Citation Nr: 1001098	
Decision Date: 01/07/10    Archive Date: 01/15/10

DOCKET NO.  01-03 511A	)	DATE
	)
	)

On appeal from the
Department of Veterans Affairs Regional Office in Jackson, 
Mississippi


THE ISSUE

Entitlement to a monetary allowance under 38 U.S.C.A. § 1805 
for a Vietnam Veteran's child on account of spina bifida.


REPRESENTATION

Appellant represented by:	Theodore C. Jarvi, Attorney


WITNESS AT HEARING ON APPEAL

Appellant


ATTORNEY FOR THE BOARD

T. Mainelli, Counsel

INTRODUCTION

The Veteran served on active duty from April 1968 to April 
1970.  He had a tour of duty in the Republic of Vietnam 
during the Vietnam War.

This case comes before the Board of Veterans' Appeals (Board) 
on appeal from a November 2000 rating decision by the 
Jackson, Mississippi, Regional Office (RO) of the Department 
of Veterans Affairs (VA).  In July 2001, the Veteran appeared 
and testified at a Travel Board hearing before Veterans Law 
Judge C. R.  By decision dated December 2001, the Board 
denied the claim of entitlement to a monetary allowance under 
38 U.S.C.A. § 1805 for a Vietnam Veteran's child on account 
of spina bifida.

The Veteran appealed this decision to the United States Court 
of Appeals for Veterans Claims (Court).  In October 2002, the 
Court granted a Joint Motion for Remand (JMR) vacating and 
remanding the Board's December 2001 decision for 
consideration of additional issues.  The Board remanded the 
case to the RO in November 2004.  

In August 2005, the Board informed the Veteran that Veterans 
Law Judge C. R. was no longer employed by the Board, and 
offered him another hearing before a Veterans Law Judge who 
would decide the case.  Later that month, the Veteran 
informed the Board that he did not desire another hearing.

In November 2005, the Board again denied the claim of 
entitlement to a monetary allowance under 38 U.S.C.A. § 1805 
for a Vietnam Veteran's child on account of spina bifida.  
The Veteran appealed this determination to the Court.  In 
January 2007, the Court granted a JMR vacating and remanding 
the Board's November 2005 decision for consideration of 
additional issues.

In July 2007, the Board remanded this case to the RO for 
further development.

The Board notes that, in July 2007, the Board referred an 
issue of whether the Veteran's November 1998 correspondence 
should be interpreted to revise a VA rating decision dated in 
July 1993 on the basis of clear and unmistakable error (CUE).  
There is an RO notation that such document is not located in 
this claims folder.  

However, the Board notes this claim has been separated from 
the Veteran's original claims folder, as the Denver RO 
currently holds jurisdiction over spina bifida claims.  
Notably, the Veteran now has a claim folder under a "C" 
number originally utilized for this case, and new "SS" 
number case for the file concerning his child currently 
before the Board.  

The Denver RO is requested to contact the RO of appropriate 
jurisdiction to ensure that the CUE claim has been acted upon 
on behalf of the Veteran.


FINDINGS OF FACT

1.  The Veteran's child was born on March [redacted], 1985.  His 
initial neonatal depression responded well to Narcan 
treatment, and his lethargy on March [redacted], 1985, was attributed 
to transient hypoglycemia that responded well to treatment.

2.  A computerized tomography (CT) scan of the head on March 
[redacted], 1985, was abnormal with the interpreting radiologist 
finding that the anterior fontanelle was full with a portion 
of the frontal poles filling the anterior fontanelle; no 
hydrocephalus was present but the findings were suggestive of 
increased intracranial pressure.

3.  A CT scan of the head performed in July 1985 was 
interpreted as showing no significant abnormalities.

4.  From March 1985 to January 1986, the child had met his 
developmental milestones, had a head circumference measured 
in the 75th percentile, and was given "OK" clinical findings 
of his head, fontanelle, neurologic system and 
musculoskeletal system.

5.  In January 1986, the child experienced a severe viral 
infection of the heart that lead to cardiopulmonary arrest 
with an hypoxic cerebral injury; this event left him severely 
neurologically impaired with spastic dyplegia, impaired 
muscle control and seizures.

6.  The preponderance of the evidence demonstrates that the 
Veteran's child does not have a form and/or manifestation of 
spina bifida.


CONCLUSION OF LAW

The criteria for a monetary allowance under 38 U.S.C.A. 
§ 1805 for a Vietnam veteran's child on account of spina 
bifida have not been met.  38 U.S.C.A. §§ 1802, 1805, 5107 
(West 2002); 38 C.F.R. § 3.814 (2009).


REASONS AND BASES FOR FINDINGS AND CONCLUSION

At that outset, the Board notes that the case is currently 
before the Board following a January 2007 Court remand, 
pursuant to the terms of a JMR.  The Board must determine 
whether those terms have been substantially complied with 
prior to reviewing the merits of this case.  See generally 
Stegall v. West, 11 Vet. App. 268, 271 (1998).

The first issue addressed in the JMR was the adequacy of 
notice, in that the Veteran was not apprised to submit all 
evidence in his possession pertaining to the claim or the 
criteria for establishing disability ratings and effective 
dates of awards should the benefit sought on appeal be 
granted.  The RO's June 2008 letter fully complies with the 
JMR terms.  

The second issue addressed in the JMR concerns the Veteran's 
opportunity to obtain additional medical opinion to support 
this claim.  Specifically, the JMR stated:

The parties further agree that, on remand, 
Appellant will be given an opportunity to obtain 
another private medical opinion, at his expense, 
with the benefit of the entire claims folder and 
curriculum vitae for any experts on which BVA 
relied in the decision on appeal.

JMR, dated January 3, 2007, p. 3.

Throughout the appellate period, the Veteran's attorney has 
repeatedly argued that VA has a duty to provide a host of 
information on "due process grounds."  The Veteran's 
attorney has also taken issue with the fact that the Board 
has obtained opinions from a Veterans Health Administration 
(VHA) expert as well as an Independent Medical Examiner 
(IME).

In an effort to impeach the validity of the VHA and IME 
opinions, the Veteran's attorney has requested copies of 
expert medical opinion reports, information regarding the 
expert including curriculum vitae, copies of all materials 
provided to the expert, correspondence leading to the 
employment of any expert, copies of internal Board case 
review leading to an expert opinion request, internal Board 
correspondence of "any kind" regarding the case and 
correspondence to the experts, copies of payment records 
reflecting planned or actual payments to the experts and/or 
his/her employer, etc.

The Board first notes that it is unaware of any "internal" 
correspondence that has been withheld from this claims 
folder.  Quite simply, when the Board's review of a record 
indicates a need for a further opinion, the Board's analysis 
is incorporated into a written document discussing the 
relevant factual history, the conflict of evidence, and the 
opinion(s) sought to resolve that conflict.  This document is 
then forwarded to the appropriate entity/examiner.  The 
Veteran's attorney has in his possession all of these 
documents, to include the billing statement for the IME.  The 
Board does not maintain separate "workproduct" folders 
which are withheld from public scrutiny.

Contrary to counsel's assertions, the Board did respond the 
Veteran's broad information request by letter dated March 12, 
2004 explaining to him which information could or could not 
be provided.  The Veteran's counsel does not agree with the 
Board's determination, and implies that the Board, or VA in 
general, has somehow skewed the record to obtain unfavorable 
VHA and IME opinions.  There is no showing to support this 
allegation, and certainly no clear evidence to rebut the 
presumption that VA officials have properly discharged their 
official duties in this case.  See generally Ashley v. 
Derwinski, 2 Vet. App. 307, 311 (1992) (citing United States 
v. Chemical Foundation, Inc., 272 U.S. 1, 14-15 (1926)); 
Mindenhall v. Brown, 7 Vet. App. 271 (1994).

The Board further finds no precedential opinion supporting 
the counsel's argument that VA's failure to respond to his 
type of information request violates any statutory, 
regulatory or constitutional law.  The Court has held, 
however, that VA's duty to assist does not extend to 
conducting a "fishing expedition."  See Counts v. Brown, 6 
Vet. App. 473, 478- 9 (1994) and Gobber v. Derwinski, 2 Vet. 
App. 470, 472 (1992).

In a letter dated June 12, 2008, the Veteran's counsel argued 
that the JMR terms "contemplates" the Veteran's access to 
the qualifications of the experts upon which the Board 
intends to rely, that the Veteran's right to such information 
has been repeatedly addressed to no avail, and that the 
Veteran's counsel has never been able to extract such 
information from any other source.  It is also asserted that 
such information was a "condition precedent" which had to 
be complied with before the Veteran was able to adequately 
provide another opinion.

The Board first notes that there is no per se legal 
requirement to provide a claimant curriculum vitae for an 
expert medical examiner.  See D'Aries v. Peake, 22 Vet. App. 
97 (2008).  Regardless, the argument advanced by Veteran's 
counsel is disingenuous and cannot withstand close scrutiny.  

First, the Veteran has been provided the entire curriculum 
vitae of the VHA physician.  Furthermore, the examination 
report from the IME identifies herself as an Instructor at 
the Department of Neurology, Department of Pediatrics, 
Division of Pediatric Neurology at The University of 
Mississippi Medical Center.  In a May 2005 "rebuttal" 
opinion, the Veteran's own expert acknowledged and attacked 
the qualifications of the IME examiner for lack of formal 
training in neuro-imaging to properly interpret CT findings.  
Notably, in November 2005, the Board found no controversy on 
that issue as it was not implicated in this case, as all of 
the experts in this case relied upon the interpretation 
provided by the interpreting radiologist at the time and that 
none were interpreting the actual CT findings.  The issue at 
controversy was the medical implications of the CT findings.

Second, the Veteran's counsel has a complete copy of the 
claims folder and acknowledged actual notice of the VHA and 
IME qualifications in argument to the Court.  Incongruent 
with the June 2008 argument, the Veteran provided the 
following admission to the Court:

The BVA decision recited the qualifications of 
the Mississippi doctor (R. at 32).  It was 
exactly this category of information which 
Appellant's representative sought time and time 
again from the BVA, but was unable to obtain.  
By refusing to respond one way or another to 
Appellant's requests for qualifications and 
processes utilized to obtain the VA medical 
opinions, the BVA also trampled the due process 
concept that both sides should have equal 
access to information upon which a decision is 
to be made.

The information sought was easily within the 
Board's access.  Certainly its own policies and 
procedures were within its reach.  The letters 
which appear of Record, which the Board sent to 
doctors soliciting their opinions, were exactly 
the type of information sought by Appellant (R. 
at 259, 497).  It would have been an easy thing 
to provide copies of those letters, but 
Appellant didn't see them until the Designation 
of Record in this case.

Appellant's Brief dated August 2006, p.14 (emphasis added).

As demonstrated by Counsel's representation to the Court, 
Veteran's counsel has "exactly the type of information" 
deemed necessary to proceed with obtaining another opinion in 
this case.

On this record, and upon review of the JMR terms, the Board 
finds that the Veteran's counsel has all necessary 
information proceed with obtaining an opinion in this case.  
The issue involves a question within the realm of neurology 
and the Veteran's attorney has been provided adequate and 
long-standing notice that the VHA and IME examiner's have 
expertise in this field.  Thus, the qualification of these 
individuals to render an opinion in this case is not subject 
to reasonable dispute.  See D'Aries, 22 Vet. App. at 105 (the 
designation of a neurologist to review an organic brain 
disorder claim was clearly adequate as such a specialist 
could reasonably be expected to provide the appropriate 
medical analysis and opinion to resolve the question posed by 
the Board).  Further delay of this case is not warranted. 

Interestingly, as addressed below, this case has little to do 
with qualifications or bias regarding any of the expert 
opinions.  The Board's November 2005 opinion explicitly 
pointed to factual errors made by the Veteran's experts and 
ambiguity in other portions of their opinions which overcame 
any potential bias or qualification issues.  Thus, the 
Veteran's counsel has known since 2005 the type of medical 
opinion necessary to rectify the factual errors found by the 
Board.

Overall, the Board finds that the Veteran's counsel has 
actual notice of the VHA and IME examiner qualifications, and 
has known this information since 2005, if not earlier.  The 
Veteran's counsel has had access to the complete claims 
folder, which is the same information reviewed by the VHA and 
IME physicians.  The Veteran's counsel has had benefit of 
notice of the explicit reasons why the Board has rejected 
Appellant's expert opinions in this case.  Furthermore, fully 
compliant notice was provided to the Veteran's counsel in 
June 2008, and more than reasonable time has passed for 
Veteran's counsel to obtain additional opinion. 

The Board finds that the Veteran's counsel has been provided 
the full notice required by law and due process, and that the 
JMR terms have been fully implemented.  The Veteran's counsel 
misconstrues the terms of the JMR, which only provided that 
the Veteran be allowed an opportunity to obtain additional 
opinion based upon consideration of the entire record as well 
as the VHA and IME qualifications.  As noted to the Court at 
that time, the Veteran's counsel conceded that he had 
"exactly" what was needed to accomplish such a task.  

In summation, the Board is of the opinion that the Veteran's 
counsel, at his own peril, has chosen to withhold availing 
the Veteran additional opportunity for medical opinion on a 
faulty premise that a "condition precedent" has not been 
met.  This "condition precedent" concerns alleged 
entitlement to further information which is a legal argument 
having no merit.  The Board cannot be concerned with the 
legal and practical consequences of the advice provided by 
Counsel in this case which withholds potentially relevant 
information based upon a legal argument.  See Turk v. Peake, 
21 Vet. App. 565, 567 (2008).  

The Board finds that VA has fully complied with the terms of 
the parties' JMR as written, and not as re-interpreted by 
Veteran's counsel.  As such, the Board finds no impediment to 
proceeding a merits review of the claim.

The Veteran served a tour of duty in the Republic of Vietnam 
during the Vietnam War.  He seeks to establish his 
entitlement to a monetary allowance under 38 U.S.C.A. § 1805 
for a Vietnam Veteran's child on account of spina bifida.  
For children of a Vietnam veteran, Congress has authorized VA 
to pay a monthly allowance, based upon the level of 
disability, to or for a child who had been determined to be 
suffering from spina bifida.  38 U.S.C.A. § 1805(a); 
38 C.F.R. § 3.814(a).

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.A. § 1802.  See 
Jones v. Principi, 16 Vet. App. 219 (2002) (holding that the 
plain language of 38 U.S.C.A. § 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 case at hand 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 an hypoxic brain injury occurring 
at the age of 9 months.  There is no dispute in this case 
that the hypoxic injury has caused many of the symptoms in 
question.

The claimant bears the burden of presenting and supporting 
his/her claim for benefits.  38 U.S.C.A. § 5107(a).  See 
Fagan v. Shinseki, 573 F.3d 1282 (Fed. Cir. 2009).  In its 
evaluation, the Board shall consider all information and lay 
and medical evidence of record.  38 U.S.C. § 5107(b).  When 
there is an approximate balance of positive and negative 
evidence regarding any issue material to the determination of 
a matter, the Board shall give the benefit of the doubt to 
the claimant.  Id.  Another way stated, VA has an equipoise 
standard akin to the rule in baseball that "the tie goes to 
the runner."  Gilbert v. Derwinski, 1 Vet. App. 49 (1990).  
Notably, the benefit of the doubt doctrine is not applicable 
based on pure speculation or remote possibility.  See 
38 C.F.R. § 3.102.  

The Board is not bound to accept any opinion, from a VA 
examiner, private physician, or other source, concerning the 
merits of a claim.  Hayes v. Brown, 5 Vet. App. 60 (1993).  
The VA benefits system also does not favor the opinion of a 
VA examiner over a private examiner, or vice versa.  See 
38 U.S.C.A. § 5125; White v. Principi, 243 F.3d 1378, 1381 
(Fed. Cir. 2001) (declining to adopt the treating physician 
rule for adjudicating VA benefits).  Regardless of the 
source, an examination report must minimally meet the 
requirement of being sufficiently complete to be adequate for 
the purpose of adjudicating the claim.  See 38 U.S.C.A. 
§ 5125; 38 C.F.R. § 4.2.

The Board has an obligation to weigh the probative value of 
the medical opinions presented based upon factors such as 
personal examination of the patient, knowledge and skill in 
analyzing the data, the knowledge and expertise of the 
examiner, the expressed rationale forming the basis of the 
opinion, ambivalence and/or exactness of diagnosis, scope of 
review of the relevant records, bias, etc.  See generally 
Guerrieri v. Brown, 4 Vet. App. 467, 470-71 (1993); 
Hernandez-Toyens v. West, 11 Vet. App. 379, 382 (1998); Sklar 
v. Brown, 5 Vet. App. 140 (1993); Elkin v. Brown, 5 Vet. 
App. 474, 478 (1993); Austin v. Brown, 6 Vet. App. 547, 551-
52 (1994).  

A medical examiner's review of the claims folder may heighten 
the probative value of an opinion, as the claims folder 
generally contains all documents associated with a veteran's 
disability claim, including not only medical examination 
reports and service treatment records (STRs), but also 
correspondence, raw medical data, financial information, RO 
rating decisions, Notices of Disagreement, materials 
pertaining to claims for conditions not currently at issue 
and Board decisions disposing of earlier claims.  See Nieves-
Rodriguez v. Peake, 22 Vet. App. 295 (2008).

However, an examiner's review of the claims folder is not 
required in each case.  See Snuffer v. Gobber, 10 Vet. App. 
400, 403-04 (1997) (review of claims file not required where 
it would not change the objective and dispositive findings 
made during a medical examination); see also D'Aries v. 
Peake, 22 Vet. App. 97, 106 (2008) (holding that it is not 
necessary for a VA medical examiner to specify review of the 
claims folder where it is clear from the report that the 
examiner has done so and is familiar with the claimant's 
extensive medical history).

A significant factor to be considered for any opinion is 
based on an accurate factual predicate, regardless of whether 
the information supporting the opinion is obtained by review 
of medical records or lay reports of injury, symptoms and/or 
treatment.  See Harris v. West, 203 F.3d 1347, 1350-51 (Fed. 
Cir. 2000) (examiner opinion based on accurate lay history 
deemed competent medical evidence in support of the claim); 
Kowalski v. Nicholson, 19 Vet. App. 171, 177 (2005) (holding 
that a medical opinion cannot be disregarded solely on the 
rationale that the medical opinion was based on history given 
by the veteran); Reonal v. Brown, 5 Vet. App. 458, 461 (1993) 
(holding that the Board may reject a medical opinion based on 
an inaccurate factual basis).

Although formal rules of evidence do not apply in the VA 
benefits system, the Court has indicated that recourse to the 
Federal Rules of Evidence may be appropriate if it assists in 
the articulation of the reasons for the adjudicator's 
decision.  Rucker v. Brown, 10 Vet. App. 67, 73 (1997).  
Within the VA benefits system, VA medical examiners and 
private physicians offering medical opinions in veterans' 
benefits cases are essentially considered expert witnesses.  
Nieves-Rodriguez, 22 Vet. App. 295 (2008).

In Nieves-Rodriguez, the Court indicated that the Federal 
Rules of Evidence for evaluating expert medical opinion 
before U.S. district courts, Fed.R.Evid. 702, are important, 
guiding factors to be used by VA adjudicators in evaluating 
the probative value of a medical opinion.  The factors 
identified in Fed.R.Evid 702 are as follows:

(1) The testimony is based upon sufficient facts 
or data; 
(2) the testimony is the product of reliable 
principles and methods; and 
(3) the expert witness has applied the principles 
and methods reliably to the facts of the case.

A layperson is generally not capable of opining on matters 
requiring medical knowledge.  Routen v. Brown, 10 Vet. App. 
183, 186 (1997).  Where the determinative issue involves 
medical causation or a medical diagnosis, there must be 
competent medical evidence to the effect that the claim is 
plausible; lay assertions of medical status generally do not 
constitute competent medical evidence.  Grottveit v. Brown, 5 
Vet. App. 91, 93 (1993); Espiritu v. Derwinski, 2 Vet. App. 
492, 494 (1992). 

However, 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, (e.g., a broken 
leg), (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.3d 1372 (Fed. 
Cir. 2007).

In essence, lay testimony is competent when it regards the 
readily observable features or symptoms of injury or illness 
and "may provide sufficient support for a claim of service 
connection."  Layno v. Brown, 6 Vet. App. 465, 469 (1994).  
See also 38 C.F.R. § 3.159(a)(2).  In this regard, the Court 
of Appeals of Veterans Claims (Court) has emphasized that 
when a condition may be diagnosed by its unique and readily 
identifiable features, the presence of the disorder is not a 
determination "medical in nature" and is capable of lay 
observation.  In such cases, the Board is within its province 
to weigh that testimony and to make a credibility 
determination as to whether that evidence supports a finding 
of the presence or absence of the claimed symptomatology.  
See Barr v. Nicholson, 21 Vet. App. 303 (2007).

In reviewing the case at hand, the Board has to determine the 
reason, or reasons, as to why the expert examiners have 
arrived at differing conclusions.  As will be addressed 
below, the Board must make findings of fact as to both the 
underlying history of chronological events and clinical 
findings in order to make this determination.  The Board will 
first cite in full each examiner's opinion, in chronological 
order, and then proceed to analyze the evidence of record in 
the entire claims folder to determine the probative value to 
be assigned to each examiner's opinion.

I.  Expert 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 parents 
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:

[redacted] March 1985 Date of Birth

[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]

[redacted] 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];

[redacted] 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 [redacted] 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 [redacted] 
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.

6.7 Neural tube defects

CLASSIFICATION
Various classification systems exist, this one is 
adapted from Lemire55.
1.  Neurulation defects: non-closure of the 
neural tube results in open lesions
A.    craniorachichisis: total 
dysraphism.  Many die as spontaneous 
abortion
B.     anencephaly: AKA exencephaly.  
Due to failure of fusion of the 
anterior neuropore.  Neither cranial 
vault nor scalp covers the partially 
destroyed brain.  Uniformly fatal.  
Risk of recurrence in future 
pregnancies: 3%
C.    meningomyecocele: most common in 
lumbar region
		1.  myelomeningocele (MM): see page 
153;
		2.  myelocele
		2.  postneurulation defects: produces skin 
covered (AKA) closed lesions (some may also 
be considered "migration abnormalities", see 
below)
A.    cranial
1.  microcephaly: see below
2.  hydranencephaly: loss of 
significant portion of cerebral 
hemispheres which are replaced 
by CSF.  Must be differentiated 
from maximal hydrocephalus (see 
page 174)
3.  holoprosencephaly: see below
4.  lissencephaly: see below
5.  porencephaly: see below to 
distinguish from schizencephaly
6.  agenesis of corpus callosum: 
see below
7.  cerebellar hypoplasia/Dandy-
Walker syndrome: see page 148
8.  macroencephaly AKA 
megalencephaly: see below

B.  spinal
1.  diastematomyelia, diplomyelia: 
see Split cord malformation, page 
160
2.  hydromyelia/syringomyelia: see 
page 338

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 patients 
disabilities he would likely best be placed in VA 
payment level III under CFR38.

(emphasis original).

Attached to the opinion letter was a chart entitled "BOYS: 
BIRTH TO 36 MONTH PHYSICAL GROWTH NCHS PERCENTILES" and the 
curriculum vitae for Dr. Bash.  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 
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. B. did not include 
the definition of magalencephaly from Greenberg, Handbook of 
Neurosurgery 2001, referenced and relied upon in his opinion 
letter.  The Board, therefore, will supplement the record 
from the definition of magalencephaly 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 11, 2003 
opinion from neurologist B.N.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 a 
veteran's child, which was born on 03-[redacted]-85.  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..."  An opinion is requested to:

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.
5.  It is further specified, "It is requested 
that the appellant not be identified by name 
in the opinion itself."  Therefore, I have 
not indicated the relevant Social Security 
Number in dictating this report and will not 
refer to the veteran or his child by name in 
this report.

REVIEW OF MEDICAL RECORDS:  The patient is not 
actually available for examination.  This is 
merely a review of the relevant records in the 
claims file and will answer the questions as 
requested.

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 
herniated 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, will actually herniated 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 herniated 
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 skeletal 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 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 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 record 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 as 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 she 
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. 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. Greenspan (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 then 
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 his 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 that the patient clearly had 
lethargy almost a year earlier on [redacted] March 
1985 (one day after birth).  It should also 
be noted that the CT scan spoken about in 
point 1 above was taken one day later on [redacted]
March 1985, 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 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 opinion an IME opinion.  A 
July 15, 2004 opinion letter from A.L.C., M.D., opines as 
follows:

Per your request, I have reviewed Claim File X XX 
XXX XXX 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 patient (J.H.) was born [redacted] March 1985 at 38 
weeks gestation to a 33 year old G3PD 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, 
J.H.'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 J.H. 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, J.H. 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, J.H. 
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 
J.H.'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, J.H. 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. 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 patient 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.

My first observation is that the SSOC and the 
opinion of Dr. [C] are inconsistent in that Dr. 
[C] states that Spina bifida can have many of the 
associated clinical conditions and sequ[e]lae 
including each of the chronic conditions of the 
patient in question where as the SSOC states "... 
child is not diagnosed with spina Bifida..."  I 
assume that this inconsistency has its origin in 
the fact that the SSOC's author is not a physician 
and is not capable of making the diagnosis of 
spina bifida or related forms and therefore the 
SSOC conclusions should be invalidated.

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.

Please feel free to contact me with any questions.

II.  Factual determinations

The Veteran's child was born on March [redacted], 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 child 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 child'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 child 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 child 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 child'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 child 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 veteran's child] since his 
birth on 3/[redacted]/85.  [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 this 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 child's medical records demonstrates 
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 veteran's child] is a patient of mine.  He 
has a diagnosis of seizure disorder and cerebral 
palsy.  The diagnosis are 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...

III.  Analysis

The Board finds that the preponderance of the evidence 
demonstrates that the Veteran's child does not have a form 
and/or manifestation of spina bifida.  The Board reaches this 
conclusion on the following facts found:  The child was born 
on March [redacted], 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) was 
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 on March [redacted], 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 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 fontanel, 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

Unfortunately, the child experienced a severe viral infection 
of the heart in January 1986 that lead to cardiopulmonary 
arrest with an 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.  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 of these 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 are necessary to 
a determination in this case.

Given that all of the examiners are relying on the 
radiologist 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 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, quite simply, 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 instances of 
lethargy in the child's first nine months of life.  Dr. B. 
offers no explanation as to how the treating physician's and 
Dr. C. have misdiagnosed the child on this point.  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, Dr. B. made the following findings of 
fact and opinion: 

Facts, Rationale/Medical theory, Other Medical 
Opinions:

[redacted] March 1985 Date of Birth

[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 [redacted] have any medical problems 
after he left the hospital in March/April 1985?  
Yes he was developmentally slow..."  [EH].

... 
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 [redacted] 
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...

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.

Conspicuously absent from Dr. B's January 2003 opinion, and 
his following opinions, is 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.  The 
Board finds no opinion or rationale by Dr. B., or Dr. M., 
that would allow the Board to reconcile how they obviously 
overlooked material pieces of evidence.  Dr. B. reviewed Dr. 
C's opinion reciting this evidence, and offered no rebuttal 
argument.  On this point, the opinion by Dr. B. is severely 
flawed.

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 [redacted] 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:

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

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.  See Lilly's An 
Introduction to the Law of Evidence, 2nd Ed. (1987), pp. 245-
46 (many state jurisdictions, including the federal judiciary 
and Federal Rule 803(4), expand the hearsay exception for 
physical conditions to include statements of past physical 
condition on the rational that statements made to physicians 
for purposes of diagnosis and treatment are exceptionally 
trustworthy since the declarent has a strong motive to tell 
the truth in order to receive proper care).  

Furthermore, Dr. B. does not offer any rationale 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.  See Reonal, 5 
Vet. App. at 460-61 (recognizing that a physician opinion 
based upon an inaccurate factual premise lessens its 
probative value).  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 examiners 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 doctors reviewed the entire 
record nor his opinions.  This argument is obviously false as 
reflected in the complete text the opinions by Drs. G. and C. 
that the Board has cited in full.  Rather, 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 examiner's 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 opinion that the lethargy was due to transient 
hypoglycemia that is entirely consistent with the impression 
of the treating physician's at the time.

Finally, 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 Veteran's 
child 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 held 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 assertion 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 examiner fully acknowledges the results from the CT 
scans of the head conducted in March and July 1985.  
Additionally, neither examiner counter's 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."

Based upon the above, the Board has determined that the 
preponderance of the evidence demonstrates that the Veteran's 
child does not have a form and/or manifestation of spina 
bifida.  Accordingly, it is concluded that the criteria for a 
monetary allowance under 38 U.S.C.A. § 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 
claimant's favor.  38 U.S.C.A. § 5107(b).  See also Ortiz v. 
Principi, 274 F. 3d. 1361, 1365 (Fed. Cir. 2001) (benefit of 
doubt rule does not apply when preponderance of evidence is 
against claim).

IV.  Duty to assist and provide notice

As provided for by the Veterans Claims Assistance Act of 2000 
(VCAA), VA has a duty to notify and assist claimants in 
substantiating a claim for VA benefits.  38 U.S.C.A. §§ 5100, 
5102, 5103, 5103A, 5107, 5126 (West 2002 & Supp. 2007); 
38 C.F.R. §§ 3.102, 3.156(a), 3.159 and 3.326(a) (2009).  

An RO letter dated June 2008 fully complied with the notice 
content requirements.  See Quartuccio v. Principi, 16 Vet. 
App. 183 (2002); Pelegrini v. Principi, 18 Vet. App. 112 
(2004); Dingess v. Nicholson, 19 Vet. App. 473 (2006).

Technically, the Board concedes that the VCAA notice in this 
case was not satisfied prior to the initial AOJ adjudication 
denying the claim.  This is so due to impossibility as the 
original AOJ determination was made prior to the passage of 
the VCAA.  After fully compliant notice was provided in June 
2008, the RO readjudicated the claim in a May 2009 
supplemental statement of the case which cured the timing 
defect.  Mayfield v. Nicholson, 444 F.3d 1328 (Fed. Cir. 
2006); Prickett v. Nicholson, 20 Vet. App. 370, 376 (2006).

The Board has also considered the potential role of 
prejudicial notice error in this case.  Such a finding would 
be patently inconsistent with evidence of record.  In an 
August 2006 brief to the Court, the Veteran's counsel 
demonstrated full knowledge of the VCAA requirements and 
obtained a remand, in part, on VCAA notice error.  The Board 
is confident that, while this argument was being pursued, the 
Veteran's counsel nonetheless undertook his obligation to 
impart his knowledge of the VCAA notice requirements to his 
client.

VA also has a duty to assist the Veteran in obtaining 
evidence necessary to substantiate a claim.  38 U.S.C.A. 
§ 5103A; 38 C.F.R. § 3.159(c).  The case at hand involves the 
medical treatment and diagnosis of the Veteran's child.  The 
claims folder includes the child's pertinent medical records, 
statements from the child's physicians, and expert medical 
opinions submitted by the Veteran.  There are no outstanding 
requests for VA to obtain evidence on behalf of the Veteran 
wherein he has authorized VA to do so.  

VA has also obtained medical opinion as necessary to 
substantiate the claim.  In July 2003, the Board obtained a 
VHA specialist opinion based upon review of the claims 
folder.  This opinion was not favorable to the Veteran's 
claim, and the claimant responded with a rebuttal medical 
opinion.  In March 2004, the Board responded to the 
attorney's Privacy Act Information discovery request 
involving the VHA opinion.

In July 2004, the Board re-reviewed the record and determined 
that the case was of such complexity and controversy that an 
IME opinion was required.  In August 2004, the Board provided 
the claimant and his attorney with a copy of that report, and 
provided them a 60-day period in which to provide additional 
evidence and/or argument.  The Veteran, through his attorney, 
responded by submitting two additional expert opinions. 

The Board takes note of the arguments advanced by the 
attorney that the Board, in obtaining an IME, has engaged in 
"development for denial" and that the process used by the 
Board in obtaining such opinions is "flawed."  It is also 
argued that the Board does not have the authority to obtain 
such opinions in the first instance due to its lack of 
developmental powers.

Congress has statutorily authorized the Board to seek IME 
opinions when deemed necessary by the complexity and 
controversy of the case, and the Secretary has authorized the 
Board to seek VHA opinions.  38 U.S.C.A. § 7109; 38 C.F.R. 
§ 20.901.  The Federal Circuit Court has upheld the Board's 
power to both obtain such opinions and adjudicate the matter 
without RO review, provided that the claimant is provided a 
copy of the examination report and an opportunity to respond.  
Disabled American Veterans, et.al, vs. Secretary of Veterans 
Affairs, 419 F.3d 1317 (Fed. Cir. 2005).

The Board notes that the pro-claimant system aspect of this 
system is reflected by the policy that VA, and not the 
claimant, be required to pay for IME opinions.  As indicated 
above, the Board has had reason to question the underlying 
bases for Dr. B.'s opinion, and the record already included 
an unfavorable VHA opinion before the IME was requested.  The 
Board requested the IME, in part, because the examiner is 
deemed "Independent" from the VA system.  Clearly, the 
issues in this case are both complex and in controversy, and 
the Board had a legitimate basis to pursue an IME opinion 
based upon a conflict of medical opinion of record.  Cf. 
Mariano v. Principi, 17 Vet. App. 305, 312 (2003).

Overall, the Board finds that the record has been fully 
developed, and the evidence and information of record, in its 
totality, provides the necessary information to decide the 
case.  38 U.S.C.A. § 5103A(d); 38 C.F.R. § 4.2.  The Board 
further finds that no reasonable possibility exists that any 
further development to the claim would be capable of 
substantiating the claim.  Thus, on appellate review, the 
Board sees no areas in which further development is needed.  


ORDER

The appeal is denied. 


____________________________________________
JOHN J. CROWLEY
Veterans Law Judge, Board of Veterans' Appeals




 Department of Veterans Affairs