M.S.B. Ex Rel. Bast v. Secretary of Health & Human Services

In the United States Court of Federal Claims
No. 01-565V
(Filed under seal July 8, 2014)
(Reissued July 25, 2014) †

*************************
*
[M.S.B.], by her mother and * Vaccine Act off-table petition; IPV,
natural guardian, TIFFANY BAST, * DTaP, Hib, hepatitis B vaccines;
* seizure disorder; reactive oxygen
* species; oxidative stress; weight of
Petitioner, * contemporaneous medical records;
* mitochondrial disorder; rechallenge;
v. * Althen prongs; unreliable medical
* theory; factual predicate not proven;
SECRETARY OF HEALTH AND * medically-inappropriate time frame.
HUMAN SERVICES, *
*
Respondent. *
*
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Clifford J. Shoemaker, Vienna, Virginia, for petitioner.

Ann D. Martin, Senior Trial Attorney, Torts Branch, Civil Division,
Department of Justice, with whom were Stuart F. Delery, Assistant Attorney
General, Rupa Bhattacharyya, Director, Vincent J. Matanoski, Deputy Director, and
Catharine E. Reeves, Assistant Director, all of Washington, D.C., for respondent.

OPINION AND ORDER

WOLSKI, Judge.

Petitioner Tiffany Bast has moved for review of then-Chief Special Master
Patricia Campbell-Smith’s decision that petitioner is not entitled to compensation
under the National Vaccine Injury Compensation Program, 42 U.S.C. §§ 300aa-10–

†
At petitioner’s request, her minor daughter’s name has been replaced with
initials. The opinion is reissued for publication with some minor, non-substantive
corrections.
300aa-34 (Vaccine Act or Act). 1 The petition, which was filed by Mrs. Bast on behalf
of her daughter, [M.S.B], on October 1, 2001, contended that [M.S.B.] suffered
“seizures, encephalopathy, and liver damage” as a result of the hepatitis B vaccine
administered on October 23, 1998. Pet. at 1–2. In later filings, it was alleged that
the inactivated polio, diphtheria-tetanus-acellular pertussis, Haemophilus
influenzae type B, and hepatitis B vaccines that [M.S.B.] received on December 4,
1998, caused her neurodevelopmental disorders and epilepsy. Pet’r’s Ex. 51 at 4;
Pet’r’s Post-Hr’g Br. at 4. Petitioner raised three objections to the Chief Special
Master’s decision denying compensation, arguing that her decision was arbitrary
and capricious and failed to follow the standards of Althen v. Sec’y of Health &
Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Pet’r’s Mot. for Rev. at 2. For the
reasons stated below, the Court DENIES petitioner’s motion and SUSTAINS the
decision of the Chief Special Master.

I. BACKGROUND

A. The Vaccinations and Medical History 2

[M.S.B.] was born on October 11, 1998, after a complicated pregnancy. Pet’r’s
Ex. 12 at 35. On March 27, 1998, at the beginning of the second trimester, Mrs.
Bast was involved in an automobile accident. Pet’r’s Ex. 4 at 2; Pet’r’s Ex. 12 at 25.
Following this incident, Mrs. Bast suffered from migraine headaches, for which she
was prescribed Vicodin. Pet’r’s Ex. 4 at 2; Pet’r’s Ex. 12 at 25. Petitioner also
contracted a respiratory infection during the second trimester, and was given
antibiotics and prescription strength Robitussin AC to treat the infection and a
cough that she developed. Pet’r’s Ex. 4 at 3. In the third trimester, Mrs. Bast fell
and tore the round ligament of her uterus. Pet’r’s Ex. 19 at 217. She was placed on
bed rest and was again prescribed Vicodin. Id.

[M.S.B.] was carried to full-term, and weighed eight pounds and thirteen
ounces at birth. Pet’r’s Ex. 12 at 29. During labor, [M.S.B.]’s umbilical cord became
wrapped tightly around her neck and had to be removed at birth. Pet’r’s Ex. 13 at
10, 20. When she was delivered, [M.S.B.]’s Apgar scores were 8 and 9, Pet’r’s Ex.
12 at 15, and her newborn exam was normal, see Pet’r’s Ex. 13 at 20. [M.S.B.] was
discharged from the hospital the day after she was born. Pet’r’s Ex. 12 at 16.

[M.S.B.] received her first hepatitis B vaccine in an office visit with her
pediatrician, Dr. Peri Gunay, M.D., twelve days after she was born. See Pet’r’s Ex.

1 The Honorable Patricia Campbell-Smith has since become the Chief Judge of our
court. This opinion will refer to her using the position she held when the decision
was issued.
2 The background facts are primarily drawn from the Chief Special Master’s

opinion, with any relevant disputes concerning these facts specifically noted.
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23 at 9. At this visit, Dr. Gunay noted slackness in her right hip, but no “clicks or
clunks,” as would be indicative of a hip joint problem. Id. On November 4, 1998,
[M.S.B.] returned to see Dr. Gunay for a sick visit, presenting with slight nasal
congestion, occasional vomiting, and mucous that had been draining from her right
eye for one day. Id. at 6. At this visit, [M.S.B.] did not have a fever, and Dr. Gunay
determined that she had conjunctivitis in her right eye. See id.

[M.S.B.] returned to Dr. Gunay’s office on December 4, 1998, for a well-child
visit. Pet’r’s Ex. 23 at 9. At this visit [M.S.B.] presented with a mild cold. See id.
Although flattening of the back of [M.S.B.]’s head was noted during her visit, no
concerns about her growth and development were noted. See id. [M.S.B.] received
the vaccinations that petitioner contends caused [M.S.B.]’s subsequent medical
problems during this visit --- specifically, her first inactivated polio (IPV),
diphtheria and tetanus toxoid with acellular pertussis (DTaP), and Haemophilus
influenzae type B (Hib) vaccines, and her second hepatitis B vaccine. See id.

At some point after this visit, [M.S.B.] developed more serious cold
symptoms. There is some dispute, however, as to the timing of the onset of these
symptoms. [M.S.B.]’s parents filed a joint affidavit contending that [M.S.B.]
developed a “pretty bad” upper respiratory infection “within ten days of the
vaccine,” requiring a visit to the pediatrician. Pet’r’s Ex. 25 at 2. Based on this
timing, [M.S.B.] would have visited the pediatrician’s office on or about December
14, 1998. However, a review of [M.S.B.]’s contemporaneous medical records
indicates that [M.S.B.] did not return to the pediatrician’s office until December 30,
1998, at which time she presented with cold symptoms that were noted as having
been present for one week. Pet’r’s Ex. 23 at 6.

There is also some dispute as to the timing of [M.S.B.]’s first seizures.
[M.S.B.]’s medical records reflect that on January 11, 1999, Mrs. Bast called the
pediatrician’s office to report that [M.S.B.] had “three brief spells involving
stiffening, eye deviation [and] rhythmic movements of extrem[ities],” each of which
lasted a few seconds. Pet’r’s Ex. 23 at 6. Doctor Gunay indicated that [M.S.B.] was
to be seen “ASAP,” and he examined [M.S.B.] later that day. Id. The notes from Dr.
Gunay’s examination indicate episodes of “seizures” that involved an “altered
mental status,” “eye deviations,” and “twitching movements” over the “past five
days.” Id. But in their affidavits, [M.S.B.]’s parents recalled that [M.S.B.] began to
have “little” tics roughly one week after her upper respiratory infection and the
associated trip to the pediatrician, which was “less than three weeks after her
immunizations.” Pet’r’s Ex. 25 at 2. This would date the onset of these symptoms
on or about December 21, 1998. The Basts further declared that these tics turned
into grand mal seizures “[b]y January 4, 1999.” Id. 3

3 The Chief Special Master accorded more weight to the contemporaneous medical
records, citing the diligence of [M.S.B.]’s parents in seeking treatment and the
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 At the January 11 visit, Dr. Gunay made note of [M.S.B.]’s recent upper
respiratory infection, in which she had nasal congestion and cough, but no fever.
Pet’r’s Ex. 23 at 6. He also consulted with Dr. Stuart Stein, M.D., a pediatric
neurologist, and concluded that [M.S.B.] should start anti-seizure medication only if
the frequency of her seizures increased. See Pet’r’s Ex. 19 at 216. [M.S.B.]’s seizure
activity increased the next day to about four or five, typically occurring after she
was fed. Id. Doctor Gunay examined [M.S.B.] again on January 13, 1999, and
started [M.S.B.] on the anticonvulsant. Id. At this visit, Dr. Gunay also ordered an
electroencephalogram (EEG) for [M.S.B.]. Id. at 210. The EEG was performed the
following day, and the results were “markedly abnormal” due to “very active
epileptiform potentials . . . in the right frontal central area.” Pet’r’s Ex. 1 at 165.

Doctor Stein examined [M.S.B.] on January 15, 1999, noting that she
appeared to have a seizure disorder. Pet’r’s Ex. 19 at 214. [M.S.B.] exhibited signs
of weakness and diminished muscle tone, Pet’r’s Ex. 15 at 93, and Dr. Stein
indicated that she may have a “possible metabolic disorder” or a “possible post
infectious encephalopathy,” Pet’r’s Ex. 19 at 214. While at Dr. Stein’s office,
[M.S.B.] had two or three seizure episodes of greater duration than usual. See id. at
214; Pet’r’s Ex. 15 at 93. Doctor Stein recommended that [M.S.B.] be admitted to
the hospital for treatment and that she receive a computed tomography (CT) scan in
order to begin to rule out some of the possible causes of her seizures --- in particular,
factors such as a brain abnormality, a metabolic disorder, an infectious process,
Guillain-Barré, or demyelinating diseases. See Pet’r’s Ex. 19 at 218.

[M.S.B.] was admitted to the hospital where she was started on the
anticonvulsant Dilantin. See Pet’r’s Ex. 23 at 166. The results of [M.S.B.]’s CT scan
and testing of her cerebrospinal fluid ruled out a post-infectious encephalopathy,
but indicated possible abnormalities in her brain formation. See Pet’r’s Ex. 1 at
162. Based on [M.S.B.]’s lab results, which indicated insufficient carnitine, Dr.
Stein questioned whether [M.S.B.] had an energy metabolic disorder. See Pet’r’s Ex.
23 at 167. [M.S.B.] also exhibited symptoms of “Todd’s paralysis” while in the
hospital --- a condition marked by temporary paralysis following seizures. See id. at
162, 166.

Before being discharged from the hospital on January 17, 1999, [M.S.B.] was
diagnosed with a seizure disorder and an absent corpus callosum. See Pet’r’s Ex. 19
at 212. She continued to take both Dilantin and Phenobarbital upon release from
the hospital in an attempt to control her seizures. See Pet’r’s Ex. 23 at 162. Doctor
Stein evaluated [M.S.B.] a few days later, and noted that at that time, he thought

thorough documentation of her medical appointments. See Bast ex rel. Bast v. Sec’y
of Health & Human Servs., No. 01-565V, 2012 WL 6858040, at *8–9 (Fed. Cl. Sp.
Mstr. Dec. 20, 2012).
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she had “an idiopathic seizure disorder,” but that the possibility that she had “a
disorder of energy metabolism” should also be considered. See Pet’r’s Ex. 23 at 167.
He started [M.S.B.] on a carnitine treatment to address the possible energy
metabolism disorder, but [M.S.B.]’s seizure activity did not decrease in response to
this treatment --- instead increasing to about twenty to thirty seizures per day. See
Pet’r’s Ex. 23 at 162–63, 168.

On January 29, 1999, [M.S.B.] was hospitalized again, this time for two days.
See Pet’r’s Ex. 11 at 90, 98. While at the hospital, a magnetic resonance imaging
(MRI) scan was taken of [M.S.B.]’s brain, and the results showed a brain
abnormality --- “[f]ocal thickening and irregularity of the right frontal lobe gray
matter” --- which suggested a “focal migrational anomaly.” See Pet’r’s Ex. 1 at 141–
42. This type of anomaly is a birth defect caused by the abnormal migration of
neurons during brain and nervous system development. See Bast, 2012 WL
6858040, at *18. The MRI report also indicated that [M.S.B.] had a “[t]iny left
frontal lobe subdural hematoma,” see Pet’r’s Ex. 1 at 142, which may have been
caused by her vacuum extraction at birth, Pet’r’s Ex. 11 at 97.

On February 5, 1999, [M.S.B.] was examined by Dr. Raman Sanker, M.D.,
another pediatric neurologist. Pet’r’s Ex. 23 at 162–63. At this visit, Dr. Sanker
noted that [M.S.B.]’s head circumference was forty-one centimeters, which put her
in the fiftieth percentile for her age, and that her “fontanelle anteriorly is soft and
open.” Id. at 163. He also noted that [M.S.B.] had a right gaze preference and
preferred to lie to the right side, and that her face appeared to be intermittently
weak on the left side. Id. Another EEG was ordered that month, and the results
were markedly abnormal. Id. at 163–64.

[M.S.B.] was referred to the Advanced Epilepsy Management Clinic at the
University of California, Irvine, where on February 15, 1999, she was seen by Dr.
Tallie Baram, M.D., a pediatric neurologist. See Pet’r’s Ex. 1 at 168; Pet’r’s Ex. 23
at 159. After another EEG, which showed a “very irritative encephalopathy,” Dr.
Baram concluded that [M.S.B.] had an “abnormal brain, likely a [neuronal]
migration abnormality, associated with a multifocal, irritative cortex” and identified
her condition as severe multifocal epilepsy. See Pet’r’s Ex. 23 at 160. Doctor Baram
also noted that [M.S.B.] had infantile spasms, and recommended that she be treated
for the spasms before addressing their source. See id. Doctor Baram recommended
that [M.S.B.] be given adrenocorticotropic hormone (ACTH) for her infantile
spasms, and that her other medications be limited to phenobarbital and pyridoxine,
a form of vitamin B6. See id. at 160–61.

Shortly thereafter, [M.S.B.] was examined by Dr. Keith DeOrio, M.D., a
family physician who offers alternative healing therapies. See Pet’r’s Ex. 36 at 2.
As of that time, Dr. DeOrio noted that [M.S.B.] was taking phenobarbital, had
elevated liver enzymes, and was having approximately fifty-five seizures per day.

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Id. On March 1, 1999, [M.S.B.] had a follow-up appointment with Dr. Baram, who
again recommended ACTH, noting that based on her prior evaluation of [M.S.B.], it
did not appear that she had “a mitochondrial disorder or any other disorders which
would preclude her from starting on ACTH.” See Pet’r’s Ex. 23 at 157.

At a follow-up appointment approximately three weeks later, on March 22,
1999, Dr. Baram noted that [M.S.B.] had “responded beautifully” to a “two-week
dose of ACTH, at a high dose.” See id. at 155. Doctor Baram indicated that
[M.S.B.]’s infantile spasms were gone, that her EEG testing had improved, and that
[M.S.B.] showed improvements in alertness and her ability to visually track and
hear. See id. [M.S.B.] was experiencing an emerging focal seizure disorder, which
Dr. Baram indicated would be treated with topiramate. Id. [M.S.B.] also
underwent testing for any infection process and the results were negative. See
Pet’r’s Ex. 1 at 121–25.

[M.S.B.]’s medical records indicate that she was tested for a variety of
conditions beginning in July of 1999. Doctor Stein examined [M.S.B.] on July 2 and
indicated that he was unsure whether [M.S.B.] had a metabolic disorder or whether
she was acidotic as a result of her frequent seizures. See Pet’r’s Ex. 1 at 105.
Doctor Stein ordered metabolic testing, and the results of the tests were normal,
except for high levels of lactic acid in her urine. See id. at 95. In August of 1999,
Dr. Sidney Gospe, M.D., another pediatric neurologist, conducted additional testing
and concluded that [M.S.B.] did not have pyridoxine-dependent seizures. Id. at 54–
55. Instead, he attributed the seizures to “a developmental brain anomaly,” and
recommended another MRI to examine this possibility. Id. at 55. Doctor Gospe also
recommended that [M.S.B.] continue to receive all regular vaccinations, indicating
that her prior evaluations failed to reveal any specific metabolic abnormalities and
that he did not believe that her epileptic encephalopathy was related to her
previous hepatitis immunization. Id. He did, however, note that [M.S.B.] showed
evidence of precocious puberty --- namely, bilateral breast development --- which
may be attributable to “exogenous estrogen ingestion” or medication that she had
taken. Id.

A brain scan in September of 1999 showed a mild decrease in the maturation
of [M.S.B.]’s brain’s white matter and a delay in the maturation of her corpus
callosum, indicating abnormal brain development. See Pet’r’s Ex. 1 at 43–44. The
issue of whether [M.S.B.] had a mitochondrial disorder was evaluated, but the
results were inconclusive for any known mitochondrial disorders. See id. at 33–34.
Based on the test results, which showed that [M.S.B.] had elevated blood and urine
lactate levels and elevated glutaric acid, Dr. Stein started [M.S.B.] on a cocktail of
vitamins for mitochondrial disorders. See id. at 34.

Testing of [M.S.B.]’s mitochondrial DNA revealed a G15257A point mutation,
which was interpreted as the mildest primary mutation of Leber’s hereditary optic

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neuropathy (LHON), a condition characterized by degeneration of the optic nerve
and progressive vision loss. Pet’r’s Ex. 1 at 36. [M.S.B.] was examined by a
pediatric ophthalmologist, Dr. Florencio Ching, M.D., who did not report any
evidence of the expression of LHON. Id. at 38. In October of 1999, [M.S.B.] had a
normal cardiac evaluation and the pediatric cardiologist concluded that it was
unlikely that [M.S.B.] had a disorder of energy metabolism. See Pet’r’s Ex. 23 at
114–15. [M.S.B.] was also tested for allergies, and the results showed that she had
“moderate” allergies to cow’s milk, soybeans, and peanuts. See Pet’r’s Ex. 1 at 20–
25.

Doctor Stein examined [M.S.B.] shortly after her first birthday (a visit which
appears to be her last documented appointment with a pediatric neurologist). See
Pet’r’s Ex. 1 at 17–19. At this time, [M.S.B.] was no longer taking “Topamax and all
usual anticonvulsant medications” or the mitochondrial cocktail she had been
prescribed. Id. at 17–18. Instead, she was only taking vitamin B6 and homeopathic
medications. Id. at 17. Doctor Stein suggested that a mitochondrial disorder might
be causing [M.S.B.]’s symptoms and recommended further investigation of this
possibility. Id. at 18–19. As of May 30, 2000, Dr. DeOrio reported that [M.S.B.]
experienced “upwards of 55 seizures per day, along with neuromuscular weakness
and poor attention and focusing abilities.” Pet’r’s Ex. 36 at 24. In December of
2000, at which time [M.S.B.] was twenty-six months old, her occupational therapist
determined that she fell into the three- to nine-month age range for various
evaluation categories. See Pet’r’s Ex. 19 at 256. In February of 2002, Dr. DeOrio
offered a written opinion that [M.S.B.]’s conjunctivitis in November of 1998 had
been a reaction to her first hepatitis B vaccine. 4 See Pet’r’s Ex. 36 at 31. He relied,
in part, on previous test results which showed extremely elevated liver enzymes ---
a possible indication of hepatitis. See id.

In May of 2003, when [M.S.B.] was four and one-half years old, she
underwent an endocrinology evaluation for precocious puberty. See Pet’r’s Ex. 41 at
44–47. The endocrinologist found “no other chronic conditions other than the
seizure disorder,” id. at 44, noting that it was “not uncommon for children with
seizure disorders or central nervous system lesions to present with early pubertal
changes,” id. at 46. At an evaluation more than one year later in July, 2004, a
previous chemistry panel was noted to have been “unremarkable,” and [M.S.B.]’s
liver enzymes were specifically mentioned. Id. at 25. It was also noted at that time
that [M.S.B.] had a medical history “significant for a seizure disorder and an as yet
uncharacterized autoimmune disorder.” Id. at 24. No medical records appear to
have been filed which diagnose [M.S.B.] with an autoimmune condition.

4 Doctor DeOrio attributed [M.S.B.]’s “brain damage” to “the Thimerosal in the
vaccines she received.” Pet’r’s Ex. 36 at 31.

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 [M.S.B.] continues to have daily seizures, and there is no record that she has
taken any medications to control her seizures since she was one year old. See Pet’r’s
Ex. 55 at 5, 34; Pet’r’s Ex. 1 at 17–19 (evaluation by Dr. Stein in 1999 indicating
that [M.S.B.] had stopped taking anticonvulsant medications). Nothing in the
record suggests that [M.S.B.] has been evaluated by a neurologist since her seizure
medication was discontinued. In July of 2006, Dr. DeOrio summarized [M.S.B.]’s
medical condition as “a severe seizure disorder resulting from a hepatitis B vaccine
given at three months of age,” and also indicated that [M.S.B.] experienced heavy
metal poisoning from the mercury preservative Thimerosal. 5 Pet’r’s Ex. 45 at 324.
[M.S.B.] is wheelchair-bound and remains significantly developmentally delayed,
although the magnitude of the delay has not been formally evaluated. See Pet’r’s
Ex. 55 at 31–32.

B. The Petition and Hearing Before the Chief Special Master

[M.S.B.]’s mother filed a petition for compensation on [M.S.B.]’s behalf under
the National Vaccine Injury Compensation Program on October 1, 2001, claiming
that the administration of [M.S.B.]’s hepatitis B vaccine on October 23, 1998,
caused [M.S.B.] to suffer from seizures, encephalopathy, and liver damage. Pet. at
1–2. Petitioner subsequently filed medical records from [M.S.B.]’s treating
physicians and hospital visits. See Pet’r’s Exs. 1–45, 50, 53–58, 93–94. Pursuant to
Vaccine Rule 4(c) of the Rules of the United States Court of Federal Claims (RCFC),
the Secretary of Health and Human Services (respondent) filed a report on the
petition for vaccine compensation, arguing that petitioner failed to demonstrate by
a preponderance of the evidence that [M.S.B.]’s vaccinations caused her health
problems. Resp’t’s Rule 4(c) Resp. at 10–11. The Secretary contended that
petitioner failed to put forth a reputable medical or scientific theory persuasively
connecting the vaccinations to the injury, and noted that the medical records filed
by petitioner did not contain any significant opinions regarding the cause of
[M.S.B.]’s injuries. See id. The report also posited that petitioner failed to show a
logical sequence of cause and effect between the vaccine and the injury. See id.

Following the filing of respondent’s report, petitioner filed expert reports
from Dr. Richard Frye, a pediatric neurologist; Dr. Mark Geier, an obstetrician with
a doctoral degree in genetics; and Dr. Joseph Bellanti, an immunologist. See Pet’r’s
Exs. 51 (Frye), 59 (Frye, Supplemental Report), 46 (Bellanti), 48 (Geier). At the
hearing before the Chief Special Master, and in her post-hearing arguments,
petitioner relied solely on Dr. Frye’s opinion and the medical literature filed in

5 Petitioner did not rely upon Dr. DeOrio’s offered opinion regarding heavy metal
toxicity at the hearing or in post-hearing briefing. Bast, 2012 WL 6858040, at *17.

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support thereof; for this reason, the Chief Special Master focused on the opinion
offered by Dr. Frye in her decision. See Bast, 2012 WL 6858040, at *2. 6

Doctor Frye received his M.D. and a Ph.D. in physiology and biophysics from
Georgetown University. Pet’r’s Ex. 52. He is board certified in general pediatrics
and in neurology, with a special competence in child neurology. Id. In his original
expert report, Dr. Frye offered two theories of causation: that vaccines can induce
autoimmunity; and that vaccines can induce or exacerbate mitochondrial
dysfunction in individuals with mitochondrial disorders by increasing oxidative
stress. Pet’r’s Ex. 51 at 3–6. Incorporated in the second theory was Dr. Frye’s belief
that “genetic studies have identified a mutation in the SCNA1 sodium channel
gene” of [M.S.B.]. Id. at 3. He explained that this mutation was associated with
“vaccine associated encephalopathy with refractory seizures and intellectual
impairment.” Id. Doctor Frye concluded that in [M.S.B.]’s case, “it is clear that
both an environmental (i.e., vaccine) and metabolic factor (i.e., mitochondrial
dysfunction), interacted with the SCNA1 mutation to unmask a severe refractory
epilepsy.” Id. at 6. Subsequently, after it came to Dr. Frye’s attention that there
was no evidence that [M.S.B.] had the SCNA1 mutation or had ever been tested for
it, Dr. Frye submitted a supplemental expert report in which the references to this
mutation were removed. See Pet’r’s Ex. 59; Bast, 2012 WL 6858040, at *2 n.7.
Otherwise, Doctor Frye’s report was unchanged. See Pet’r’s Exs. 51, 59.

Under his first theory, Dr. Frye posits that vaccine-induced autoimmunity
and over-activation of the immune system can cause the types of symptoms that
[M.S.B.] experienced, and may be related to several neurological disorders. See
Pet’r’s Ex. 59 at 3–4. Doctor Frye’s second theory of causation is that [M.S.B.] had
an underlying mitochondrial disorder, 7 which made it difficult for her mitochondria
to handle reactive oxygen species (ROS), and which ultimately caused her seizures
and neurological damage. See id. at 4–6. According to Dr. Frye’s theory, if
mitochondria are not functioning properly, they may not be able to properly process
oxidants, leading to an excess of ROS within the cell. Id. If this occurs, the
oxidative stress caused by the ROS can lead to metabolic decompensation and a
neurodegenerative event, such as the seizures and developmental delays suffered by

6The Chief Special Master noted that Dr. Geier’s license to practice medicine in
Maryland has been suspended due to requirements of public health, safety, and
welfare, and that six other states subsequently suspended his license to practice
medicine pending the outcome of the Maryland disciplinary proceeding. Bast, 2012
WL 6858040, at *1 n.5.
7
Mitochondria are organelles within cells that produce energy; if they do not
function properly, various organs in the body may be adversely affected. See
Resp’t’s Ex. A at 4; Resp’t’s Ex. C at 2; Tr. of Oral Arg. Before Sp. Mstr. (Dec. 6,
2010) at 18.

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[M.S.B.]. Id. Doctor Frye contends that [M.S.B.]’s December 4, 1998 vaccinations
activated her immune system and caused an increase in oxidative stress --- to which
she was particularly susceptible due to having a mitochondrial disorder --- and
ultimately caused the damage that led to both her seizures and her other
neurodevelopmental disorders. Id.

In response, respondent filed two expert reports of her own: from Dr. Gerald
Raymond, an M.D. and expert in pediatric neurology and neurogenetics; and Dr.
Dean Jones, a Ph.D. and expert in mitochondrial oxidative stress. See Resp’t’s Exs.
A–D. Respondent also filed medical literature in support of her position. See
Resp’t’s Exs. E–H. Doctor Raymond received his M.D. from the University of
Connecticut, and served a residency in pediatrics at Johns Hopkins Hospital and a
residency in neurology at Massachusetts General Hospital. Resp’t’s Ex. B. He is
currently a professor of neurology at Johns Hopkins University and is board
certified in pediatrics, clinical genetics, and neurology, with a special qualification
in child neurology. Resp’t’s Ex. B. Doctor Jones received a Ph.D. in biochemistry
from Oregon Health Sciences University, and is currently a professor in the
Department of Biochemistry at Emory University School of Medicine. Resp’t’s Ex.
D. Doctor Jones has published between 150 and 200 papers on oxidative stress and
has conducted numerous lectures on this topic. See id.; Tr. of Oral Arg. Before Sp.
Mstr. (Dec. 6, 2010) (Sp. Mstr. Tr.) at 207–08.

Doctor Raymond’s report discusses the fact that [M.S.B.] appears to have the
mitochondrial point-mutation associated with LHON, but emphasizes that [M.S.B.]
has neither manifested symptoms of LHON, nor been shown to have any other
mitochondrial defect which might lead to the chain of events described by Dr. Frye.
See Resp’t’s Ex. A. Although he notes that the diagnostic criteria for mitochondrial
disorders are quite broad and the possibility that [M.S.B.] has a mitochondrial
disorder “cannot be excluded,” Dr. Raymond explains that a mitochondrial disorder
has “not been substantiated as a cause of her epileptic syndrome.” Id. at 6. Doctor
Raymond indicates that [M.S.B.] would be listed in the “possible to probable range”
for a mitochondrial disorder, but then goes on to explain that “nearly any individual
with a neurologic condition would be so listed.” Id. In his report, Dr. Raymond also
discusses the literature relied upon by Dr. Frye and rejects both of Dr. Frye’s
proposed theories of causation. See id. at 6–7. With respect to the autoimmunity
theory, Dr. Raymond explains that Dr. Frye did not identify any medical “literature
that demonstrates autoantibodies to any portion of the mitochondria as a result of
immunization.” Id. at 6. Doctor Raymond also rejects Dr. Frye’s contention that
oxidative stress could have caused [M.S.B.]’s medical problems, stating that “there
is no clinical evidence that vaccines may affect individuals with mitochondrial
disease” in the manner proposed by Dr. Frye, and that even if this were possible,
[M.S.B.]’s upper respiratory infection would be “the more suitable trigger” for the
injury. See id. at 7.

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 Respondent’s other expert, Dr. Jones, submitted a report which also criticizes
Dr. Frye’s theories of causation. See Resp’t’s Ex. C. Doctor Jones’s report primarily
focuses on Dr. Frye’s theory of oxidative stress, rejecting that theory as “not sound,”
and as reflecting “some degree of obfuscation.” See id. at 4. Doctor Jones explains
that oxidants are essential for normal cell signaling, and opines that the scientific
evidence does not support the proposition that vaccines can stimulate enough
oxidation to cause the symptoms that [M.S.B.] experienced in the time frame in
which her symptoms occurred. See id. at 4–5. Doctor Jones is also critical of the
literature relied upon by Dr. Frye, noting that many of the studies are about
responses to infections, which are “not equivalent” to those following vaccinations.
See id. With respect to Dr. Frye’s autoimmune theory, Dr. Jones rejects the theory
as “not supported by evidence that [M.S.B.] had symptoms or laboratory tests
consistent with an autoimmune response activated by vaccination.” Id. at 5.

On December 6, 2010, the Chief Special Master held a hearing in this
matter. Doctor Frye, testifying for petitioner, was accepted as an expert in child
neurology and pediatrics. Sp. Mstr. Tr. at 11. At the hearing, he focused on
oxidative stress as the causation mechanism, indicating that his theory of causation
does not depend on the autoimmunity theory. See Sp. Mstr. Tr. at 109. 8 Doctor
Frye provided detailed testimony regarding the petitioner’s theory of oxidative
stress, and stated that, in his expert opinion, and to a reasonable medical
probability, the vaccines that [M.S.B.] received caused her injuries. See id. at 12–
22. Explaining the oxidative stress theory, Dr. Frye posited that vaccines can cause
an increase in oxidative stress, which can damage the mitochondria --- particularly
when the mitochondria contain a mutation affecting the electron transport chain ---
and that this can cause an excess of ROS, which in turn, causes more damage to the
mitochondria. See id. at 13. As Dr. Frye explains it, “the vaccine would activate
immune processes, which through cytokine and other processes would increase
reactive oxygen species.” Id. at 49. His theory is that this “vicious cycle” can lead to
metabolic decompensation and a neurodegenerative event. See id. Dr. Frye also
discussed three potential “pathways” through which this chain of events could
occur. Id. at 52–60. 9

8 The autoimmune theory was also not discussed in petitioner’s post-hearing brief.
See Pet’r’s Post-Hr’g Br. Although Dr. DeOrio, a family practitioner with no
apparent expertise in immunology, made conclusory statements that [M.S.B.] has
an autoimmune disorder, the basis for this contention is unexplained. See Pet’r’s
Ex. 36 at 27; Pet’r’s Ex. 45 at 324. Moreover, Dr. Bellanti, petitioner’s expert
immunologist, refrained from concluding that [M.S.B.] had an autoimmune
condition. See Pet’r’s Ex. 46 at 10.
9 These “pathways” were an immune response in the brain to excess ROS, a
mitochondrial dysfunction in which enough energy is not produced to support the
brain, and the diversion of antioxidants from the brain to compensate for the
reactive oxygen species. See Sp. Mstr. Tr. at 59–60.
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 During the hearing, Dr. Frye provided an overview of the medical literature
upon which he relies in support of his theory of oxidative stress. See Sp. Mstr. Tr.
at 24–43. He also explained in detail the basis for his opinion that [M.S.B.] has a
mitochondrial disorder, discussing the diagnostic criteria for mitochondrial
disorders set forth in an article co-authored by Dr. F.P. Bernier. Id. at 31–34; see
also Pet’r’s Ex. 63 (F.P. Bernier et al., Diagnostic Criteria for Respiratory Chain
Disorders in Adults and Children, 59 Neurology 1406 (2002)) (Bernier).
Specifically, Dr. Frye opined that under that article’s classification system, [M.S.B.]
has a “probable” mitochondrial disorder because she meets at least one of the
“major” criteria of the article --- the clinical criterion requiring an unexplained
combination of multi-systemic symptoms in at least three organ systems (in
[M.S.B.]’s case, the neurologic, hepatic, and endocrine systems) --- and two of the
“minor” criteria, the molecular and the metabolic. See Sp. Mstr. Tr. at 33–34; Pet’r’s
Ex. 63 at 2. 10 Doctor Frye identified [M.S.B.]’s mitochondrial DNA mutation and
her exhibition of metabolic indicators of impaired respiratory chain function (in the
form of lactate elevation) as fulfilling two of the minor criteria. See Sp. Mstr. Tr. at
33–34. In addition, Dr. Frye discussed the timing of the onset of [M.S.B.]’s
symptoms and explained that, in his opinion, the timing of her symptoms is
consistent with the expected timing under his theory of causation and the medical
literature filed in support thereof --- two to four weeks from the date of vaccination.
Id. at 71.

On cross-examination, Dr. Frye was questioned at length about the literature
upon which he relied in forming his opinion regarding the cause of [M.S.B.]’s
medical problems. See, e.g., Sp. Mstr. Tr. at 60–78. The respondent also challenged
Dr. Frye’s focus on the vaccines that [M.S.B.] received as the cause of her injuries,
rather than her subsequent upper respiratory infection. See id. at 117–18. In

10 Under the Bernier criteria, one is defined as having a “probable” mitochondrial
disorder when “either one major plus one minor criterion or at least three minor
criteria” are met. Pet’r’s Ex. 63 at 2. In [M.S.B.]’s case, Dr. Frye contends that one
major criterion and two minor criteria are met. The majority of the discussion by
the experts and the Chief Special Master focused on one of the major criteria --- a
clinical mitochondrial cytopathy --- and its three conditions. The three conditions,
which petitioner contends [M.S.B.] meets, are: (1) an unexplained combination of
multi-systemic symptoms involving at least three organ systems; (2) a progressive
clinical course with episodes of exacerbation; and (3) that other possible metabolic
or nonmetabolic disorders have been excluded by appropriate testing. See id.; Sp.
Mstr. Tr. at 31–34.

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response, Dr. Frye stated that he thought that the “multiple vaccines that she
received probably caused more activation to the immune system than a . . . mild
viral infection would have.” Id. at 118. The Chief Special Master inquired as to Dr.
Frye’s assessment that [M.S.B.] experienced a developmental “regression,” eliciting
the explanation that he used the term “regression” to include the mere failure to
acquire additional skills, rather than its customary meaning that previously
acquired skills were lost. 11 See id. at 121–22.

Doctors Raymond and Jones testified as expert witnesses for respondent,
with the former found to be qualified as an expert in neurology and genetics and the
latter found to be qualified as an expert in the field of oxidative stress. Sp. Mstr.
Tr. at 130, 208. Doctor Raymond testified that, in his opinion, [M.S.B.]’s December
4, 1998 vaccinations did not cause her current neurologic condition. Id. at 131.
Instead, it was his opinion that [M.S.B.] has an epileptic syndrome, and that “there
is very limited evidence that she has a mitochondrial disorder” --- something about
which he “would not be overly concerned” were he [M.S.B.]’s treating physician. See
id. He opined that there was “limited evidence of multisystem disorder” and “really
no evidence” of episodes of regression, despite Dr. Frye’s testimony to the contrary.
See id. Noting that [M.S.B.] does have the mutation associated with LHON, but not
LHON itself, Dr. Raymond reiterated that he is “not convinced that we have enough
evidence that she has a mitochondrial disorder.” See id. at 131–32.

In explaining his opinion that there was insufficient evidence to conclude that
[M.S.B.] has a mitochondrial disorder, Dr. Raymond discussed the Bernier criteria
and how [M.S.B.]’s symptoms fit within that framework. See id. at 134–152. Doctor
Raymond indicated that he would look for more consistently abnormal lab readings,
in contrast to [M.S.B.]’s lab results, which he considered to be fairly normal, with a
few elevations. See id. at 134. For example, Dr. Raymond testified that testing
performed in January of 1999 revealed lactate levels on the “high end of normal,” a
pyruvate level that was normal, a normal amino acid profile, an “essentially”
normal cerebral spinal fluid examination, normal aldolase, normal ketones in
[M.S.B.]’s blood, and normal levels of the enzymes alanine aminotransferase (ALT)
and aspartate aminotransferase (AST). See id. at 135–38. Testing in February of
1999 indicated abnormal liver functioning, but Dr. Raymond testified that the
anticonvulsants that [M.S.B.] was taking are known to “rev up the liver function
system,” the result of which would be an elevated liver function test. See id. at 139.

During his testimony, Dr. Raymond also called into question whether
[M.S.B.] had the type of multi-systemic symptoms contemplated by the Bernier
article. See id. at 145. While he did not dispute that [M.S.B.] had neurologic

11 Doctor Frye stated in his expert report that [M.S.B.]’s case is similar to another
case “in which immunizations triggered developmental regression, brain injury and
the subsequent development of a seizure disorder.” Pet’r’s Ex. 59 at 6.

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symptoms, Dr. Raymond noted that he did not think that she had hepatic or
endocrine abnormalities that would be typical of a mitochondrial disorder, and that
with respect to her gastrointestinal system, constipation was “so common in
children with intellectual disabilities” that he would hesitate to consider that a sign
of a multisystem abnormality. See id. at 145, 147. Doctor Raymond also indicated
that the Bernier criteria are meant to help determine which patients are
appropriate candidates to be tested for mitochondrial disorders via muscle biopsies,
and that he thinks that the authors were “trying to lower the criteria” to expand the
use of these biopsies. See id. at 146. Moreover, Dr. Raymond disputed that [M.S.B.]
had the type of “progressive clinical course with episodes of exacerbation”
contemplated by the article, see id. at 147, noting that, by definition, a seizure
disorder involves periods of exacerbation, see id. at 150. Instead, he contended that
the criteria encompassed mitochondrial disease that was progressive in nature,
although allowing for periods of recovery. See id. at 150–51. The fact that other
possible disorders had not been excluded through appropriate testing, despite
substantial developments in the ability to do so in recent years, was also mentioned
by Dr. Raymond as a reason the Bernier criteria were not met in [M.S.B.]’s case.
See id. at 151. He later added that [M.S.B.] also had “unremarkable” MRIs, which
he would not have expected if she were suffering from neurodegeneration. See id. at
167–68.

On cross-examination, Dr. Raymond was asked about [M.S.B.]’s 2008 alanine
to lysine ratio of 3.4, which Dr. Raymond conceded was significantly outside the
expected range of 1.5 to 2.5. See Sp. Mstr. Tr. at 174. Doctor Raymond indicated,
however, that the test did not involve a fasting sample, which could have skewed
the results. See id. He was also asked about [M.S.B.]’s 2008 lactate level of 87.5,
which was well above the expected upper-limit of 19.8. See id. at 174–75; Pet’r’s Ex.
50 at 18. Doctor Raymond responded that he believed that the lactate level was
artificially high, likely due to the mishandling of the sample, see Sp. Mstr. Tr. at
175–76, and that he did not think that this “outrageous lactate” level “would
actually be consistent with anyone’s condition,” id. at 180, 192. Petitioner’s counsel
also asked Dr. Raymond to apply to [M.S.B.]’s case the criteria for diagnosing
mitochondrial disease advanced in an article co-authored by Dr. E. Morava, which
was included among respondent’s exhibits. See id. at 176–81; Resp’t’s Ex. H (E.
Morava et al., Mitochondrial Disease Criteria: Diagnostic Applications in Children,
67 Neurology 1823 (2006)). Using the point system from the Morava article, Dr.
Raymond acknowledged that [M.S.B.] could have totaled as many as six points,
putting her in the probable (five to seven) range for a mitochondrial disorder. Sp.
Mstr. Tr. at 180. He elaborated, however, that he would want to confirm [M.S.B.]’s
lab results, particularly the elevated lactate level. Id.

Doctor Raymond later clarified on re-direct examination that if he were
[M.S.B.]’s treating physician he would not have assigned her a score within the
probable range without retesting her lactate level. See id. at 192–94. He

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emphasized that at the time when one would have expected [M.S.B.]’s alleged
mitochondrial disease to be “in full force,” there was “very limited” evidence of any
sort of dysfunction concerning her electron transport chain. Id. at 194. Doctor
Raymond would not have assigned a point for gastrointestinal tract disease,
reducing the maximum point score to five (including two based on the dubious
lactate measurement). Id. at 193.

Doctor Raymond also discussed Dr. Frye’s characterization of [M.S.B.]’s
genetic mutation associated with LHON, explaining that no evidence links this
specific point mutation with seizures. See id. at 158–61, 184. He also testified that
if it were assumed that [M.S.B.] had a mitochondrial disorder affecting her electron
transport chain, her upper respiratory infection would produce a much “more
enhanced” response than a vaccine and thus would more likely be the cause of her
injuries. Id. at 185–86.

Doctor Raymond criticized Dr. Frye’s reliance on certain literature as
supporting his theory of oxidative stress. One article, whose lead author was Dr.
Rahul N. Khurana, see Pet’r’s Ex. 75, 12 had been described as showing that a
vaccine could result in an increase in reactive oxygen species, Sp. Mstr. Tr. at 23.
Doctor Raymond believed that this animal model, in which bovine retina were
injected into rats “to get a horrendous response,” has “absolutely nothing to do with
vaccination of children,” and that to rest a theory concerning the latter on the study
was “just nonsensical.” Sp. Mstr. Tr. at 171–72. Another article, co-authored by Dr.
Joseph L. Edmonds, see Pet’r’s Ex. 79, 13 was cited as demonstrating that infections
are associated with the neurodegenerative episodes in children with mitochondrial
disorders. Sp. Mstr. Tr. at 38, 65. Doctor Raymond noted that [M.S.B.]’s point
mutation was not among the disorders identified; that the article did not establish
causality; and that it discusses infections, rather than vaccines. See id. at 187–90,
195. He did acknowledge that “there’s nothing that excludes the possibility that” a
combination of infection and vaccination could “bring mitochondrial dysfunction to a
clinical level,” id. at 191, but emphasized that none of the literature discusses such
a “synergistic event,” id. at 195. And when asked about two case reports cited by
Dr. Frye, see Pet’r’s Exs. 67 & 68, Dr. Raymond emphasized that in contrast to the
patients discussed in the reports, there was no evidence that [M.S.B.] experienced a
fever at the time that her seizures first presented, Sp. Mstr. Tr. at 198–200.

Respondent’s second expert, Dr. Jones, an expert in the field of oxidative
stress, testified that he did not think that Dr. Frye’s theory of oxidative stress was
12
R.N. Khurana et al., Mitochodria Oxidative DNA Damage in Experimental
Automimmune Uveitis, 49 Investigative Ophthalmology & Visual Sci. 3299 (2008).
13
J.L. Edmonds et al., The Otolaryngological Manifestations of Mitochondrial
Disease and the Risk of Neurodegeneration with Infection, 128 Archives
Otolaryngology Head & Neck Surgery 355 (2002).
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reliable, as research in the last decade has changed how oxidants are understood to
affect the body. Id. at 208–09. According to Dr. Jones, the old concept was one of
“imbalance” --- if antioxidants did not balance out the oxidants in the body,
oxidative stress would result, with a deleterious effect on the body. See id. at 209–
14. Doctor Jones explained, however, that recent research has shown that this
theory is incorrect, as enzymes purposefully generate oxidants because the latter
are necessary for normal cell signaling. See id. at 214–17. Moreover, Dr. Jones
notes that there is no evidence that an excess of oxidants is actually harmful, as Dr.
Frye’s theory contends, although in certain other contexts, oxidative stress may
have an impact on health. 14 See id. at 216–22. For example, Dr. Jones explained
that oxidants seem to contribute to aging, although the time frame for those effects
would be different by orders of magnitude from the time frame proposed by Dr.
Frye. See id. at 221–22. While Dr. Jones indicated that some things, such as toxic
chemicals, can inhibit electron transfer flow in the mitochondria, see id. at 255, he
reiterated that any oxidants produced though vaccine-induced activation of the
immune system would operate as part of the normal cell signaling process, see id. at
263.

The difference between how an infection might produce excess oxidants and
how a vaccine might do so was also discussed by Dr. Jones, who noted that Dr.
Frye’s reliance on studies involving infections involved some degree of “obfuscation.”
See id. at 223–25. One reason that the “scientific folklore” of oxidative stress as a
central mechanism has persisted, according to Dr. Jones, is because oxidants are
difficult to detect and quantify, creating confusion about their impact on disease
processes. See id. at 224–25. Despite this confusion, Dr. Jones made clear that he
does not think that it is possible that oxidants generated at the site of a vaccination
could travel to the brain and cause the types of injuries that [M.S.B.] experienced
because oxidants are locally metabolized. Id. at 227. Moreover, the brain has a
rigorous antioxidant system, which, in Dr. Jones’s opinion, could not be overcome by
oxidants produced as a result of activation of the immune system by a vaccine. See
id. at 228–29. Instead, Dr. Jones noted that it would require a level of oxygen a
thousand-fold greater than that which is present in the body to create enough
oxidants to overload the body’s antioxidant system and cause an injury, see id. at
232–34, and thus he believed that Dr. Frye’s proposed causation theory is “not
quantitatively reasonable,” id. at 244.

14 Doctor Jones elaborated that while it was clear that an imbalance between
oxidants and antioxidants does not itself create oxidative stress or otherwise harm
the body, a different type of oxidative stress can affect the body. See Sp. Mstr. Tr.
at 215–18. He viewed this concept of oxidative stress as a disruption in the
signaling pathways, which could be caused by an inhibitor that blocks signaling
pathways or by the creation of an abnormal pathway. See id.

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 Doctor Jones also discussed several of the articles relied upon by Dr. Frye,
indicating that the articles do not support Dr. Frye’s causation mechanism. See Sp.
Mstr. Tr. at 236–42. In conclusion, Dr. Jones explained that reactive oxygen species
play a beneficial role in cell signaling, id. at 275, and that he did not think that Dr.
Frye’s theory of oxidative stress as the cause of [M.S.B.]’s injuries was at all
plausible, id. at 244.

In her post-hearing brief, petitioner argued that she had met her burden of
proof under all three of the Althen prongs, and was therefore entitled to relief.
Petitioner relied upon Dr. Frye’s theory of oxidative stress, and did not discuss the
autoimmunity theory. See Pet’r’s Post-Hr’g Br. Applying the Althen factors to
[M.S.B.]’s case, petitioner contended that she met the burden of proof by
demonstrating that Dr. Frye’s theory of oxidative stress causally connects [M.S.B.]’s
December 4, 1998 vaccinations with her injuries, by presenting a logical sequence of
cause and effect that the vaccinations triggered the underlying mitochondrial
dysfunction to cause [M.S.B.]’s injuries, with or without demonstrating a proof of a
“rechallenge” event; 15 and by showing a proximate temporal relationship between
the vaccination and the onset of [M.S.B.]’s symptoms. Id. at 4, 11.

Respondent filed a post-hearing memorandum, arguing that petitioner failed
to meet her burden of proof for each of the Althen factors. See Resp’t’s Post-Hr’g
Mem. With respect to the first prong, respondent argued that Dr. Frye’s theory
“lacks reliable scientific support” and “is just plain wrong.” Id. at 8–9. Explaining
this position, respondent noted that Dr. Frye’s causation theory was based on an
imbalance theory of oxidative stress, which “is inconsistent with the current
understanding,” and therefore, did not meet the reliability standards set forth in
Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). Resp’t’s Post-
Hr’g Mem. at 10–11. Citing Dr. Jones’s hearing testimony, respondent also
contended that it is “scientifically implausible” that vaccines could produce enough
ROS to overwhelm the body’s antioxidant system. Id. at 12–14.

With respect to the second prong of Althen, respondent argued that petitioner
failed to demonstrate by preponderant evidence that [M.S.B.] actually had
dysfunctional mitochondria at the time of her vaccination, or at any time thereafter.
See id. at 14. Respondent noted that no evidence has been presented that the point
mutation identified for [M.S.B.] causes seizures; rather, Dr. Frye seemed to
reference the fact that [M.S.B.]’s point mutation is in the same protein complex as
other point mutations that may do so, and cited this as evidence that [M.S.B.] has
dysfunctional mitochondria making her susceptible to epilepsy and
neurodevelopmental delays. See id. at 15–16. In addition, respondent argued that

15 Rechallenge is the occurrence of an adverse event after each administration of
the same vaccine in the same individual, without worsened symptoms. See
Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1322 (Fed. Cir. 2006).

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[M.S.B.]’s clinical course was not consistent with mitochondrial dysfunction, and
discussed the symptoms which Dr. Frye contended establish that she has a probable
mitochondrial disorder. See id. at 18–25. Lastly, according to respondent,
petitioner failed to provide reliable evidence of a “rechallenge” event, which was
raised by petitioner for the first time in her post-hearing brief. See id. at 25–27.

Regarding the third Althen factor, respondent argued that petitioner failed to
meet her burden of proof because the evidence did not support Dr. Frye’s proposed
timeframe for the onset of symptoms as medically acceptable, and also did not
support the contention that [M.S.B.]’s symptoms occurred within the proposed
timeframe. See id. at 27–30. Challenging Dr. Frye’s proposed timeframe,
respondent contended that the timeframe “lacks a scientific basis,” and according to
Dr. Jones, “would be off by [orders] of magnitude.” Id. at 29. Moreover, respondent
noted that [M.S.B.]’s medical records place the onset of her seizures just past the
two- to four-week timeframe proposed by Dr. Frye, while the parents’ affidavits
would place her symptoms “somewhere between 10 days and two weeks after the
vaccine,” barely within the expected timeframe. Id. at 28–29.

In her reply, petitioner disputed respondent’s contention that she did not
advance a sufficient medical theory connecting the vaccines to [M.S.B.]’s injuries,
noting that Althen’s preponderance standard allows “the finding of causation in a
field bereft of complete and direct proof of how vaccines affect the human body.”
Pet’r’s Reply Br. to Resp’t’s Post-Hr’g Mem. (Pet’r’s Reply) at 3 (quoting Althen, 418
F.3d at 1280). Petitioner contended that while Dr. Jones has suggested an
“alternative approach to oxidative stress,” respondent has “offered very little
evidence to support her assertion that the scientific and medical communities have
completely dismissed the imbalance theory as a viable explanation for oxidative
stress.” Id. at 4. Instead, petitioner argued, the evidence offered by respondent did
not demonstrate that Dr. Jones’s theory is correct, or that it “has supplanted the
imbalance theory.” Id. Petitioner also addressed respondent’s argument that the
studies relied upon by Dr. Frye do not support petitioner’s theory, see id. at 5–7, and
noted that two of the articles relied upon by respondent actually use “the
oxidant/antioxidant balance theory that Respondent claims is no longer viable,” id.
at 7 (citing Resp’t’s Exs. T and U).

Petitioner also discussed the second Althen factor, and, in particular, the
respondent’s characterization of Dr. Frye’s attempt to explain how [M.S.B.]’s genetic
mutation could cause her seizures. See id. at 8–9. According to petitioner, Dr. Frye
did not claim that [M.S.B.]’s point mutation has been shown to lead directly to
epilepsy or neurodegenerative events, but rather testified that “this mutation is in
cytochrome b, and other mutations similarly affecting cytochrome b have been
shown to cause epilepsy” --- meaning that [M.S.B.]’s mutation may also do so after a
vaccine triggers a disruption in mitochondrial function. Id. Petitioner contended
that she had presented sufficient evidence to show that [M.S.B.]’s mutation did

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disrupt her electron transport chain, despite “a lack of definitive experimental proof
that [the mutation] causes seizures or neurodevelopmental delay.” Id. at 9.

Responding to the argument that petitioner failed to prove that [M.S.B.] had
the underlying mitochondrial disorder upon which Dr. Frye’s theory is predicated,
petitioner argued that she had proven by preponderant evidence that [M.S.B.] has
such a mitochondrial disorder. See id. at 10–13. Petitioner contended that
[M.S.B.]’s symptoms fit within the diagnostic criteria for mitochondrial disorders,
and disputed various aspects of Dr. Raymond’s testimony discussing those criteria.
Id. Finally, petitioner’s discussion of the third Althen prong set forth the basis for
Dr. Frye’s opinion that two to four weeks was a medically appropriate timeframe for
the onset of symptoms following [M.S.B.]’s vaccinations, and argued that the onset
of [M.S.B.]’s symptoms did, indeed, fall within that timeframe. See id. at 13–15.

C. The Chief Special Master’s Decision Denying Compensation

In her December 20, 2012 decision, the Chief Special Master determined,
based on the preponderance of the evidence and after a thorough review of the
record, that [M.S.B.]’s December 4, 1998 vaccinations did not cause her subsequent
injuries. See Bast, 2012 WL 6858040, at *1. The Chief Special Master found that
petitioner failed to meet her burden for each of the Althen factors under either the
vaccine-induced autoimmunity theory or the mitochondrial dysfunction theory. See
id. Beginning with a discussion of the credibility of the experts who testified in the
case, the Chief Special Master noted that while all of the experts were
“unquestionably competent,” respondent’s experts possessed superior expertise, and
their testimony “cogently rebutted petitioner’s offered medical theory.” Id. at *4–5.

In discussing the first Althen prong --- whether the petitioner put forth a
biologically plausible theory explaining how the vaccines could have caused the
sustained injury --- the autoimmunity theory was first considered. Finding no
evidence that [M.S.B.] has suffered from an autoimmune condition, other than an
unsupported opinion from Dr. DeOrio, the Chief Special Master found that
petitioner failed to meet her burden of establishing that [M.S.B.] had the proposed
condition upon which the autoimmunity theory rests. See id. at *26. The Chief
Special Master also noted that Dr. Frye indicated at the hearing that his theory of
causation does not depend on the autoimmunity theory. Id.

Regarding the mitochondrial dysfunction theory, the Chief Special Master
examined Dr. Frye’s testimony and concluded that Dr. Frye’s understanding of
oxidative stress “is not supported by sound and reliable science.” Id. at *27–28.
The Chief Special Master noted that Dr. Frye’s theory offers an “older view of
oxidative stress” than is currently held by the scientific community, and that Dr.
Frye relied upon literature of “questionable relevance.” Id. at *28. The Chief
Special Master explained that Dr. Frye failed to rebut the evidence that oxidants

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play a necessary role in normal cell signaling; that the body possesses robust levels
of antioxidants which make it very unlikely that reactive oxygen species generated
by a vaccine could cause the type of harm alleged; and that the distance between
[M.S.B.]’s injection site and the brain make it very unlikely that the briefly-existing
reactive oxygen species adversely impacted her brain. See id. at *28–33. In
discussing the literature relied upon by Dr. Frye, the Chief Special Master found
Dr. Frye’s extrapolation from the effects of infections to that of vaccinations
unpersuasive. See id. at *33–34. She also noted that the case studies discussed by
Dr. Frye, which involved children with purported mitochondrial disorders, highlight
the role of fever in metabolic decompensation --- a symptom which [M.S.B.] notably
did not have. See id. at *34–38. Thus, the Chief Special Master concluded that
petitioner failed to meet her burden under the first Althen prong under either of Dr.
Frye’s theories of causation. See id. at *38–39.

The Chief Special Master then discussed the second Althen prong, under
which petitioner must prove “a logical sequence of cause and effect showing that the
vaccination was the reason for the injury.” Id. at *39–48 (quoting Althen, 418 F.3d
at 1278). The medical theory offered by Dr. Frye was predicated on the premise
that [M.S.B.] actually had dysfunctional mitochondria at the time of her
vaccinations --- a premise which the Chief Special Master found petitioner failed to
prove by preponderant evidence. See id. In reaching this conclusion, the Chief
Special Master noted that [M.S.B.]’s point mutation, which is associated with
LHON, does not, without more, demonstrate that [M.S.B.] had dysfunctional
mitochondria at the time of her vaccination. Id. at *39–40. Turning to a discussion
of the Bernier criteria, the Chief Special Master evaluated each of the diagnostic
criteria relied upon by Dr. Frye and determined that preponderant evidence does
not establish that [M.S.B.] meets the criteria for mitochondrial dysfunction. See id.
at *40–48. Moreover, the Chief Special Master noted that the petitioner
downplayed the role of [M.S.B.]’s upper respiratory infection in late December of
1998. See id. at *47. By contrast, Dr. Raymond testified that this “clear infectious
event” was far more likely to have acted as the trigger pursuant to Dr. Frye’s theory
than the vaccinations [M.S.B.] received. See id. Finally, the Chief Special Master
rejected petitioner’s rechallenge argument, which was raised for the first time
during post-hearing briefing, indicating that petitioner offered little evidence to
establish the vaccine-relatedness of [M.S.B.]’s conjunctivitis and upper respiratory
infection. See id. at *47–48.

Finally, the Chief Special Master found that petitioner failed to meet her
burden under the third Althen prong, because the latter did not establish by
preponderant evidence that [M.S.B.]’s injury occurred within a time frame that is
medically appropriate for the alleged causal mechanism. See id. at *48–50. In his
expert report, Dr. Frye indicated that [M.S.B.]’s symptoms began “approximately 10
days after [her] 2 month vaccinations,” apparently relying on the affidavits of
[M.S.B.]’s parents. See id. at *49 (citing Pet’r’s Ex. 59 at 1). At the hearing, Dr.

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Frye offered his opinion that the medically appropriate time frame in which one
would expect to see symptoms caused by oxidative stress would be two to four
weeks. See id. The Chief Special Master gave greater credence to [M.S.B.]’s
contemporaneously documented medical records, which place the onset of her
symptoms narrowly beyond the time frame proposed by Dr. Frye. See id. But the
Chief Special Master made clear that petitioner failed to meet her burden under
prong three of Althen for other reasons as well. Specifically, the Chief Special
Master rejected the causation mechanism proposed by Dr. Frye, and the articles
that he cited as support for his proposed time frame. See id. at *49–50. Relying on
Dr. Jones’s testimony, the Chief Special Master indicated that even if she were to
accept Dr. Frye’s theory of oxidative stress, the two- to four-week time frame that
he proposed is much too short, by decades, to cause the types of injuries alleged.
See id.

Having determined that petitioner failed to meet her burden under each of
the prongs set forth in Althen, the Chief Special Master concluded that petitioner
was not entitled to compensation.

D. Petitioner’s Motion for Review

On January 22, 2013, petitioner filed a motion for review and memorandum
of objections pursuant to Vaccine Rules 23 and 24, raising three objections to the
Chief Special Master’s decision. See generally Pet’r’s Mot. for Rev. (Pet’r’s Mot.).
First, petitioner argues that the Chief Special Master’s rejection of petitioner’s
theory of oxidative stress was arbitrary and capricious. See id. at 2. Second,
petitioner argues that the Chief Special Master’s rejection of Dr. Frye’s reliance on
[M.S.B.]’s parents’ affidavits regarding the onset of her symptoms, as well as her
“selective reading of the medical record,” which precluded a finding of a logical
sequence of cause and effect was arbitrary and capricious. See id. Finally,
petitioner argues that the Chief Special Master’s “limitation” of the medically-
appropriate temporal association was arbitrary and capricious. See id.

The Secretary of Health and Human Services responded to petitioner’s
motion for review. See Resp’t’s Resp. to Pet’r’s Mot. for Rev. (Resp’t’s Resp.).
Respondent contends that the Chief Special Master properly determined that
petitioner did not meet her burden under all three Althen prongs. Id. The Court
held oral argument on petitioner’s motion. After careful consideration of the
medical records, testimony, medical literature in the record, the decision below, and
the arguments of counsel, this opinion issues.

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 II. DISCUSSION

A. Legal Standards

1. The Court’s Standard of Review of a Special Master’s Decision

Under the Vaccine Act, a special master must award compensation if, “on the
record as a whole,” she finds “that the petitioner has demonstrated by a
preponderance of the evidence” the claims of the petition. 42 U.S.C. § 300aa-
13(a)(1)(A) (2012). By this same standard, a special master must find that nothing
else is responsible for causing the injury. Id. § 300aa-13(a)(1)(B). “The special
master or court may not make such a finding based on the claims of a petitioner
alone, unsubstantiated by medical records or by medical opinion.” Id. § 300aa-
13(a)(1). A special master must consider all the “relevant medical and scientific
evidence contained in the record,” including any “diagnosis, conclusion, medical
judgment, or autopsy . . . regarding the nature, causation, and aggravation of the
petitioner’s illness, disability, injury, condition, or death” and “the results of any
diagnostic or evaluative test which are contained in the record and the summaries
and conclusions.” Id. § 300aa-13(b)(1). The Act further specifies that “[a]ny such
diagnosis, conclusion, judgment, test result, report, or summary shall not be binding
on the special master or court.” Id. A special master is entrusted with evaluating
the “weight to be afforded to any” of these sources of information. Id. A special
master’s “assessments of the credibility of the witnesses” are “virtually
unchallengeable on appeal.” Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1362 (Fed. Cir. 2000). This deference rests on the special master’s “broad
discretion in determining credibility because he saw the witnesses and heard the
testimony,” Bradley v. Sec’y of Dep’t of Health & Human Servs., 991 F.2d 1570, 1575
(Fed. Cir. 1993), and extends to assessments of expert testimony. See Moberly v.
Sec’y of Health & Human Servs., 592 F.3d 1315, 1325–26 (Fed. Cir. 2010).

Medical records “warrant consideration as trustworthy evidence.” Cucuras v.
Sec’y of Dep’t of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
These records are “generally contemporaneous to the medical events,” and “accuracy
has an extra premium” because a patient’s proper treatment is “hanging in the
balance.” Id. Moreover, because medical records are contemporaneous
documentary evidence, conflicting oral testimony “deserves little weight.” Id. (citing
United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1947)).

In reviewing a special master’s decision, our court may “set aside any
findings of fact or conclusion of law of the special master found to be arbitrary,
capricious, an abuse of discretion, or otherwise not in accordance with law and issue
its own findings of fact and conclusions of law.” 42 U.S.C. § 300aa-12(e)(2)(B)
(2012). Findings of fact are to be reviewed under the “arbitrary and capricious”
standard; legal questions are to be reviewed under the “not in accordance with law”

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standard; and an abuse of discretion standard is used for discretionary rulings. See
Munn v. Sec’y of Dep’t of Health & Human Servs., 970 F.2d 863, 870 n.10 (Fed. Cir.
1992). With respect to the arbitrary and capricious review, “no uniform definition of
this standard has emerged,” but it is “a highly deferential standard of review” such
that “[i]f the special master has considered the relevant evidence of record, drawn
plausible inferences and articulated a rational basis for the decision, reversible
error will be extremely difficult to demonstrate.” Hines ex rel. Sevier v. Sec’y of
Dep’t of Health & Human Servs., 940 F.2d 1518, 1527–28 (Fed. Cir. 1991).

2. The Standard of Causation in Vaccine Cases

A special master may award compensation through an “off-table” or
“causation-in-fact” case. Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352,
1355 (Fed. Cir. 2006). Causation-in-fact --- the basis for the legal entitlement to
compensation when a petitioner’s injury is either not listed in the Vaccine Injury
Table or did not occur within the time period set forth in the Table --- must be
proven under two formulations adopted by the Federal Circuit. See Pafford, 451
F.3d at 1355. Petitioners must establish that the vaccine was both a “but-for” cause
of the injury and a substantial factor in causing the injury. See Shyface v. Sec’y of
Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Under a three-part
test more recently articulated by the Circuit, petitioners must prove “(1) a medical
theory causally connecting the vaccination and the injury; (2) a logical sequence 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 injury.”
Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). 16
Petitioners bear the burden of proving causation by preponderant evidence. See 42
U.S.C. § 300aa-13(a)(1)(A).

A petitioner must show more than a proximate temporal relationship
between the vaccination and the injury to meet her burden of showing actual
causation. Althen, 418 F.3d at 1278; see also Grant v. Sec’y of Dep’t of Health &
Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). Furthermore, “[t]here may
well be a circumstance where it is found that a vaccine can cause the injury at issue
and where the injury was temporally proximate to the vaccination, but it is illogical
to conclude that the injury was actually caused by the vaccine.” Capizzano v. Sec’y
of Health & Human Servs., 440 F.3d 1317, 1327 (Fed. Cir. 2006). A petitioner could
meet the first and third prongs of the Althen test without “satisfying the second
prong when medical records and medical opinions do not suggest that the vaccine
caused the injury, or where the probability of coincidence or another cause prevents
the claimant from proving that the vaccine caused the injury by preponderant

16 Although the Federal Circuit has described the Althen test as an “alternative,”
the very same opinion makes plain that the Althen “prongs must cumulatively
show” that the Shyface standard is met. See Pafford, 451 F.3d at 1355.

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evidence.” Id. The sequence only has to be “‘logical’ and legally probable, not
medically or scientifically certain,” and thus can be established by “epidemiological
evidence and [a] clinical picture,” even “without detailed medical and scientific
exposition on the biological mechanisms.” Knudsen v. Sec’y of Dep’t of Health &
Human Servs., 35 F.3d 543, 548–49 (Fed. Cir. 1994). Nonetheless, the Federal
Circuit has stated that while “epidemiological studies are probative medical
evidence relevant to causation,” they are not necessarily dispositive. Grant, 956
F.2d at 1149.

“The government . . . is permitted to offer evidence to demonstrate the
inadequacy of the petitioner’s evidence on a requisite element of the petitioner’s
case[-]in-chief.” de Bazan v. Sec’y of HHS, 539 F.3d 1347, 1353 (Fed. Cir. 2008). If
a petitioner satisfies her burden, she is entitled to compensation “unless the
[government] shows, also by a preponderance of evidence, that the injury was in fact
caused by factors unrelated to the vaccine.” Althen, 418 F.3d at 1278 (quoting
Knudsen, 35 F.3d at 547) (alteration in original).

B. The Chief Special Master’s Decision Was Not Arbitrary and Capricious

In her motion for review, petitioner challenges as arbitrary and capricious
the determinations of the Chief Special Master regarding each of the three prongs of
Althen. Pet’r’s Mot. at 2, 10–20. Before addressing each specific objection,
petitioner’s paper contains a prolonged discussion of the evidentiary standard
employed in Vaccine Act cases. See id. at 4–10. In the course of this discussion, she
alleges that the Chief Special Master “misinterpret[ed]” the Act by “requiring
‘cause-in-fact,’ ‘truth,’ and/or scientific certainty.” See id. at 5. The only elaboration
of this claim is the general charge (with no citation to the opinion below) that the
Chief Special Master engaged in “over-analysis” and “ignored the reasonable
reliability of . . . Dr. Frye’s theories, the strong temporal relationship [and] the
totality of the record and required too much of [M.S.B.].” Id. at 8.

Nothing in the Chief Special Master’s decision suggests she employed any
standard other than the “causation in fact” standard adopted by the Federal Circuit
for Vaccine Act cases. See, e.g., Bast, 2012 WL 6858040, at *20–23. If, despite the
Act’s use of the phrase “caused by a vaccine,” 42 U.S.C. § 300aa-11(c)(1)(C)(ii)(I)–
(II), and the Federal Circuit’s frequent use and explanation of the “causation in
fact” standard, see Moberly, 592 F.3d at 1322, petitioner objects to the Federal
Circuit’s interpretation of the Act, this criticism should be directed to Congress or
the Federal Circuit, and not to our court. In any event, requiring that a medical
theory of causation be proven reputable by a preponderance of the evidence is not
the same thing as requiring scientific certainty. See id.

Petitioner seems to be arguing for a lower standard, under which she prevails
as long as her expert claims to have a reliable medical theory of causation,

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regardless of any testimony to the contrary by respondent’s experts. But the
Federal Circuit has made it quite clear that it is the job of our special masters to
assess conflicting testimony of expert witnesses in determining whether a reputable
theory has been proven. See Porter v. Sec’y of Health & Human Servs., 663 F.3d
1242, 1250–51 (Fed. Cir. 2011) (collecting cases). As we will see, the Chief Special
Master well and ably discharged this duty, by a careful and thorough evaluation of
the evidence and a rational articulation of her reasoning.

1. The Chief Special Master Properly Found Petitioner’s Theory to Be
Unreliable

Petitioner contends that she satisfied the first Althen prong through Dr.
Frye’s theory of oxidative stress, and that the Chief Special Master’s rejection of
this theory of causation was arbitrary and capricious. 17 See Pet’r’s Mot. at 10–14.
To support her argument, she cites another case (now on appeal) in which Dr. Frye
advanced the same theory and our court reversed the special master’s
determination that the theory was unreliable. See Pet’r’s Mot. at 13–14 (citing
Paluck v. Sec’y of Dep’t of Health & Human Servs., 104 Fed. Cl. 457 (2012), appeal
docketed, No. 14-5080 (Fed. Cir. May 1, 2014)). At the hearing, petitioner’s counsel
identified statements by respondent’s experts which purportedly undermine their
credibility, and argued that the Chief Special Master should have accordingly
discounted their testimony. Counsel also argued that the literature relied upon by
respondent’s experts was of little relevance to [M.S.B.]’s case because she was
already ill on the day of her vaccines and allegedly had dysfunctional mitochondria.

The first prong of Althen requires “a medical theory causally connecting the
vaccination and the injury” that is based on a “‘reputable medical or scientific
explanation.’” Althen, 418 F.3d at 1278 (quoting Grant, 956 F.2d at 1148). It is
clear that the standard of proof under the Vaccine Act “is a simple preponderance of
evidence; not scientific certainty.” Bunting v. Sec’y of Dep’t of Health & Human
Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). But as the Federal Circuit has explained,
under the preponderance standard, “petitioner must do more than demonstrate a
‘plausible’ or ‘possible’ causal link between the vaccination and the injury.” W.C. v.
Sec’y of Dep’t of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013)
(citing Moberly, 592. F.3d at 1322).

The Court finds that the Chief Special Master did not act arbitrarily and
capriciously in rejecting petitioner’s theory that oxidative stress resulting from the
December 4, 1998 vaccinations caused [M.S.B.]’s injuries. The Chief Special Master
based this determination primarily on the testimony of Dr. Jones, a frequently-
published expert in oxidative stress. See Bast, 2012 WL 6858040, at *4–6, *26–39.

17Petitioner does not discuss the rejection of the autoimmunity theory in her
motion for review.

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She accurately recounted his testimony that an imbalance in reactive oxygen
species could not have caused injuries such as [M.S.B.]’s --- including his opinions
that the amount of antioxidants available in the human body could not possibly be
overwhelmed by the amount of oxidation resulting from a vaccination; that the
reactive oxygen species was too short-lived and localized to have harmed [M.S.B.]’s
brain; and that the human body’s reaction to infection is too different from the
reaction to vaccines for studies concerning the former to be used to explain the
latter. Id. at *29–30, *32–34, *38–39; see Sp. Mstr. Tr. at 209–15, 221–22, 224–29,
232–34; Resp’t’s Ex. C at 2–4. She appropriately noted that much of Dr. Jones’s
testimony was not rebutted. Bast, 2012 WL 6858040, at *33–34. The Chief Special
Master also discussed the medical literature upon which Dr. Frye relied and
explained why she did not find it to support his theory, crediting the criticisms of
respondent’s experts. Id. at *30–32; see also Sp. Mstr. Tr. at 171–72, 230, 236–44.
And she discounted the relevance of case reports in which neurodegeneration
followed a fever --- a symptom from which [M.S.B.] did not suffer. Bast, 2012 WL
6858040, at *34–38.

Based on the foregoing, it is quite clear that the Chief Special Master did not
reach her conclusion under prong one of Althen in an arbitrary and capricious
manner, but instead reviewed the entire record and based her determination on the
evidence before her. Petitioner appears to contend that her expert should have been
found more persuasive than respondent’s experts. See Pet’r’s Mot. at 13. But, as
the Federal Circuit has frequently held, in reviewing Vaccine Act cases courts “do
not reweigh the factual evidence, assess whether the special master correctly
evaluated the evidence, or examine the probative value of the evidence or the
credibility of the witnesses --- these are all matters within the purview of the fact-
finder.” Porter, 663 F.3d at 1249 (citing Broekelschen v. Sec’y of Health & Human
Servs., 618 F.3d 1339, 1349 (Fed. Cir. 2010) (citing Munn, 970 F.2d at 871)). As
long as the record evidence which was relied upon “was not wholly implausible,”
Lampe, 219 F.3d at 1363, the conclusion resting upon it cannot be found arbitrary
upon review.

But instead of trying to show the implausibility of the opinions of
respondent’s expert witnesses, petitioner argues that her expert’s opinion was found
sufficiently reliable in an unrelated case --- in which neither Dr. Jones nor Dr.
Raymond testified. See Pet’r’s Mot. at 13–14 (citing Paluck, 104 Fed. Cl. at 471,
477); Paluck, 104 Fed. Cl. at 462 n.4 (identifying respondent’s expert witness).
Based on the evidence before the court in that case, it was noted that Dr. Frye’s
theory was “under active, continuing scientific investigation by a range of
researchers, showing that it is sufficiently worthy and reliable to merit that
extensive scientific inquiry.” Pet’r’s Mot. at 13 (quoting Paluck, 104 Fed. Cl. at
475). But decisions from our court on questions of law are merely persuasive
authority. See CBY Design Builders v. United States, 105 Fed. Cl. 303, 332 n.23
(2012); Vessels v. Sec’y of Dep’t of Health & Human Servs., 65 Fed. Cl. 563, 569

-26-
(2005). It is hard to see how a decision concerning a question of fact could even be
persuasive, when there are differences in evidentiary records. 18

Special masters are “neither bound by their own decisions nor by cases from
the Court of Federal Claims, except, of course, in the same case on remand.”
Hanlon v. Sec’y of Dep’t of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998),
aff’d, 191 F.3d 1344 (Fed. Cir. 1999). As the Federal Circuit has explained: “A
special master’s acceptance of a theory in one case does not require him or her to
accept the theory in subsequent cases involving similar facts or the same vaccine.
Rather a different evidentiary record can lead to different outcomes.” Rickett v.
Sec’y of Dep’t of Health & Human Servs., 468 Fed. App’x 952 (Fed. Cir. 2011)
(unpublished). Significantly, unlike in the present case, the record in Paluck did
not include testimony from experts (including an expert in oxidative stress) who
credibly rejected Dr. Frye’s theory as outdated and not scientifically sound. 19 Here,
the Chief Special Master carefully considered the expert testimony, expert reports,
and the medical literature filed in support thereof, and concluded that a
preponderance of the evidence did not support Dr. Frye’s theory. The Court can
find no error in this determination.

At the hearing on the motion for review, petitioner’s counsel supplemented
the grounds covered in the motion with additional arguments, presumably
attempting to show the implausibility of respondent’s evidence. First, a supposed
admission by Dr. Jones was noted, as on cross-examination he was asked if “it’s
possible that oxidative stress can potentially result in seizures in a system where
the cells cannot effectively handle [it].” Sp. Mstr. Tr. at 265. He responded, “I’m
really not qualified to answer that question at all.” Id. According to petitioner, this
exchange shows that by Dr. Jones’s own admission, he is not qualified to assess the
key issue in this case --- whether, as posited by Dr. Frye, oxidative stress could
potentially result in the symptoms [M.S.B.] experienced.

Even if the statement could be taken as such an admission, the Court doubts
that it could appropriately find a decision to be arbitrary based on one sentence of

18 At the hearing before the Court, petitioner suggested that the doctrine of
collateral estoppel should bar respondent from challenging a medical theory that
was accepted in another case. It has long been recognized, however, that the
doctrine of offensive nonmutual collateral estoppel does not extend to the United
States government. See United States v. Mendoza, 464 U.S. 154, 159–62 (1984).

19 In Paluck, “the only objection to the Palucks’ general theory presented by the
government’s expert was that oxidative stress from vaccines has not been
established in humans. . . . Putting aside that objection, then, [the government’s
expert] otherwise conceded that Dr. Frye’s general theory was plausible.” 104 Fed.
Cl. at 476.

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testimony that the petitioner did not even see fit to mention in either of her post-
hearing briefs before the Chief Special Master --- much less identify in her motion
for review. But in any event, the context shows that Dr. Jones was reluctant to
speculate on the causes of seizures. In response to a follow-up question regarding
whether oxidative stress could cause seizures by damaging brain cells, Dr. Jones
clarified: “As I said, I’m not really qualified to answer that question. I really don’t
know the causes of seizures and [the likely] causes of seizures.” Id. This hardly
detracts from his testimony in his area of expertise, oxidative stress. As was noted
above, Dr. Jones persuasively testified that any reactive oxygen species from a
vaccination in the thigh were too few, short-lived and localized to injure the brain,
so whether it was possible that oxidative stress in the brain could result in seizures
is beside the point. See id. at 225–34.

The other statement identified at the hearing is no more availing for
petitioner. On cross-examination, Dr. Raymond was asked about a vaccination
followed by the type of upper respiratory infection suffered by [M.S.B.]: “And
there’s nothing that excludes the possibility that when you combine these two small
infections they can function to bring mitochondrial dysfunction to a clinical level?”
Sp. Mstr. Tr. at 191. Doctor Raymond agreed with the statement. Id. 20 Even
putting aside the predicate of mitochondrial dysfunction, with which Dr. Raymond
disagreed, see Sp. Mstr. Tr. at 131–52, not excluding a possibility is far from
conceding a probability. The preponderance of the evidence standard requires more
than proof of a mere possibility. See Moberly, 592 F.3d at 1322.

Finally, petitioner’s counsel contended that the Chief Special Master
arbitrarily failed to discount the articles relied upon by respondent’s experts,
arguing that [M.S.B.]’s case can be distinguished on the grounds that she was
already ill and had dysfunctional mitochondria. But if the medical literature is to
be so distinguished or limited, this is a question of fact requiring contrary testimony
by petitioner’s expert, not just the argument of her counsel. No expert opinion to
this effect has been identified. Moreover, under the deferential review standard, a
court is not to reweigh the evidence that was before the Chief Special Master and
reach its own conclusion as to the viability of Dr. Frye’s theory. See Munn, 970 F.2d
at 871. It is the task of a special master to examine the evidence and determine
both its relevance and weight. Our court can only ensure that the Chief Special
Master considered all relevant evidence, drew plausible inferences, and articulated
a rational basis for her decision. Hines, 940 F.2d at 1527. The issue of whether the
respondent’s studies can be distinguished from [M.S.B.]’s case was one for the Chief
Special Master to consider, and it is clear from her detailed discussion of the
literature, see Bast, 2012 WL 6858040, at *30–38, that she thoroughly examined the
evidence of record. All told, her determination that petitioner failed to prove a

20 Although not mentioned in the motion for review, this statement was included in
the post-hearing reply brief before the Chief Special Master. See Pet’r’s Reply at 14.
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reliable theory of causation under the first prong of Althen was far from arbitrary.
Petitioner’s first objection is accordingly rejected.

2. The Chief Special Master Did Not Err in Finding That Petitioner Failed to
Prove a Logical Sequence of Cause and Effect

Petitioner also objects to the Chief Special Master’s conclusions regarding the
second Althen prong. Under this prong, a petitioner must establish a “logical
sequence of cause and effect showing that the vaccination was the reason for the
injury.” Althen, 418 F.3d at 1278; Capizzano, 440 F.3d at 1326 (“‘A logical sequence
of cause and effect’ means what it sounds like – the claimant’s theory of cause and
effect must be logical.”). The 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.” Althen, 418 F.3d at 1278 (quoting Shyface, 165 F.3d at 1352). While
circumstantial evidence may be used to meet petitioner’s burden, “[t]here may well
be a circumstance where it is found that a vaccine can cause the injury at issue and
where the injury was temporally proximate to the vaccination, but it is illogical to
conclude that the injury was actually caused by the vaccine” --- for example, “where
the probability of coincidence or another cause prevents the claimant from proving
that the vaccine caused the injury by preponderant evidence.” Capizzano, 440 F.3d
at 1327.

The Chief Special Master’s analysis under the second Althen prong centered
on the issue of whether [M.S.B.] had an underlying mitochondrial disorder --- the
“factual predicate” upon which Dr. Frye’s theory of oxidative stress is based. See
Bast, 2012 WL 6858040, at *39–48. The Chief Special Master first explained that
[M.S.B.]’s point mutation, which is associated with LHON, “does not, without more,
establish that she had a mitochondrial dysfunction.” Id. at *39–40. She then
discussed the Bernier criteria relied upon by Dr. Frye, concluding that “the
constellation of [M.S.B.]’s symptoms do not preponderate in favor of a finding that
[M.S.B.] has a mitochondrial disorder, as defined by the Bernier criteria.” Id. at
*40–41. In reaching these conclusions, the Chief Special Master examined the
testimony of the expert witnesses, as well as the Bernier article itself and [M.S.B.]’s
medical records. See id. at *40–46.

The remainder of the Chief Special Master’s analysis under the second prong
of Althen addressed how petitioner “diminished the role of [M.S.B.]’s intercurrent
upper respiratory infection” and petitioner’s rechallenge argument. See id. at *47–
48. With respect to the rechallenge argument, which the Chief Special Master
noted was raised for the first time in petitioner’s post-hearing brief, the Chief
Special Master concluded that the argument was “unavailing” because petitioner
offered “little more than her own assertions regarding the vaccine-relatedness” of
the prior symptoms allegedly part of the rechallenge scenario. See id.

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 In the motion for review, petitioner did not argue that the Chief Special
Master was arbitrary in finding that petitioner failed to prove the existence of a
mitochondrial disorder. Instead, petitioner first reargued the rechallenge argument
from the post-hearing brief. See Pet’r’s Mot. at 14–16. She then contended that
prong two was satisfied by Dr. Frye’s testimony alone, on the assumption that
prongs one and three have separately been met. See id. at 16 (citing Andreu, 569
F.3d at 1375; Capizzano, 440 F.3d at 1326).

Taking the second argument first, as we have just seen, petitioner did not
prove a reliable theory of causation to satisfy the first prong of Althen, which is
sufficient to doom this argument. Petitioner’s points concerning the temporal
association of [M.S.B.]’s vaccinations and symptoms will be addressed below under
the prong three objection, which the Court also rejects. Moreover, while petitioner
is correct that the second Althen prong may be established through medical opinion
testimony alone, the Chief Special Master is not required to blindly rely on such
testimony merely because petitioner has offered it. After all, “there is nothing in
Andreu that mandates that the testimony of a treating physician is sacrosanct –
that it must be accepted in its entirely and cannot be rebutted.” Snyder ex rel.
Snyder v. Sec’y of Dep’t of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009).
More fundamentally, in [M.S.B.]’s case, her treating physicians did not attribute her
condition to an underlying mitochondrial disorder and vaccine-induced oxidative
stress. 21 As explained by the Chief Special Master, this theory was only put
forward by Dr. Frye, petitioner’s expert:

[M.S.B.]’s treating physicians attributed her health issues variously to
congenital brain abnormalities, an evolving seizures disorder that may
have been caused by a metabolic disorder, and the effects of [M.S.B.]’s
anticonvulsant medications. It is the petitioner’s expert, Dr. Frye, who
offers the singular opinion that [M.S.B.]’s health problems resulted
from a vaccine-induced cascade of events—including the development
of a seizure disorder—that was facilitated by [M.S.B.]’s mitochondrial
point mutation and in turn, produced detrimental levels of excess
reactive oxygen species, a condition known as oxidative stress.

Bast, 2012 WL 6858040, at *5 (emphasis added); see also id. at *26 n.78.

21 The Chief Special Master explains that of [M.S.B.]’s treating physicians, only Dr.
Stein indicated that [M.S.B.] might have a mitochondrial disorder. See Bast, 2012
WL 6858040, at *46. He initiated treatment for a “possible” mitochondrial disorder
because he was uncertain about the cause of [M.S.B.]’s symptoms, and noted that
there was little danger in treating her for a mitochondrial disorder, even if it turned
out that she did not actually have such a disorder. See id. (citing Pet’r’s Ex. 23 at
108).

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 But most importantly, regardless of whether Dr. Frye’s testimony alone could
be sufficient to prove a logical sequence of cause and effect, it is the Chief Special
Master who is charged with determining whether his testimony did prove this
under the second prong of Althen. Petitioner has failed to identify any error in the
making of this determination.

Turning to her first argument, after explaining how [M.S.B.]’s symptoms
purportedly demonstrate a rechallenge scenario, petitioner contends that she “has
no burden to present any evidence of specific mechanisms of cause, because the
cause and effect are understood to be occurring.” Id. at 14–16 (citing Capizzano v.
Sec’y of Health & Human Servs., No. 00-759V, 2003 U.S. Claims LEXIS 219, at *15
(Fed. Cl. Sp. Mstr. Aug. 5, 2003)). This argument rests on Dr. Frye’s testimony that
[M.S.B.]’s conjunctivitis following her October 23, 1998 hepatitis B vaccination, and
her upper respiratory infection following the December 4, 1998 vaccinations, were
“adverse effect[s]” of the vaccinations. See Sp. Mstr. Tr. at 17–18, 93–94; Pet’r’s
Mot. at 14–15. But the Chief Special Master noted that no supportive evidence was
filed showing an association between the hepatitis B vaccination and conjunctivitis,
Bast, 2012 WL 6858040, at *48, and petitioner does not identify any to the contrary.
A review of the transcript does not reveal any discussion by Dr. Frye concerning
whether the reactions which followed the vaccinations would meet the standards for
rechallenge identified by the Institute of Medicine or, indeed, anyone. Given this
record, the Chief Special Master accurately concluded that “[p]etitioner has offered
little more than her own assertions regarding the vaccine-relatedness of [M.S.B.]’s
conjunctivitis and upper respiratory infection,” and properly did not “accord much
weight to these assertions.” Id. While a rechallenge event may be strong evidence
of causality, petitioner has failed to show that the Chief Special Master’s rejection of
the rechallenge contention was arbitrary and capricious.

The motion for review ignored the Chief Special Master’s critical finding that
petitioner failed to prove by preponderant evidence that [M.S.B.] had an underlying
mitochondrial disorder at the time of the December 4, 1998 vaccinations. But at the
hearing before the Court, petitioner’s counsel added an argument challenging the
Chief Special Master’s reliance on Dr. Raymond’s testimony concerning this issue. 22
Petitioner’s counsel noted that while being cross-examined about [M.S.B.]’s score
under the Morava criteria, see Resp’t’s Ex. H, Dr. Raymond acknowledged that
[M.S.B.] could receive a score of six, which would put her in the “probable” range for
a mitochondrial disorder. 23 See Sp. Mstr. Tr. at 180. Doctor Raymond qualified this

22A variation on this argument was included in the post-hearing reply brief below.
See Pet’r’s Reply at 10–13.

23 Doctor Raymond also explains that the significance of a “probable” score is that it
indicates that the patient would be an appropriate candidate for a muscle biopsy,
something which was never performed on [M.S.B.]. Sp. Mstr. Tr. at 180.

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statement by saying that he would want to see repeat laboratory reports for
[M.S.B.]’s lactate levels, which he described as “outrageous.” Id. On re-direct, Dr.
Raymond clarified that he would not assign [M.S.B.] a point for her gastrointestinal
symptoms. 24 He further explained that while rigid application of the criteria would
assign two points based on the dubious lactate levels, “as a practicing clinician” he
would not base a diagnosis on those results but rather would order another test. 25
Id. at 192–94.

Doctor Raymond elaborated that when [M.S.B.] originally presented with
symptoms, “when the mitochondrial disease should be in full force, we have very
limited evidence of a biochemical dysfunction of the electron transport chain . . .
Frankly, this is the period of time when I would have thought okay, this is when
these would be evident and we’re not seeing that.” Id. at 194. In addition, although
Dr. Raymond indicated in his expert report that the possibility that [M.S.B.] has a
mitochondrial disorder “cannot be excluded,” he explained that “nearly any
individual with a neurologic condition would be so listed.” Resp’t’s Ex. A at 6.

A full review of Dr. Raymond’s testimony shows that, far from conceding that
[M.S.B.] suffered from a mitochondrial disorder, respondent’s expert believed to the
contrary. He explained why he did not believe that a score in the “probable” range
under the Morava criteria was a reliable indicator of her condition. The Chief
Special Master fully considered his views in reaching her conclusion on this issue.
See Bast, 2012 WL 6858040, at *41–46 & nn.117–18. Again, in reviewing these
decisions courts “do not reweigh the factual evidence, assess whether the special
master correctly evaluated the evidence, or examine the probative value of the
evidence or the credibility of the witnesses.” Porter, 663 F.3d at 1249 (citations
omitted). The Chief Special Master undertook a thorough review of the evidence
and expert testimony and reasonably concluded that preponderant evidence did not
establish that [M.S.B.] had an underlying mitochondrial disorder. This
determination was not arbitrary, and petitioner’s second objection is rejected.

24Earlier, Dr. Raymond testifed that “chronic constipation is extraordinarily
common in children with intellectual disabilities, autism and a variety of other
neurologic features. It really doesn’t speak to a specific mitochondrial
characteristic.” Sp. Mstr. Tr. at 177.
25 As noted, Dr. Raymond testified that the reported lactate levels were so high that
he did not think they “would actually be consistent with anyone’s condition.” Sp.
Mstr. Tr. at 192.

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 3. The Chief Special Master Did Not Err in Her Analysis of Petitioner’s
Proposed Time Frame for the Onset of Symptoms

Petitioner also objects to the Chief Special Master’s analysis of the third
Althen prong, which requires that petitioners establish “a proximate temporal
relationship between vaccination and injury.” Althen, 418 F.3d at 1278. The
Federal Circuit has held that this proximate temporal relationship must occur
within a “medically acceptable” timeframe. See de Bazan, 539 F.3d at 1352;
Pafford, 451 F.3d at 1358; Porter, 663 F.3d at 1266. The Chief Special Master
determined that petitioner did not meet her burden under this prong for two
reasons --- petitioner did not sufficiently prove that [M.S.B.]’s symptoms actually
occurred within the timeframe proposed, and moreover did not establish that the
timeframe was medically acceptable. Bast, 2012 WL 6858040, at *48–51.

In her motion for review, petitioner challenges both of these determinations.
Petitioner first argues that [M.S.B.]’s parents’ affidavits establish that [M.S.B.]’s
symptoms occurred within the two- to four-week timeframe proposed by Dr. Frye,
and that the Chief Special Master improperly discounted these affidavits. See
Pet’r’s Mot. at 16–19. The Chief Special Master explained in her opinion that the
parents’ recollections of the timing of [M.S.B.]’s symptoms differ from the timing
reflected in [M.S.B.]’s medical records, see Bast, 2012 WL 6858040, at *8, 26 and
indicated that she would rely upon the contemporaneous medical records to the
extent that the affidavit testimony “conflicts with or is unsupported by the medical
records,” id. at *6 (citing Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525
(Fed. Cir. 1993)). Petitioner challenges this decision as arbitrary and capricious,
contending that the two forms of evidence do not contradict each other, but rather
reflect an absence of correlative evidence in the record, making it improper not to
afford more weight to the parents’ affidavits. See Pet’r’s Mot. at 16–17 (citing
Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), Campbell ex.

26 As the Chief Special Master explained, “[M.S.B.]’s parents asserted that ‘within
ten days of the vaccine[,]’ [M.S.B.] developed a ‘pretty bad’ upper respiratory
infection which required a pediatric visit.” Bast, 2012 WL 6858040, at *8. Since the
vaccinations were administered December 4, the recounted visit would have
occurred “on or about December 14, 1998,” but [M.S.B.]’s contemporaneous medical
records indicate that she saw the pediatrician on December 30, 1998, for cold
symptoms present by that time for one week. Id. (citing Pet’r’s Ex. 23 at 6).
[M.S.B.]’s parents also recalled that [M.S.B.] began having “tics” on or about
December 21, 1998, and that she was having grand mal seizures by January 4,
1999. Id. at *8 n.24 (citing Pet’r’s Ex. 23 at 6). The Chief Special Master noted that
there were no references to tics or tremors in the records from [M.S.B.]’s December
30, 1998 sick visit, and the records from her January 11, 1999 visit indicated that
she had been experiencing stiffening and rhythmic moving of her extremities for
about five days. Id.

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rel. Campbell v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006), and
Camery v. Sec’y of Health & Human Servs., 42 Fed. Cl. 381, 391 (1998)).

While petitioner is correct that an absence of correlative evidence is certainly
less significant than the existence of evidence that actually negates a witness’s
recollection, it is still the task of the Chief Special Master to weigh such evidence
and the Court affords much deference to the Chief Special Master’s determination.
Here, the Chief Special Master carefully examined the evidence before her
regarding the timing of the onset of [M.S.B.]’s symptoms. She detailed the extent of
the conflicts between the parents’ affidavits and the medical records, and noted the
diligence of [M.S.B.]’s parents in seeking treatment during this time period. See,
e.g., Bast, 2012 WL 6858040, at *8. She also made note of the general presumption
in favor of contemporaneous medical records over later-recorded recollections. 27 See
id. at *6. Moreover, the parents’ recollection of the onset of upper respiratory
infection symptoms was directly contradicted by the medical records, as the latter
indicate that as of December 30, 1998, [M.S.B.]’s cold symptoms were present for
one week --- which would be nineteen days after the vaccinations. See Pet’r’s Ex. 23
at 6.

The Court can find no error in the Chief Special Master’s decision to afford
greater weight to the contemporaneous medical records than to the parents’ later-
recorded recollections, particularly in light of the extensive documentation of
[M.S.B.]’s doctor visits when her symptoms first began to appear. But the decision
on the timing of the onset of symptoms was of slight significance compared with the
Chief Special Master’s determination that Dr. Frye’s proposed timeframe of two to
four weeks is “much too short a period of time for oxidative stress to have caused
the degree of injury alleged.” Bast, 2012 WL 6858040, at *49. This was the primary
reason for the finding that petitioner did not meet her burden under the third prong
of Althen.

Petitioner also challenges this aspect of the Chief Special Master’s decision
under prong three of Althen. Pet’r’s Mot. at 18–19. Petitioner’s argument boils
down to noting that another judge in another case reversed a special master for
basing the onset of symptoms under Dr. Frye’s oxidative stress theory on “a hard
and fast limit of two weeks.” Id. (quoting Paluck, 104 Fed. Cl. at 482). The
relevance of this eludes the Court. The Chief Special Master relied on the

27
In Campbell, a special master’s decision not to conduct an evidentiary hearing
was found arbitrary and capricious in light of a similar tension between medical
records and later recorded recollections. See Campbell, 69 Fed. Cl. 775, 779–80
(2006). Here, in contrast, a hearing was held, at which petitioner was present and
chose not to testify. See Bast, 2012 WL 6858040, at *6.

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testimony of Dr. Jones that, even if it were possible for [M.S.B.]’s symptoms to occur
as alleged by Dr. Frye, it would take decades, not weeks, for such harm to occur.
See, e.g., Bast, 2012 WL 6858040, at *50. A decision, based on a different factual
record, that it was arbitrary to require that symptoms manifest within fourteen
days, hardly shows that the decision under review was reached in an arbitrary
manner.

It is clear to the Court that the Chief Special Master properly examined the
evidence before her, including the reports and testimony of all of the experts, in
reaching her conclusion that Dr. Frye’s testimony was not persuasive concerning
Althen prong three. See id. at *28–30, *48–50. Petitioner does not even attempt to
identify any errors in the Chief Special Master’s understanding of the crucial
testimony of Dr. Jones. Instead, petitioner again cites Paluck, in which a special
master was purported to have based his assessment of Dr. Frye’s testimony on
matters of style. Pet’r’s Mot. at 19 (citing Paluck, 104 Fed. Cl. at 475–76 n.26). But
nothing of the sort has been identified in the decision under review. The Chief
Special Master thoroughly explained her reasons for finding the testimony of
respondent’s experts to be more persuasive than Dr. Frye’s, in general and as
pertaining to the prong three analysis. See, e.g., Bast, 2012 WL 6858040, at *4–6,
*23–25, *48–50. The assessment of the reliability of expert testimony is
particularly entrusted to special masters as the finders of fact. See Porter, 663 F.3d
at 1250–51; Moberly, 592 F.3d at 1325–26. The Chief Special Master has
“considered the relevant evidence in the record, drawn plausible inferences, and
articulated a rational basis for the decision,” Hines, 940 F.2d at 1528, and the
evidence relied upon “was not wholly implausible,” Lampe, 219 F.3d at 1363. Her
determination that petitioner failed to prove a medically-appropriate time frame
under the third prong of Althen was not arbitrary but instead quite rational.
Petitioner’s third objection to the decision under review is thus rejected.

III. CONCLUSION

For the reasons stated above, the petitioner’s motion for review is DENIED
and the decision of the Chief Special Master is SUSTAINED. The Clerk of Court is
directed to enter judgment for respondent.

IT IS SO ORDERED.

s/ Victor J. Wolski
VICTOR J. WOLSKI
Judge

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