Court Opinion

ID: 2651322
Source: CourtListenerOpinion
Date Created: 2014-01-28 17:13:08.735031+00
Date Added: 2024-06-11T09:10:23.657107
License: Public Domain

NOTE: This disposition is nonprecedential.

  United States Court of Appeals
      for the Federal Circuit
               ______________________

JED SNYDER AND LILIA SNYDER, Parents of N.S.,
            Petitioners-Appellees,

                          v.

     SECRETARY OF HEALTH AND HUMAN
                 SERVICES,
             Respondent-Appellant.
            ______________________

                     2013-5068
               ______________________

    Appeal from the United States Court of Federal
Claims in No. 07-VV-0059, Judge Susan G. Braden.

             ----------------------

 FRANK HARRIS, Parent of JORDAN HARRIS, a
                   minor,
            Petitioner-Appellee,

                          v.

     SECRETARY OF HEALTH AND HUMAN
                 SERVICES,
             Respondent-Appellant.
            ______________________

                     2013-5072
2                                            SNYDER   v. HHS

                 ______________________

    Appeal from the United States Court of Federal
Claims in No. 07-VV-0060, Judge Susan G. Braden.
                 ______________________

               Decided: January 28, 2014
                ______________________

   JOSEPH PEPPER and SYLVIA CHIN-CAPLAN, Conway,
Homer & Chin-Caplan, P.C., of Boston, Massachusetts,
argued for Petitioners-Appellees. On the brief was
RONALD C. HOMER.

    VORIS E. JOHNSON, JR., Assistant Director, Torts
Branch, Civil Division, United States Department of
Justice, of Washington, DC, argued for Respondent-
Appellant. With him on the brief were STUART F. DELERY,
Acting      Assistant     Attorney     General,    RUPA
BHATTACHARYYA, Director, VINCENT J. MATANOSKI, Depu-
ty Director, and CATHERINE E. REEVES, Assistant Director.
                  ______________________

Before O’MALLEY, BRYSON, and WALLACH, Circuit Judges.
WALLACH, Circuit Judge.
     Petitioners-Appellees, by and through their parents,
filed suits under the National Childhood Vaccine Injury
Act of 1986, 42 U.S.C. § 300aa–1 to 300aa–34 (2006)
(“Vaccine Act”), alleging that they suffered from epilepsy
or a seizure disorder, as a direct result of the diphtheria
and tetanus toxoids and acellular pertussis vaccine
(“DTaP”). The same Special Master presided over Peti-
tioners’ cases and denied compensation finding, in part,
that a genetic mutation was the sole cause of the seizure
disorders in both cases. Harris v. Sec’y of Health & Hu-
man Servs., No. 07-60V, 2011 WL 2446321 (Fed. Cl. Spec.
Mstr. May 27, 2011); Snyder v. Sec’y of Health & Human
SNYDER   v. HHS                                           3

Servs., No. 7-59V, 2011 WL 3022544 (Fed. Cl. Spec. Mstr.
May 27, 2011). Upon review, the Court of Federal Claims
reversed the Special Master in favor of Petitioners.
Harris v. Sec’y of Health & Human Servs., 102 Fed. Cl.
282 (2011); Snyder v. Sec’y of Health & Human Servs.,
102 Fed. Cl. 305 (2011). On remand, the Special Master
determined the amount of compensation and entered
judgment in these cases. E.g., Snyder v. Sec’y of Health &
Human Servs., No. 07-59, 2013 WL 391169 (Fed. Cl. Spec.
Mstr. Jan. 8, 2013). This court finds in favor of the Secre-
tary of Health and Human Services (“government” or
“Secretary”). Therefore, we reverse the Court of Federal
Claims’ decisions and direct the court to reinstate the
Special Master’s decisions denying compensation. The
Special Master’s decisions awarding compensation there-
fore are vacated.
                       BACKGROUND
     These Vaccine Act cases involve an examination of the
relationship between the DTaP vaccine and the seizure
disorders from which the Petitioners suffer. Severe
Myoclonic Epilepsy of Infancy (“SMEI”), also known as
Dravet Syndrome, is a rare disorder that is characterized
by generalized tonic, clonic, and tonic-clonic seizures,
which are typically induced by fever and begin during the
first year of life. Typically, SMEI is first manifested as a
seizure that occurs when the child is between six and nine
months in the context of a fever. While a child’s early
development is normal, SMEI stagnates mental develop-
ment in the second year of life.
     The SCN1A gene provides instructions for making so-
dium ion channels. These channels play a key role in a
cell’s ability to generate and transmit electrical signals.
Abnormal function of these sodium ion channels may
cause a person to have seizures. For example, although
not definitive, variant SCN1A genes have been associated
with, depending on the range of symptoms, familial
4                                           SNYDER   v. HHS

hemiplegic migraines, generalized epilepsy with febrile
seizures plus (“GEFS+”), and SMEI. GEFS+ is a disorder
that is considered sufficiently similar to SMEI that they
are sometimes described as falling on one spectrum.
GEFS+ is milder than SMEI, but GEFS+ occurs more
frequently than SMEI.
    Minors Jordan Harris and N.S. are the Petitioners-
Appellees in these cases. Jordan was born on March 6,
2004. On May 7, 2004, Jordan received his first set of
immunizations, including the DTaP vaccine. Several
hours after these vaccinations, Jordan was taken to the
emergency room upon experiencing a seizure preceded by
a fever. Jordan was discharged two days later.
    On July 7, 2004, Jordan received a set of immuniza-
tions, including a second dose of DTaP, and subsequently,
on September 3, 2004, a third dose of DTaP. On Septem-
ber 28, 2004, when he was six months old, Jordan experi-
enced a second seizure. He was admitted to a hospital
and was examined by a neurologist. Jordan’s magnetic
resonance imaging (“MRI”), computed tomography scan
(“CT scan”), and electroencephalogram (“EEG”) results
were all normal and he was discharged.
    Over the next several years, Jordan experienced occa-
sional seizures, and in August 2006, Jordan was referred
for genetic testing. The genetic testing report identified
two DNA variants in Jordan, one of which was a variant
in the SCN1A gene. This variant was “predicted to dis-
rupt the structure of the protein [that is encoded by the
SCN1A gene] and alter its function.” Harris, 2011 WL
2446321, at *2 (internal quotation marks omitted). The
report further opined that the results were “consistent
with a diagnosis of, or a predisposition to developing,
SMEI or [Severe Myoclonic Epilepsy Borderline], the
severe phenotype associated with SCN1A mutations.” Id.
(internal quotation marks omitted). The report neverthe-
SNYDER   v. HHS                                          5

less noted that Jordan’s specific mutation has not been
definitively demonstrated to be associated with SMEI.
    Petitioner N.S. was born in November 2004. He de-
veloped normally through March 2005. On March 4,
2005, when he was four months old, N.S. received a dose
of the DTaP vaccination. The next day, he experienced a
seizure that was associated with a slight fever. N.S. was
taken to the emergency room. In the hospital, N.S. had
various tests, including a CT scan, which produced mostly
normal results.
    Upon discharge, N.S. saw a neurologist. The neurolo-
gist indicated that “[t]his could have been a febrile sei-
zure” and noted the “seizure was several hours after
getting the [DTaP] shot.” Snyder, 2011 WL 3022544, at
*2 (internal quotation marks omitted). The neurologist
recommended careful observation but no medication, and
an EEG was recommended, although the record reflects
this test was not conducted.
    N.S. continued to experience occasional seizures
through the end of 2005. After one such occasion, N.S.
returned to the neurologist, at which time an EEG and an
MRI were administered. Results were normal.
    After more seizures, N.S. was admitted to the hospital
in May 2006, and a pediatric neurologist ordered genetic
testing to rule out SMEI. N.S.’s genetic testing was
positive for a mutation of the SCN1A gene. The pediatric
neurologist thereafter diagnosed N.S. with Dravet syn-
drome (or SMEI).
    In January 2007, Frank Harris, parent of Jordan, and
Jed and Lilia Snyder, parents of N.S., invoked the juris-
diction of the Court of Federal Claims and the special
master under 42 U.S.C. § 300aa-12(a), claiming the DTaP
vaccination was a substantial cause of Petitioners’ seizure
disorders. On July 3, 2008, the cases were assigned to
one Special Master because the cases presented the same
6                                            SNYDER   v. HHS

issues, were based on similar evidence, and were advocat-
ed by the same attorneys. On May 27, 2011, the Special
Master issued his decisions denying compensation to
Petitioners.
     Specifically, the Special Master found the Secretary’s
arguments persuasive, stating it was not necessary to
determine “whether DTaP can cause a significant neuro-
logical injury . . . because even if [Petitioners] were as-
sumed to have met [their] burden of proof[,] . . . [t]he
evidence convincingly shows” that the SCN1A gene muta-
tion identified in both children was the “sole cause” of
their seizure disorders. Harris, 2011 WL 2446321, at *1;
Snyder, 2011 WL 3022544, at *1. The Special Master
based his decisions on the Secretary’s proffered expert
opinions of Dr. Max Wiznitzer and Dr. Gerald V. Ray-
mond, while discounting Petitioners’ expert, Dr. Marcel
Kinsbourne. The Special Master found that none of the
scientific literature introduced during testimony in the
record “clearly suggest[ed]” that an environmental factor,
e.g., a vaccination, is “necessary to cause symptoms.”
Harris, 2011 WL 2446321, at *16 (internal quotation
marks omitted); Snyder, 2011 WL 3022544, at *16 (inter-
nal quotation marks omitted).
    While finding that Petitioners’ genetic mutations were
the sole cause of their seizure disorders, the Special
Master alternatively found that Petitioners failed to show
causation, in part, because “Dr. Kinsbourne did not offer
any ideas” of how Petitioners’ seizure disorders would
have been “but for” the vaccine. Harris, 2011 WL
2446321, at *33; Snyder, 2011 WL 3022544, at *34. The
Special Master noted that “when asked whether the
seizure disorders in these cases would not have been
manifest ‘absent the receipt of the DTaP’ vaccine, Dr.
Kinsbourne testified that he has ‘no knowledge of that.
That would be speculation . . . .’” Harris, 2011 WL
2446321, at *33; Snyder, 2011 WL 3022544, at *34.
SNYDER   v. HHS                                           7

    The Special Master further determined that “[t]he un-
certainty about [Petitioners’] outcome but for the vaccina-
tion that is inherent in Dr. Kinsbourne’s testimony is not
present in the testimony of Dr. Wiznitzer and Dr. Ray-
mond.” Harris, 2011 WL 2446321, at *33; Snyder, 2011
WL 3022544, at *35. These doctors testified that the
DTaP vaccine did not cause Petitioners’ seizure disorders.
Based on this record, the Special Master concluded Peti-
tioners’ SCN1A mutations were the sole cause of their
seizure disorders.
     The Court of Federal Claims reversed the Special
Master’s decisions and entered final judgment in favor of
N.S. on January 14, 2013, and in favor of Jordan on
January 23, 2013. The Court of Federal Claims reversed
on the basis that the Special Master had required Peti-
tioners to satisfy a standard of scientific certainty rather
than preponderance of the evidence, and had therefore
applied the wrong standard of proof. Also, the Court of
Federal Claims found that the Special Master erred in
finding that the Secretary demonstrated alternate causa-
tion. According to the court, the Special Master unrea-
sonably credited the Secretary’s expert testimony over Dr.
Kinsbourne’s testimony. The Court of Federal Claims
“view[ed] the entirety of the record on alternative causa-
tion as a classic case of ‘conflicting’ experts,” and stated
that in such circumstances the Special Master was re-
quired to find in favor of Petitioners. Harris, 102 Fed. Cl.
at 304 (quoting Knudsen v. Sec’y of Health & Human
Servs., 35 F.3d 543, 550–51 (Fed. Cir. 1994)); Snyder, 102
Fed. Cl. at 325 (quoting Knudsen, 35 F.3d at 551). The
Court of Federal Claims thus set aside the Special Mas-
ter’s decisions and made its own findings, ultimately
determining that Petitioners carried their burden of
demonstrating that their conditions were caused-in-fact
by the DTaP vaccination. On remand, the Special Master
calculated the amount of compensation due to the Peti-
8                                             SNYDER   v. HHS

tioners. The Secretary appeals both decisions. This court
has jurisdiction under 42 U.S.C. § 300aa-12(f).
                       DISCUSSION
    The Secretary contends the record supports a finding
that the SCN1A gene mutation is the sole cause of Peti-
tioners’ seizure disorders. Petitioners allege that admin-
istration of the DTaP vaccination was a substantial cause
of the SMEI from which Petitioners suffer. Although
these cases were appealed separately, the cases were
consolidated and this court considers them together
because of the substantial overlap of the evidence and
issues in the two cases.
    “We review an appeal from the Court of Federal
Claims in a Vaccine Act case de novo, applying the same
standard of review as the Court of Federal Claims applied
to its review of the special master’s decision.” Carson v.
Sec’y of Health & Human Servs., 727 F.3d 1365, 1368
(Fed. Cir. 2013) (internal quotation marks and citation
omitted). We give no deference to the Court of Federal
Claims’ or Special Master’s determinations of law, but
uphold the Special Master’s findings of fact unless they
are arbitrary or capricious. Id.; 42 U.S.C. § 300aa–
12(e)(2)(B). As we have noted:
        Congress assigned to a group of specialists,
    the Special Masters within the Court of Federal
    Claims, the unenviable job of sorting through
    these painful cases and, based upon their accumu-
    lated expertise in the field, judging the merits of
    the individual claims. The statute makes clear
    that, on review, the Court of Federal Claims is not
    to second guess the Special Masters [sic] fact-
    intensive conclusions; the standard of review is
    uniquely deferential for what is essentially a judi-
    cial process. Our cases make clear that, on our
    review . . . we remain equally deferential. That
    level of deference is especially apt in a case in
SNYDER   v. HHS                                            9

    which the medical evidence of causation is in dis-
    pute.
Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958,
961 (Fed. Cir. 1993) (internal citations omitted).
    The Vaccine Act created the National Vaccine Injury
Compensation Program through which claimants can
petition the Court of Federal Claims to receive compensa-
tion for vaccine-related injuries or death. In crafting the
Program, Congress created the Vaccine Injury Table, 42
U.S.C. § 300aa-14(a), which sets forth “a list of vaccines, a
parallel list of adverse medical conditions commonly
associated with the use of each vaccine, and, for certain
medical conditions, a time period in which the first symp-
toms should become apparent following vaccination.”
Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302,
1307 (Fed Cir. 1999). “For cases involving injuries that do
not fall within the Vaccine Injury Table, 42 U.S.C. §
300aa–14(a)—the so-called ‘off-Table’ cases—the petition-
er has the burden to prove causation by a preponderance
of the evidence.” Stone v. Sec’y of Health & Human
Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (citing 42
U.S.C. § 300aa–13(a)(1)(A)).
    To prove causation in an off-Table case, “a petitioner
must show that the vaccine was not only a but-for cause
of the injury but also a substantial factor in bringing
about the injury.” Id. (quoting Shyface v. Sec’y of Health
& Human Servs., 165 F.3d 1344, 1352–53 (Fed. Cir.
1999)). This court has held that the causation standard
in off-Table Vaccine Act cases is to be applied consistently
with the principles set forth in the Second Restatement of
Torts. Id. In making this showing, a petitioner must
provide the following: (1) a medical theory causally con-
necting the vaccination and the injury; (2) a logical se-
quence of cause and effect showing that the vaccination
was the reason for the injury; and (3) a showing of a
proximate temporal relationship between vaccination and
10                                             SNYDER   v. HHS

injury. Moberly v. Sec’y of Health & Human Servs., 592
F.3d 1315, 1322 (Fed. Cir. 2010) (quoting Althen v. Sec’y
of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir.
2005)) (“Althen test”). Under these standards, it is the
petitioner’s burden to “prove ‘actual causation’ or ‘causa-
tion in fact’ by a preponderance of the evidence.” Id. at
1321.
    Once a petitioner establishes her prima facie case by
satisfying the Althen test, the burden shifts to the Secre-
tary to show by a preponderance of the evidence that the
injury is due to factors unrelated to the administration of
the vaccine. 42 U.S.C. § 300aa–13(a)(1)(B). In order to
meet that burden, the Secretary must “identify[ ] a par-
ticular . . . factor (or factors) and present[ ] sufficient
evidence to establish that it was the sole substantial
factor in bringing about the injury.” de Bazan v. Sec’y of
Health & Human Servs., 539 F.3d 1347, 1354 (Fed. Cir.
2008).
    Here, the record fully supports the Special Master’s
finding that it was more likely than not that Jordan’s and
N.S.’s SCN1A gene mutations were the sole cause of their
seizure disorders. As an initial matter, Petitioners argue
that the Special Master legally erred by placing the
burden on the Petitioners, and not on the Secretary, to
show that other alternative triggers or factors unrelated
to the vaccine did not cause the seizure disorders. The
Special Master however properly considered the entire
record and determined the Secretary met its burden of
proof.
    This court recently addressed this same issue when
faced with the question of
     whether, in assessing whether a prima facie show-
     ing of causation has been made in an off-Table
     case, a special master may consider evidence of
     other possible causes for the injury in question, or
     whether evidence of other possible causes may be
SNYDER   v. HHS                                        11

   considered only in connection with the “factors
   unrelated” defense on which the government has
   the burden of proof.
Stone, 676 F.3d at 1379. In assessing a petitioner’s prima
facie case for causation, a special master may consider
evidence of other possible causes for the injury in ques-
tion. Id. That evidence is relevant to “whether a prima
facie showing has been made that the vaccine was a
substantial factor in causing the injury in question,” as
well as to a “‘factors unrelated’ defense on which the
government has the burden of proof.” Id. Therefore,
Stone concluded that “the special master is entitled to
consider the record as a whole . . . , and no evidence
should be embargoed from the special master’s considera-
tion simply because it is also relevant to another inquiry
under the statute.” Id. at 1380.
    As in Stone, the Special Master did not err by examin-
ing the record in its entirety, and subsequently, finding
that the Secretary proved by preponderant evidence its
“factors unrelated” defense by showing that the gene
mutations were the sole cause of the seizure disorders. In
addition, by examining the record as a whole, the Special
Master did not require Petitioners to shoulder the burden
of eliminating all possible alternative causes in making
their prima facie case nor did he effectively place the
burden of showing “factors unrelated” to the vaccine on
Petitioners. See id. Rather, the Special Master was clear
that his determinations were based on the Secretary’s
evidence, which he found to be convincing. We according-
ly turn to these determinations to examine whether they
were arbitrary or capricious. See 42 U.S.C. § 300aa–
12(e)(2)(B).
    The Special Master found persuasive the Secretary’s
experts, Dr. Wiznitzer and Dr. Raymond. In particular,
the Special Master noted the extensive background and
experience of Drs. Wiznitzer and Raymond. The Special
12                                            SNYDER   v. HHS

Master found that Dr. Wiznitzer has an active clinical
practice in pediatric neurology. The Special Master also
found that Dr. Wiznitzer teaches medical students about
child neurology and conducts research, including on topics
related to the effectiveness of medications for epilepsy.
The record further shows that Dr. Wiznitzer has been
interested in Dravet syndrome since the 1980s, and has
treated children with that condition.
    The record also reflects that Dr. Raymond, board-
certified in neurology and clinical genetics, is an associate
professor of neurology at Johns Hopkins University and
the director of neurogenetic research at the Kennedy
Krieger Institute. Dr. Raymond conducts research, teach-
es medical students and residents about neurology and
genetics, and maintains a clinical practice. Among his
patients, approximately half suffer from epilepsy, includ-
ing those diagnosed with Dravet syndrome.
    Drs. Raymond and Wiznitzer attributed Jordan’s and
N.S.’s seizure disorders solely to their SCN1A mutations,
and as a result, testified that Jordan and N.S. would have
suffered seizures eventually, whether or not they received
the DTaP vaccine. In reaching their opinions, they con-
sidered several factors generally relied upon by research-
ers in the relevant field and from which Drs. Raymond
and Wiznitzer consider when counseling their patients.
See Terran v. Sec’y of Health & Human Servs., 195 F.3d
1302, 1316 (Fed. Cir. 1999) (applying Daubert factors to
the Special Master’s evaluation of expert witnesses in
Vaccine Act cases). 1 The Special Master found the meth-

     1 The Daubert factors for analyzing the reliability of
testimony are: (1) whether a theory or technique can be
(and has been) tested; (2) whether the theory or technique
has been subjected to peer review and publication; (3)
whether there is a known or potential rate of error and
whether there are standards for controlling the error;
SNYDER   v. HHS                                            13

odology these experts applied convincing.           See, e.g.,
Snyder, 2011 WL 3022544, at *4; see also Kumho Tire Co.
v. Carmichael, 526 U.S. 137, 152 (1999) (“[The objective of
Daubert’s gatekeeping requirement] is to make certain
that an expert, whether basing testimony upon profes-
sional studies or personal experience, employs in the
courtroom the same level of intellectual rigor that charac-
terizes the practice of an expert in the relevant field.”).
     According to Dr. Raymond, Petitioners’ SCN1A muta-
tions were not inherited from either parent, and therefore,
their mutations were “de novo” mutations, which are
more likely to present a severe disease. Harris, 2011 WL
2446321, at *14; Snyder, 2011 WL 3022544, at *15. Dr.
Raymond also opined that Petitioners’ mutations are
located in the region of the genome that is highly con-
served across different species, which presumably is
strong circumstantial evidence that the mutation is
pathogenic. With respect to Jordan, Dr. Raymond indi-
cated that Jordan’s genetic mutation “is a change in the
sequence of amino acids that control how DNA is tran-
scribed into messenger RNA,” and such “splice site”
mutations tend to indicate a disease. Harris, 2011 WL
2446321, at *14. With respect to N.S., Dr. Raymond
observed that N.S.’s mutation occurred within the DNA
that codes the pore of the sodium ion channels, and that
“[a]lmost all mutations that have been found in the pore
region of the sodium channel have been found in cases of
SMEI.” Snyder, 2011 WL 3022544, at *15.
    Drs. Wiznitzer and Raymond further opined that the
cases reported in scientific literature supported their
conclusion that Petitioners’ genetic mutations were the

and, (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community. Daub-
ert v. Merrell Dow Pharms., Inc., 509 U.S. 579, 592–95
(1993).
14                                            SNYDER   v. HHS

sole cause of their seizure disorders. For example, Drs.
Wiznitzer and Raymond testified that the exact mutation
Jordan has was reported in a 2009 article by Kumakura
et al. 2 The example showed, according to the experts,
that this particular mutation tends to control the person’s
development. With respect to N.S., Drs. Wiznitzer and
Raymond provided that N.S.’s variant has been reported
to be disease-associated and such cases were reported in
literature by, for example, Ohmori et al. and Claes et al. 3
According to Drs. Wiznitzer and Raymond, these exam-
ples show that this particular mutation tends to control
the person’s development, and both experts opined that
children who had this exact mutation also developed
SMEI.
    While finding Drs. Wiznitzer and Raymond persua-
sive, the Special Master found Petitioners’ expert, Dr.
Kinsbourne, unconvincing. First, the Special Master
noted the relative difference in experience among Dr.
Kinsbourne, Dr. Wiznitzer, and Dr. Raymond as “one
reason for finding that the evidence establishes that the
genetic mutation was the sole cause of [Petitioners’]
developmental change.” Harris, 2011 WL 2446321, at
*11; Snyder, 2011 WL 3022544, at *12.
    The Special Master found that “[i]n his entire career,
Dr. Kinsbourne has not focused on genetics or seizure
disorders. The basis of Dr. Kinsbourne’s opinions comes

     2   Akira Kumakura, et al., Novel de novo splice-site
mutation of SCN1A in a patient with partial epilepsy with
febrile seizures plus, 31(2) Brain & Dev. 179 (2009).
    3    Iori Ohmori, et al., Significant correlation of the
SCN1A mutations and severe myoclonic epilepsy in infan-
cy, 295(1) Biochemical & Biophysical Research Comm. 17
(2002); Lieve Claes, et al., De novo SCN1A mutations are
a major cause of severe myoclonic epilepsy of infancy, 21(6)
Human Mutation 615 (2003).
SNYDER   v. HHS                                          15

from his interpretation of medical articles about genetic
epilepsies. This research was done for the purpose of
presenting an opinion in this case.” Harris, 2011 WL
2446321, at *4; Snyder, 2011 WL 3022544, at *6. In
addition, the Special Master noted “Dr. Kinsbourne
essentially stopped practicing pediatric neurology in
1981,” and therefore, “Dr. Kinsbourne was not a practic-
ing pediatric neurologist in 2000, when the SCN1A muta-
tion started being linked to GEFS and SMEI.” Harris,
2011 WL 2446321, at *21; Snyder, 2011 WL 3022544 at,
*21–22. Although the Special Master acknowledged “Dr.
Kinsbourne read literature on SCN1A to support his work
as an expert witness,” he found it “difficult to see how Dr.
Kinsbourne’s efforts can equal the knowledge gained by
Dr. Wiznitzer and Dr. Raymond.” Harris, 2011 WL
2446321, at *21; Snyder, 2011 WL 3022544, at *22.
    Indeed, the record shows that both Dr. Wiznitzer and
Dr. Raymond study neurologic problems associated with
genetic abnormalities as a regular part of their full-time
careers, and they counsel patients with genetic mutations
that cause neurological problems. The Special Master
noted that “[t]heir professional duties give them a depth
of knowledge that is not matched by Dr. Kinsbourne. For
example, Dr. Wiznitzer attended an international confer-
ence about SCN1A just before the hearing in this case.”
Harris, 2011 WL 2446321, at *21; Snyder, 2011 WL
3022544, at *22. Accordingly, the Special Master con-
cluded Drs. Wiznitzer’s and Raymond’s opinions “merit
consideration” and determined that Dr. Kinsbourne’s
testimony was not persuasive. Harris, 2011 WL 2446321,
at *22; Snyder, 2011 WL 3022544, at *22. This court does
not discern error in this conclusion. Porter v. Sec’y of
Health & Human Servs., 663 F.3d 1242, 1249 (Fed. Cir.
2011) (On review, we do “not reweigh the factual evi-
dence, assess whether the special master correctly evalu-
ated the evidence, or examine the probative value of the
16                                           SNYDER   v. HHS

evidence or the credibility of the witnesses—these are all
matters within the purview of the fact finder.”).
     The Special Master likewise found Drs. Wiznitzer’s
and Raymond’s opinions were consistent with scientific
literature. For example, the researchers of the Berkovic
article did not believe that “avoiding vaccination, as a
potential trigger, would prevent onset of this devastating
disorder in patients who already harbor the SCN1A
mutation.” 4 In yet another article by Claes et al., re-
searchers studying observable physical manifestations of
carrying SCN1A mutations determined that “genotype-
phenotype correlations seem to be fairly strict.” 5 The
same conclusion was reached in the Ceulemans article:
“detailed analyses of all published patients for whom
sufficient clinical and genetic information is available
clearly demonstrate phenotype/genotype correlation.” 6
Most significantly, the McIntosh article analyzed medical
and vaccination records to investigate whether there was
an association between vaccination and onset of seizures
in patients with Dravet syndrome who had mutations in
the SCN1A gene. 7 It concluded that the vaccine had no

     4  Samuel F. Berkovic, et al., De novo mutations of
the sodium channel gene SCN1A in alleged vaccine en-
cephalopathy: a retrospective study, 5 Lancet Neurology
488, 491 (2006).
    5   Lieve Claes, et al., The SCN1A variant database:
a nonvel research and diagnostic tool, 30 Human Muta-
tion E904, E910 (2009).
    6   Berten P.G.M. Ceulemans, et al., Clinical correla-
tions of mutations in the SCN1A gene: From febrile sei-
zures to severe myoclonic epilepsy in infancy, 30(4)
Pediatric Neurology 236, 241 (2004).
    7   Anne M. McIntosh, et al., Effects of vaccination on
onset and outcome of Dravet syndrome: a retrospective
study, 9 Lancet Neurology 592 (2010).
SNYDER   v. HHS                                            17

effect on the outcome of children with SCN1A mutation.
The Special Master further found that Petitioners’ medi-
cal records and statement of treating doctors supported
Drs. Wiznitzer’s and Raymond’s theory. These determi-
nations were not arbitrary or capricious. Lampe v. Sec’y
of Health & Human Servs., 219 F.3d 1357, 1363 (Fed. Cir.
2000) (“[If] the special master’s conclusion [is] based on
evidence in the record that [is] not wholly implausible, we
are compelled to uphold that finding as not being arbi-
trary or capricious.”).
    The Court of Federal Claims views the record in a dif-
ferent light. Upon review of the experts’ testimony, the
Court of Federal Claims found all the experts “helpful and
instructive.” Harris, 102 Fed. Cl. 303 n.29; Snyder, 102
Fed. Cl. at 325 n.35. Thus, the court characterized the
record as a “classic case of ‘conflicting experts,’” where the
evidence was in “equipoise,” requiring a finding against
the Secretary for failure to meet its burden of proof estab-
lishing that the SCN1A mutation was the sole cause of
Petitioners’ seizure disorders. Harris, 102 Fed. Cl. at 303
(quoting Knudsen, 35 F.3d at 550–51); Snyder, 102 Fed.
Cl. at 325 (quoting Knudsen, 35 F.3d at 550–51). This,
however, is not that “classic case of conflicting experts,”
nor is the evidence in these cases in “equipoise.”
    The Special Master in these cases made particular
findings, supported by the record, in favor of the Secre-
tary. Although a true equipoise of evidence may defeat
the party with the burden of proof, the Special Master
here did the analysis necessary to decide the Secretary
had the stronger case based on testimony and the intellec-
tual strength of the evidence, as well as the arguments
presented. Andrew Corp. v. Gabriel Elecs., Inc., 847 F.2d
819, 824 (Fed. Cir. 1988) (quoting United States v. Gen-
eral Motors Corp., 561 F.2d 923, 933 (D.C. Cir. 1977))
(“The mere fact that experts disagree does not mean that
the party with the burden of proof loses. The finder of
fact has to make the effort to decide which side has the
18                                            SNYDER   v. HHS

stronger case. This can be based on the demeanor of the
witnesses (if so, the trial judge should say so) or the
intellectual strength of the evidence and arguments based
thereon.”).
     In particular, the Special Master found that Dr. Kins-
bourne “did relatively little to rebut” Drs. Wiznitzer and
Raymond’s testimony, and Dr. Kinsbourne failed, for
instance, to “explain why the conclusion of the research-
ers [in the McIntosh article] was wrong.” Harris, 2011
WL 2446321, at *23; Snyder, 2011 WL 3022544, at *23.
Also, the Special Master noted that “when asked whether
the seizure disorders in these cases would not have been
manifest ‘absent the receipt of the DTaP’ vaccine, Dr.
Kinsbourne testified that he has ‘no knowledge of that,’”
and “[w]hen asked to explain how [Jordan and N.S.]
would have been different today if [they] had not received
the vaccine, Dr. Kinsbourne stated that he did not know.”
Harris, 2011 WL 2446321, at *33; Snyder, 2011 WL
3022544, at *34. The Special Master thus concluded that
“[t]o the extent that Dr. Kinsbourne’s opinion has been
informed by reading medical articles, the articles general-
ly do not support the arguments [Petitioners advance].
The studies that investigated whether a pertussis vaccine
affected the development of a person with an SCN1A
mutation concluded that the vaccine did not cause the
epilepsy.” Harris, 2011 WL 2446321, at 24; Snyder, 2011
WL 3022544, at 25.
    These findings were not arbitrary or capricious, and
in turn, show that the Secretary met her burden of proof
with preponderant evidence. To the extent Petitioners
argue otherwise, we cannot reweigh the evidence and
substitute our judgment for that of the Special Master.
                       CONCLUSION
    Based on the foregoing, we reverse the Court of Fed-
eral Claims’ decisions and direct the court to reinstate the
Special Master’s decisions denying compensation. The
SNYDER   v. HHS                                       19

Secretary has shown that the evidence supports a finding
that the SCN1A gene mutation was, more likely than not,
the sole cause of Petitioners’ seizure disorders. We also
vacate the Special Master’s decisions awarding compensa-
tion.
                     REVERSED