Citation Nr: 20004583 Decision Date: 01/21/20 Archive Date: 01/21/20 DOCKET NO. 01-03 511A DATE: January 21, 2020 ORDER Entitlement to compensation under 38 U.S.C. § 1805 for a child of a Vietnam veteran born with spina bifida is denied. FINDING OF FACT The preponderance of the evidence is against a finding that the appellant has any form and/or manifestation of spina bifida. CONCLUSION OF LAW The criteria for establishing benefits under the provisions of 38 U.S.C. § 1805 for a child born with spina bifida have not been met. 38 U.S.C. §§ 1802, 1805; 38 C.F.R. § 3.814.   REASONS AND BASES FOR FINDING AND CONCLUSION The Veteran served on active duty from April 1968 to April 1970, including in the Republic of Vietnam. The appellant is the Veteran’s son. This matter is before the Board of Veterans’ Appeals (Board) on appeal from a November 2000 rating decision of a Department of Veterans Affairs (VA) Regional Office (RO). In July 2001, a hearing was held before a Veterans Law Judge. A transcript of the hearing is of record. In December 2001, the Board denied the claim. The Veteran appealed the Board’s December 2001 decision to the United States Court of Appeals for Veterans Claims (Court). In October 2002, the Court granted a Joint Motion for Remand (Joint Motion) vacating and remanding the Board’s December 2001 decision. The Board remanded the appeal to the Agency of Original Jurisdiction (AOJ) in November 2004. In August 2005, the Board informed the Veteran that the VLJ who held his hearing in July 2001 was no longer employed by the Board and offered him another hearing before a different VLJ. Later that month, the Veteran informed the Board that he did not want another hearing. Therefore, his Board hearing request is deemed satisfied. See 38 C.F.R. § 20.704. In November 2005, the Board again denied the claim. In January 2007, the Court granted a second Joint Motion and vacated and remanded the Board’s November 2005 decision. In July 2007, the Board again remanded the case to the AOJ. In January 2010, the Board again denied the claim. In November 2010, the Court granted a third Joint Motion and vacated and remanded the Board’s January 2010 decision. In February 2012, the Board again remanded the case to the AOJ. In January 2013, the Board again denied the claim. In April 2015, the Court reversed the Board’s January 2013 finding that VA had met its duty to assist the Veteran and vacated and remanded the Board’s January 2013 decision. In March 2016, the Board again remanded the case to the AOJ for further development. The Board notes that as requested in the March 2016 remand, VA requested the Social Security Administration (SSA) records of the Veteran’s son, and private treatment records, including records from Dr. E. and Dr. P. A June 2017 response from the SSA National Records Center reflects that the Veteran’s son’s medical records had been destroyed. Private treatment records from Dr. E. and Dr. P. have been added to the claims file and have been reviewed by the Board. Legal Criteria VA will provide certain benefits, including monthly monetary allowance, for an individual who suffers from a form or manifestation of spina bifida and whose biological father or mother is a Vietnam veteran. See 38 U.S.C. §§ 1802, 1805; 38 C.F.R. § 3.814; see also, e.g., 72 Fed. Reg. 32,395 (June 12, 2007) and 79 Fed. Reg. 20,308 (April 14, 2014) (both providing that benefits for birth defects other than spina bifida may not be presumed based on Vietnam-era herbicide agent exposure of parents). The term “Vietnam veteran” means a person who performed active military service in the Republic of Vietnam during the period beginning on January 9, 1962, and ending on May 7, 1975, without regard to the characterization of the person’s service. Service in the Republic of Vietnam includes service in the waters offshore and service in other locations, if the conditions of service involved duty or visitation in the Republic of Vietnam. 38 C.F.R. § 3.814(c)(1). The U.S. Court of Appeals for Veterans Claims (Court) has held that “Republic of Vietnam” includes the 12-nautical mile territorial sea. See Procopio v. Wilkie, 913 F.3d 1371 (Fed. Cir. 2019) (en banc). The Veteran had verified service in Vietnam from April 1969 to March 1970, during the Vietnam War era, and is thus, a Vietnam veteran. Spina bifida is the only birth defect which warrants an award of monetary benefits based on the herbicide agent exposure of a Vietnam veteran who is the father of the child at issue. Jones v. Principi, 16 Vet. App. 219, 225 (2002). For purposes of benefits under 38 U.S.C. § 1805, “the term ‘spina bifida’ means any form and manifestation of spina bifida except spina bifida occulta.” 38 U.S.C. § 1802; 38 C.F.R. § 3.814(c)(4). To qualify for a monthly allowance on the basis of other birth defects, the appellant must show that the Vietnam veteran who was exposed to herbicide agents is his or her mother. 38 U.S.C. §§ 1812, 1815; 38 C.F.R. § 3.815. In this case, the appellant, through the Veteran, contends that he is entitled to a monetary allowance under 38 U.S.C. § 1805 for spina bifida. The appellant asserts that his father’s in-service herbicide agent exposure while on active service in the Republic of Vietnam caused or contributed to the appellant developing symptoms consistent with spina bifida following a hypoxic event which occurred when he was 9 months old. The Veteran served in the Republic of Vietnam during the Vietnam era. Therefore, he has verified service in Vietnam during the Vietnam era. As noted above, the term “spina bifida,” in the context of this law, is defined as “all forms and manifestations of spina bifida except spina bifida occulta.” 38 U.S.C. § 1802. See Jones v. Principi, 16 Vet. App. 219 (2002) (holding that the plain language of 38 U.S.C. § 1802 does not limit the definition to spina bifida per se but includes other “forms and manifestations” of spina bifida except for spina bifida occulta). The question before the Board is whether the appellant has had symptoms of a form or manifestation of spina bifida, other than spina bifida occulta. Factual Background The case involves a Vietnam Veteran’s child who currently manifests clinical symptoms as seen in cases of children manifesting a form of spina bifida, but a controversy exists among experts as to whether any and/or all of those clinical symptoms may be indicative of an underlying form of spina bifida in this particular child, or may be exclusively attributed to a hypoxic brain injury occurring at the age of 9 months. The appellant was born in March 1985 at Golden Triangle Regional Medical Center (GTRMC). A “PHYSICIAN’S RECORD OF NEWBORN” noted that the child was treated “FOR NEOTAL DEPRESSION 2d TO DEMERAL [PATIENT] RESPONDED WELL TO NARCAN. APGAR 6/6.” On March [REDACTED], 1985, he was noted to be “LETHARGIC & HYPOTHERMIC” otherwise described as “INFANT SLEEPY, BUT RESPONSIVE TO STIMULATION.” He had a “GOOD RESPONSE” to intravenous medication (IV) and continued to have his blood glucose monitored. A March [REDACTED], 1985 CT scan of the head was interpreted by radiologist M.L.S.G., M.D., as follows: CRANIAL CT: (without contrast enlargement) The study was done without contrast enhancement. Five millimeter contiguous tomographic slices were obtained through the cranium. There are no focal intracranial defects. No subdural effusions are apparent. There is no dilation of the intracerebral ventricular system. The anterior fontanelle is full. Specifically, a portion of the frontal poles appears to be filling the anterior fontanelle. OPINION: 1. No hydrocephalus is apparent. 2. The study is suggestive of increased intracranial pressure, although, the etiology can not be determined from this examination. The appellant was discharged on April 9, 1985, with a diagnosis of “Newborn, term living male, borderline, small for gestational age” and “Hypoglycemia.” It was noted that a lumbar puncture was performed on April 1, 1985. The appellant’s 4-week follow-up visitation on April 24, 1985 noted that his head circumference (HC) was at the 75th percentile with his anterior fontanel open and soft. Otherwise, an evaluation of his other bodily systems, including neurological and musculoskeletal, were noted as “OK.” His 8-week follow-up visitation, dated May 18, 1985, noted blisters in the mouth. An examination conducted on May 22, 1985 again noted an HC at the 75th percentile with an open anterior fontanelle. There was also a notation of slight “sunset” eye appearance. A CT of the head was ordered. A July 26, 1985 clinical record noted HC at the 75th percentile and noted that he was still with sunset eyes. An evaluation of his other bodily systems, including the head, fontanelles, neurological and musculoskeletal, were noted as “OK.” He was given an assessment of rule out (R/O) hydrocephalus noting that his head CT scan demonstrated no significant abnormalities (NSA). A September 8, 1985, examination only noted the presence of conjunctivitis. A clinical evaluation on October 15, 1985 noted that examination of the head, fontanelles, neurological and musculoskeletal systems were “OK.” On January 9, 1986, he was treated for purulent rhinitis. On January 13, 1986, he was assessed with bronchitis. On January 15, 1986, the appellant was admitted to GTRMC due to upper respiratory congestion, decreased urination and an inability to tolerate oral feedings. On admission, he was noted to have the usual childhood illnesses with no significant injuries. His physical examination was significant for a soft anterior fontanelle, decreased skin turgor, somewhat sunken eyes, bilateral rhonchi, and faint rales. He was placed on IV fluids and given antibiotics based upon diagnoses of pneumonitis and dehydration. A chest x-ray demonstrated gross cardiomegaly. He was referred to the University of Mississippi Medical Center (UMC) for suspected cardiomyopathy. On January 16, 1986, the appellant was admitted to the UMC. His admission history noted that the child “had been doing well until about three weeks prior to admission when he developed cold-like symptoms, fever, nasal congestion and a slight cough.” Another intake record noted that the child was in his “usual state of excellent health” until he developed his cold symptoms. His past medical history was recorded as follows: Feeding: ? Prosebee Prior to illness pt eating table food G& D: Pt sat [with] support @ 6 mo, turns over, back to front & reverse, reaches for toys The appellant’s initial physical examination showed him to be “normocephalic.” He was immediately intubated with chest x-ray examination showing marked cardiomegaly and pulmonary edema. A 2D echocardiogram showed dilated left ventricle, left atrium, right ventricle, and poor left ventricular contractility. An electrocardiogram (EKG) showed an axis of +60 and positive for T waves in V1 with deep S waves. He was begun on Dopamine, Nipride, Lasix and Cefuroxime. However, he developed shock, bradycardia with PVC’s and had a full cardiopulmonary arrest. He failed to respond until intracardiac Epinephrine was given. Due to a lethargic mental status, a neurological workup was obtained. A head CT scan, dated January 31, 1986, was interpreted by radiologist Drs. M. and R. as follows: CLINICAL INFORMATION: 9 month old black male with probable hypoxic ischemic brain injury. S/P cardiopulmonary arrest... CT OF THE HEAD WITHOUT & FOLLOWING CONTRAST: There is a slight amount of generalized cerebral atrophy. No mass effects, hypodense areas suspicious for infarction, or evidence of midline shift is seen. No other intracranial abnormalities are identified. An electroencephalogram (EEG) showed diffuse slowing indicative of a generalized cerebral dysfunction. There were no epileptiform activities noted, but the appellant had been observed to have some seizure activity two days after the cardiac arrest. A lumbar puncture was normal. He was placed on Phenobarbital for his seizure activity, and required continuous nasoduodenal feedings due to poor suck and swallow reflexes. He was discharged with diagnoses of cardiomyopathy, status post cardiopulmonary arrest, and hypoxic cerebral injury. An October 26, 1989 letter from R.L.B., M.D., of the Columbus Children’s Clinic, stated as follows: I have followed [the appellant] since his birth . . . . [He] experienced an illness known as cardiomyopathy when he was 9 months old. This is a severe viral infection of the heart. [He] had a cardiopulmonary arrest during his illness and suffered hypoxic cerebral injury. This has left him severely neurologically impaired. He presently has spastic dyplegia and is impaired in muscle control of his trunk, head, and neck as well as all extremities. He suffers seizures which require daily antiseizure medication. [He] also has recurrent urinary tract infections which require treatment frequently. [His] daily medications as well as his frequent trips to the physician and his future rehabilitation cost are expected to be extremely high. The remainder of the appellant’s medical records demonstrate severe developmental delay with neurologic impairment, impaired muscle control and seizure activity. A CT of the head on September 17, 1999 was interpreted by radiologist P.S. as follows: CT HEAD WITHOUT CONTRAST: 09/17/99 Multiple computerized tomograms of the head demonstrate the cerebral ventricular system to be normal in appearance. Specifically, no evidence of hydrocephalus or shift of midline structures can be identified. No infarction or hemorrhage is present. No evidence of a subdural hematoma is seen. CONCLUSION: CT examination of the head demonstrates no abnormality. An April 7, 2000 letter from P.S., M.D., stated as follows: [The appellant] is a patient of mine. He has a diagnosis of seizure disorder and cerebral palsy. The diagnosis [is] secondary following a cardiomyopathy. He has severe developmental delay and mental retardation. He is confined with muscular atrophy, diffusely and contractures to arms and legs. Several times a day, he has tonic/clonic seizures. He cannot perform any activities of daily living. He is incontinent of bowel and bladder. His speech is not intelligible to anyone. He takes physical therapy and occupational therapy with no changes, thus far. A May 2012 private treatment record from Dr. O.E. reflects that the appellant had severe organic brain syndrome with seizures. The record noted that the appellant had been severely disabled since he had an acute illness, possibly viral myocarditis, at 9 months of age. The appellant’s private treatment records do not note any treatment or diagnosis of spina bifida. Medical Opinions In January 2003, VA received an opinion from C.N.B., M.D., who represented himself as a Neuro-Radiologist, that stated as follows: At your request, I have reviewed the patient’s C-folder and medical records for the purpose of making a medical opinion concerning his brain disorder and if it was caused by his parent’s exposure to Agent Orange in Viet Nam. In order to make this decision I have carefully reviewed the following information: Medical records; Rating decisions; Statements of the Case; Veterans and Agent Orange Updates 1996 and 1998; Medical literature review. Definition of terms: The terms central nervous system defects/neural tube defects and “... all forms and manifestations of spina bifida...” describe the same pathologic process and will therefore be considered synonymous within this report. Facts, Rationale/Medical theory, Other Medical Opinions: [Birth Date] [REDACTED] March 1985 “...Infant noted to be lethargic & hypothermic at 1:00 AM today...” Dr. ? [REDACTED] March 1985 Head CT scan “...a portion of the frontal pole appears to be filling the anterior fontanelle... This study suggestive of increased intracranial pressure, although the etiology can not be determined from this examination...” Dr. [G.]; 16 Jan 1986 “...EEG showed diffuse slowing indicative of a generalized cerebral dysfunction...” Dr. [W.] 29 Jan 1986 “...HC 48...1/18...has stiffness/slowing episodes - 3 seizures... eyes midportion or...deviated to R.A. Probable hypoxic-ischemic brain injury with [increasing] head circumference-etiology unknown...” Dr. [P.]; 31 Jan 1986 “...There is a slight amount of generalized cerebral atrophy...” Drs. [M. & R.]; 29 Oct 1989 “...9 months old suffered hypoxic cerebral injury...” Dr. [B.] 17 July 2000 “...This child has organic brain syndrome...” Dr. [E.]; Dec 2002 Patient’s medical history as remembered by mother “...Did [child] have any medical problems after he left the hospital in March/April 1985? Yes he was developmentally slow...” [E.H.]. Summary: In review of the record it is clear that this patient had a very serious illness in Jan of 1986, which resulted in shock, bradycardia with PVC’s and cardiopulmonary arrest, and which further necessitated the use of intracardiac epinephrine for response. It is also clear that this patient was not mentally normal prior to this near-death clinical episode because his mother states that he was developmentally slow, his Head CT scan on 29 March 1985 showed the following “...a portion of the frontal pole appears to be filling the anterior fontanelle... This study suggestive of increased intracranial pressure, although the etiology can not be determined from this examination...”, which was thought to represent increased intracranial pressure by Dr. [G.], and his head circumference was increasing at an increasing rate from birth until his Jan 1986 (see attached Head circumference chart with the 29 Jan 1986 data added). These findings all indicate that this patient had an abnormality within his brain prior to his episode of near death in Jan 1986. I understand that this patient’s father was exposed to Agent Orange in Viet Nam and that there is a positive association between Agent Orange exposure and central nervous system defects/neural tube defects/all forms and manifestations of spina bifida as supported by the Institute of Medicine 1996 and 1998 Veterans and Agent Orange updates. Thirteen of the sixteen or 81% studies below, from the 1998 update, show an Estimated Risk of greater 1 which means that nervous system/neural tube defects/all forms and manifestations of spina bifida occurs more often in siblings of exposed individuals than the rest of the population. Furthermore, the table includes three studies in which these [sic] is a statically [sic] significant association between nervous system defects/neural tube defects/ all forms and manifestations of spina bifida and Agent Orange as supported by the fact that the entire range of the confidence interval in these three studies in above 1. Table 9-1 Selected Epidemiologic Studies - Neural Tube Defects... It is my opinion that this patient had a brain defect prior to his 1986 near death episode and that this brain defect contributed substantially to his current mental deficits and that these defects are due to his parent’s exposure to Agent Orange for the following reasons: 1. His head CT findings of 1985 are consistent with the spectrum of findings that I would expect to see in a patient with Central nervous system defects/neural tube defects secondary to Agent Orange. In fact this patient had “...a portion of the frontal pole appears to be filling the anterior fontanalle...” which is very consistent with magalencephaly, which is described below in the neurulation defect sub-classification of Neural tube defects (see Greenberg below). It is my opinion that this patient’s abnormal Head CT finding in 1985 were likely due to the spectrum of terms central nervous system defects/neural tube defects/all forms and manifestations of spina bifida and that these defects were likely due to the parent’s exposure to Agent Orange. This is a serious brain defect and therefore likely substantially contributes to his current disabilities. … 2. The patient had an abnormally enlarging head circumference prior to his near death episode in Jan 1986, which is consistent with the spectrum of cranial problems associated with Neural tube defects. It is my opinion that this patient’s abnormal head circumference was due to the spectrum of problems associated with terms central nervous system defects/neural tube defects/all forms and manifestations of spina bifida neural tube defects caused by Agent Orange and likely substantially contributes to his current disabilities. 3. The patient had developmental delay according to his mother prior to the Jan 1986 incident and developmental delay is consistent with megalencephaly according to Greenberg page 151 and that this developmental delay likely substantially contributes to his current disabilities. 4. Due to the severity of this patient[’]s disabilities he would likely best be placed in VA payment level III under CFR38. Attached to the opinion letter was a chart entitled “BOYS: BIRTH TO 36 MONTH PHYSICAL GROWTH NCHS PERCENTILES” and the curriculum vitae for Dr. C.N.B. His training and education includes earning his medical doctorate at the Uniformed Services University of the Health Sciences (USUHS), an internship and residency in radiology at The George Washington University Hospital, a clinical fellowship in neuroradiology at the University of Maryland, and a clinical research fellowship and guest researcher in neuroradiology at the National Institutes of Health (NIH) Laboratory of Diagnostic Radiology Research (LDRR). His employment has included being the President and Director of Radiology Consulting, Deputy Director of Medical Services for the Paralyzed Veterans of America, Assistant Professor and Clinical Instructor of Radiology and Nuclear Medicine at USUHS, Neuroradiologist at Laurel Diagnostic Imaging, Staff/Senior Fellow at NIH/LDRR, Neurology Fellow at the University of Maryland Medical Systems, and Chief of Radiology at White River Indian Hospital. His certifications include being a Senior Member of the American Society of Neuroradiology (ASNR), Board certified in Diagnostic Radiology and a Member of the National Board of Medical Examiners. The Board notes that the submission by Dr. C.N.B. did not include the definition of macroencephaly (aka megalencephaly) from Greenberg, Handbook of Neurosurgery 2001, referenced and relied upon in his opinion letter. The Board, therefore, will supplement the record with the definition of macroencephaly from the 2001 Greenberg edition stating as follows: MACROENCEPHALY AKA macroencephaly, AKA megalencephaly (not to be confused with macrocephaly, which is enlargement of the skull (see page 880). Not a single pathologic entity. An enlarged brain which may be due to: hypertrophy of gray matter alone, gray and white matter, presence of additional structures (glial overgrowth, diffuse gliomas, heterotopias, metabolic storage diseases...) May be seen in neurocutaneous syndromes (especially neurofibromatosis). Brains may weigh up to 1600-2850 grams. IQ may be normal, but developmental delay, retardation, spasticity and hypotonia may occur. Head circumference is 4-7 cm above mean. The usual signs of hydrocephalus (frontal bossing, bulging fontanelle, “setting sun” sign, scalp vein engorgement) are absent. Imaging studies (CT or MRI) show normal sized ventricles and can be used to rule out extra-axial fluid collections. In June 2003, the Board referred the claims folder for an opinion by a neurology expert at the VHA. A July 2003 opinion from neurologist, Dr. G., reads as follows: GENERAL REMARKS: This is a specialist opinion for Compensation and Pension purposes. The letter requesting this opinion states that it is in regard to questions regarding a case of the Veteran’s child, who was born in March 1985. The child had experienced an illness known as cardiomyopathy, a severe viral infection of the heart when nine months old. The child had experienced cardiopulmonary arrest during that illness and suffered hypoxic cerebral injury, leaving the child severely neurologically impaired. The child had spastic diplegia and was impaired in muscle control of his truck [sic], head, and neck, as well as all extremities. An April 2000 letter from a private physician reflects that the Veteran’s child had a diagnosis of seizure disorder and cerebral palsy. These were secondary following the cardiomyopathy. The child had severe developmental delay and mental retardation and was confined with muscular atrophy diffusely and contractures to the arms and legs. The child had tonic/clonic seizures daily and could not perform any activities of daily living. A private medical opinion dated January 2003 included the opinion that the Veteran’s child’s condition “was due to the spectrum of problems associated with the term central nervous system defect/neural tube defect/all forms and manifestations of spina bifida neural tube defects...” . . . HISTORY: The first question as to what the defining characteristics of spina bifida are: Spina bifida is a congenital condition resulting from failure of the neural tube to close normally which usually happens in the third to fourth week of prenatal development in the uterus. Spina bifida generally refers to those cases in which the spinal cord does not close correctly but has a deficit. I will refer to open spina bifida or spina bifida aperta because that appears to be the relevant condition that is in question here. There is also a condition spina bifida occulta in which there is not actual protrusion of neurologic tissue through the bony defect and this is often asymptomatic and is not at issue in this case, and I will not discuss it further. In spina bifida there is a bony defect in the spinal column or perhaps in the skull and either the meninges will herniate through this defect, or both meninges and neural tissue such as nerve roots in the spine or perhaps brain tissue in the case of a skull defect, actually herniate through the opening in the bone. I will quote from the Nelson Textbook of Pediatrics, 15th Edition, published by W.B. Saunders. This edition was published in 1996. “Meningocele which is one form of open spina bifida is formed when the meninges herniate through a defect in the posterior vertebral arches. The spinal cord is usually normal, and assumes the normal position in the spinal canal although there maybe tethering syringomyelia or diastematomyelia. A fluctuant midline mass that may transilluminate occurs along the vertebral column usually in the low back. There may be an association with hydrocephalus in some cases.” To quote from this section on myelomeningocele, this is more severe because there is actually neural tissue that is herniated through bony defect. The clinical manifestations include dysfunction of many organs and structures, including the skeleton skin and genitourinary tract in addition to the peripheral nervous system and the central nervous system. A myelomenigocele can be located anywhere along the neuroaxis, but the lumbosacral region accounts for at least 75% of the cases. The extent and degree of the neurologic depend on the location. A lesion in the low sacral region accounts for at least 75% of the cases. The extent and degree of the neurologic deficit depends on the location... A lesion in the low sacral region causes bowel and bladder incontinence and anesthesia in the peroneal area but no impairment of motor function. The newborn with a defect in the mid-lumbar region typically has “a sack-like cystic structure covered by a thin layer of partially epithelialized tissue...” An examination of the infant shows a flaccid paralysis of the lower extremities and absence of deep tendon reflexes, a lack of response to touch and pain and a high incidence of postural abnormalities of the lower extremities, including clubbed feet and subluxation of the hips. Constant urinary dribbling in a relaxed anal sphincter may be evident. Hydrocephalus in association with a type II Chiari defect develops in at least 80% of patient’s [sic] with myelomeningocele. Generally, the lower the deformity in the neuroaxis, the less likely will be the risk of hydrocephalus. Ventricular enlargement may be indolent and slow-growing or it may be rapid causing a bulging anterior fontanel, dilated scalp veins, a setting sun appearance of the eyes, irritability, and vomiting associated with increased head circumference. Not infrequently infants with hydrocephalus in the Chiari II malformation develop symptoms of hindbrain dysfunction, including difficulty feeding, choking, stridor, apnea, vocal cord paralysis, pooling of secretions, and spasticity of the upper extremities which, if untreated, can lead to death. Encephalocele (Nelson’s Textbook of Pediatrics, p. 1679). There are two major forms of dysraphism affecting the skull resulting in protrusion of tissue through a bony midline defect called cranium bifidum. A cranial meningocele consists of a CSF-filled meningeal sac only, and a cranial encephalocele contains the sac plus cerebral cortex, cerebellum or portions of the brain stem. The cranial defect occurs most commonly in the occipital region at or below the inion but in certain parts of the world frontal or nasofrontal encephaloceles are more prominent. Infants with a cranial encephalocele are at increased risk for developing hydrocephalus due to aqueduct stenosis, a Chiari malformation, or the Dandy-Walker syndrome. Examination may show a small sac with a pedunculated stalk or a large cyst-like structure that may exceed the size of the cranium. The lesion may be completely covered with skin but areas of denuded skin can occur... Children with a cranial meningocele generally have a good prognosis, whereas patient’s [sic] with an encephalocele are at risk for visual problems, microcephaly, mental retardation, and seizures. Generally, children with neural tissue within the sac and associated hydrocephalus have the poorest prognosis. Finally, there is anencephaly. The anencephalic infant presents a distinctive appearance with a large defect of the calvaria meninges and scalp associated with a rudimentary brain... (Nelson’s, p. 1680) Because it is clear that the Veteran’s child considered in this case does not have anencephaly. Those children rarely survive very long beyond birth.” So that is the response to the first question about the defining characteristics of spina bifida in its different manifestations. The second question is, “Identify all currently diagnosed chronic disorders of the Veteran’s child’s nervous and skeletal systems.” As to the skeletal system there is really not mention of specific anomalies. With regard to the child’s nervous system, although not strictly neurological diagnosis: 1. The child is status post a cardiomyopathy which was believed secondary to viral myocarditis occurring when the child was nine months of age. 2. The child is status post cardiopulmonary arrest secondary to the cardiomyopathy. The records that are in the claims file show that the child when being treated for the cardiomyopathy and after being hospitalized in pediatric intensive care unit, did go into cardiac and pulmonary arrest and was difficult to resuscitate responding only to intracardiac epinephrine. 3. Hypoxic ischemic cerebral injury resulting from the cardiopulmonary arrest which occurred in January of 1986 which is diagnosis No. 2, already mentioned. 4. Spastic diplegia elsewhere referred to in the record as spastic quadriparesis which is secondary to diagnosis No. 3, the hypoxic ischemic cerebral injury. 5. Seizure disorder, which again, appears to be secondary to the hypoxic cerebral injury which is diagnosis No. 3. Generalized encephalopathy manifested by severe cognitive impairment, unintelligible speech, lack of control of the bowels and bladder according to a letter from the Veteran’s child’s doctor dated April 7, 2000, which is in the claims file and which was also cited in the request for a specialist opinion already quoted. Question three requested for the opinion is for each chronic disorder identified, indicate whether, or not it is a form of spina bifida. Spina bifida can produce symptoms such as spastic quadriparesis, a seizure disorder and encephalopathy as already mentioned in my response to question 1. However, the history of this child’s problems is most consistent with these chronic disorders being secondary to the cardiopulmonary arrest producing hypoxic cerebral injury and this was related to cardiomyopathy that the child suffered and was treated for in January of 1986 when the child was nine months of age. The records from the neonatal period do indicate that the child was not entirely normal at the time the child was born. A CT scan of the head done at two days of age showed fullness of the anterior fontanelle; however, there was not actually hydrocephalus. The radiologist said that these findings were consistent with some increase in intracranial pressure, although no specific etiology could be identified from the radiological images. The child was born as a full-term delivery by a vaginal delivery for which no complications were mentioned on the records from that delivery and the APGAR scores at one minute was 6, and the APGAR at five minutes was also 6, which is a low score. The baby weighed 6 pounds 12 ounces but was felt to be small for his gestational age. Additionally, as a newborn, the Veteran’s child was observed to be hypoglycemic. However, the infant did not have a prolonged hospitalization at that time but was apparently discharged within a few days to home and there is no mention of further symptoms or complaints requiring medical attention until about three weeks before the admission in January of 1986 when the infant had some systemic signs of infection and was seen several times by a doctor who treated him with antibiotics prior to becoming more ill and being found to have a severely enlarged heart and requiring ventilation and admission to an intensive care unit in January of 1986 when the child was nine months of age. Now, although the child had an abnormal CT scan in the neonatal period with fullness of the anterior fontanelle, and there is a mention that part of the frontal poles of the brain was protruding into the anterior fontanelle area. But it is not abnormal for a newborn baby to have a fontanelle, that is, that does not constitute a developmental skull defect and there is no mention of an actual skull defect which might be an indication of a spina bifida type of condition that is an actual dysraphism with an encephalomeningocele. So, this CT scan in itself does not provide evidence of a condition that would fall into the category of spina bifida, although it does suggest that the child in the neonatal period had some increased intracranial pressure. Some note from the child’s admission in January of 1986 when he was severely ill state as far as his development, he could sit without supports at six months, turn over back to front and reverse, and was able to reach for toys, and had been eating table food prior to that illness which he experienced at about nine months of age. So, there is not really documentation that the child was experiencing developmental delay prior to this illness that he suffered at nine months of age. So, in conclusion, I would have to say that for the chronic disorders which were mentioned in response to item 2, that in this case they do not seem to be manifestations of spina bifida, but rather, seem to be related to the child’s cardiopulmonary arrest that he suffered at the age of nine months as a result of a cardiomyopathy and are not manifestations of spina bifida, as such. Item #4 is whether the chronic disorders are manifestations of spina bifida, I think the chronic disorders that are mentioned in this particular case of this child are not a form or manifestation of spina bifida, but seen [sic] most plausibly to be attributable to the child’s cardiopulmonary arrest due to his cardiomyopathy that he suffered at nine months. While there is some documentation that the child did not have completely normal neurologic function when he was born, and had an abnormal CT scan at that time. There is not documentation specifically that he had a condition which would fall under the definition of spina bifida. I think that is all I can say in regard to the questions which I am asked to address in this opinion. Attached to the VHA opinion were definitional sections from Chapter 542 of Nelson’s Textbook of Pediatrics, 15th edition (1996), entitled Congenital Anomalies of the Central Nervous System. A later received curriculum vitae indicates that the specialist earned her medical doctorate at the University of Miami. She is board certified in neurology. Her occupational experience includes an internship at St. Elizabeth Hospital, a residency in neurology at Dartmouth-Hitchcock Hanover, a fellowship in neurology in GeriNeuro at the Boston, Massachusetts, VA Medical Center (VAMC), a staff neurologist at the Newington, Connecticut VAMC, Clinical Staff Assistant at Hartford Hospital, and Assistant Clinical Professor in the Department of Neurology at the University of Connecticut. A January 2004 rebuttal opinion letter from Dr. C.N.B. stated as follows: At your request, I have re-reviewed this patient’s medical records for the purpose of making a medical opinion concerning his brain disorder. I have paid particular attention to the recent 6-page opinion by Dr. G. I note that Dr. G provides a nice summary of the findings in spina bifida, which includes “...an association with hydrocephalis...[and] Ventricular enlargement may be indolent and slow-growing...bulging the anterior fontanel... increased head circumference....” I also note that Dr. G. in her answers to the questions, that she was presented, that she basically stated that [t]he CT scan was not abnormal and that the scan by “...in itself does not provide evidence of a condition that would fall into the category of spina bifida...” I disagree with her opinion and have discounted her assessments for the following reasons: 1. The initial CT scan was abnormal as dictated by the radiologist. If Dr. G would like to interpret the scan differently than this scan should be obtained and shown to her for a change in interpretation. Please note that Dr. G did not correlate the CT findings with the clinical record that shows that this patient had a head circumference that was greater than 50% of children for age and that this circumference was increasing in percentage such that it measured 80% at 10 months of age (see attached chart). 2. I do not think that Dr. G had the entire record to review because she infers that the patient’s problems originate from the Jan 1986 episode of hypoxic injury when the records shows [sic] that the patient clearly had lethargy almost a year earlier . . . (one day after birth). It should also be noted that the CT scan spoken about in point 1 above was taken one day later . . . , therefore this patient’s clinical lethargy, CT scan findings, and head circumference changes all occurred near birth and significantly predated the hypoxic injury of Jan 1986 that Dr. G attributes this patient’s current problems. 3. While Dr. G acknowledges that the patient had “...some documentation that the child did not have a complete normal neurological function when he was born, and had an abnormal CT scan at that time. There is no documentation specifically that he had a condition which would fall under the definition of spina bifida...” she does not explain why or how these findings are inconsistent with spina bifida or what other diagnosis she would offer to explain the abnormalities or why it is not at least as likely as not that a newborn patient with symptoms and signs of increasing percentile head circumference, lethargy, and abnormal CT scan could not represent the first signs and symptoms of a form of spinal bifida. 4. Dr. G does not provide any literature to support her opinion that a newborn patient with symptoms and signs of increasing head percentile circumference, lethargy, and abnormal CT scan are not early sings [sic] and symptoms of spinal bifida. In fact, the literature that she quotes actually supports my opinion because she states the following: “... an association with hydrocephalis...[and] Ventricular enlargement may be indolent and slow-growing...budging the anterior fontanel...increased head circumference...” which is totally consistent with the record which refers to hydrocephalis (which is often manifest by increasing percentile head circumference and an abnormal CT scan), the abnormal CT findings and the clinical findings of lethargy. 5. Finally, she does not comment on my previous opinion, which also makes me think that she did not have the full record to review. In summary I do not see anything in the recent opinion by Dr. G that would make me change my previous opinion because I have discounted Dr. G’s opinion for the above stated reasons. In July 2004, the Board requested an Independent Medical Expert (IME) opinion. A July 2004 opinion letter from A.L.C., M.D., opines as follows: Per your request, I have reviewed [the appellant’s claims file] and all supporting documents contained therein including but not limited to: Hospital Records Private Physician Records (Primary care physician and specialists) Home Health Records Independent Medical Evaluation (2003, 2004) VA Physician Report (2003) Radiology Reports In addition, I have reviewed selected medical literature on Spina Bifida (references listed at the end of this opinion). Essentially, I have been asked to provide an opinion regarding the following issues: (1) What are the defining characteristics of “spina bifida” (spina bifida aperta)? (2) Identify all currently diagnosed chronic disorders of the Veteran’s child’s nervous and skeletal systems. (3) For each chronic disorder identified in (2), indicate whether or not it is a form of spina bifida (4) For each chronic disorder identified in (2), indicate whether or not it is a manifestation of spina bifida The available history reveals the following: The [appellant] was born [in] March 1985 at 38 weeks gestation to a 33 year old G3P2 via vaginal delivery. APGAR scores were 6 at 1 minute and 6 at 5 minutes. Neonatal depression at the time of delivery was felt to be secondary to narcotic medication administered to the mother, and the patient responded well to Narcan. On [REDACTED] March 1985, he was noted to be lethargic and was found to be hypoglycemic. On March [REDACTED], 1985, he underwent a CT scan of the head without contrast. These films are not available for my review; however, the scan reportedly showed “... The anterior fontanelle is full. Specifically, a portion of the frontal pole appears to be filling the anterior fontanalle... No hydrocephalus is present. The study is suggestive of increased intracranial pressure, although, the etiology can not be determined from this examination.” There is no report of any follow-up scan done at that time. No other records are available from the neonatal admission except the neonatal discharge summary sheet. However, according to the history and physical done at the time of the patient’s admission to University Medical Center for his viral cardiomyopathy, “...Nursery course complicated by a “blood infection” & the pt remained in the nursery for 10 days for IV antibiotics.” Over the course of the next 2 months, according to private physician records, [the appellant’s] head circumference was at the 75th percentile but the anterior fontanelle was open. He had a repeat CT head. Again, films are not available, but according to the physician’s notes, there was no hydrocephalus present. At four months of age, there is another note that the head circumference was still 75th percentile. It appears that [the appellant] did relatively well until January 1986 when at the age of 9 months, he developed a viral illness for which he was admitted to the local hospital. He was subsequently transferred to University Medical Center (UMC) with a suspected viral cardiomyopathy. According to the history and physical done at that time, [the appellant] had met the following milestones: sat without support at 6 months, able to turn over back to front and reverse, was reaching for toys, and was eating table food. Shortly after arrival to UMC, as a complication of his cardiomyopathy, [the appellant] developed shock, bradycardia, and cardiopulmonary arrest that responded only to intracardiac epinephrine (Discharge summary dated 2/6/86). He was subsequently felt to have suffered hypoxic-ischemic brain injury. Other documentation from the claims file: 1/31/86: CT of the head without & following contrast: “...generalized cerebral atrophy...no other intracranial abnormalities...” 10/26/89: letter from private physician describes [the appellant’s] condition as “severely neurologically impaired...spastic dyplegia...impaired in muscle control...seizures...recurrent urinary tract infections” 9/17/99: CT examination of the head demonstrates no abnormality 7/20/00: Clinic note from pediatric neurologist documenting chronic organic brain syndrome, intractable seizures, hyperflexia, and spasticity. With regard to the question asked in your letter, my opinion is as follows: (1) Spina bifida is a neural tube defect caused by incomplete closure of the spinal column during the first month of conceptual life. This can result in a spectrum of disorders that can range from an opening in one or more of the vertebrae without damage to the spinal cord (spina bifida occulta) to an opening in the vertebrae with protrusion of the meninges and/or the spinal cord itself (spina bifida manifesta or aperta). These may vary in location and occur anywhere along the neuroaxis with the most common location involving the lumbosacral spine. When the cranial area is involved these are referred to as cranial meningocele (meninges only) or encephalocele (meninges plus cerebral tissue) and may be located in the occipital or frontal regions. In the case of anencephaly, the most severe spinal dysraphism, there is absence of the calvarium, scalp, and cerebrum. For the purpose of this opinion, further reference to spina bifida will refer to spina bifida aperta unless otherwise specified. Spina bifida can have many associated complications including: paralysis, spasticity, loss of bowel and bladder control, hydrocephalus, seizures, cognitive impairments, and learning problems. Spina bifida is a congenital problem that is present from birth and in most cases, signs and symptoms are also present at birth. An imaging study (preferably magnetic resonance imaging) of the affected area can rapidly confirm the diagnosis even in the absence of clinical signs as is the case of spina bifida occulta. (2) This patient’s birth was uncomplicated; however, he had documented lethargy related to transient hypoglycemia. This was appropriately evaluated and he was ultimately treated with antibiotics for an infection. His CT head at birth was reported as abnormal due to fullness of the anterior fontanel. However, this was not diagnostic of hydrocephalus. The patient had follow-up CT two months later that showed no evidence of hydrocephalus and in the absence of placement of a shunt, one would expect that congenital hydrocephalus would still be present and in fact would have worsened over that period of time. At the time of his admission for viral cardiomyopathy, he was appropriately meeting developmental milestones. This would suggest the absence of cognitive impairment and developmental delay prior to the cardiomyopathy. Unfortunately, [the appellant] suffered a severe hypoxic cerebral insult as a result of the arrest resulting in cognitive impairment, muscle weakness, seizures, spastic diplegia/spastic quadriparesis, unintelligible speech, and recurrent urinary tract infections. It would appear from the records available that these are the current chronic conditions of the Veteran’s child. (3) Spina bifida can have many associated clinical conditions and sequelae including each of the chronic conditions of the patient in question. However, as all of these conditions followed the hypoxic cerebral injury and none of them were present at birth, or documented as present at the time of his admission for the cardiomyopathy, it is unlikely that they are the result of spina bifida. In addition, with the exception of the abnormal CT scan at birth, there is no other neuroimaging that suggests a primary CNS abnormality. Even this CT scan is not consistent with failure of closure of the neural tube as the anterior fontanel is a normal physiologic finding in the newborn. So, I do not feel that this represents a form of spina bifida. (4) While each of the patient’s chronic conditions may represent a complication or manifestation of spina bifida, I do not feel that this is what they represent in this patient. Rather, I feel that his chronic conditions represent residual deficits and sequelae of hypoxic injury given the chronological occurrence of events. The IME opinion letter indicates that Dr. C. is an instructor at the Departments of Neurology and Pediatrics, Division of Pediatric Neurology, at the University of Mississippi Medical Center. In an opinion letter dated May 2005, Dr. C.N.B. provided the following rebuttal opinion: I have re-reviewed this patient’s medical records for the third time in order to make an opinion concerning his current brain damage. Special Knowledge: I have special knowledge in the area of the imaging of brain abnormalities, as I am board certified Radiology sub specialist and three Fellowship trained Neuro-Radiologist and I am a Senior Member of the American Society of Neuro-Radiology (ASNR). I have performed and/or interpreted plain x-rays, CT scans, nuclear medicine scans, angiograms, PET scans and MRI scans on thousands of patients with brain disorders and I have correlated my findings with the clinical record. This patient’s case includes several of the above imaging studies. (attached C.V.). In my recent review of this case I noticed some new information from Dr. [C.] and a new VA SSOC dated 20 April 2005. … I also note several inconsistencies in the report by Dr. [C.]. She states that the patient had an abnormal CT scan in the face of lethargy but that i[t] was not diagnostic of hydrocephalus even though the radiologist stated “... suggestive of increased intracranial pressure...” She does not explain her expertise in neruo-imaging [sic] or document that she reread the imagines [sic] in question. She also does not provide any rationale that does not support an association between hydrocephalus and lethargy. In fact she fails to acknowledge the opinion of Dr. [G.] of “...is suggestive of increased intracranial pressure...” and/or she does not attempt to attribute it to another cause and/or she fails to say how this abnormality is not due to a form of spina bifida. She also states that this patient had multiple head circumference measurements that were increasing at an increasing rate consistent with the CT scan findings of increased intracranial pressure, which is consistent with a form of spina bifida. Dr. [C.] also fails to provide any literature to support her hypothesis that increasing head circumferences and an abnormal head CT scan is not consistent with a form of spina bifida. I think that many of Dr. [C.]’s incorrect opinions likely stem from her unfamiliarity with the neuro-imaging studies as I note she is an Instructor in pediatric neurology and therefore likely does not have any formal training in neuroimaging and/or she did not have the full record to review as she apparently overlooked or did not have the comments by Dr. [G.]/longitudinal head circumference measurements and/or she does not understand the full spectrum of the forms of spina bifida and/or she does not understand the VA concept of benefit of the doubt as it relates to the terms of “as likely as not.” In summary, I have discounted the recent SSOC and the opinion of Dr. [C.] for the reason stated above and I do not find any new information in the record that would make be [sic] change my previous two opinions. In June 2005, an opinion letter was authored by H.M., M.D., opinion stating as follows: I have reviewed the patient’s medical records and accompanying statements by Dr. [B.] and [C.]. Special Knowledge: I am board certified Radiologist with specialty training and certification in Pediatric Radiology. I have completed dual residencies in Pediatrics, followed by Radiology with fellowship training in Pediatric Radiology and while on active duty, served as the Chief of Pediatric Radiology at Walter Reed Army Medical Center. In addition to having been the primary care provider for hundreds of pediatric patients, I have performed and/or interpreted various imaging studies on thousands of pediatric patients, to include plain film, CT and MRI. While it is unclear to what extent [the patient’s] current neurologic deficits are congenital, it is clear that he was neurologically abnormal from birth. His APGARS were low at 6 and 6, and although this was attributed to maternal narcotics, there is no objective way to establish this. Additionally, the mother describes developmental delay and a head CT read by Dr. M.L.S. [G.] in day 2 of life describes a “portion of the frontal poles... filling the anterior fontanelle” and “findings suggestive of increased intracranial pressure.” The presence of the frontal poles within the fontanelle is significant because with normal intracranial pressure, the fontanelle should be flat. Other than increased intracranial pressure, the only other reasonable etiology for the finding would be encephalococele, which is also congenital abnormality and falls into the category of neural tube defects. The patient’s growth chart also supports the diagnosis of intracranial pressure in that the head circumference increased from 75 percentile at birth and 8 weeks, to 80th percentile at 4 months, while his length and weight remained relatively stable at the 30th and 60th percentiles, respectively. Lastly, a head CT obtained two weeks following the cardiac arrest, read by Drs [M. and R.], showed “generalized atrophy... without infarction.” The absence of CT evidence of infarction, which is expected sequelae of lack of oxygen to the brain, raises the possibility that the CT abnormality (generalized atrophy) predated the ischemic event, particularly when the optimal time for imaging hypoxic brain injury is after 2 weeks. Typically, “the repeat scan in 14 days will show a return to near normal in those patients who will have relatively mild deficits, whereas cystic or hemorrhagic parenchymal degeneration and progressive atrophy indicate a more guarded prognosis.” (Barkovich, Pediatric Neuroimaging). None of these findings were described on the CT. I have also reviewed the expert opinions of Dr.’s [B. and C.]. I disagree with Dr. [C.] for several reasons. She neglects to mention the increasing head circumference, fails to acknowledge the developmental delay as described by the mother. She describes normal developmental milestones, but nowhere in the record is a full developmental assessment. Additionally she states that an “anterior fontanelle is a normal physiologic finding in the newborn.” This is correct. But what was described on the initial head CT is much more than a physiologically normal fontanelle; the frontal portions of the brain were described as filling the anterior fontanelle. That is not a normal finding and is most likely what lead the interpreting physician to suggest the presence of increased intracranial pressure. Finally, Dr. [C.] contradicts herself and her own argument stating that “spina bifida can have many associated clinical conditions and sequela including each of the chronic conditions of the patient in question.” I agree with Dr. [B.]’s conclusion that the lethargy described in the newborn period, the abnormal head CT, increasing head circumference, and developmental delay are likely manifestations of spina bifida and contribute substantially to the current disabilities. Analysis The Board finds that the preponderance of the evidence is against a finding that the appellant has a form and/or manifestation of spina bifida. The Board reaches this conclusion on the following facts found: The child was born in March 1985. There is no dispute of record that his APGAR scores (appearance (color), pulse (heart rate), grimace (reflex, irritability), activity (muscle tone), and respiration (score reflecting condition of newborn) were abnormally low. He was initially thought to be suffering from neonatal depression and responded well to Narcan. See GTRMC “PHYSICIAN’S RECORD OF NEWBORN”; July 2004 opinion by Dr. C., p. 1. His documented lethargy in March 1985, was attributed to transient hypoglycemia for which he had a “GOOD RESPONSE” to IV treatment. GTRMC “PHYSICIAN’S RECORD OF NEWBORN”; July 2004 opinion by Dr. C., p. 2. There is also no dispute of record that a CT scan of the head performed on March [REDACTED], 1985 was abnormal. The interpreting radiologist found that the anterior fontanelle was full with a portion of the frontal poles filling the anterior fontanelle. Drs. C. and M. agree that an anterior fontanelle is a normal physiologic finding in a newborn. See July 2004 opinion by Dr. C., p. 3; June 2005 opinion by Dr. M., p.2. The interpreting radiologist specifically diagnosed “[n]o hydrocephalus is apparent.” A follow-up CT of the head in approximately July 1985 is reported by the child’s treating physician as showing no significant abnormalities. Review of the child’s medical records from his treating physicians indicate concern that the HC was in the 75th percentile, but that a considered diagnosis of hydrocephalus was not borne out by CT scan results. The child’s follow-up visitation records, dated April 24, 1985, May 18, 1985, July 26, 1985, September 8, 1985, October 15, 1985 and January 13, 1986, do not document any concerns that the child displayed developmental delay or cognitive impairment. Rather, aside from the findings of HC at the 75th percentile, an open and soft anterior fontanelle, slight “sunset” eye appearance and conjunctivitis, the child’s clinical evaluations of his head, fontanelles, neurological and musculoskeletal systems were noted as “OK” for his first 9 months of life. The lay history of developmental and cognitive status most contemporaneous in time to the hypoxic injury that occurred in January 1986 consists of a UMC intake assessment wherein the parent(s) reported as follows: Feeding: ? Prosebee Prior to illness pt eating table food G& D: Pt sat [with] support @ 6 mo, turns over, back to front & reverse, reaches for toys The Board finds the evidence shows that unfortunately, the child experienced a severe viral infection of the heart in January 1986 that led to cardiopulmonary arrest with a hypoxic cerebral injury. This event left him severely neurologically impaired with spastic dyplegia, impaired muscle control, and seizures. Based upon the facts found, the Board places the greatest probative weight on the July 2004 opinion by Dr. C. as it discusses all the relevant evidence and information of record, and provides an opinion that is well analyzed and consistent with the known factual evidence of record. Further, as an Instructor in the Department of Neurology and Pediatrics in the Division of Pediatric Neurology at the University of Mississippi Medical Center, the Board finds that she is highly qualified to speak to the question at hand. Dr. C. acknowledges all of the abnormal findings relied upon by Drs. B. and M. in arriving at a different conclusion, analyzes all of the findings in the context of all the relevant information and evidence of record, and references medical treatise materials as supplementing her own medical knowledge at arriving at her ultimate conclusion. Dr. C. concluded that there was no evidence of hydrocephalus documented in the child which is consistent with the radiologist interpretations of CT scans performed in March 1985 and July 1985. She further concluded that there was no evidence of developmental or cognitive impairment that is consistent with the parent’s recollections at the time of the UMC intake summary. This finding is also consistent with the clinical records and October 26, 1989 letter from Dr. B. wherein he does not note any observable evidence of developmental or cognitive impairment during his first nine months. Dr. C. also concluded that the child’s current neurologic, musculoskeletal and neurologic impairments are due to his hypoxic cerebral injury. This conclusion is consistent with the documented evidence of record to include the diagnoses of Dr. B., the physicians who treated the child for the hypoxic injury at UMC and the current treating physician Dr. S. The Board finds that the opinions offered by Drs. B. and M. hold less probative value as the basis for the opinions are not supported by the factual record. First, the Board finds the credentials of both specialists as impressive but not any more so than Dr. C. Dr. B. argues that Dr. C.’s opinion should be given less weight based upon the fact that she does not have formal training in neuroimaging and has failed to review the actual CT scan themselves. The Board finds that this reasoning is misplaced. In his three opinions of record, Dr. B. recites the radiologist interpretations but does not give any indication that he reviewed the CT scan results himself. Rather, like Drs. M., C. and G., Dr. B. has accepted the interpretation provided by the reviewing radiologist as a matter of fact. All the specialist opinions are equal on this point, and none have determined that actual reading of the films is necessary to a determination in this case. Given that all of the opinion providers are relying on the radiologist’s interpretation, the Board fails to discern any reason why a neuroimaging specialist has better qualifications than a board-certified pediatric neurologist for the particular facts of this case. A specialty in neuroimaging may have some benefit if that specialist reviewed the actual CT head scans and reached a different conclusion as to findings by the radiologist. As indicated above, however, all of the expert opinions rely on the same radiologist’s opinion of the CT head scan results. Additionally, the basis for the diagnosis that the child in question has a form or manifestation of spina bifida is based upon clinical and not diagnostic findings that would appear better suited for an individual with the expertise of Dr. C. The opinions offered by Dr. B. are not based upon an accurate recitation of the evidence of record. Dr. B. concludes that the child demonstrated a manifestation or form or spina bifida during his first 9 months based upon the following assumptions of fact: A. The child demonstrated lethargy on March [REDACTED], 1985; B. The child had an abnormal CT head scan on March [REDACTED], 1985; C. The child was developmentally slow during his first 9 months; and, D. The child had an increasing head circumference during his first 9 months The record is clear that the child demonstrated lethargy with low APGAR scores during his first two days after birth. As indicated above, the child’s treating physicians and Dr. C. attribute these findings to neonatal depression responding well to Narcan, and then an instance of transient hypoglycemia. There is no other documented instance of lethargy in the child’s first nine months of life. Dr. B. offers no explanation as to how the treating physicians and Dr. C. have misdiagnosed the child on this point, undermining the medical opinion provided. The best that could be offered is Dr. M.’s argument that there is no objective way to establish that maternal narcotics was a cause of the low APGAR scores. The factual evidence demonstrates that the child responded well to medication treatment with no documentation of any further episodes of lethargy during his first nine months. On this point, the Board finds that Dr. B. has relied upon a factual assumption not supported by the factual record. Dr. B. next relies on the assumption that the child’s abnormal March 1985 CT scan and increasing head circumferences evidenced a brain abnormality. In the January 2003 opinion letter and in his following opinions, Dr. B. did not include any discussion that the March 1985 CT scan of the head was interpreted as showing no hydrocephalus and that the CT scan of the head in July 1985 was interpreted as showing no significant abnormalities. Dr. B. also relies upon a factual proposition that the child was developmentally slow during his first nine months. The particulars of the low APGAR scores immediately following birth have been discussed above. A careful review of the record contains only one instance where the parents reported developmental delay. This comes in the January 2003 report by Dr. B. reported as follows: Dec 2002 Patient’s medical history as remembered by mother “...Did [the appellant] have any medical problems after he left the hospital in March/April 1985? Yes he was developmentally slow...” [E.H.] The Board makes several observations on the above-mentioned evidence: First, the mother’s report, when taken at face value, holds very little, if any, evidentiary value. The recollection is vague and does not offer a single example of how the child was observed to be developmentally slow. It is also the product of a leading question. Dr. B. accepts this vague statement as establishing, as a matter of fact, that the child had developmental delay. Second, this report is inconsistent with the report of lay history offered at the time of the child’s UMC admission in January 1986 wherein the child was noted: Prior to illness pt eating table food G& D: Pt sat [with] support @ 6 mo, turns over, back to front & reverse, reaches for toys This UMC report is consistent with the fact that the treating physician during the first 9 months did not document any observable signs of developmental delay or cognitive impairment. The Board places the greatest probative weight on the lay history provided by the child’s parents at the time of the UMC admission as more contemporaneous in time to the symptoms in question and in the context of seeking proper treatment of the child at the time. Furthermore, Dr. B. does not offer any rationale as to why he discounts the developmental milestones reported by the child’s parents at the time of the UMC admission, or why Drs. G. and C. are incorrect in their conclusion that the child had met his developmental milestones. Thus, the Board finds that 3 of the 4 bases relied upon by Dr. B. at arriving at his opinion are based upon an inaccurate recitation of the factual record. The lethargy displayed upon birth has been attributed to medical causes other than a form of manifestation of spina bifida, the opinion inexplicably fails to acknowledge the diagnosis of no hydrocephalus on the March 1985 CT scan of the head, fails to acknowledge the normal CT head scan results of July 1985, and relies upon a parent’s vague history of developmental slowness reported 7-years after the fact in the context of seeking benefits that contradicts a more reliable history provided contemporaneous in time to the time period in question to examiners requiring honesty to properly treat the child. The Board also observes that Dr. B. makes mistakes of fact in his opinion letters discounting the opinions of both Drs. G. and C. He argues that neither doctor reviewed the entire record nor his opinions. This argument is false as reflected in the complete text of the opinions by Drs. G. and C. that the Board has cited in full. Drs. C. and G. did not find that the claimed lethargy and developmental slowness was demonstrated by the record. The Board has also come to this conclusion based upon the facts found as reported by the child’s treating physicians. In his January 2004 opinion, Dr. B. argued that Dr. G. “basically stated that [t]he [March 1985] CT scan was not abnormal” and that she was interpreting it “differently” than the radiologist. The opinion from Dr. G., however, included an extensive discussion of the “abnormal CT scan in the neonatal period” and accepted as fact the radiologist’s interpretation. Dr. B. also argues that neither of the examiners explained how the abnormality of the CT scan of March 1985 should not be deemed indicative of a form or manifestation of spina bifida. Dr. G. opined that the abnormal CT scan was not indicative of hydrocephalus which is in exact agreement with the radiologist who interpreted the March 1985 CT scan. Dr. C. referred to the normal CT scan of the head performed in July 1985 and discounted hydrocephalus. Again, Dr. B. has selectively ignored that the radiologist found no hydrocephalus at the time of the March 1985 CT scan and that the CT scan findings in July 1985 were unremarkable. As for the relationship between hydrocephalus and lethargy, Dr. C. offered an opinion that the lethargy was due to transient hypoglycemia that is entirely consistent with the impression of the treating physicians at the time. Also, there is no dispute among any of the experts that the child’s HC had increased from the time of his birth to the age of 9 months. This factor was considered by Drs. G. and C. in arriving at their opinions. The Board, upon review of the medical literature provided by the specialists, finds no basis on this fact alone to determine that the appellant has a form or manifestation of spina bifida. The Board has also given careful consideration of the opinion offered by Dr. M. Dr. M agreed with Dr. B’s conclusion “that the lethargy described in the newborn period, the abnormal head CT, increasing head circumference, and developmental delay are likely manifestations of spina bifida and contribute substantially to the current disabilities.” Again, the Board has found that the assumptions of lethargy and developmental delay are incorrect based upon the facts found. Dr. M. acknowledges the previous report of the child meeting developmental milestone at the age of 9 months, but argues that “nowhere in the record is a full developmental assessment.” For the reasons discussed above, the best evidence as to developmental milestones comes from the January 1986 UMC intake assessment. Additionally, Dr. M. does not acknowledge the interpretation of no hydrocephalus at the time of the March 1985 CT head scan nor the normal results from the July 1985 CT scan of the head. So, as is the case with Dr. B’s opinion, the Board finds that 3 out of the 4 assumptions underlying the opinion by Dr. M. are factually incorrect. The Board also disagrees with Dr. M’s factual assertions that Dr. C. contradicted her opinion by stating “spina bifida can have many associated clinical conditions and sequelae including each of the chronic conditions in questions.” This quote is taken out of context, wherein Dr. C. continues “However, as all of these conditions followed the hypoxic cerebral injury and none of them were present at birth, or documented as present at the time of his admission for the cardiomyopathy, it is unlikely that they are the result of spina bifida.” The Board further finds that the opinions by Drs. B. and M. are ambiguous as to the actual diagnosis offered other than that the child manifests a form or manifestation of spina bifida. Dr. M. argues that, with regard to the increased intracranial pressure, “the only other reasonable etiology for the finding would be encephalocele” while Dr. B. finds that the child’s March 1985 CT head findings were “very consistent with magalencephaly.” As stated previously, neither physician fully acknowledges the results from the CT scans of the head conducted in March and July 1985. Additionally, neither physician counters the following assertion by Dr. C.: “The patient had a follow-up CT two months (after the March 1985 CT scan) that showed no evidence of hydrocephalus and in the absence of placement of a shunt, one would expect that congenital hydrocephalus would still be present and in fact would have worsened over that period of time.” Finally, Dr. B. asserted that his training and experience were superior to that of Dr. G. in interpreting the facts of this case. However, that is a simple complaint without any satisfactory explanation. The Veteran and his attorney have been supplied with the curricula vitae for Drs. G. and C. and have not identified any short comings that would make the opinions of these physicians less qualified. Further, their analysis covers all the relevant findings and integrates the known facts of this case with the applicable medical knowledge. In a November 2019 statement, the appellant’s representative asserted that the evidence of record is in equipoise as to whether the appellant has spina bifida. However, as discussed above, the Board finds that the July 2003 opinion from Dr. G. and the July 2004 opinion from Dr. C. have more probative value than the private opinions of record. Dr. G. and Dr. C.’s opinions are highly probative because they are based on an accurate medical history and provide explanations that contain clear conclusions and supporting data. Nieves-Rodriguez v. Peake, 22 Vet. App. 295, 304 (2008). As discussed in detail above, the Board finds that the private opinions of record are based, in part, on an inaccurate factual history and therefore have little probative value. See Reonal v. Brown, 5 Vet. App. 458, 460-61 (1993). The Board notes that the Veteran has asserted that his son a manifestation of spina bifida. The issue is medically complex, as it requires knowledge of pathology and interpretation of complicated diagnostic medical testing. Therefore, it is outside the competence of the Veteran in this case because the record does not show that he has the medical training or credentials to make such a determination. Jandreau v. Nicholson, 492 F.3d 1372, 1377 n.4 (Fed. Cir. 2007); see also Kahana v. Shinseki, 24. Vet. App. 428 (2011). Spina bifida is the only birth defect which warrants an award of monetary benefits based on the herbicide agent exposure of a Vietnam veteran who is the father of the child at issue. Jones v. Principi, 16 Vet. App. 219, 225 (2002). To qualify for a monthly allowance on the basis of other birth defects, the evidence must show that the Vietnam veteran who was exposed to herbicide agents was the children’s biological mother. 38 U.S.C. §§ 1812, 1815; 38 C.F.R. § 3.815. The evidence does not show, and the Veteran has not asserted that the appellant’s biological mother was a Vietnam veteran. As the appellant is not the child of a biological mother who is a Vietnam veteran, he does not qualify for a monthly allowance on the basis of birth defects, other than spina bifida. 38 U.S.C. §§ 1811, 1812, 1815; 38 C.F.R. § 3.815.   Based upon the above, the Board has determined that the preponderance of the evidence is against a finding that the appellant has had a form and/or manifestation of spina bifida, other than spina bifida occulta. Thus, it is concluded that the criteria for a monetary allowance under 38 U.S.C. § 1805 for a Vietnam veteran’s child on account of spina bifida have not been met. There is no doubt of material fact to be resolved in the appellant’s favor. 38 U.S.C. § 5107(b); see Ortiz v. Principi, 247 F.3d 1361, 1365 (Fed. Cir. 2001). M. SORISIO Veterans Law Judge Board of Veterans’ Appeals Attorney for the Board K. Marenna, 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.