particularly to dioxin (TODD), the toxic contaminant in Agent Orange could have aggravated the progression and severity of [the Veteran's] neurofibromatosis beyond its natural hereditary course.

His service treatment records document unusually active disease during service, including multiple neurofibromas requiring excision, involvement of the chest wall, eyelid, and mediastinal structures, and early signs of systemic spread. Post-service records reveal continued acceleration, including orbital and temporal tumors, recurrent eyelid lesions, plexiform neurofibromas of the cervical and lumbar spine, and eventual spinal cord compression requiring multilevel laminoplasty an aggressive pattern not typical for stable NFl.

The biological effects of TCDD exposure oxidative stress, mitochondrial dysfunction, epigenetic remodeling, altered MAPK and growth-factor pathways, disruption of immune surveillance, and stromal microenvironment dysregulation all directly intersect with the known drivers of NFl tumor expansion, Schwann cell proliferation, and malignant potential. These mechanisms provide a plausible and medically reasonable causal chain by which herbicide related toxicant injury could exacerbate tumor burden, accelerate lesion recurrence, and amplify the systemic manifestations of NFl.

Therefore, when the mechanistic evidence is integrated with the documented clinical trajectory in [the Veteran's] record, it is compellingly supported that his neurofibromatosis was at least as likely as not secondary to aggravation from in-service herbicide exposure." See November 2025, Medical Opinion (R.P., DO).

Analysis

The Board finds
and growth-factor pathways, disruption of immune surveillance, and stromal microenvironment dysregulation all directly intersect with the known drivers of NFl tumor expansion, Schwann cell proliferation, and malignant potential. These mechanisms provide a plausible and medically reasonable causal chain by which herbicide related toxicant injury could exacerbate tumor burden, accelerate lesion recurrence, and amplify the systemic manifestations of NFl.

Analysis

The Board finds this November 2025 medical opinion probative. The Board observes that the physician details the Veteran's treatment during service and cites pertinent evidence, combined with scientific literature and research to support the conclusion, to a degree as likely as not, that the Veteran's neurofibromatosis was aggravated by service beyond the normal progression. The Board also finds the December 2019 VA medical opinion probative. Essentially, the December 2019 VA examiner determined that nothing in the environment could aggravate the Veteran's neurofibromatosis. Although the Board could reasonably infer that this conclusion would encompass herbicide exposure, the Board notes that the examiner did not specifically address this issue. With consideration of these two probative medical opinions, the Board finds that the VA has not met its burden to show that the Veteran's pre-existing neurofibromatosis, which clearly and unmistakably pre-existed service was not clearly and unmistakably-not aggravated by service beyond the normal progression.

Therefore, with reasonable doubt in favor of the Veteran, the Board finds that service connection for neurofibromatosis based on the theory of aggravation is warranted and the claim is hereby granted. See 38 C.F.R. § 3.306 (b)

The Board construes this award as a full grant, satisfying the Veteran's appeal; therefore, further discussion regarding entitlement to service connection for neurofibromatosis under any other theory of entitlement is not warranted. See also, November 26, 2025, Post-Hearing Memorandum, pg. 1.

Entitlement to service connection for a ptosis disability

The Veteran contends that his current ptosis stems from his active-duty military service, to include Agent Orange. See July 2013 Notice of Disagreement (NOD); April 2017 Board Hearing transcript, pgs. 11-12; July 2022, Board Hearing transcript re: Agent Orange theory raised by the Veteran's counsel, pgs. 5-6.

The Veteran contends that he was not aware that he had a diagnosis of ptosis until service. The Veteran also asserts that he never informed his eye doctors that he had ptosis since the age of three. See Board Hearing transcript, pg. 11; See also August 2017 Affidavit.

At the outset, the Board notes that the Veteran's counsel submitted an October 2022 medical opinion which asserts that the Veteran's condition was related to Agent Orange exposure; however, the Board also notes that the medical opinion is based an inaccurate factual premise as to the Veteran's diagnosed condition and consequently has no probative value in this adjudication.

Conversely, the Board finds that a September 2019 VA examination and medical opinion, in tandem with the March 2013 VA examination, adequate for purposes of adjudication as the September 2019 VA examination is based on an accurate factual history of the Veteran's treatment and medical history and provides sufficient detail to fully inform the Board on its medical question. See Nieves-Rodriguez v. Peake, 22 Vet. App. 295 (2008).

In addition, as referenced above, the Board considers the medical opinion submitted by counsel in November 2025 in support of his claim for purposes of this adjudication.

The evidence shows that the Veteran's ptosis pre-existed service, as it was noted on entry.

The Veteran's service treatments records include a March 1968 entrance examination which notes partial ptosis due to an old injury. See March 1968 Entrance examination re: partial ptosis due to old injury.

In March 2013 and September 2019 VA examinations, the examiners who reviewed the Veteran's records determined that the Veteran's ptosis pre-existed service. See March 2013 and September 2019 VA examinations.

The Board, therefore, finds that the Veteran's entrance examination noted a pre-existing ptosis disability. See 38 U.S.C. § 1111 (West 2012); 38 C.F.R. § 3.304 (b) (2018).

The Board must then determine whether the Veteran's
treatments records include a March 1968 entrance examination which notes partial ptosis due to an old injury. See March 1968 Entrance examination re: partial ptosis due to old injury.

The Board, therefore, finds that the Veteran's entrance examination noted a pre-existing ptosis disability. See 38 U.S.C. § 1111 (West 2012); 38 C.F.R. § 3.304 (b) (2018).

The Board must then determine whether the Veteran's pre-existing ptosis, underwent an increase in severity during his period of active military service, thereby triggering the presumption of aggravation. See Maxson v. West, 12 Vet. App. 453 (1999) (the presumption of aggravation is generally triggered by evidence that a pre-existing disability has undergone an increase in severity in service); see also Sondel v. West, 13 Vet. App. 213 (1999).

The Board notes that March 1970, October 1971and November 1971 service treatment records show that the Veteran had treatment for his ptosis. In November 1971, the Veteran had a levator resection for his ptosis, right eye, benign. See March 1970, October 1971 and November 1971 STR's.

Based on these facts, the Board finds that it is as likely as not that the Veteran pre-existing ptosis disability underwent an increase in severity during service. See Maxson v. West, 12 Vet. App. 453 (1999) (the presumption of aggravation is generally triggered by evidence that a pre-existing disability has undergone an increase in severity in service); see also Sondel v. West, 13 Vet. App. 213 (1999).

Therefore, the Board finds that the presumption of aggravation has been triggered in this case.

Pursuant to the Board's December 2018 remand directives, the Veteran was afforded an Eye Conditions Examination and Medical Opinion in September 2019 with regards to the nature of his pre-existing ptosis disability. In this September 2019 medical examination and medical opinion, the examiner reasoned that it was clear and unmistakable that any increase in the Veteran's pre-existing ptosis disability was due to the natural progression of the Veteran's disease. The examiner noted review of the Veteran's medical history, including his [diagnosis of] neurofibromatosis 2 with ptosis of the right upper eyelid due to a neurofibroma. The examiner noted the Veteran's ptosis repair in 1970, and subsequently 3 further revisions in 1971, 1984, and 1998. See September 2019 VA Eye Conditions examination, pg. 2. The examiner noted that post service, the Veteran suffered a perforated cornea of the right eye that required a corneal transplant. The Veteran subsequently received 3 more corneal transplants post service, his last being in 2009. After his last transplant failed, the Veteran reported that he had been left with no light perception vision for the last 10 years. Id.

With regards to whether the Veteran's pre-existing ptosis disability was aggravated beyond its natural progression, the examiner noted that the Veteran developed ptosis secondary to a neurofibroma in his right upper eyelid. He had 2 of the 3 ptosis surgeries while in service. During this time, he did not have any visual complaints. The examiner reported that the Veteran's ptosis was aggravated by his neurofibromatosis. It was not aggravated by any activity performed while in military service. The Veteran subsequently became blind in his right eye between 2003-2009, but this was due to a corneal perforation with multiple corneal surgeries and not related to his prior ptosis repair. See September 2019 VA Medical Opinion; See also, September 2019, Eye Conditions examination. (Attending Physician).

As referenced above, in November 2025, the Veteran (through counsel), submitted a private opinion in support of his claim. The private opinion was authored by a licensed physician who indicated review of the Veteran's claims file, to include service treatment records, post-service treatment records, VA examinations and medical opinions of record.

After review of the pertinent evidence of record, the physician determined that the Veteran's ptosis was caused or aggravated by his underlying neurofib
2009, but this was due to a corneal perforation with multiple corneal surgeries and not related to his prior ptosis repair. See September 2019 VA Medical Opinion; See also, September 2019, Eye Conditions examination. (Attending Physician).

After review of the pertinent evidence of record, the physician determined that the Veteran's ptosis was caused or aggravated by his underlying neurofibromatosis, which itself shows clear evidence of having been aggravated by his active military service.

The physician first stated that there is clear evidence of having been aggravated by his active military service. The physician noted that the Veteran's "service treatment records document early neurofibromatosis-related lesions of the eyelid, repeated surgeries, and progressive structural deformities that directly contributed to the development and worsening of ptosis. The physician noted that over time, this progressed to significant functional impairment, including lagophthalmos, multiple corneal injuries, and ultimately profound vision loss in the right eye.

The physician reasoned that because neurofibromatosis is the medically recognized driver of his ptosis, and because the neurofibromatosis was demonstrably accelerated during his service, it follows that the ptosis was likewise at least as likely as not secondary to service-aggravated neurofibromatosis.

The physician supported this conclusion with the following clinical discussion:

"Ptosis in patients with neurofibromatosis (NF) is a clinically significant manifestation that reflects the diverse pathways through which NF can involve the ocular adnexa, eyelid structures, and orbit. In the context of [the Veteran] whose service and post-service medical records document repeated tumor excisions from the right upper eyelid, chronic lid distortion, and progressive eyelid dysfunction culminating in lagophthalmos and severe visual impairment, the established mechanisms of NF-associated ptosis align closely with his ocular course. Neurofibromatosis type 1 (NFl), an autosomal dominant disorder caused by mutations in the NFl gene encoding neurofibromin, predisposes to the development of plexiform and cutaneous neurofibromas that infiltrate periocular tissues, distort the eyelid architecture, and impair levator function key pathways that underpin the development of ptosis (Tamura, 2021).

Clinically, ptosis in NF may be congenital or acquired and can arise via mechanical, myogenic, neurogenic, or sympathetic pathways, depending on the location and biological behavior of the underlying tumors (Finsterer, 2003; Huggins et al., 2017). These mechanisms are supported by a broad literature describing eyelid and orbital neurofibromas as well as foundational reviews on ptosis etiology. Synthesizing this evidence demonstrates that mechanical infiltration by plexiform neurofibromas (PNFs) is the dominant mechanism of NF-related ptosis, though myogenic and neurogenic components may also contribute, particularly in casessuch as [the Veteran's] were repeated surgeries and progressive tumor growth alter eyelid integrity over time (Chaudhry et al., 2011; Mancini et al.

The principal mechanism of NF-related ptosis is mechanical, arising when PNFs infiltrate or compress eyelid tissues or orbital structures. In Mr. [REDACTED]'s case, multiple right upper eyelid excisions beginning in service strongly support a mechanical etiology, as the recurrent neurofibromas produced progressive architectural distortion of the lid, eventually contributing to lagophthalmos, keratinization, and significant visual loss. Published cases describe similar processes: for example, NFl-related lower-eyelid tumors causing mechanical ectropion and ptosis demonstrate how neurofibromas can deform the lid margin through mass effect (Sethi et al., 2022). In orbitofacial NFl, ptosis frequently accompanies orbital soft-tissue masses, reinforcing that orbital infiltration is one of the most consistent pathways linking PNFs to functional eyelid descent (Mancini et al., 2025; Chaudhry et al., 2011).

Isolated orbital neurofibromas, even in individuals without systemic NFl, have been shown to cause ptosis through localized mass effect on the levator or lid margin (Alshomar et al., 2018). Descriptions of pulsatile exophthalmos in NF further illustrate how orbital soft-tissue expansion can alter eyelid position by changing the resting relationships between the globe, orbit, and lid Sivaramasubrahmanyam,
ofacial NFl, ptosis frequently accompanies orbital soft-tissue masses, reinforcing that orbital infiltration is one of the most consistent pathways linking PNFs to functional eyelid descent (Mancini et al., 2025; Chaudhry et al., 2011).

Isolated orbital neurofibromas, even in individuals without systemic NFl, have been shown to cause ptosis through localized mass effect on the levator or lid margin (Alshomar et al., 2018). Descriptions of pulsatile exophthalmos in NF further illustrate how orbital soft-tissue expansion can alter eyelid position by changing the resting relationships between the globe, orbit, and lid Sivaramasubrahmanyam, 1965). These mechanical pathways closely match [the Veteran's] documented clinical trajectory, where plexiform tumor burden contributed to recurrent deformity of the right upper eyelid and ultimately resulted in loss of eyelid competence.

Beyond mass effect on the eyelid, direct involvement of the levator palpebrae superioris or its aponeurosis constitutes a second major pathway of ptosis in NF. Neurofibromas infiltrating the upper eyelid can disrupt the levator insertion or impair its contractile function, creating a combined myogenic mechanical form of ptosis. Imaging and surgical assessments of orbitotemporal NFl consistently show that levator-aponeurosis distortion is common in advanced disease, and that ptosis may result as much from levator dysfunction as from the weight of the mass (Mancini et al., 2025).

Case descriptions of NFl-related eyelid infiltration producing an S-shaped lid contour illustrate this dual mechanism: the lesion both weighs down the eyelid and disrupts the structural continuity of the levator aponeurosis, impairing effective eyelid elevation (Mancini et al., 2025)."

The physician reasoned that "this aligns directly with [the Veteran's] long history of repeated eyelid surgeries for neurofibroma removal, each producing additional scar tissue, adhesions, and progressive attenuation of the levator mechanism. Broader ptosis literature corroborates that myogenic and aponeurotic involvement can develop secondarily to infiltrative or surgical processes (Finsterer, 2003; Huggins et al., 2017), which is precisely the pattern reflected in [the Veteran's] chronic right upper eyelid dysfunction."

The physician further explained that "neurogenic ptosis arises when cranial nerve function is compromised, most classically from oculomotor nerve (Ill) palsy or disruption of the sympathetic chain producing Homer syndrome. While NFl more commonly produces peripheral nerve sheath tumors and plexiform neurofibromas, neurogenic ptosis is documented across the broader neurofibromatosis spectrum, particularly in cases involving cranial nerve schwannomas or orbital nerve involvement. Reports of oculomotor nerve schwannomas presenting with ptosis illustrate a direct mechanism in which cranial nerve compression or infiltration produces eyelid droop; although such cases are more characteristic of NF2, they demonstrate the plausibility of neurogenic mechanisms in neurofibromatosis-associated ptosis when cranial nerves are affected (Saggar & Saggar, 2010).

NF2-related cases describing bilateral oculomotor nerve schwannomas with ptosis highlight how neurogenic impairment can occur in NF disorders broadly and underscore the potential for similar pathways in individuals with NFl whose tumor burden, surgical history, or adjacent tissue distortion may place cranial nerves at risk (Saggar & Saggar, 2010).

In NF1/NF2 contexts, neurogenic ptosis may arise from tumor proximity, compression, or infiltration involving cranial nerves supporting eyelid elevation and ocular motility. Although explicit reporting of isolated Ill nerve palsy in NFl is less common in the literature, the broader NF evidence base confirms that cranial nerve involvement can produce ptosis in related NF disorders (Saggar & Saggar, 2010; Chaudhry et al., 2011).

In the context of [the Veteran], whose long-standing neurofibromatosis required repeated surgeries adjacent to the levator complex, orbit, and temporal region and whose periocular tumor burden extended into structurally sensitive areas the possibility of neurogenic contributions to his ptosis cannot be dismissed.

The combination of chronic mass effect, multiple resections, and progressive tumor recurrence in periorbital tissues creates a biologically plausible environment in which even subtle cranial nerve disturbance could aggravate his eyelid function. The available NF2-related data, though involving a different genetic subtype, reinforce the broader principle that neurogenic ptosis is a recognized mechanism across neurofibromatosis syndromes and may arise when cranial nerves are affected by tumor biology or surgical manipulation (Saggar & Saggar,
-standing neurofibromatosis required repeated surgeries adjacent to the levator complex, orbit, and temporal region and whose periocular tumor burden extended into structurally sensitive areas the possibility of neurogenic contributions to his ptosis cannot be dismissed.

The combination of chronic mass effect, multiple resections, and progressive tumor recurrence in periorbital tissues creates a biologically plausible environment in which even subtle cranial nerve disturbance could aggravate his eyelid function. The available NF2-related data, though involving a different genetic subtype, reinforce the broader principle that neurogenic ptosis is a recognized mechanism across neurofibromatosis syndromes and may arise when cranial nerves are affected by tumor biology or surgical manipulation (Saggar & Saggar, 2010). Homer syndrome related ptosis, resulting from sympathetic denervation, represents another neurogenic mechanism relevant to NF patients.

In the NF literature, Homer syndrome has been reported in NFl and NF2 patients due to tumors or associated pathologies involving the sympathetic chain. Case reports describe Homer's syndrome occurring in the NF1/NF2 setting secondary to tumor involvement or secondary malignancy, including a report of diffuse large B cell lymphoma presenting with Homer syndrome in a patient with NFl, highlighting that a diverse range of pathologies can produce sympathetic-chain disruption in individuals with NF (Lueangarun & Auewarakul, 2012).

While the specific mechanism varies, the literature confirms that sympathetic pathway injury whether from direct tumor involvement, mass effect, associated lesions, or secondary processes can generate a distinct form of ptosis in neurofibromatosis patients. Broader ptosis reviews categorize Homer-type sympathetic mechanisms alongside myogenic, aponeurotic, and mechanical etiologies, affirming that neurogenic contributions must be considered when evaluating ptosis in individuals with complex neurocutaneous disorders (Huggins et al., 2017)."

The physician further explained that in "NF1/NF2 cases where sympathetic pathways are affected by tumor infiltration or secondary pathology, Homer-type ptosis may occur and must be distinguished from mechanical and myogenic etiologies (Lueangarun & Auewarakul, 2012; Huggins et al., 2017).

This diversity of mechanisms is particularly relevant to [the Veteran], whose extensive and recurrent periorbital neurofibromas created a multifactorial environment for eyelid dysfunction. His long history of right upper eyelid tumor excision, postoperative scarring, and surrounding tissue involvement raises the possibility that sympathetic fibers or oculomotor nerve branches may have been affected over time, contributing to the progression of ptosis alongside mechanical and myogenic components. Clinically, Homer's syndrome type ptosis emphasizes the importance of differentiating sympathetic denervation from levator dysfunction or lid mass effect, reinforcing the multifactorial nature of ptosis in neurofibromatosis and the plausibility that his service aggravated NF could have led to worsening neurogenic contributions to his condition."

The physician stated that in summary, "the full body of evidence strongly supports a multifactorial mechanism through which [the Veteran's] ptosis was aggravated as a direct consequence of the progression of his neurofibromatosis, which itself shows clear signs of acceleration during his military service. His clinical course marked by early eyelid tumor formation in service, repeated excisions of neurofibromas, progressive distortion of the right upper eyelid, scarring, levator disruption, lagophthalmos, and eventual visual loss is entirely consistent with the well documented mechanical, myogenic, and neurogenic pathways described in the neurofibromatosis and ptosis literature. The scientific evidence demonstrates that plexiform and diffuse neurofibromas can infiltrate eyelid tissue, alter levator function, deform orbital structures, and even involve cranial or sympathetic pathways, all of which were present or plausibly involved in his case.

When these mechanisms are integrated with the documented timeline of his tumor recurrence, surgical burden, and progressive ocular dysfunction beginning during active duty and continuing throughout his life the pattern reflects aggravation beyond what would be expected from the natural progression of isolated congenital ptosis. Therefore, the record supports that it is at least as likely as not secondary that [the Veteran's] ptosis was aggravated by his service-aggravated neurofibromatosis." See November 2025, Medical Opinion (R.P., D.O).

Analysis

The Board finds this November 2025 Medical Opinion probative. The Board also finds the September 2019 examiner's opinion probative. The Board notes that the November 2025 Medical Opinion reflected a thorough review of the Veteran's in-service treatment records and an extensive review of the medical and scientific literature to support the conclusion that the Veteran's pre-existing ptosis was aggravated beyond the normal progression, secondary to his now service-connected neurofibrom
congenital ptosis. Therefore, the record supports that it is at least as likely as not secondary that [the Veteran's] ptosis was aggravated by his service-aggravated neurofibromatosis." See November 2025, Medical Opinion (R.P., D.O).

Analysis

The Board observes that both the November 2025 physician and September 2019 VA examiner determined that the Veteran's ptosis was aggravated by neurofibromatosis, barring the distinction that November 2025 physician determined that the Veteran's neurofibromatosis was aggravated by service due to the Veteran's presumed exposure to herbicides, which in turn, aggravated the Veteran's ptosis beyond the normal progression of the disease.

(Continued on next page.)

In light of the above, the Board finds that the VA has not met it burden to show that the Veteran's pre-existing ptosis, clearly and unmistakably-was not aggravated beyond the normal progression of the disease. Consequently, the Board resolves all doubt in the Veteran's favor and finds that his ptosis was aggravated by his service-connected neurofibromatosis. See 38 U.S.C. § 5107; 38 C.F.R. § 3.102. As such, service connection for ptosis based on aggravation is warranted. 38 U.S.C. § 1131; 38 C.F.R. § 3.306.

The Board construes this award as a full grant, satisfying the Veteran's appeal; therefore, further discussion regarding service connection for ptosis under any other theory of entitlement is not warranted. See also, November 26, 2025, Post-Hearing Memorandum, pg. 1.

Michael A. Pappas

Veterans Law Judge

Board of Veterans' Appeals

Attorney for the Board Little, Calvin

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.

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