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) †

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*

[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).

-15-

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.

-23-

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,

-24-

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.

-25-

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.

-27-

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.

-28-

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.

-29-

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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