# In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS
No

. 0 9

- 0585 V (Filed: June 5 , 2013 ) (Reissued for Case Caption : June 21 , 2013)

* * * * * * * * * * * * * * * * * * * * * * *
LAMONA DODD

, parent of *
S.S.

, a minor, * PUBLISHED

* Petitioner, * Entitl ement, Seizure Disorder,

* Epilepsy, MMR Vaccination,

v. * Insufficient Proof of Causation

*
SECRETARY OF HEALTH AND * HUMAN SERVICES, *

* Respondent. *

*

* * * * * * * * * * * * * * * * * * * * * * *

Ronald C. Homer

, Conway, Homer & Chin

- Caplan, P.C., Boston, MA, for petitioner.

Voris E. Johnson , United States Department of Justice, Washington, DC, for respondent.

DECISION 1

On September 4, 2009, Lamona Sow ( “ petitioner ” or “ Mrs. Sow ” ) filed a

p etition under the National Childhood Vaccine Injury Act ( “ Vaccine Act ” ) 2

1 When this decision was originally issued, the parties were notified that the
decision would be post ed on the United States Court of Federal Claims’ website,
in accordance with the E

- Government Act of 2002, Pub. L. No. 107

- 347, § 205, 116 Stat. 2899, 2913 (codified as amended at 44 U.S.C. § 3501 note (2006)). The parties were also notified that they may seek redaction pursuant to 42 U.S.C.A. §
300aa

- 12(d)(4)(B ); Vaccine Rule 18(b) . Petitioner made a timely request for redaction and this decision is being reissued with the name of the minor child redacted to initials and the birthdate of the minor child redacted to the year only. Except for this footnote, no o ther substantive changes have been made. on2 behalf of her minor son, alleging that the injuries S.S. sustained were caused by
the vaccinations he received on October 1, 2007. Petition at 1. In particular, petitioner attributed S.S. ’s epilepsy and developmental delay to the measles

mumps

- rubella (“MMR”) and Diphtheria

- Tetanus

- acellular

- Pert ussis ( “ DTaP ” ) vaccines administered on October 1, 2007. 3 Id. Petitioner requested a ruling on
the record or alternately, summary judgment in her favor

. Id. at 27

- 28; See Vaccine Rule 8(d) (which incorporates the procedures set forth in Rule 56 of the Rules of the U.S. Court of Federal Claims ( “ RCFC ” ) )

.

The chief difficulty with the asserted claim is that petitioner’s theory of
vaccine

- related causation turned on a type of seizure that S.S. did not have when his disorder first presented. For this reason, as more fully explained below, petitioner’s claim cannot stand.

I. Procedural History

O n September 18 , 2009

, tw o weeks after filing her petition, petitioner filed (1) her affidavit; (2) S.S. ’s medical records, includ ing a list of the vaccines he had received; (3) a Vaccine Adverse Event Reporting System ( “ VAERS ” ) report filed

on S.S. ’s behalf; and (4) S.S. ’s school records

. See P et ’ r ’ s Ex s

. 1

- 17. Petitioner
asserted th at the “documents provide [d] preponderant evidence ... [ that S.S. ’s] vaccines were the likely cause of his epilepsy, and subsequent developmental
de lay.” Petition at 18.

R espondent file d her Rule 4(c) report in December of 2009

, recommending against compensation because the medical records upon which petitioner relied did not establish that she was entitled to Program compensation

. Respondent’s Report

2 The National Vaccine Injury Compensation Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99

- 660, 100 Stat. 3755, codified as amended, 42 U.S.C.A. §§ 300aa

- 10 et. seq. ( 2006). Hereinafter, individual section references will be to 42 U.S.C.A. § 300aa of the Vaccine Act.

3 Although petitioner identified both the MMR and DTaP vaccines in her petition as the causal agents, her subsequently retained expert opined that the

MM R vaccine singularly provoked S.S. ’s injuries. See Petitioner’s Exhibits (“Pet’r’s Exs.”) 18 at 5 (Expert Report of Dr. Kinsbourne filed June 3, 2010); 20 at 4 (Supplemental Expert Report of Dr. Kinsbourne filed December 21, 2010).
Consistent with her ex pert’s opinion, petitioner focused her attention in the post hearing briefing on the MMR vaccine alone. See Petitioner’s Post Hearing Brief (“Pet’r’s Br.”), Jun. 10, 2011, at 1; Petitioner’s Reply to Respondent’s Post Hearing Brief (“Pet’r’s Reply to Resp ’t’s Br.”), Aug. 12, 2011, at 1.3 ( “ R esp’t ’s R eport ” ) at 2 , 8

- 9

. Respondent asse r ted that “if the Special Master were to rule upon petitioner’s Motion for a Ruling on the Record, the appropriate ruling would be dismissal of the Petition for a failure of proof.” Id. at 1 n.1.

The formerly assigned special master held a status conference i n December
of 2009

, afford ing the parties an opportunit y to discuss settlement options before ordering p etitioner to file an expert report. Order

, Dec

. 10, 2009. The parties failed to reach a settlement, and the then

- assigned special master ordere d petitioner to file “ an expert r eport, [the] curriculum vitae of the opining expert, and copies of any articles of medical literature relied upon [by the expert] in forming the [offered] opinion .” Order, Jan. 6, 2010. Petitioner requested and
received several extension s of time to comply with the order

. See, e.g

. , Order

, Mar

. 23, 2010.

I n March 2010, the case was reassigned to the undersigned. Three months later, o n June 3, 2010, petitioner filed an expert report from Dr. Marcel
Kinsbourne

, a pediatric neurologist. Accompanying the expert report w as his
curriculum vitae and nine articles upon which he had relied in forming his opinion

. See P et’r ’s Exs. 18 (including Tabs A

- I); 19. Dr. Kins bourne posited that the
MMR vaccin e S.S. received on October 1, 2007

, caused a n encephalopathy that
manifested first as a seizure disorder , and later as developmental delay and hyperactivity with attention deficits

. P et’r ’s Ex. 18 at 4.

In July 2010, the undersigned held a status conference with the parties to clarify whether S.S. ’s initial seizures were accompanied by fever. See Order

, Sept

. 14, 2010 . P etitioner’s counsel indicated that S.S. ’s presenting seizures were
without fever. Id. At that time, t he undersigned afford ed the Secretary sixty days
to file her responsive expert report. Id.

In September 2010, respondent filed the expert report and curriculum vitae
of Dr. John McDonald, a pediatric neurologist. See Respondent’s Exhibits (“R esp’t’s Ex s

. ”) A ; B. Respondent also filed several supporting articles to which
Dr. McDonald cited in his report

. See R esp’t ’s Ex. A (Tabs 1

- 3). Dr. McDonald disagreed with Dr. Kinsbourne’s opinion of vaccine

- related causation

. Resp’t’s
Ex. A at 3. He attribut ed S.S. ’s seizure disorder , developmental delay and attentional problems to an “ underlying genetic basis

, ” but he acknowledged th at th e results of any standardized genetic and metabolic testing were not included in
the filed medical records. Id. at 4.

In a subsequently filed sta tus report, petitioner clarifie d that she wa s not alleging a n e ncephalopathy as defined by the Vaccine Injury Table and had
discussed the afebrile nature of S.S. ’s seizures with Dr. Kinsbourne. She asked to
file a supplemental ex pert report to describe petitioner’s theory more clearly

.4 Petitioner’s Status Report, Oct. 22, 2010, at 2. The undersigned grant ed petitioner’s request. First Order, Oct. 28, 2010.

P etitioner filed her supplemental expert report from Dr. Ki nsbourne in
December 2010 . P et’r ’s Ex . 20 (including Tabs A

- E). In his supplementa l report,
Dr. Kinsbourne asse r ted that S.S. had not suffered an encephalopathy

-- as defined by the Program ’s Vaccine Table Injury

-- but instead ha d suffered a medical encephalopathy

, as more broadly defined by the Institute of Medicine ( “ IOM ” ).

P et’r ’s Ex. 20 at 1; compare 42 C.F.R. § 100.3(b)(2) with P et’r ’s Ex. 18, Tab G (1994 IOM report) 4 at 137. Dr. Kinsbourne further asserted that when a seizure occurs within a medically reasonable time frame after an MMR immunization, it
need not be accompanied by fever to establish vaccine

- related causation. P et’r ’s
Ex. 20 at 2.

P etitioner filed a dditional medical records in February and March 2011

, f

urther to a subpoena issued by the undersigned. See First Order, Feb. 28, 2011 ;

s ee also, e.g

. , P et’r ’s Ex s

. 23; 24 ( Medi cal Records filed Mar. 21, 2011 )

.

On March 18, 2011, t he undersigned heard the testimony of the experts

. The reafter, the parties file d post

- hearing briefing.

Th e c laim i s now ripe for a ruling

.

II. S.S. ’s Medical History

S.S. was born in 2003. P et’r ’s Ex. 3 at 19 . He was delivered without complications at 37 weeks

, weigh ing seven pounds. His head circumference
measured 1 9.5 inches, and he displayed no observ able abnormalities. Id. at 19. His Apgar score was 9 at both one and five minutes. 5

4 Kathleen R. Stratton, et al., Adverse Events Associated With Childhood Vaccines: Evidence Bearing on Causality , Institute of Medicine 1

- 464 (1994). B oth his hearing and

5 An Apgar score is “a numerical expression of the condition of a new born infant . . . [determined by] the sum of points gained on assessment of the heart rate, respiratory effort, muscle tone, reflex, irritability, and color.” Dorland’s Illustrated Medical Dictionary 1682 (32nd ed. 2012). The scale ranges from 0 (the
low est score) to 10 (the highest score). U.S. National Library of Medicine, MedlinePlus, Apgar, http://www.nlm.nih.gov/medlineplus/ency/article/003402.htm (last visited on April 17, 2013).5 metabolic screening tests were satisfactory

. Id. at 23, 29. S.S. and his mother were discharged from the hospital two days after his birth. Id. at 26.

From birth until four years of age

, S.S. received the scheduled complement
of routine childhood vaccinations. See P et’r ’s Ex. 13 at 1. H e also experienced

common childhood ai l ments

, including runny nose s , cough ing , sore throat s , diarrhea, fever s , and ear infection s. H is doctors attributed the se various ailments to either upper respiratory infections or aller gies. E.g.

, P et’r’s Exs. 3 at 56; 5 at 3.
S.S. also contracted strep pharyngitis once and conjunctivitis (o ften referred to as pink eye) twice. P et’r ’s Ex. 5 at 1, 10, 11. 6

In August of 2005

, at 23 months of age, S.S. re quired emergent care for a
fall during which he bumped his head. See P et’r ’s Ex. 3 at 86

- 102

. The records
from the emergency room v isit appear to indicate that S.S. exhibited “c onfusion ”
after his head injury , but admittedly the term “confusion” is not clear in the
records. Id. at 92. S.S. was discharged with instructions to petitioner to return if
her son’s symptoms persist ed or worsen ed after th ree days

. Id. at 98.

Nearly seven months later, a t two and one half years of age

, S.S. began attending daycare. P et’r ’s Ex. 1 6 at 1. H e exhibited no health problems. P et’r ’s
Ex. 1 0 at 1.

S.S. began attending pre

- kindergarten at four years of age

, in August 2007

. See P et’r ’s Ex. 1 1 at 1. An early screen ing test administered shortly after he
started school showed that his articulation skills were “ fair

. ” I d. at 3. His progress report s , however, showed a decrease in his a bilities between the second and third
quarter s

-- as evidenced by the change in his skill categor y rankings from “in progress” to “non

- mastered” in a number of areas. Id. at 7.

O n O ctober 1, 2007

, S.S. received the MMR and DTaP vaccination s of which petitioner has complained in this vaccine claim. See P et’r ’s Ex. 13 at 1. In
the VAERS report petitioner filed on S.S. ’s behalf

, she stated that one week after
his vaccination s , S.S. developed a cough and fever of approximately 100 degrees

, but “ continued ” to attend sc hool. P et’r ’s Ex. 12 at 1.

On October 15, 2007, two weeks after S.S. ’s vaccinations, he was not feeling well again

. Although he did not have a fever, he did have a headache

, abdominal pain, nausea with vo miting, and an e pisode of diarrhea l incontinence during the day

. Pet’r’s Ex. 3 at 169. Later that day

, S.S. experienced a left

- sided

,

6 S.S. also suffered a foot injury in January 2006; it resolved ind ependently
after a week of rest. Pet’r’s Ex. 5 at 6

- 7.6 focal tonic

- clonic seizure that prompted petitioner to seek care at the h ospital. 7

P et’r ’s Ex. 16 at 2; accord. P et’r ’s Ex. 3 at 167, 169 , 177

- 178

.

On admission to the hospital, S.S. was examined by Dr. Phillip Norsworthy, the attending emergency room physician. See P et’r ’s Ex. 3 at 169. Dr. Norsworthy administered a d ose of Ativan , an anti

- epileptic medication, to S.S. and ordered several tests

, including a comput ed tom ography ( “ CT ” ) scan of
S.S. ’s head

. 8 Id. S.S. ’s test results returned as normal , but were suggestive of
sinus disease. Id. A fter discussions with Dr. Hemant Aga r wal

, a specialist in pediatric critical care, Dr. Norsworthy transferred S.S. to the pediatric intensive
care unit “for

. . . further evaluation ” and an ele ctroencephalo gram ( “ EEG ” ). 9 Id.

Dr. Agarwal observed and treated S.S. until hi s discharge (the day after his admission). Pet’r’s Ex. 3 at 167. During hi s hospital admission, S.S. experienced
left

- sided weakness that resolved. Id. His seizures were managed by the two anti

seizure medication s

-- Ativan and fosphentoin

-- t he combination of which appe ared
to assist S.S. ’s return to “normal ” before his discharge

. Id.

After consulting with pediatric neurolog ists at Vanderbilt Children’s

Ho spital, Dr. Agarwal placed S.S. on K eppra, another anti

- seizure medication

, to

7 The record evidence offers conflicting accounts regarding when S.S. first began feeling ill. Compare Pet’r’s Ex. 16 at 2 (petitioner’s affidavit indicating
S.S. stayed home from school), with P et’r’s Ex. 3 at 177 (pediatric records indicating that S.S. vomited at school, necessitating an early school pickup by his grandmother), and Pet’r’s Ex. 3 at 169 (hospital’s records indicating S.S. became sick that evening). But each of the accounts consi stently state that S.S. first experienced multiple staring spells followed by seizure activity on the evening of October 15, 2007. See, e.g. , Pet’r’s Ex. 3 at 169.

8 A CT scan produces a three

- dimensional view of body structures by “passing x

- rays through the body organs at many angles through 360 degrees.” Mosby’s Manual of Diagnostic and Laboratory Tests 1030 (4th ed. 2010). “Each degree of density is given a numer ic value called a density coefficient, which is digitally computed into a shade of gray.” Id. A head CT scan will give a “well imaged” view of the brain. Id. at 1080. It “is useful in the diagnosis of brain tumors, infarction, bleeding and hematomas.” Id.

9 “The EEG is a graphic recording of the electrical activity of the brain.” Id. at 573. It “is invaluable in the investigation of epileptic states.” Id. “[S]eizure activity is characterized by rapid, spiking waves,” while “[p]atients with cer ebral lesions (e.g. tumors, infarctions) will have abnormally slow EEG waves.” Id.7 be administered twice daily. Pet’r’s Ex. 3 at 167. Dr. Agarwal also prescribed
Diastat , an ad ditional anti

- epileptic medication

, to be administered rectally in the
event of a seizure last ing more than five minutes

. Id. S.S. was discharged on October 16, 2007

, with a referral to the Pediatric N eurology Clinic at Vanderbilt Children’s Hospital for a follow

- up visit

. Id.

T he results of S.S. ’s EEG

, dated one week later

, showed that he had experienced subtle slowing throughout his right cerebral hemisphere

. Pet’r’s Ex. 3
at 207. B ut

, it did not show any seizure activity

. Id.

Nearly six weeks later, o n December 9 , 2007, petitioner took S.S. back to the emergency room fo r a second seizure episode. Pet’r’s Ex. 3 at 240. D r. Geoffrey Fleming, t he examining physician during that emergency room visit

, noted that S.S. presented following an “ approximately 45

- minute generalized
tonic

- clonic seizure [that] requir[ed] multiple medications ” to control. Id.

P etitioner explained that S.S. had been napping on her lap during a church meeting when he awakened

, “stiffened and drooled for a while .” Pet’r’s Ex. 3 at 252. Once back at home

, S.S. returned to his nap and could not be a wakened

. Again, he stiffened and “vomited several times. ” Id. Concerned about S.S. ’s presentation, p etitioner took him to the hospital for evaluat i on

. Id.

“En route to the emergency room , he went from tonic to clonic convulsive

movements

. ” Pet’r’s Ex. 3 at 252. He still was convulsing when he arriv ed at the hospital

, and he required anti

- epileptic medication “to break his seizure.” Id. S.S.

was noted to be afebri le . H is head CT scan and laboratory results were normal.
Id. at 240. H e slowly returned to his neurologic baseline after a two

- day hospital
stay

. Id.

Petitioner acknowledged during that hospital visit that she had stopped giving S.S. the medication he began taking after his first seizure event in October
because it made him “ very dizzy and restless

. ” 10

10 As mentioned in Dr. Fleming’s notes, petitioner complained that the
medication made S.S. sleepy. Pet’r’s Ex. 3 at 240. Also mentioned in the notes of
the case worker

-- who observed S.S. and conferred with petitioner during the December hospitalization

-- was petitioner’s concern that the prescribed seizure medicine was contributing to S.S. ’s dizziness. Id. at 281. The case worker reported that she too had observed S.S. ’s dizziness and unsteady gait. Id. P et ’ r’ s Exs. 3 at 281; 16 at 2.

P etitioner further acknowledged that she had not taken S.S. for his follow

- up visit

, as directed, after his first seizure episode. P et’r ’s Ex. 3 at 252, 281. Dr. Fleming

, the attending p hysician during S.S. ’s hospitalization f ollowing his second seizure8 event, urged petitioner to continue to administer S.S. ’s seizure medication and to schedule an appointment for S.S. with Dr. Ahmad Alhamda, a pediatric neurologist affiliated with a f acility preferred by petitioner. Id. at 240, 253, 281.

T wo weeks later, o n December 21, 2007, petitioner took S.S. to see Dr.
Alh amda . Dr. Alhamda made note of S.S. ’s two earlier emergency room visits
and his “family history ” of “ epilepsy in an aunt

, ” whose seizure disorder began in early childhood. 11 P et’r ’s Ex. 8 at 10 . Dr. Alh amda described S.S. as “a 4 year old with [a] history consistent with generalized secondary epilepsy.” Id. He
ordered an EEG and a magnetic resonance imag e ( “ MRI ” ) of S.S. ’s brain

. Id. He
also i ncreased S.S. ’s dosage of Keppra, and provid ed pet itioner with a calendar to track S.S. ’s seizure activity

. Id.

Two week s later, o n January 9 , 2008, petitioner again sought emergen t care for S.S. for his hourly episodes of minute

- long

, tonic

- clonic seizures

. P et’r ’s Ex. 7
at 46. The attending physician, Dr. Kathryn McVicar

, made note of a family history of epilepsy in an aunt and ordered both an MRI and an EEG

. Id. at 4. The

MRI was n ormal , b ut S.S. ’s EEG showed seizure activity in his fronto

- temporal region. P et’r’s Exs. 7 at 46, 48

- 49 ; 8 at 7. T wo medication s , Ativan and fosphenytoin

, were administered to halt the seizures , and the anti

- epileptic Zonegran was added to S.S. ’s prescription regimen for b etter seizure control

. P et’r ’s Ex. 7 at 46.

Nearly one week later, o n January 15, 2008, S.S. saw Dr. Alhamda for a follow

- up visit . Pet’r’s Ex. 8 at 5. Dr. Alhamda noted S.S. ’s emergency room visit earlier in the month and observed that S.S. ’s gait was still slightly unsteady.
Id. Without comment, Dr. Alham d a recorded the Sow s ’ impression that the prescribed anti

- epileptic medication had exacerbated S.S. ’s seizures

. Id. Similarly, h e recorded Mrs. Sow’s belief that S.S. ’s seizure disorder began shortly after his vaccinations and the Sows’ concern regarding immunizations. Id. Dr.
Alhamda observed that S.S. ’s “[s]eizures seem [ed] to be consistent with [a] frontal [ lobe

- ]type epilepsy, ” a type of seizure condition accompanied by behavioral changes. Id. at 6; see also , Pet’r’s Ex. 7 at 46 (the EEG results show S.S. suffered approximately seven seizures). Dr. Alhamda increased the dosage of S.S. ’s anti

seizure medications

. Id. H e asked to see S.S. regularly and indicated that he was

eager to arrange for a “comprehensive epileptic evaluation” of S.S

. Id.

11 Dr. Fleming’s notes from S.S. ’s October visit to the emergency room also
made reference to S.S. ’s aunt’s seizure condition. Pet’r’s Ex. 3 at 169. Although Dr. Agarwal, another attending physician during that sa me hospital stay, noted that there was “no family history of seizures,” Id. at 17, the records contain a number
of indications that S.S. , in fact, had an aunt with epilepsy. See Pet’r’s Exs. 7 at 4; 14 at 4, 17 (referencing S.S. ’s great aunt who had epile psy.)9 The next week, Dr. Alhamda noted a decrease in the number of S.S. ’s
seizure s . He was experiencing only two episodes a day, but the seizures w ere now longer in duration. Pet’r’s Ex. 8 at 3

. Although Dr. Alhamda found S.S. ’s
restlessness to be suggestive of A ttention Deficit Hyperactivity Disorder ( “ ADHD ” )

, he a cknowledged that some of S.S. ’s attentional issues m ay have emerged as a “side effect” of the seizure medication

. Id. at 3

- 4. Dr. Alhamda adjusted the dosage and combination of S.S. ’s medication s. Id.

S.S. returned to Dr. Alhamda one month later. His seizures had ceased , and his hyperactivity was diminished

. Pet’r’s Ex. 8 at 1. Dr. Al hamda indicated in his

notes that since S.S. ’s last visit, petitioner had stopped administering the K eppra , had continu ed to administer the prescribed dosage of Zonegran

, and had failed to
add the Topamax he had prescribed

. Id. Dr. Alhamda increased S.S. ’s prescription for Zonegran and urged petitioner to consult with him before altering
S.S. ’s seizures medication s

. Id. at 1

- 2.

Nearly six weeks later, o n April 10, 2008, S.S. saw another neurologist, Dr.
Eric Pina

- Garza at the Vanderbilt Children ’s Hospital. Pet’r’s Ex. 14 at 17. Dr.
Pina

- Garza not ed that S.S. was taking a daily dosage of Zonegran and had last
seiz e d ten days earlier. Id. He recorded a family history of seizures in a maternal
great aunt and described S.S. ’s epilepsy as having an “ unclear etiology.” Id. He
started S.S. on Depakote , another anti

- epileptic medication, and ordered an EEG.

T h at EEG

, which was performed two weeks later, was n ormal

. Id. at 13.

S.S. continued to see Dr. Pi na

- Garza

. See

, e.g. , P et’r ’s Ex. 23 at 19. He also received more regular care at the East Jackson Family Medical Center. See

P et’r ’s Ex. 6. Although h is seizures were well

- managed , the administered
medication s made S.S. drowsy and caused him to sleep during school

. Id

. at 11

. S.S. also began to exhibit serious behavior al problems. Id. at 15.

Four months after Dr. Pina

- Garza began to treat S.S. , he added a new ant i

epileptic medication, Trileptal

, to S.S. ’s prescriptive regimen and began to de creas e S.S. ’s dosage of Depakote

. P et’r ’s Ex. 14 at 11. Three months later , Dr.
Pina

- G arza reported that S.S. was no longer experiencing seizures

, i d. at 4, and was no longer sleeping at school

. P et’r ’s Ex. 6 at 7. In addition, he was behaving
much better. Id. Not withstanding the noted improvement, S.S. was directed in to a

s pecial e ducation p lacement at school and was encouraged to repeat pre

k indergarten. P et’r ’s Ex. 15 at 27.

Two years later, S.S. began taking Adderall , on the recommendation of his treating physicians, to manage his hyperactivity. See, e.g.

, P et’r ’s Ex. 21 at 11.10 III. Expert Reports and Testimony

The parties offered the opinions of expert witnesses.

A. Petitioner’s Expert

1. His Professional Qualifications

Petitioner offered the expert opinion of Marcel Kinsbourne, M.D., a pediatric neurologist. Transcript of Testimony (“Tr.”) at 18. Dr. Marcel
Kin sbourne was educated at Oxford University and received his medical degree in
1955. P et’r ’s Ex. 19 at 1 (Curriculum Vitae of Dr. Kinsbourne). He continued his education at Oxford, earning additional degrees in the fields of neurology and pediatrics. In 1 967, he received his medical license from the state of North Carolina and became an associate professor of neurology and pediatrics at the Duke University Medical Center and a Senior Research Associate at the Center for the Study of Aging and Human Development. Id

. In 1974, Dr. Kinsbourne
moved to Canada

, accepting appointments as a professor of psychology at the University of Waterloo and a professor of pediatric neurol ogy at the University of

Toronto. Id. He returned to the United States in 1980 to become the Director of
the Behavioral Neurology Department at the Eunice Kennedy Shriver Center. Id. at 1, Tr. at 5. He currently is a professor of psychology at the New School located
in New York C ity. Id.

At the New School, Dr. Kinsbourne teaches graduate students in clinical psychology and oversees a laboratory employing twelve research assistants. Tr. at
6. Although he often sees children during the course of his research and did so during his work at the Eunice Kennedy Shriver Center, Dr. K insbourne does not provide active care. Tr. at 32. His work does not “involve the diagnosis or
treatment of seizure disorders.” Tr. at 32

- 33.

During his testimony

, Dr. Kinsbourne a cknowledged th at th e focus of his
work has been on behavioral disorders and not on seizure disorders . He further

a cknow ledged t hat he has not “seen a pediatric patient on an acute basis for the diagnosis and treatment of a neurological illness, other than a behavioral disorder,
since at least 1981 ” (now more than 30 years ago) Tr. at 34. Dr. Kinsbourne
ind icated that appr oximately fifty

- five to sixty percent o f his income comes from
medical work in legal cases

. Tr. at 31.

Based on Dr. Kinsbourne’s documented training and experience, the undersigned accepted his tendered expertise as a medical consultant on issues of

pe diatric neurology, specifically involving behavioral disorders

. Id.11 2. His Opinion of Causation

Dr. Kinsbourne pr epared an initial and a supplemental expert report

. See

P et’r ’s Ex . 18 (Expert Report filed J une 3, 2010); P et’r ’s Ex. 20 (Supplemental Expert Report filed December 21, 2010). He opined that the MMR vaccine
administered to S.S. on Oct ober 1, 2007

, caused him to develop a seizure disorder
and in turn

, led to his severe hyperactivity and developmental delay

. P et’r ’s Ex.
18 at 3 , 5

. A l t ernatively, Dr. Kinsbourne asserted that the seizure s S.S. first experienced on October 15, 2007 , led to a l owering of his seizure threshold and
allowed his subsequent injuries to develop . P et’r’s Exs. 18 at 4; 20 at 1 ; Tr. at 83

- 84

.

a. The Triggering of S.S. ’s Seizure Disorder

Dr. Kinsbourne held the MMR vaccine S.S. received in October 2007 responsible for the onset of his seizure disorder . He reasoned that S.S. experienced his first seizure event two weeks after his MMR immunization, which
is an acceptable time frame for an adverse reaction to the MMR vaccine

-- p articularly if there is no other explanation for seizure onset

. P et’r ’s Ex. 18 at 2;
Tr. at 28.

A dmitt ing that he could not describe the particular m echanism by which the
administered MMR vaccin e caused S.S. ’s seizure di s order

, 12 Dr. Kinsbourne
identified S.S. ’s first seizure episode o n October 15, 2007

, as the beginning of his epileptic condition

. Tr. at 25, 43 , 87

. Dr. Kinsbourne posite d that becau se the
wild m easles virus can cause seizures

, the measles vaccine ( an attenuated but live
viral vaccine ) also c an cause seizures

, a l beit “far less frequently.” P et’r ’s Ex. 18
at 3 ; accord. Tr. at 19

- 20 . He theorized that the m echanism by which the measles
virus and the measles vaccine could trigger seizures would be the same

. Tr. at 43.

Citing several studies and 1994 IOM report

, Dr. Kinsbourne averred t hat “[s]eizures after MMR vaccination have been rep eatedly documented [and] [t]heir peak incidence [occurs ] within the second week after vaccina tion

. ” 13

12 Dr. Kinsbourne testified that “[i]t’s not believed that the measles virus actually invades the brain.” Tr. at 25. P et’r ’s Ex.

13 The studies and report by the IOM were filed with Petitioner’s Exhibit 18

as:

Tab A: R. Alderslade et al., The National Childhood Encephalopathy Study 79

- 183 (1981). Tab D: Philip J. Landrigan, M.D., et al., Neurologic Disorders Following Live12 18 at 3

. He observed that S.S. ’s seizure event on October 15, 2007

, occurred during the second week after his MMR immunization and thus

, implicated that particular vaccine. Tr. at 42. But, Dr. Kinsbourne conce ded that timing alone is
not sufficient to prove causation

. Tr. at 49

- 50.

To bolster his opinion of vaccine

- related causation, Dr. Kinsbourne averred
that no other cause for S.S. ’s seizure event existed. P et’r ’s Ex. 18 at 2

. Discounting the record evidence of a “distant relative” with epilepsy , Dr.
Kinsbourne di smissed the likelihood that a genetic underpinning was primarily responsible for S.S. ’s seizure condition

. Dr. Kinsbourne instead insist ed that
adverse environmental f actor s

-- s pecifically, the administered vaccines

-- acted in

concert with S.S. ’s latent genetic predisposition to trigger the e xpress ion of a
seizure condition . Tr

. at 24, 28.

Dr. Kinsbourne unwaveringly pointed to the MMR vaccine as the causal trigger for S.S. ’s initial afebrile seizure event . R eferencing s everal case reports of
seizures occurring in afebrile subjects w ith gastrointestinal illness es , 14 h e asserted
that sei zures do not occur sole l y as a “ reaction to a rise in body temperature.”

P et’r ’s Ex. 20 at 1

- 2

. H e acknowledg ed , however, that fever and rash are the two

most com mon symptoms that accompany wild measles viremia 15

Measles

- Virus Vaccination, 223(13) JAMA 1459

- 62 (1973). -- which reaches its peak two weeks after a measles infection. Tr. at 61. H e further acknowledge d

Tab G: Kathleen R. Stratton, et al., Adverse Events Associated With
Chil dhood Vaccines: Evidence Bearing on Causality , Institute of Medicine

1

- 464 (1994). Tab I: Robert E. Weibel, M.D., et al., Acute Encephalopathy Followed by Permanent Brain Injury or Death With Further Attenuated Measles
Vaccines: a Review of Claims Submi tted to the National Vaccine Injury Compensation Program , 101 (13) Pediatrics 383

- 87 (1998).

14 These studies were filed with Petitioner’s Exhibit 20 as:

Tab C: Wei

- Ling Lee, et al., Afebrile Seizures Associated with Minor Infections: Comparison with Febrile Seizures and Unprovoked Seizures

, 31(3) Pediatric Neurology 157

- 164 (2004). Tab D: Hassib Narchi, Benign afebrile cluster convulsions with gastroenteritis: an observational study , published at
www.biomedcentral.com/1471

- 2431/4/2 (an open access site) on MBC Pediatrics 4:2 (2004).

15 Viremia is “the presence of viruses in the blood.” Dorland’s at 2058.13 that this is the first instance in which he ha s “offered the opinion that the MMR
vaccine caused an afebrile seizure.” Tr. at 30.

Dr. K insbourne recognized that neither f ever nor rash

-- “the mo st prominent
clinical symptoms”

-- during the peak period

, of measles viremia, Tr. at 61, were present at the time of S.S. ’s October 15, 2007 seizure event

, Tr. at 39

- 40, not even in the milder form of presentation that might appear after an administration of the
attenuated viral measles vaccine. In an effort to explain the absence of the most common symptoms of m easles

- associated viremia in S.S. ’s case, Dr. Kinsbourne
offered that “neither of [ the symptoms] are seen” in cases involving a measles

induced inflam mation known as measles encepha litis, which can lead to serious brain damage and death . Tr. at 61; See also Robert M. Kliegman et. al., Nelson
Textbook of Pediatrics 1072 (19th ed. 2011) (describing t he “unf avorable

outcome s ” in children afflict ed with measles encephalit is).

Dr. Kinsbourne posited that the fever S.S. is alleged to have developed 16
( one week before his seizure event on October 15, 2007 ) wa s attributable to the MMR vaccine and thus, furnished “evidence of viremia

. ” P et’r ’s Ex. 20 at 1 ; Tr.
at 61

. He did not address, however, the subsequent symptoms of vomiting and
diarrhea that S.S. developed shortly before his first seizure event; such symptoms may have been associated with a gastrointestinal illness.

b. All e gations of a Seizure

- Induced Encephalopathy

In Dr. Kinsbourne ’s view, S.S. ’s initial seizure was a vaccine

- precipitated
event that caused brain damage and led to a seizure disorder . He posited th at the
MMR vaccine S.S. received caused the first seizure event i n October 2007 , and effectively, l owered S.S. ’s seizure threshold

, which allow ed him to experience seizures more easily.

Dr. Kinsbourne clarified that S.S. did not suffer an encephalopathy as
de fined by the Vaccine Injury Table

. P et’r ’s Ex. 20 at 1. Rather, Dr. Kinsbourne explained

, S.S. suffered an encephalopathy

, a s more broadly defined by the IOM

. According to the IOM , an encephalopathy is “any acute or chronic

, acquired abnormality of, or injury to, or impairment of function of the brain.” P et’r ’s Ex. 18, Tab G (1994 IOM report)

, at 137

.

16 Petitioner claimed in the VAERS report she filed on S.S. 's behalf, that S.S.
de veloped a fever a week after his vaccination. See Pet’r’s Ex. 12 at 1.14 Citing s everal filed articles

, 17 Dr. Kinsbourne asserted that “prolonged or recurrent seizure activity . . . can irreversibly alter the way the immature br ain develops.” P et’r ’s Ex. 18 at 4. But

, he a dmitted that the seizures S.S. first experienced on Octo ber 15, 2007

, could not be characterized as the type of prolonged seizure capable of causing brain damage . As he described S.S. ’s initial seizure event, it involved staring spell s last ing less than a minute

, followed by a later episode last ing only a few minutes. Tr. at 37. Although the episode was

unsett l ing to petitioner, it was not protracted.

Dr. Kinsbourne also relied on the results of S.S. ’s earliest EEG (the day after his first seizure event) to su pport his theory of vaccine

- related causation.

P et’r ’s Ex. 20 at 1. That EEG showed “a right hemisphere abnormality

. ” Id. But,
Dr. Kinsbourne conceded

-- when questioned further

-- that the EEG results were “consistent with a postictal state” following seizure and were not dispositive of permanent damage. Tr. at 41

- 42

. After more questioning, Dr. Kinsbourne acknowledged that S.S. behaved “ normally ” a nd s h owed “ no neurological symptoms” the day after his first seizure episode

. Tr. at 39.

Dr. Kinsbourne posited that after S.S. ’s f irst seizure event

, he was merely in “an abnormal neurological state.” Tr. at 86. However, after his subsequent seizure episode on December 9, 2007

, S.S. “began to experience . . . severe epilepsy” that radically changed his behavior and school achievements

. 18

17 These articles were filed with Petitioner’s Exhibit 18 as: Tr. at

Tab B: Bruce Hermann, et al., The Neurodevelopmental Impact of Childhood

onset Temporal Lobe Epilepsy on Brain Structu re and Function , 43(9) Epilepsia 1062

- 71 (2002). Tab C: Gregory L. Holmes and Yehezkiel Ben

- Ari, The Neurobiology and Consequences of Epilepsy in the Developing Brain , 49 (3) Pediatric
Research 320

- 25 (2001). Tab F: Carl E. Stafstrom, Assessing the behavi oral and cognitive effects of seizures on the developing brain , 135 Progress in Brain Research 377

- 390 (2002). Tab H: Thomas P. Sutula, Mechanisms of epilepsy progression: current theories and perspectives from neuroplasticity in adulthood and development , 60 Epilepsy Research 161

- 171 (2004).

18 S.S. experienced behavioral problems at school. Pet’r’s Ex. 6 at 15. In addition, his performance decreased from “in progress” to “non

- mastered” in a
number of the skills that were assessed between th e second and third quarters of the school year. Pet’r’s Ex. 11 at 8. On December 15, 2008, S.S. ’s Individual15 13. Dr. Kinsbourne explained that the f irst seizure episode left S.S. os tensibly still

“ within the mainstream” because there was no mention in the medical records of

any change in his conduct

. Tr. at 22

- 23. It was o nly after hi s second seizure event and subsequent seizure episodes that S.S. ’s developmental delay and hyperactivity
manifest ed

. Id.

c. The Emerg ence of S.S. ’s ADHD and Developmental Delay

Dr. Kinsbourne also opined that S.S. ’s hyperactivity and his developmental delay were caused either by his vaccine

- induced epilepsy or the seizure

- related
medication he was prescribed

. Pet’r’s Exs. 18 at 4

- 5; 20 at 3

- 4. Comparing
S.S. ’s condition before and after he received the MMR vaccine, Dr. Kinsbourne
averred that the MMR vaccine S.S. received impaired his n ormal functioning and left him performing at “a special education level.” Tr. at 66. But when directly questioned about S.S. ’s intellect before his vaccination , Dr. Kinsbourne acknowledged that accurate IQ testing cannot be performed prior to “the four th year of life

. ” Tr. at 62

- 64

. The record indicates that S.S. was four years old when
his se izure disorder first manifested, s ee Pet’r ’s Ex. 3 at 19; at the same time, he reached the appropriate age for intelligence testing.

d. Pondering the Genetic Influences on S.S. ’s Condition

Dr. Kinsbourne commented that no “underlying genetic disorder” had been
established in S.S. ’s case. Pet’r’s Ex. 20 at 3. He note d that as a former clinical pediatric neurologist

, he would not have recommended genetic testing for a child
wh o

-- similar to S.S.

-- had presented “with a sei zure disorder, a low IQ and [hyperactivity] ” b ecause such t esting woul d not have inform ed t he child’s

treatment. Tr. at 59

- 60. Nonetheless, the undersigned notes that s uch testing could provide a better understanding of the nature of S.S. ’s seizure disorder.

B. Respondent’s Expert

1. His Professional Qualifications

Respondent offered John McDonald , M.D., as an expert in the field of pediatric neurology

. Dr. McDonald was educated at the University of Michigan

. R esp’t ’s Ex. B at 1 (Curriculum Vitae of Dr. McDonald). After two years of
service in the United States Na vy, Dr. McDonald attended medical school at the University of Miami

. Id. He is board certifi ed in pediatric neurology. Tr. at 89.

Education Program (“IEP”) team recommended a special education placement for
him. Pet’r’s Ex. 15 at 27.16 Dr. McDonald is currently an Assistant Professor at the University of Minnesota Medical School, Department of Pediatrics . R esp’t ’s Ex. B at 1. He
testified that his duties include monitoring hospitalized patients one week each
month , staffing the pediatric neurology clinic twice a week, occasionally assisting at the bone marrow clinic, teaching medical students , and conduct ing research. Tr.
at 90. Dr. McDonald ’s patients r ange from the unborn to eighteen years of age.

Tr. at 91. He estimated seeing between 30 and 50 patients each week. Id. As an integral part of his clinical practice, h e diagnoses and treats chi ldren with seizure
disorde rs and instructs medical students about such conditions. Tr. at 92.

The undersigned accepted Dr. McDonald as an expert in pediatric neurology who actively treats children with seizure disorders

. Tr. at 94.

2. His Opinion Regarding Causation

Dr. McDonald disagreed with Dr. Kinsbourne ’s view that S.S. ’s seizure
disorder resulted from the immunizations he received on October 1, 2007.

R esp’t ’s Ex. A at 3. Dr. McDonald observ ed that the medical records contain n o

e vidence

, other than timing, to link the two events. R esp’t ’s Ex. A at 3; Tr. at 102.
None of S.S. ’s “treating physicians associate d the immunizations directly with [ his ] seizure s or developmental delays/ADHD.” Resp’t’s Ex. A at 3. N o r is there evidence suggesting that an acute encephalopathy occurred after S.S. ’s
vaccinations. Tr. a t 95

- 96.

a. Challenging the Vaccine

- Relatedness of S.S. ’s Seizure
Disorder

Dr. McDonald a cknowledged that the “natural measl es disease can cause
seizures.” Tr. a t 124. He indicated that although he has seen seizures occur in patients with measles encephalitis, a n often debilitating (and occasionally fatal )
condition caused by brain inflammation that develops as a patient recovers from a
measles infection, i d.

, there is no evidence of measles enceph alitis , in this case

. Tr. at 95, 99. Dr. Kinsbourne agreed with respondent’s assertion that S.S. showed no signs of having contracted measles encephalitis

. Tr. at 87

- 88

.

Dr. McDonald explained that the measles vac cine “is an attenuat[ed]
version of the natural measles virus ” and thus bear s a substantially diminished
viral load ; due to its significantly reduced virulence

, it is much less likely than
wild measles vir us to cause seizures. Tr. at 125. Dr. McDonald criticized the studies relied upon by Dr. Kinsbourne for the proposition that the measles vaccine
could provoke seizure events because th ose studies involved small, poorly defined

groups. Id.17 Dr. McDonald also questioned whether

, in fact, S.S. ’s seizu re disorder may have begun to be expressed befo re he received the MMR vaccine i n October of
20 07

, See R esp’t ’s Ex. A . P ointing to the record evidence of S.S. ’s unwitnessed fall on August 19, 2005

, i d. at 2

- 3

, Dr. McDonald observed that “many children
with epilepsy are found to have episodes of suspicious seizure activity that predate their first hospital admiss ion [after] a witnessed seizure, ” i d. at 2.

b. Refuting the Allegations of a Seizure

- Induced Encephalopathy

Refuting Dr. Kinsbourne ’s theory that S.S. ’s vaccine

- induced seizures
caused irreversible brain damage, Dr. McDonald stated that the IOM’s definition of encephalopathy is a very broad one

. Tr. at 130

- 32. He explained that, as the term is understood more narrowly by neurologists who evaluat e seizure patients, an encephalopathy refers to any damage that persists beyond the seizure event and
the attendant recovery period. Tr. at 132 . Dr. McDonald observed that
“convulsions and

. . . [ the transient] post

- convulsive effects” are distinguish able
from those functional disruptions that produce mental changes

, but are unrelated to

a seizure event. Id.

Pointing to S.S. ’s EEG on October 16, 2007

-- the day following his first recogniz ed seizure

-- Dr. McDonald stated t hat the test results s howed “very subtle slowing, . . . [but] not an ongoing epileptic process

. ” Tr. at 97. He added that

s uch results were not “consistent with an en cephalopathy ” when found in a seizure patient. Tr. at 99.

C hallenging petitioner’s assertion that S.S. su ffer e d an encephalopa t hy , Dr.
McDonald addressed the investigators’ findings in the 2001 Holmes articl e

-- filed by petitioner and cited by Dr. Kinsbourne. T he authors of the 2001 H olmes study
determined that “the im mature brain is less vulnerable to seizure

- induced injury
than the mature brain.” R esp’t ’s Ex. A at 3 (quoting the 2001 Holmes article, filed
as Pet’r’s Ex

. 18, Tab C ). 19 But, t he authors observe d that “seizures in the developing brain [could] result in i rreversible alterations in neuroma connectivity

, and thereby affect brain functioning

. ” Tr. at 116.

Building upon the observations of the authors in the 2001 Holmes study

, D r. McDonald stat ed that repetitive seizures ( as occur in a patient with status epilepticus ) c an caus e additional seizure activity by lowering a patient’s seizure
threshold

-- which allows for increased susceptibility to seizures . Tr. at 117. Dr.

19 Holmes, supra note 17, at 320

- 25.18 McDonald explained that a lower ed seizure threshold can result from seizure

induced brain damage caused either by alter ations to nerve pathways or by changes in the nerve impulse transmissions that protect against seizures. Tr. at
117

- 18. A lthough certain seizure activity c an result in the lowering of a subject’s
seizure thre s hol d

, he asserted that S.S. did not experience th at type of activity during his first s eizure event i n October of 2 007. T r. at 134.

c. The Emergence of S.S. ’s ADHD and Developmental Delay

Dr. McDonald expressed the view similarly expresse d by at least one of
S.S. ’s tr eaters, that the prescribed anti

- epileptic medication could have cause d
S.S. ’s attentional and behavioral issues

. Tr. at 106. Dr. McDonald also considered the possibility that S.S. ’s developmental delay and attentional probl ems were co

- morbid conditions “unrelated to his epilepsy.” R esp’t ’s Ex. A
at 2. He a dded that most likely, S.S. ’s diminished intellectual skills and his hyperactivity were genetic ally

- triggered

. T r. at 105, 133. But, e ven if S.S. ’s
various conditions were not genetically

- based, Dr. McDonald noted that none of
S.S. ’s treaters associated his health issues with the MMR vaccination he received.

Tr. at 105

.

d. Pondering the Genetic Influences on S.S. ’s Condition

Dr. McDonald asserted that S.S. ’s seizure disorder most likely arose from “an underlying genetic basis.” R esp’t ’s Ex. A at 4; accord. Tr. at 105. Although convinced of a genetic underpinning, Dr. McDonald recognized that without
results from “standardized genetic and metabolic testi ng , ” the relevant genetic
influence s could not be established. R esp’t ’s Ex. A at 4 ; accord. Tr. at 134.

IV. Applicable Legal Standard s

Under the Vaccine A ct, a petitioner may prevail on her claim if the
vaccinee for whom she seeks compensation has “sustained, or endured the significant aggravation of any illness, disability, injury, or condition ” set fo rth in the Vaccine Injury Table (the Table)

. § 11(c)(1)(C)(i). T he most recent version
of the Table , which can be found at 42 C.F.R. § 100.3, identifies the vaccines covered under the Program , the corresponding injuries

, and the time period in
which the particular injuries must occur after vaccination. § 14(a). I f p etitioner
establishes that the vaccine e has suffered a “Table Injury

, ” causati on is presumed

.

I f , however, the vaccinee suffered an injury that either is not listed in the
Table or did not occur w ithin the prescribed time frame, petitioner mu s t prove that
the administered vaccine caused injury to receive Progra m compensation on behalf19 of the vaccinee

. § 11(c)(1)(C)(ii) and (iii). In such circumstances, p etitioner

asserts a “non

- Table or [an ] off

- Table ” claim and to prevail, p e titioner must prove her claim by prepo nder ant evidence. 20 § 13(a)(1)(A). Th is standard is “one of . . . simple preponderance, or ‘more probable than not’ causation.” Alth en v . Sec’y of
Health & Human Servs. , 418 F.3d 1274, 1279

- 80 (Fed. Cir. 2005) (referencing Hellebrand v. Sec’y of Health & Human Servs. , 999 F.2d 1565, 1572

- 73 (Fe d. Cir. 1993).

The Federal Cir cuit has held that to establish an off

- Table injur y, petitioner s must “prove

. . . that the vaccine was not only a but

- for cause of the injury but also a substantial factor in bringing about the injury.” Shyface v. Sec’y
of Health & Human Servs. , 165 F.3d 1344, 1351 (Fed. Cir 1999). Id. at 1352.
The received vaccine , however, need not be the predominant cause of the injury

. Id. at 1351.

T he Circuit Court has indicated that petitioner s “must show ‘a medical theory causally connecting the vaccination a nd the injury’ ” to establish that the
vaccine was a substantial facto r in bringing about the injury. Shyface , 165 F.3d at
1352

- 53 (quoting Grant v. Sec’y of Health & Human Servs. , 956 F.2d 1144, 1148 (Fe d. Cir. 1992) ) . The Circuit C ourt added that " [t]here must be a ‘logical sequence of cause and effect showing that the vaccination was the reason for the injury.’” Id.

The Federal Circuit subsequently reiterated these requirements in its Althen
decision

. See 418 F.3d at 1278

. Althen requires a petitioner

to show by preponderant evidence that the vaccination brought about her injury by providing : (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.

20 Under Section 13(a)(1)(A) of the Act, a petitioner must demonstrate, by a preponderance of the evidence, that all requirements for a petition set forth in section 11(c)(1) have been satisfied. Section 11(c)(1) contains additional vaccine claim requirem ents concerning the type of vaccination received and where it was administered, the duration or significance of the injury, and the lack of any other
award or settlement. See § 11(c)(1)(A),(B),(D) and (E ).20 Id. All three prongs of Althen must be satisfied

. Id. “ U nlike an on

- Table case, proof of causation in an off

- Table case must comprise more than just a literal temporal association between the onset of the injury and the vaccination.” Pafford v. Sec’y of Health & Human Servs.

, 64 Fed.Cl. 19, 24 (Fed. Cl. 2005) ; see also
Grant , 956 F.2d at 1148

.

T he Federal Circuit has instructed that a petitioner may satisfy he r evidentiary burden by relying either on “ medical records or medical opinion.”
Althen , 418 F.3d at 1279 (emphasis in original). Any offered expert testimony must be scientifically reliable and may be analyzed using the four factors
enumerated by the Supreme Court in Daubert

. Te rran v. Sec’y of Health &

Human Ser vs. , 195 F.3d 1301, 1316 (Fed. Cir. 1999) (referring to Daubert v. Merrell Dow Pharmaceuticals, Inc. , 509 U.S. 579 (1993)). Circumstantial
evidence also might be used. Capizzano v. Sec’y of Health & Human Serv s

. , 440 F.3d 1317, 1325

- 26 (Fed. Cir. 2006). E vidence that satisf ies one prong might assist in proving another prong as well. Id. at 1326.

T he Vaccine Act further requires “that there is not a preponderance of the evidence that the illness, disability, injury, condition, or death described in the petition is due to factors unrelated to the administration of the vaccine described in the petition.” § 13(a)(1)(B). Thus, even if a petitioner sat i s fies the three

- prong ed
Althen test , compensation cannot be awarded if respondent establishes an alternat e cause of injury , not related to the administered vaccine

. To defeat petitioner’s

recovery on c e petitioner has met her evidentiary burden, r espondent must prove

, by preponderant evidence

, that an alternat e cause of injury exists. Knudsen v. Sec’y of Health & Human Serv s

. , 35 F.3d 543, 549 (Fed. Cir. 1994).

The Federal Cir c uit has stated that “close calls regarding causation are
resolved in favor of injured claimants.” Althen , 418 F. 3d at 1280.

V. Evaluating Petitioner’s Claim

A. Summary of Petitioner’s Theory of Causation

P etitioner al lege s that the MMR vaccine administered on October 1, 2007

, caused S.S. to develop epilepsy

, developmental delay , and hyperactivity. 21

21 In her petition and later filings, petitioner asserts that S.S. ’s epilepsy and developmental delay were vaccine

- caused. See, e.g. , Pet’r’s Br. at 18. However, during his testimony and in his supplemental expert report, Dr. Kinsbourne also
describes S.S. ’s hyperactivity as a vaccine

- caused injury. Pet’r’s Ex. 20 at 3; Tr.
at 27.21 P etitioner a sse r ts that the seizure episode S.S. suffered on October 15, 2007

, signal ed the onset of his seizure disorder

. Petitioner’s expert , Dr. Kinsbourne,
contends that because the onset of S.S. ’s seizures occurred within two weeks of his receipt of the MMR vaccine , the resultant seizure condition is likely vaccine

related . Dr. Kinsbourne reasons that S.S. suffered first his seizure during the period of increased viremia associated with the attenuated measl es component in
the MMR vaccine. P et’r’s Exs. 18 at 2; 20 at 1

- 2; Tr

. at 25

- 26.

To explain S.S. ’s later seizures

, Dr. Kinsbourne asserted that S.S. ’s initial
seizure event caused sufficient brain damage t o lower S.S. ’s seizure threshold and
increase S.S. ’s susceptibility to another s eizure event two months later, on December 9, 2007 and thereafter

, with increas ing frequency

. See P et’r ’s Ex. 20 at

1 ; Tr. at 65

- 66, 83

- 84

. Dr. Kinsbourne a dded t hat the later seizures caused further brain damage that resulted in S.S. ’s developmental delay and hyperactivity.

Dr. Kinsbourne’s arguments

-- although forcefully presented

-- lack
coherence. Dr. Kinsbourne focused solely on the seizures that S.S. experienced on October 15, 2007 , w hen discussing whether the measles vaccine could cause seizures in the same manner as the measles infection during the two week period following v accine exposure. Tr. at 1 2 , 42

- 43

. But, he focused specifically on the seizure events that occurred on December 9, 2007

, and later when discussing the
seizure s that allegedly caused th e brain damage that result ed in S.S. ’s developmental delay and a ttentional issues

. Tr. at 66

- 67. 22

Dr. Kinsbourne ’s circular logic , that one event was caused by another simply because the second event occurred

, is also u navailing. In support of his
assertion that the seizures S.S. experienced on October 15, 2007, led to a lowering
of his seizure threshold and caus ed him to suffer seizure events on December 9,
2007 ( and thereafter )

, Dr. Kinsbourne relie s heavily on the fact that the later
seizures occurred. Tr. at 83

- 84. In addition, in support of his assertion that S.S. experienced severe brain damage as a result of his seizures, Dr. Kinsbourne pointed to S.S. ’s diminished mental capacity as evidence of earlier brain damage

. Tr. at 66.

As discussed further below, a lthou gh the individual components of Dr.
Kinsbourne’s theo ry seem medically sound, the combination of the components underlying his theory of causation is not . N or does the cobbled theory of

22 Dr. Kinsbourne testified that “after” the seizure event S.S. suffered on December 9, 2007, “he began to experience a really severe epilepsy with seizures multiple times every day.” Tr. at 13.22 causation provide a logical connect ion between the received vac cination and S.S. ’s injuries. For these reasons, petitioner’s claim cannot stand.

B. The Filed Medical Literature Does Not Assist P etitioner 23

Essential to Dr. Kins bourne’s theory is the postulate that similar to a natural
measles virus, the attenuated viral measles vaccine can reach a sufficient viral load (that is, peak viremia) within the two

- week period after vaccination to provoke
seizures , and that it did so in S.S. ’s case

. To account for S.S. ’s later seizure

events , Dr. Kinsbourne asserts that the seizure episode S.S. experienced on October 15, 2007, was adequately severe to lower his seizure threshold and thus, allow the subsequent seizure events to occur. In support of this particular assertion, Dr. K insbourne cites a number of studies. P et’r ’s Ex. 18 at 4. The undersigned addresses

, in turn

, the studies on which petitioner primarily depended.

1. The 1973 Landrigan Study and 1998 Weibel Study

In the 1973 Landrigan study, t he authors evaluated 84 cases of n eurologic disorders that appeared within one month of receipt of a live measles

- virus vaccine and were reported between the years of 1963 and 1971

. P et ’ r’ s Ex. 18, Tab D (1973 Landrigan study ) , at 1460. The cases were intended to provide epidemiologic detail about the relation ship between neurologic disorders

, the
measles vaccine

, and t he risk s posed by vaccination

. Id. at 1459

. The case s were divided into four group s based on the reported clinical and laboratory findings. Id.
at 1460.

The findings presented for Group 3 and Grou p 4 a re the most relevant here. Subjects in Group 3 who had experienced episodes of brief

, generalized
convulsions with fever

-- but had no other clinical or laboratory evidence of
cerebral infection or intoxication

, and had no sequelae

-- were deemed to have
suffered febrile convulsions. Id. (emphasis added). E leven patients in Group 3
met the cri teria for febrile convulsions, and t he auth ors speculated that the
convulsions were related to the subjects’ febrile response to the administered
vaccine. Id. These eleven patients had a convulsive onset within 6 to 13 days
after the MMR vaccination , which was a period of time that fell within the expected time frame for a febrile response. 24

23 The parties submitted a total of 17 articles and studies; only those articles on which the parties appeared to rely most heavily are discussed in detail in this
section. Id.

24 The median age of Group 3 patients was two years, and the group consisted of eight girls, two boys, and one patient whose sex was not reported. P et ’ r’ s Ex.23 The s ubjects in the largest group, Group 4

, experienced seizures with no
identified cause and suffered more extensive or permanent neurologic effects than
did th ose in Group 3. Id. Some of the subje ct s in Group 4 were diagnosed with
either encephalomyelitis, aseptic meningitis, spinal cord disorders, or disorders of the peripheral nervous system. Id. at 1461. O f the 59 subject s in Group 4 with
serious neurologic disorders

, five of the disorders were fatal. Id. at 1460.

Symptoms of the various neurologic disorders began to manifest between 1
and 25 days after vaccination. Id. Forty

- five subjects in G roup 4 had symptom

onset between 6 and 15 days after vaccination , the period of time during which
vir al replication is at its height. 25 Id.

Thirty

- six subjects in Group 4 were deemed to have suffered an encephalopathy. Id. at 1461. Twenty

- seven of those subjects had convulsions that
were either prolonged or focal

. Id. Twenty

- four subjects in this group were

younger than two years old. Id.

The interval between vaccination and symptom onset ranged between 2 and
25 days, but 72% of the group ( 26 subjects ) experienced onset between 6 and 15 days. Id. Follow

- up data for 31 subjects in t he group showed that five died, ten

rec overed fully, and sixteen were left with neurologic residua that ranged from
mild hyperactivity to profound retardation. Id.

The authors of the 1973 Landrigan study were unable to establish a causa l relationship in any single case between vaccination and the subsequent neurologic
disorder. Id. at 1462. Although the epidemiologic evidence suggest ed that some of the cases may have been caus ally related to the vaccine administration , the
stud y’s authors concluded that the cause of the disorders was “not clear” and “more thorough investigation might demonstrate agents other than measles” caused the observed injuries. Id.

Dr. Kinsbourne appeared initially to rely on t he study for the proposition that the measles vaccine could cause seizures. But, o n cross examination

, he

18, Tab D (1973 Landrigan study), at 1460. Follow

- up data was obtained from eight of the participants. All patients had a full recovery, with no ongoing seizure problems and no residual neurologic imp airment. Id.

25 In the Group 4 cases reported between 1963 and 1964, the median age of the subjects was seven years; between 1965 and 1966, the median was three years of age, and between 1967 and 1971, the median was one year of age. Id. There

w ere 53 girls, 20 boys, and 4 patients whose sex was not reported. Id.24 limited the scope of his reliance on the 1973 Landrigan study , asserting only that

t he study established the time frame within which neurologic injur y might appear
after vaccination. Tr. at 50

- 51.

In the 1998 Weibel study filed by petitioner , the authors examined pediatric cases of encephalopathy following MMR vaccination

-- whether “with or without an inflammatory response.” P et’r ’s Ex. 18, Tab I (1998 Weibel s tudy) , at 383 . Of
the 403 reviewed cases , the authors d etermined that only 48 of the children met the criteria for an acute encephalopathy between the 2nd and 15th day after vaccination, i d. at 384 , and f ever preceded onset “ by sev eral hours to several days in forty

- three of [the] forty

- eight children.” Id. at 385 (emphasis added) . In the majority of the children (32 of 34)

, who experienced either generalized or focal seizures, the seizures were associated with fever. Id. In one case, a seven month old girl developed a rash and a fever seven days after she receiv ed an MMR
vaccination. Id. She was hospitalized for recurring seizures (status epil e pticus) with a fever of 106 degrees three days later ( which was approximately 10 days
after v accination). Id.

Here, the part ies do not dispute that S.S. ’s initial seizures occurred without
fever. The VAERS report filed on March 28, 2008 indicated that S.S. exp erienced a slight fever seven days prior to his first seizure event but not during his seizure

e pisode

. See P et’r ’s Ex. 12 at 1. Because the 1998 Weibel study focus ed on the incidence of febrile seizures, it does not lend significant support to petitioner’s theory that the MMR vaccine S.S. received caused him to develop a seizure
disor der beca use his brief, initial seizure event was not associated with fever.

Of note, t he authors of the 1973 Landrigan study and the authors of the 1998 Weibel study concluded that “the incidence of reported neurologic disorders following live, attenuated measles

- virus vaccination is extremely low.” P et’r ’s Ex. 18, Tab D (197 3 Landrigan s tudy)

, a t 1642; accord. P et’r ’s Ex. 18, Tab I (1998 Weibel s tudy)

, at 387. The a uthors also observed that “the lack of
controlled stud ies that distinguish [ed] background rates of encephalopathy of undetermined cause in unvaccinated populations ” ma de an assessment of potential
vaccine

- related causation difficult. P et’r ’s Ex. 18, Tab I (1998 Weibel s tudy)

, at 386; accord. P et’r ’s Ex. 18, Tab D (1973 Landrigan s tudy)

, at 1642.

2. The 2004 Ong Study and the 2004 Narchi Study

Petitioner did file two articles involving the onset of afebrile seizures ; b ut both the 2004 Ong study and the 2004 Narchi study focused on children who had developed severe seizures after suffering g astrointestinal illnesses. P et’r ’s Exs. 20 at Tab C (2004 Ong s tudy) , at 1 57 ; 20 at Tab D (2004 Narchi s tudy)

, at 1. T he
authors of the 2004 Narchi study specifically observed that “the occurrence of25 afebrile seizures during viral gastroenteritis without dehydration or electrolyte
imbalance is little known in Western countries

, ” P et’r ’s Ex. 20 at Tab D (200 4
Narchi s tudy) , at 3 (emphasis added)

, and t he autho r s of both studies concluded
that afebrile seizure events that occur in the context of a gastrointestinal illness are typically “benign

. . . and carry an excellent prognosis.” Id. at 4; accord. Pet’r’s Ex. 20 at Tab C (2004 Ong s tudy) , at 161, 164.

The records suggest that S.S. may have experienced his critical seizure event in the context of a gastrointestinal illness because he was reported to have symptoms of nausea, vomiting, and diarrhea before he began seizing. Pet’r’s Ex.
3 at 169. Ho wever, he was not shown to be dehydrated or suffering from an electrolyte imbalance. And contrary to Dr. Kinsbourne’s suggestion

, the literature petitioner filed indicates that S.S. ’s initial, brief

, afebrile seizure event was much
more lik ely than not to have been benign in its impact on S.S. ’s neurologic health

.

3. The 1994 IOM R eport

As previously discussed, the authors of the 1994 IOM report defined the

term encephalopathy broadly

, and they drew a careful distinction between th e expansive definition accorded an encephalopathy and the more narrow definition
of an enc ephalitis. Pet’r ’s Ex. 18, Tab G (1994 IOM report) at 122. As the authors explained

, an “[e]ncephalitis refers to an encephalopathy caused by an inflammatory response in the brain.” Id. Observing that “the occurrence of encephalitis following a natural measles vi rus infection is well described, ” i d. at
123 , the authors turned to examine the encephalopathic effects of the attenuated
measles vaccine.

While acknowledging that “[t]here is demonstrated biological plausibility
that measles vaccine might cause [an] encephalopathy,” Id. at 129 (emphasis added) , the authors concluded that “the [incidence] rates quoted are impossible to distinguish from backgr ound rates

. ” I d. T he authors specifically lamented the lack of “[g]ood case control or controlled cohort studies of these conditions in similar unvaccinated populations, which are necessary for determining the casual relationship between measles and mump s and encephalopathy and encephalitis.”
Id. at 1 29

- 30 (emphasis added) . The authors found that “no conclusive evidence of the occurrence of encephalopathy or encephalitis resulting from the
administration of the measles vaccine [had been] identified.” I d. at 130

.

4. The 1981 NCES S tudy

The 1981 NCES study filed by petitioner was a case

- control study. I ts primary purpose was to identify potential adverse events following a pertussis
immunization. P et’r ’s Ex. 18, Tab A (1981 NCES s tudy)

, at 80. Dr. Kinsbourne26 argued that the portion of the study which addressed the potential adverse effects
of the measles vaccine was a meaningful part of the study . H e further argued that
the authors ’ advisory concerning the possible over

- reporting of cases applied o nly to the conclusions involving the pertussis vaccine. Tr. at 52, 75

- 76; see P et’r ’s Ex. 18, Tab A (1981 NCES s tudy)

, at 145

.

T he majority of the considered cases involved seizures associated with fever, and consistent with the guidelines provided to physicians , case referrals
were limited to child ren who had suffered a convulsion lasting more than 30 minutes, or a convulsion followed by a two or more hour

- long coma, or a convulsion followed by paralysis or other neurological event lasting 24 or more
h ours. P et’r ’s Ex. 18, Tab A (1981 NCES s tudy) , at 157

. As Dr. Kinsbourne acknowledged, S.S. ’s case did not meet this criteria. Tr. at 54

- 55.

As noted in the NCES study , 16 children developed illness seven to ten days after vaccination. P et’r ’s Ex. 18, Tab A (1981 NCES s tudy) at 140. Of the 16 children, two had prior abnormalities. Of the remaining 14 children, nine had experienced “simple or febrile convulsions

. . . and [ had suffered either an] encephalitis or encephalopathy.” Id. “All but two children with mild defects

. . . made an apparently complete neurological recovery when followed up .” Of the
two others

, each had a febrile convulsion on a later occasion.” Id. (emphasis added). The authors of the NCES observed that the serious neurologic reactions “associated with the measles vaccine are thought to [have been] cause d b y a mechanism similar to that responsible for post

- infectious encephalitis.” P et’r ’s Ex. 18, Tab A ( 1981 NCES s tudy)

, at 142. T he NCES study was criticiz ed later in the 1994 IOM report for i t s observation about the measles vaccine because “a separate analysis of those diagnosed with encephalitis and encephalopathy was not performed.” P et’r ’s Ex. 18, Tab G (1994 IOM report)

, at 144; see also P et’r ’s Ex, 18, Tab I (1998 Weibel s tudy)

, at 384 (the authors noted that the 1981 NCES

s tudy did not separate convulsions from cases of acute encephalopathy).

T he recorded seizure events in the 1981 NCES study were accompanied by fever and were more prolonged or severe than those suffered by S.S. In addition

, the subjects of the 1981 NCES study enjoyed substantial recov eries; the outcome
for those subjects was materially different from S.S. ’s.

5. The 2001 Holmes article

The autho rs of the 2001 Holmes study dis cussed the long

- term consequences of seizures in the developing versus the mature brain. Pet’r’s Ex.
18

, Tab C (2001 Holmes s tudy) , at 320. Pointing to animal models, the authors observed that adult animals have greater deficits in learning, memory, and behavior following seizure activity, id. at 322, but the authors allowed that27 significant deficits can occur as a result of seizure activity i n neonatal subjects. Id. at 324. The results of the animal study led the authors to conclude that “prolonged or recurrent seizure activity . . . can irreversibly alter the way the immature brain develops and forms synapses.” Id.

The auth ors specifically identifi ed “precipitating factors such as fever” as the agents likely to trigger seizures in children

. Id. at 322. Although the authors concluded that the immature brain is more susceptible to seizures, they found that
the immature brain was less vulnerable to long

- term consequence of these
seizures. Id.

When questioned at the hearing about the 2001 Ho l mes study

, Tr. at 115

- 23

, Dr. McDonald s tated that the findings of the “ pretty convincing ” animal model

s tudy showed that repetitive seizures can cause “actual alterations in nerve pathways in the brain.” Tr. at 117. He explained that repetitive seizures could cause brain damage and lead to more seizures by harming the “nerve cells and
chemicals that may help to dampen a se iz ure.” Tr. at 116

- 17. But he observed
that the authors of the 2001 Holmes article had determined that the immature brain is “relatively resilient

, ” Tr. at 120, and thus, cannot be harmed as readily as the

mature (or adult ) brain. Tr. at 116

.

The 200 1 Holmes article, as discussed by Dr. MacDonald, helpfully
delineates those circumstances in which seizures could l ead to the type of brain damage petitioner claims that S.S. suffered

. But such circumstances we re absent
when S.S. first began seizing and thus, t he 2001 Holmes article furnishes modest support for petitioner’s claim that the received vaccine caused S.S. ’s injuries.

6. Conclusion Regarding the Filed Medical Literature

The medical literature submitted by petitioner provides little or no
evi dentiary support for her theory of causation as applied to S.S. ’ s circumstances

.

The authors of the 1973 Landrigan study

, 1998 Weibel study, and 1994 IOM report acknowledge d they could not establish a causal connection between
the measles vaccine and neurologic disorders, encephalopathy or encephalitis. See

P et’r ’s Ex. 18, Tab D (197 3 Landrigan s tudy)

, a t 1642; P et’r ’s Ex. 18, Tab I (1998
Weibel s tudy) , at 38 6

- 87 ; Pet’r ’s Ex. 18, Tab G (1994 IOM report) at 130. The
authors of the 2001 Holmes study co nclude d that although more likely to experience seizures, the immature brain is less susceptible to the long term consequences of seizures. Pet’r’s Ex. 18, Tab C (2001 Holmes s tudy) , at 322.

I n the 1998 Weibel and 1981 NCES studies, the investigators c onsidered
cases of seizure onset that was accompanied by fever or was more prolonged and28 severe than the seizure events suffered by S.S. P et’r ’s Ex. 18, Tab I (1998 Weibel

s tudy) , at 385; P et’r ’s Ex. 18, Tab A (1981 NCES s tudy) , at 157

. The authors of the 2004 Ong and 2004 Narchi studies determined that afebrile seizure that occur in the context of gastrointestinal illnesses, are generally benign. Moreover, t he
authors of the 2004 Ong and 2004 Narchi studies found that afebrile seizures caused by viral gastroenteritis do not occur in the Western countries unless accompanied by dehydration or electrolyte imbalance. Even if S.S. was shown to have suffered a gastrointestinal illness, the records do not indicate that he
exhibited either of t h e accompanying conditions of dehydration or electrolytic imbalance. And unlike the subjects of the 2004 Ong and 2004 Narchi studies, S.S. required ongoing medical attention for his seizures

.

As the Federal Circuit held in Moberly , “studies provide no evidence pertinent to persons not within the parameters of the test group.” Moberly , 592
F.3d at 1324. Because the literature petitioner filed does not pertain to the factual
circumstances of S.S. ’s case, it merits limited evidentiary weight.

C. The Three

- Prong ed Al then Test

To prove vaccine causation, petitioner must satisfy all three prongs of the
Althen test. Althen , 418 F.3d at 1278. R espondent does not dispute that petitioner
has established a temporal relationship between the administered MMR vaccine
and thus , has satisfi ed the third Althen prong . Respondent argues , however, that
because “petitioner’s claim rests on nothing more than a temporal relationship, [it] is legally insufficient to establish vaccine causation.” R esp’t’s Br. at 1.

Even if t he undersigned were to conclude that petitioner has satisfied the third prong of Althen, respondent has correctly asserted that proving timing alone is not enough. See Grant , 956 F.2d at 1148. Pet itioner contends she has
established the first and second prongs of the Althen test . P et’r’s Br. at 34; P et’r ’s Reply to R esp’t’s Br. at 13. Respondent disagrees, insisting that “[ p ] etitioner has
failed to provide [both] a reliable medical theory of causation and . . . adequate proof of a logical sequence of cause and effect linking [Sheik’s] vaccinations and his injuries.” R esp’t’s Br. at 24.

To evaluate petitioner’s claim properly, t he undersigned turn s now to consider the first and second prongs of the Althen analysis.

1. Considering t he First and Second Althen Prongs

T he analyses under the first and second prongs of the Althen test may involve a review of the same evidence to examine different aspects of the
causation issue

. See Doe 9 3 v. Sec’y of Health & Human Servs. , 98 Fed. Cl. 553,29 567 (Fed. Cl. 2011). T he first prong focuses on general causation , that is whether
the administered vaccine c an cause the particular injury which th e vaccin e e suffers 26 and, t he second prong focuses on specific causation , that is whe ther the
administered vaccine did cause the injury. 27 See Pafford , 451 F.3d at 1355

- 56;

2. First Althen Prong

To satisfy the first prong of the Althen test, petitioners must provide “a
medical theory casually connecting the vaccination and the injury.” Althen

, 418 F.3d at 1278 (quoting Grant, 956 F.2d at 1148). P etitioners must show that it is more likely than not that the received vaccine can cause the alleged injury.

T he offered medical theory must be reputable , reliable, and biologically plausible. See, e. g. , Pafford

, 451 F.3d at 1355 (reputable) ; Moberly v. Sec’y of
Health & Human Servs. , 592 F.3d 1315, 1324 (Fed. Cir. 2010) (reliable); Andreu

v. Sec’y of Health & Human Serv s. , 569 F.3d 1367, 1375 (Fed. Cir. 2009) ( b iologically plausible )

. Petitioners must prove this prong by preponderan t evidence. Broekelschen v. Sec’y of Health & Human Serv s. , 618 F.3d 1339, 1350 (Fed. Cir. 20 10 )

.

Dr. Kinsbourne offer ed a theory of causation, based on a few critical
components. First, he asserted that the me asles vaccine can cause seizures during the period of peak viremia which occurs two week s after vaccination. P et’r ’s Ex. 18 at 3; Tr. at 19

- 20. Unable to identify the exact mechanism involved

-- and not required to do so, s ee Knudsen , 35 F.3d at 549

, Dr. Kinsbourne averred that the
measles vaccine c ould cause harm in the same manner that the wild measles virus
does

. Tr. at 43. Respondent’s expert, Dr. McDonald, did not disagree with Dr. Kinsbourne, and he stated that he was “willing” to accept as biologically plausible the proposition that the measles vaccine c ould cause seizures under certain
circumstan ces

-- particularly those invol v ing fever and gastrointestinal illness

. Tr.
at 130.

When d iscussing the seizures that S.S. experienced during the period of peak viremia after he received the measles vaccine, Dr. Kinsbourne posited th at S.S. ’s initial seizure event c ould have cause d sufficient brain damage t o lower h is

s eizure threshold and mak e h i m more susceptible to future seizure event s. See

26 See generally

, Veryzer v. Sec’y of Health & Human Servs. , 100 Fed. Cl. 344 (Fed. Cl. 2011) (petitioner failed to satisfy the first Althen prong).

27 See generally

, Hibbard v. Sec’y of Health & Human Servs.

, 698 F.3d 1355 (Fed. Cir. 2012) (petitioner failed to satisfy the second Althen prong).30 P et’r ’s Ex. 20 at 1; Tr. at 65

- 66, 83

- 84. Dr. McDonald acknowledged that certain types of seizures could lead to additional seizure activity, but e mphasiz ed such
seizures must be prolonged or repetitive to lower a seizure threshold . Tr. at 1 16

- 17.

Finally, Dr. Kinsbourne maintained that epileptic seizures

-- such as those
S.S. experienced on Dece m ber 9, 2007 and thereafter

-- c ould c ause brain damage
and lead to developmental delay and hyperactivity. P et’r’s Exs. 18 at 4; 20 at 3

- 4.
Dr. McDonald challenged this aspect of Dr. Kinsbourne’s testimony, asserting that
S.S. ’s seizures, developmental delay, and hyperactivity were mostly likely part of
the sa me underlyi ng genetic disorder , if related at all to each other

. Resp’t’s Ex. A at 4; Tr. at 133.

Based on careful consideration of the record evidence, t he undersigned
finds that in rare circumstances, the measles vaccine can trigger

-- within fourteen days of adm inistration

-- seizures if accompanied by fever or in the context o f a gastrointestinal illness. A finding t hat prolonged or repetitive seizures can result
in the lowering of a seizure threshold and lead to additional seizures as well as
d evelopmental delay is also supported by the expert testimony and filed literature
introduced here. Although the record c ontains some evidence that hyperactivity
can result from seizure medications , the undersigned is not persuaded on the weight of this record that hyperactivity can r esult from MMR vaccine

- induced seizure activity.

To prevail on her vaccine claim, h owever, petitioner also must prove that
the MMR vaccine S.S. received i n October of 2007 cause d his injuries in the manner proposed b y Dr. Kinsbourne.

3. S econd Althen Prong

To satisfy the second prong of the Althen test

, 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 1 278. In other words, petitioner must show
that it is more l ikely than not that the received vaccine cause d the allege d injury. See Capizzano , 440 F.3d at 1326

. The sequence of cause and effect need only be “logical and legally probable, not medically or scientifically certain.” Knudsen

, 35 F.3d at 548

- 49; accord

. Capizzano , 440 F.3d at 1326. Testimony from a treating physician may assist petitioner in meeting her burden of proof under the
second Althen prong. Capizzano , 440 F.3d at 1326.

P etitioner contends that she has “demonstrated that the MMR vaccine caused [ S.S. ’s] epilepsy and subsequent developmental delay

, ” P et’r ’ s Br. at 25

, that S.S. ’s “injury occurred within a medically appropriate time frame after the31 MMR vaccine” and that “no other likely cause of [ S.S. ’s] injury [ has been ]
identified

. ” Id

. at 26

.

P etitioner’s claim that S.S. ’s treating physicians attributed his injuries to his
vaccination does not persuade. The only mention in the medical records of a possible causal connection between S.S. ’s injuries and MMR vaccine originated
with petitioner who questioned whether such a connection might exist

. See e.g. , P et’r ’s Ex. 8 at 5

. S.S. ’s treating physicians did not know the cause of S.S. ’s epilepsy

. See, e.g.

, P et’r ’s Ex 14 at 17.

Moreover, t he theory advanced by Dr. Kinsbourne is not supported by the
facts of this case. 28 Even with the undersigned’s accept ance of Dr. Kinsbourne’s theory that the measles vaccine can cause seizures in rare c i r cum stances involving fever on gastrointestinal illn ess and that prolonged or repetitive se izures can result
in the lowering of a person’s seizure threshold and additional seizure activity

, petitioner has failed to prove , and the evidence of record is insufficient to show,
that either event occurred in this case.

Dr. Kinsbourne admitted that the seizure event S.S. experie nced on October 15, 2007

, consisted of several “staring spells, each lasting for less than a minute” and a seizure that lasted a few minutes. Tr. at 37. Moreover, Dr. Kinsbourne
acknowl edged that S.S. was “behaving normally and had no neurological
symptoms the day after his hospital admission

, and that th is EEG was consisten t with a postictal state and show ed no evidence of seizure activity or brain damage

. Tr. at 37

- 39 , 41

- 42

. As Dr. McDonald testified , and the undersigned similarly finds, S.S. ’s brief seizure and staring spells on October 15, 2007

, were not of the prolonged and repetitive nature needed to lower S.S. ’s seizure threshold. Tr. at
11 3.

O ther than the temporal relationsh ip

, there is nothing to suggest that the
seizures S.S. suffered on October 15, 2007

, were caused by the measles vaccine.
S.S. experienced a slight fever of 100 degrees on October 8, 2007

. Dr.
Kinsbourne a greed that fever and rash are the two most common symptoms of
measles v iremia

. Tr. at 61. Howev er, S.S. ’s fever occurred and abated seven days prior to his October 15, 2007 seizures. T he studies relied upon by Dr. Kinsbourne mentioned fever occurring a few days prior to and usually continuing during the
time of the seizure. See P et’r ’s Ex . 18, Tab I (1998 Weibel s tudy) , at 4; Tab A (1981 NCES s tudy)

, at 63. And as previously mentioned

, none of S.S. ’s treating physicians causally associated the measles vaccine with S.S. ’s seizures.

28 Even if the first Althen prong is met or assumed to be met, the proposed theory must be applicable to the facts in the case in order to satisfy the second
Althen prong. See Hibbard , 698 F.3d at 1362

- 63.32 Although “the Vaccine Act does not require [a] petitioner to bear the burden of eliminating alternative causes where the other evidence on causation is sufficient to establish a prima facie case,” a petitioner “ may be required to eliminate potential altern ative causes where the petitioner's other evidence on
causation is insufficient.” Walther v. Sec’y of Health & Human Servs. , 485 F.3d 1146, 1149

- 50 (Fed. Cir. 2007) (citing Pafford , 451 F.3d at 1359). Here, petitioner asserts that no alternat e explanatio n exists for S.S. ’s injury

. Yet, a s reflected in his medical records, S.S. had a maternal great aunt with epilepsy, s ee
supra note 11, and thus, a likely genetic predisposition to have a seizure condition.

While petitioner has propos ed a theory by which the MMR vaccine could cause injuries such as those suffered by S.S. , p etitioner has failed to establish a logical sequence of cause and effec t

-- consistent with her proposed theory

-- provi ng that the measles vaccine S.S. received on October 1, 2007 did cause his injuries

. Thus

, petitioner has failed to satisfy the second prong of the Althen test.

VI. Conclusion

The Federal Circuit stated in Althen that “neither a mere showing of a proximate temporal relationship between vaccination and injury, nor a simplistic elimination of other potential causes of the injury suffices, without more, to meet the burden of showing actual causation.” 418 F.3d at 1278. In this case, petitioner relied primarily on a proximate temporal relationship which she proved and her
dubious claim that no other potential cause for S.S. ’s injuries existed. For the reasons more fully detailed above, t he undersigned is persuaded that p etitioner has
satisfied the first and third prong s of the Althen test but finds that petitioner has failed to establish the requirements of the second Althen prong on a factual record
that is not close . B ecause petitioner c annot establish a logical causal sequence, petitioner’s claim must be denied.

Petit ioner has failed to prove that she is enti tled to compensation under the
Vaccine P rogram. The petition for compensation SHALL BE DISMISSED, and the Clerk of Court shall enter judgment consistent with this decision. 29

IT IS SO ORDERED.

s/Patricia E. Campbell

- Smith Patricia E. Campbell

- Smith Chief Special Master

29 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of notice renouncing the right to seek review.