Lamona Dodd, Parent of S.S., a Minor v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 09-0585V
(Filed: June 5, 2013)
(Reissued for Redaction and Amended Caption: June 19 and 21, 2013)1

***********************
LAMONA DODD, parent of *
S.S., a minor, * PUBLISHED
*
Petitioner, * Entitlement, 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.

1
When this decision was originally issued, the parties were notified that the
decision would be posted 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 was reissued on June 19, 2013, with the name of the
minor child redacted to initials and the birth date of the minor child redacted to the
year only. Two days later, petitioner moved to amend the caption as she is no
longer married to S.S.’s father and has changed her name back to Lamona Dodd.
The decision was reissued on June 21, 2013 with the amended caption, and
petitioner’s name was corrected throughout the decision. Except as noted in this
footnote, no other substantive changes have been made.
 DECISION

On September 4, 2009, Lamona Dodd (“petitioner” or “Ms. Dodd”) filed a
petition under the National Childhood Vaccine Injury Act (“Vaccine Act”)2 on
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-Pertussis (“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

On September 18, 2009, two weeks after filing her petition, petitioner filed
(1) her affidavit; (2) S.S.’s medical records, including 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 Pet’r’s Exs. 1-17. Petitioner
asserted that the “documents provide[d] preponderant evidence … [that S.S.’s]
vaccines were the likely cause of his epilepsy, and subsequent developmental
delay.” Petition at 18.

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
MMR 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 expert’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.

2
 Respondent filed 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
(“Resp’t’s Report”) at 2, 8-9. Respondent asserted 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 in December
of 2009, affording the parties an opportunity to discuss settlement options before
ordering petitioner to file an expert report. Order, Dec. 10, 2009. The parties
failed to reach a settlement, and the then-assigned special master ordered
petitioner to file “an expert report, [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 extensions of time to comply with the order. See, e.g., Order,
Mar. 23, 2010.

In March 2010, the case was reassigned to the undersigned. Three months
later, on June 3, 2010, petitioner filed an expert report from Dr. Marcel
Kinsbourne, a pediatric neurologist. Accompanying the expert report was his
curriculum vitae and nine articles upon which he had relied in forming his opinion.
See Pet’r’s Exs. 18 (including Tabs A-I); 19. Dr. Kinsbourne posited that the
MMR vaccine S.S. received on October 1, 2007, caused an encephalopathy that
manifested first as a seizure disorder, and later as developmental delay and
hyperactivity with attention deficits. Pet’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. Petitioner’s counsel indicated that S.S.’s presenting seizures were
without fever. Id. At that time, the undersigned afforded 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
(“Resp’t’s Exs.”) A; B. Respondent also filed several supporting articles to which
Dr. McDonald cited in his report. See Resp’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 attributed S.S.’s seizure disorder, developmental delay and
attentional problems to an “underlying genetic basis,” but he acknowledged that
the results of any standardized genetic and metabolic testing were not included in
the filed medical records. Id. at 4.

3
 In a subsequently filed status report, petitioner clarified that she was not
alleging an encephalopathy 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 expert report to describe petitioner’s theory more clearly.
Petitioner’s Status Report, Oct. 22, 2010, at 2. The undersigned granted
petitioner’s request. First Order, Oct. 28, 2010.

Petitioner filed her supplemental expert report from Dr. Kinsbourne in
December 2010. Pet’r’s Ex. 20 (including Tabs A-E). In his supplemental report,
Dr. Kinsbourne asserted that S.S. had not suffered an encephalopathy--as defined
by the Program’s Vaccine Table Injury--but instead had suffered a medical
encephalopathy, as more broadly defined by the Institute of Medicine (“IOM”).
Pet’r’s Ex. 20 at 1; compare 42 C.F.R. § 100.3(b)(2) with Pet’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. Pet’r’s
Ex. 20 at 2.

Petitioner filed additional medical records in February and March 2011,
further to a subpoena issued by the undersigned. See First Order, Feb. 28, 2011;
see also, e.g., Pet’r’s Exs. 23; 24 (Medical Records filed Mar. 21, 2011).

On March 18, 2011, the undersigned heard the testimony of the experts.
Thereafter, the parties filed post-hearing briefing.

The claim is now ripe for a ruling.

II. S.S.’s Medical History

S.S. was born in 2003. Pet’r’s Ex. 3 at 19. He was delivered without
complications at 37 weeks, weighing seven pounds. His head circumference
measured 19.5 inches, and he displayed no observable abnormalities. Id. at 19.
His Apgar score was 9 at both one and five minutes.5 Both his hearing and

4
Kathleen R. Stratton, et al., Adverse Events Associated With Childhood
Vaccines: Evidence Bearing on Causality, Institute of Medicine 1-464 (1994).
5
An Apgar score is “a numerical expression of the condition of a newborn
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
lowest score) to 10 (the highest score). U.S. National Library of Medicine,
MedlinePlus, Apgar,
4
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 Pet’r’s Ex. 13 at 1. He also experienced
common childhood ailments, including runny noses, coughing, sore throats,
diarrhea, fevers, and ear infections. His doctors attributed these various ailments
to either upper respiratory infections or allergies. E.g., Pet’r’s Exs. 3 at 56; 5 at 3.
S.S. also contracted strep pharyngitis once and conjunctivitis (often referred to as
pink eye) twice. Pet’r’s Ex. 5 at 1, 10, 11.6

In August of 2005, at 23 months of age, S.S. required emergent care for a
fall during which he bumped his head. See Pet’r’s Ex. 3 at 86-102. The records
from the emergency room visit appear to indicate that S.S. exhibited “confusion”
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 persisted or worsened after three days. Id. at 98.

Nearly seven months later, at two and one half years of age, S.S. began
attending daycare. Pet’r’s Ex. 16 at 1. He exhibited no health problems. Pet’r’s
Ex. 10 at 1.

S.S. began attending pre-kindergarten at four years of age, in August 2007.
See Pet’r’s Ex. 11 at 1. An early screening test administered shortly after he
started school showed that his articulation skills were “fair.” Id. at 3. His progress
reports, however, showed a decrease in his abilities between the second and third
quarters--as evidenced by the change in his skill category rankings from “in
progress” to “non-mastered” in a number of areas. Id. at 7.

On October 1, 2007, S.S. received the MMR and DTaP vaccinations of
which petitioner has complained in this vaccine claim. See Pet’r’s Ex. 13 at 1. In
the VAERS report petitioner filed on S.S.’s behalf, she stated that one week after
his vaccinations, S.S. developed a cough and fever of approximately 100 degrees,
but “continued” to attend school. Pet’r’s Ex. 12 at 1.

http://www.nlm.nih.gov/medlineplus/ency/article/003402.htm (last visited on
April 17, 2013).
6
S.S. also suffered a foot injury in January 2006; it resolved independently
after a week of rest. Pet’r’s Ex. 5 at 6-7.

5
 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 vomiting, and an episode of diarrheal incontinence
during the day. Pet’r’s Ex. 3 at 169. Later that day, S.S. experienced a left-sided,
focal tonic-clonic seizure that prompted petitioner to seek care at the hospital.7
Pet’r’s Ex. 16 at 2; accord. Pet’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 Pet’r’s Ex. 3 at 169.
Dr. Norsworthy administered a dose of Ativan, an anti-epileptic medication, to
S.S. and ordered several tests, including a computed tomography (“CT”) scan of
S.S.’s head.8 Id. S.S.’s test results returned as normal, but were suggestive of
sinus disease. Id. After discussions with Dr. Hemant Agarwal, a specialist in
pediatric critical care, Dr. Norsworthy transferred S.S. to the pediatric intensive
care unit “for . . . further evaluation” and an electroencephalogram (“EEG”).9 Id.

Dr. Agarwal observed and treated S.S. until his discharge (the day after his
admission). Pet’r’s Ex. 3 at 167. During his hospital admission, S.S. experienced
left-sided weakness that resolved. Id. His seizures were managed by the two anti-

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 Pet’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 consistently 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 numeric 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 cerebral
lesions (e.g. tumors, infarctions) will have abnormally slow EEG waves.” Id.

6
seizure medications--Ativan and fosphentoin--the combination of which appeared
to assist S.S.’s return to “normal” before his discharge. Id.

After consulting with pediatric neurologists at Vanderbilt Children’s
Hospital, Dr. Agarwal placed S.S. on Keppra, another anti-seizure medication, to
be administered twice daily. Pet’r’s Ex. 3 at 167. Dr. Agarwal also prescribed
Diastat, an additional anti-epileptic medication, to be administered rectally in the
event of a seizure lasting more than five minutes. Id. S.S. was discharged on
October 16, 2007, with a referral to the Pediatric Neurology Clinic at Vanderbilt
Children’s Hospital for a follow-up visit. Id.

The 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. But, it did not show any seizure activity. Id.

Nearly six weeks later, on December 9, 2007, petitioner took S.S. back to
the emergency room for a second seizure episode. Pet’r’s Ex. 3 at 240. Dr.
Geoffrey Fleming, the 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.

Petitioner 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 awakened.
Again, he stiffened and “vomited several times.” Id. Concerned about S.S.’s
presentation, petitioner took him to the hospital for evaluation. 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 arrived at the
hospital, and he required anti-epileptic medication “to break his seizure.” Id. S.S.
was noted to be afebrile. His head CT scan and laboratory results were normal.
Id. at 240. He 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 Pet’r’s Exs. 3 at 281; 16 at 2.

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
7
Petitioner further acknowledged that she had not taken S.S. for his follow-up visit,
as directed, after his first seizure episode. Pet’r’s Ex. 3 at 252, 281. Dr. Fleming,
the attending physician during S.S.’s hospitalization following his second seizure
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 facility preferred by petitioner. Id. at 240, 253, 281.

Two weeks later, on December 21, 2007, petitioner took S.S. to see Dr.
Alhamda. 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 Pet’r’s Ex. 8 at 10. Dr. Alhamda 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 image (“MRI”) of S.S.’s brain. Id. He
also increased S.S.’s dosage of Keppra, and provided petitioner with a calendar to
track S.S.’s seizure activity. Id.

Two weeks later, on January 9, 2008, petitioner again sought emergent care
for S.S. for his hourly episodes of minute-long, tonic-clonic seizures. Pet’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 normal, but S.S.’s EEG showed seizure activity in his fronto-temporal
region. Pet’r’s Exs. 7 at 46, 48-49; 8 at 7. Two medications, Ativan and
fosphenytoin, were administered to halt the seizures, and the anti-epileptic
Zonegran was added to S.S.’s prescription regimen for better seizure control.
Pet’r’s Ex. 7 at 46.

Nearly one week later, on 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. Alhamda recorded the impression of S.S.’s parents that
the prescribed anti-epileptic medication had exacerbated S.S.’s seizures. Id.
Similarly, he recorded Ms. Dodd’s belief that S.S.’s seizure disorder began shortly
after his vaccinations and the concern of S.S.’s parents regarding immunizations.

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.
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 same 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 epilepsy.)
8
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. He asked to see S.S. regularly and indicated
that he was eager to arrange for a “comprehensive epileptic evaluation” of S.S. Id.

The next week, Dr. Alhamda noted a decrease in the number of S.S.’s
seizures. He was experiencing only two episodes a day, but the seizures were now
longer in duration. Pet’r’s Ex. 8 at 3. Although Dr. Alhamda found S.S.’s
restlessness to be suggestive of Attention Deficit Hyperactivity Disorder
(“ADHD”), he acknowledged that some of S.S.’s attentional issues may 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 medications. 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. Alhamda indicated in his
notes that since S.S.’s last visit, petitioner had stopped administering the Keppra,
had continued 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 medications. Id. at 1-2.

Nearly six weeks later, on 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 noted that S.S. was taking a daily dosage of Zonegran and had last
seized 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.
That EEG, which was performed two weeks later, was normal. Id. at 13.

S.S. continued to see Dr. Pina-Garza. See, e.g., Pet’r’s Ex. 23 at 19. He
also received more regular care at the East Jackson Family Medical Center. See
Pet’r’s Ex. 6. Although his seizures were well-managed, the administered
medications made S.S. drowsy and caused him to sleep during school. Id. at 11.
S.S. also began to exhibit serious behavioral problems. Id. at 15.

Four months after Dr. Pina-Garza began to treat S.S., he added a new anti-
epileptic medication, Trileptal, to S.S.’s prescriptive regimen and began to
decrease S.S.’s dosage of Depakote. Pet’r’s Ex. 14 at 11. Three months later, Dr.
Pina-Garza reported that S.S. was no longer experiencing seizures, id. at 4, and
was no longer sleeping at school. Pet’r’s Ex. 6 at 7. In addition, he was behaving
much better. Id. Notwithstanding the noted improvement, S.S. was directed into a

9
special education placement at school and was encouraged to repeat pre-
kindergarten. Pet’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., Pet’r’s Ex. 21 at 11.

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
Kinsbourne was educated at Oxford University and received his medical degree in
1955. Pet’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 1967, 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 neurology 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 City. 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. Kinsbourne 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 acknowledged that the focus of his
work has been on behavioral disorders and not on seizure disorders. He further
acknowledged that 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

10
indicated that approximately fifty-five to sixty percent of 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
pediatric neurology, specifically involving behavioral disorders. Id.

2. His Opinion of Causation

Dr. Kinsbourne prepared an initial and a supplemental expert report. See
Pet’r’s Ex. 18 (Expert Report filed June 3, 2010); Pet’r’s Ex. 20 (Supplemental
Expert Report filed December 21, 2010). He opined that the MMR vaccine
administered to S.S. on October 1, 2007, caused him to develop a seizure disorder
and in turn, led to his severe hyperactivity and developmental delay. Pet’r’s Ex.
18 at 3, 5. Alternatively, Dr. Kinsbourne asserted that the seizures S.S. first
experienced on October 15, 2007, led to a lowering of his seizure threshold and
allowed his subsequent injuries to develop. Pet’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--
particularly if there is no other explanation for seizure onset. Pet’r’s Ex. 18 at 2;
Tr. at 28.

Admitting that he could not describe the particular mechanism by which the
administered MMR vaccine caused S.S.’s seizure disorder,12 Dr. Kinsbourne
identified S.S.’s first seizure episode on October 15, 2007, as the beginning of his
epileptic condition. Tr. at 25, 43, 87. Dr. Kinsbourne posited that because the
wild measles virus can cause seizures, the measles vaccine (an attenuated but live
viral vaccine) also can cause seizures, albeit “far less frequently.” Pet’r’s Ex. 18
at 3; accord. Tr. at 19-20. He theorized that the mechanism 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 that
“[s]eizures after MMR vaccination have been repeatedly documented [and] [t]heir

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

11
peak incidence [occurs] within the second week after vaccination.”13 Pet’r’s Ex.
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 conceded 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. Pet’r’s Ex. 18 at 2.
Discounting the record evidence of a “distant relative” with epilepsy, Dr.
Kinsbourne dismissed the likelihood that a genetic underpinning was primarily
responsible for S.S.’s seizure condition. Dr. Kinsbourne instead insisted that
adverse environmental factors--specifically, the administered vaccines--acted in
concert with S.S.’s latent genetic predisposition to trigger the expression 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. Referencing several case reports of
seizures occurring in afebrile subjects with gastrointestinal illnesses,14 he asserted

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 Live
Measles-Virus Vaccination, 223(13) JAMA 1459-62 (1973).
Tab G: Kathleen R. Stratton, et al., Adverse Events Associated With
Childhood 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 Submitted 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).
12
that seizures do not occur solely as a “reaction to a rise in body temperature.”
Pet’r’s Ex. 20 at 1-2. He acknowledged, however, that fever and rash are the two
most common symptoms that accompany wild measles viremia15--which reaches
its peak two weeks after a measles infection. Tr. at 61. He further acknowledged
that this is the first instance in which he has “offered the opinion that the MMR
vaccine caused an afebrile seizure.” Tr. at 30.

Dr. Kinsbourne recognized that neither fever nor rash--“the most 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 measles-associated viremia in S.S.’s case, Dr. Kinsbourne
offered that “neither of [the symptoms] are seen” in cases involving a measles-
induced inflammation known as measles encephalitis, 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 the “unfavorable
outcomes” in children afflicted with measles encephalitis).

Dr. Kinsbourne posited that the fever S.S. is alleged to have developed16
(one week before his seizure event on October 15, 2007) was attributable to the
MMR vaccine and thus, furnished “evidence of viremia.” Pet’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. Allegations 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 that the
MMR vaccine S.S. received caused the first seizure event in October 2007, and
effectively, lowered S.S.’s seizure threshold, which allowed him to experience
seizures more easily.

Dr. Kinsbourne clarified that S.S. did not suffer an encephalopathy as
defined by the Vaccine Injury Table. Pet’r’s Ex. 20 at 1. Rather, Dr. Kinsbourne

15
Viremia is “the presence of viruses in the blood.” Dorland’s at 2058.
16
Petitioner claimed in the VAERS report she filed on S.S.'s behalf, that S.S.
developed a fever a week after his vaccination. See Pet’r’s Ex. 12 at 1.

13
explained, S.S. suffered an encephalopathy, as 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.” Pet’r’s Ex.
18, Tab G (1994 IOM report), at 137.

Citing several filed articles,17 Dr. Kinsbourne asserted that “prolonged or
recurrent seizure activity . . . can irreversibly alter the way the immature brain
develops.” Pet’r’s Ex. 18 at 4. But, he admitted that the seizures S.S. first
experienced on October 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 spells lasting less than a minute, followed by a
later episode lasting only a few minutes. Tr. at 37. Although the episode was
unsettling 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 support his theory of vaccine-related causation.
Pet’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” and showed “no neurological
symptoms” the day after his first seizure episode. Tr. at 39.

Dr. Kinsbourne posited that after S.S.’s first 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

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

Tab B: Bruce Hermann, et al., The Neurodevelopmental Impact of Childhood-
onset Temporal Lobe Epilepsy on Brain Structure 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 behavioral 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).

14
epilepsy” that radically changed his behavior and school achievements.18 Tr. at
13. Dr. Kinsbourne explained that the first seizure episode left S.S. ostensibly 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 only after his second seizure event
and subsequent seizure episodes that S.S.’s developmental delay and hyperactivity
manifested. Id.

c. The Emergence 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 normal 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 fourth
year of life.” Tr. at 62-64. The record indicates that S.S. was four years old when
his seizure disorder first manifested, see 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 noted that as a former clinical
pediatric neurologist, he would not have recommended genetic testing for a child
who--similar to S.S.--had presented “with a seizure disorder, a low IQ and
[hyperactivity]” because such testing would not have informed the child’s
treatment. Tr. at 59-60. Nonetheless, the undersigned notes that such testing
could provide a better understanding of the nature of S.S.’s seizure disorder.

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 the second and third quarters of
the school year. Pet’r’s Ex. 11 at 8. On December 15, 2008, S.S.’s Individual
Education Program (“IEP”) team recommended a special education placement for
him. Pet’r’s Ex. 15 at 27.
15
 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.
Resp’t’s Ex. B at 1 (Curriculum Vitae of Dr. McDonald). After two years of
service in the United States Navy, Dr. McDonald attended medical school at the
University of Miami. Id. He is board certified in pediatric neurology. Tr. at 89.

Dr. McDonald is currently an Assistant Professor at the University of
Minnesota Medical School, Department of Pediatrics. Resp’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 conducting research. Tr.
at 90. Dr. McDonald’s patients range 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, he diagnoses and treats children with seizure
disorders 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.
Resp’t’s Ex. A at 3. Dr. McDonald observed that the medical records contain no
evidence, other than timing, to link the two events. Resp’t’s Ex. A at 3; Tr. at 102.
None of S.S.’s “treating physicians associated the immunizations directly with
[his] seizures or developmental delays/ADHD.” Resp’t’s Ex. A at 3. Nor is there
evidence suggesting that an acute encephalopathy occurred after S.S.’s
vaccinations. Tr. at 95-96.

a. Challenging the Vaccine-Relatedness of S.S.’s Seizure
Disorder

Dr. McDonald acknowledged that the “natural measles disease can cause
seizures.” Tr. at 124. He indicated that although he has seen seizures occur in
patients with measles encephalitis, an often debilitating (and occasionally fatal)
condition caused by brain inflammation that develops as a patient recovers from a
measles infection, id., there is no evidence of measles encephalitis, in this case.

16
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 vaccine “is an attenuat[ed]
version of the natural measles virus” and thus bears a substantially diminished
viral load; due to its significantly reduced virulence, it is much less likely than
wild measles virus 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 those studies involved small, poorly defined
groups. Id.

Dr. McDonald also questioned whether, in fact, S.S.’s seizure disorder may
have begun to be expressed before he received the MMR vaccine in October of
2007, See Resp’t’s Ex. A. Pointing to the record evidence of S.S.’s unwitnessed
fall on August 19, 2005, id. 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 admission [after] a witnessed seizure,” id. 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 evaluate 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 distinguishable
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
recognized seizure--Dr. McDonald stated that the test results showed “very subtle
slowing, . . . [but] not an ongoing epileptic process.” Tr. at 97. He added that
such results were not “consistent with an encephalopathy” when found in a seizure
patient. Tr. at 99.

Challenging petitioner’s assertion that S.S. suffered an encephalopathy, Dr.
McDonald addressed the investigators’ findings in the 2001 Holmes article--filed
by petitioner and cited by Dr. Kinsbourne. The authors of the 2001 Holmes study
determined that “the immature brain is less vulnerable to seizure-induced injury
than the mature brain.” Resp’t’s Ex. A at 3 (quoting the 2001 Holmes article, filed

17
as Pet’r’s Ex. 18, Tab C).19 But, the authors observed that “seizures in the
developing brain [could] result in irreversible alterations in neuroma connectivity,
and thereby affect brain functioning.” Tr. at 116.

Building upon the observations of the authors in the 2001 Holmes study,
Dr. McDonald stated that repetitive seizures (as occur in a patient with status
epilepticus) can cause additional seizure activity by lowering a patient’s seizure
threshold --which allows for increased susceptibility to seizures. Tr. at 117. Dr.
McDonald explained that a lowered seizure threshold can result from seizure-
induced brain damage caused either by alterations to nerve pathways or by
changes in the nerve impulse transmissions that protect against seizures. Tr. at
117-18. Although certain seizure activity can result in the lowering of a subject’s
seizure threshold, he asserted that S.S. did not experience that type of activity
during his first seizure event in October of 2007. Tr. at 134.

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

Dr. McDonald expressed the view similarly expressed by at least one of
S.S.’s treaters, that the prescribed anti-epileptic medication could have caused
S.S.’s attentional and behavioral issues. Tr. at 106. Dr. McDonald also
considered the possibility that S.S.’s developmental delay and attentional
problems were co-morbid conditions “unrelated to his epilepsy.” Resp’t’s Ex. A
at 2. He added that most likely, S.S.’s diminished intellectual skills and his
hyperactivity were genetically-triggered. Tr. at 105, 133. But, even 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.” Resp’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 testing,” the relevant genetic
influences could not be established. Resp’t’s Ex. A at 4; accord. Tr. at 134.

19
Holmes, supra note 17, at 320-25.

18
IV. Applicable Legal Standards

Under the Vaccine Act, 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 forth in
the Vaccine Injury Table (the Table). § 11(c)(1)(C)(i). The 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). If petitioner
establishes that the vaccinee has suffered a “Table Injury,” causation is presumed.

If, however, the vaccinee suffered an injury that either is not listed in the
Table or did not occur within the prescribed time frame, petitioner must prove that
the administered vaccine caused injury to receive Program compensation on behalf
of the vaccinee. § 11(c)(1)(C)(ii) and (iii). In such circumstances, petitioner
asserts a “non-Table or [an] off-Table” claim and to prevail, petitioner must prove
her claim by preponderant evidence.20 § 13(a)(1)(A). This standard is “one of . . .
simple preponderance, or ‘more probable than not’ causation.” Althen 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 (Fed. Cir.
1993).

The Federal Circuit has held that to establish an off-Table injury,
petitioners 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.

The Circuit Court has indicated that petitioners “must show ‘a medical
theory causally connecting the vaccination and the injury’” to establish that the
vaccine was a substantial factor 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
(Fed. Cir. 1992)). The Circuit Court added that "[t]here must be a ‘logical

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 requirements 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).

19
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.

Id. All three prongs of Althen must be satisfied. Id. “Unlike 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.

The Federal Circuit has instructed that a petitioner may satisfy her
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. Terran v. Sec’y of Health &
Human Servs., 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 Servs., 440
F.3d 1317, 1325-26 (Fed. Cir. 2006). Evidence that satisfies one prong might
assist in proving another prong as well. Id. at 1326.

The 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 satisfies the three-pronged
Althen test, compensation cannot be awarded if respondent establishes an alternate
cause of injury, not related to the administered vaccine. To defeat petitioner’s
recovery once petitioner has met her evidentiary burden, respondent must prove,
by preponderant evidence, that an alternate cause of injury exists. Knudsen v.
Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994).

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

20
V. Evaluating Petitioner’s Claim

A. Summary of Petitioner’s Theory of Causation

Petitioner alleges that the MMR vaccine administered on October 1, 2007,
caused S.S. to develop epilepsy, developmental delay, and hyperactivity.21
Petitioner asserts that the seizure episode S.S. suffered on October 15, 2007,
signaled 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 measles component in
the MMR vaccine. Pet’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 to lower S.S.’s seizure threshold and
increase S.S.’s susceptibility to another seizure event two months later, on
December 9, 2007 and thereafter, with increasing frequency. See Pet’r’s Ex. 20 at
1; Tr. at 65-66, 83-84. Dr. Kinsbourne added that 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, when discussing whether the measles vaccine could cause
seizures in the same manner as the measles infection during the two week period
following vaccine exposure. Tr. at 12, 42-43. But, he focused specifically on the
seizure events that occurred on December 9, 2007, and later when discussing the
seizures that allegedly caused the brain damage that resulted in S.S.’s
developmental delay and attentional issues. Tr. at 66-67.22

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.
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.

21
 Dr. Kinsbourne’s circular logic, that one event was caused by another
simply because the second event occurred, is also unavailing. In support of his
assertion that the seizures S.S. experienced on October 15, 2007, led to a lowering
of his seizure threshold and caused him to suffer seizure events on December 9,
2007 (and thereafter), Dr. Kinsbourne relies 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, although the individual components of Dr.
Kinsbourne’s theory seem medically sound, the combination of the components
underlying his theory of causation is not. Nor does the cobbled theory of
causation provide a logical connection between the received vaccination and S.S.’s
injuries. For these reasons, petitioner’s claim cannot stand.

B. The Filed Medical Literature Does Not Assist Petitioner23

Essential to Dr. Kinsbourne’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. Kinsbourne cites a number of studies. Pet’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, the authors evaluated 84 cases of neurologic
disorders that appeared within one month of receipt of a live measles-virus vaccine
and were reported between the years of 1963 and 1971. Pet’r’s Ex. 18, Tab D
(1973 Landrigan study), at 1460. The cases were intended to provide
epidemiologic detail about the relationship between neurologic disorders, the
measles vaccine, and the risks posed by vaccination. Id. at 1459. The cases were
divided into four groups based on the reported clinical and laboratory findings. Id.
at 1460.

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.

22
 The findings presented for Group 3 and Group 4 are 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). Eleven patients in Group 3
met the criteria for febrile convulsions, and the authors 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 timeframe for a febrile response.24 Id.

The subjects in the largest group, Group 4, experienced seizures with no
identified cause and suffered more extensive or permanent neurologic effects than
did those in Group 3. Id. Some of the subjects in Group 4 were diagnosed with
either encephalomyelitis, aseptic meningitis, spinal cord disorders, or disorders of
the peripheral nervous system. Id. at 1461. Of the 59 subjects 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 Group 4 had symptom
onset between 6 and 15 days after vaccination, the period of time during which
viral 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 the group showed that five died, ten

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. Pet’r’s Ex.
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 impairment. 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
were 53 girls, 20 boys, and 4 patients whose sex was not reported. Id.
23
recovered 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 causal
relationship in any single case between vaccination and the subsequent neurologic
disorder. Id. at 1462. Although the epidemiologic evidence suggested that some
of the cases may have been causally related to the vaccine administration, the
study’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 the study for the proposition
that the measles vaccine could cause seizures. But, on cross examination, he
limited the scope of his reliance on the 1973 Landrigan study, asserting only that
the study established the time frame within which neurologic injury 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.” Pet’r’s Ex. 18, Tab I (1998 Weibel study), at 383. Of
the 403 reviewed cases, the authors determined that only 48 of the children met
the criteria for an acute encephalopathy between the 2nd and 15th day after
vaccination, id. at 384, and fever preceded onset “by several 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 received an MMR
vaccination. Id. She was hospitalized for recurring seizures (status epilepticus)
with a fever of 106 degrees three days later (which was approximately 10 days
after vaccination). Id.

Here, the parties do not dispute that S.S.’s initial seizures occurred without
fever. The VAERS report filed on March 28, 2008 indicated that S.S. experienced
a slight fever seven days prior to his first seizure event but not during his seizure
episode. See Pet’r’s Ex. 12 at 1. Because the 1998 Weibel study focused 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
disorder because his brief, initial seizure event was not associated with fever.

Of note, the 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.” Pet’r’s
Ex. 18, Tab D (1973 Landrigan study), at 1642; accord. Pet’r’s Ex. 18, Tab I

24
(1998 Weibel study), at 387. The authors also observed that “the lack of
controlled studies that distinguish[ed] background rates of encephalopathy of
undetermined cause in unvaccinated populations” made an assessment of potential
vaccine-related causation difficult. Pet’r’s Ex. 18, Tab I (1998 Weibel study), at
386; accord. Pet’r’s Ex. 18, Tab D (1973 Landrigan study), at 1642.

2. The 2004 Ong Study and the 2004 Narchi Study

Petitioner did file two articles involving the onset of afebrile seizures; but
both the 2004 Ong study and the 2004 Narchi study focused on children who had
developed severe seizures after suffering gastrointestinal illnesses. Pet’r’s Exs. 20
at Tab C (2004 Ong study), at 157; 20 at Tab D (2004 Narchi study), at 1. The
authors of the 2004 Narchi study specifically observed that “the occurrence of
afebrile seizures during viral gastroenteritis without dehydration or electrolyte
imbalance is little known in Western countries,” Pet’r’s Ex. 20 at Tab D (2004
Narchi study), at 3 (emphasis added), and the authors 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 study), 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. However, 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 likely than not to have been benign in its impact on S.S.’s neurologic health.

3. The 1994 IOM Report

As previously discussed, the authors of the 1994 IOM report defined the
term encephalopathy broadly, and they drew a careful distinction between the
expansive definition accorded an encephalopathy and the more narrow definition
of an encephalitis. 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 virus infection is well described,” id. 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

25
distinguish from background rates.” Id. The 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 mumps and encephalopathy and encephalitis.”
Id. at 129-30 (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.” Id. at 130.

4. The 1981 NCES Study

The 1981 NCES study filed by petitioner was a case-control study. Its
primary purpose was to identify potential adverse events following a pertussis
immunization. Pet’r’s Ex. 18, Tab A (1981 NCES study), at 80. Dr. Kinsbourne
argued that the portion of the study which addressed the potential adverse effects
of the measles vaccine was a meaningful part of the study. He further argued that
the authors’ advisory concerning the possible over-reporting of cases applied only
to the conclusions involving the pertussis vaccine. Tr. at 52, 75-76; see Pet’r’s Ex.
18, Tab A (1981 NCES study), at 145.

The majority of the considered cases involved seizures associated with
fever, and consistent with the guidelines provided to physicians, case referrals
were limited to children 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
hours. Pet’r’s Ex. 18, Tab A (1981 NCES study), 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. Pet’r’s Ex. 18, Tab A (1981 NCES study) 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] caused by a
mechanism similar to that responsible for post-infectious encephalitis.” Pet’r’s
Ex. 18, Tab A (1981 NCES study), at 142. The NCES study was criticized later in
the 1994 IOM report for its observation about the measles vaccine because “a
separate analysis of those diagnosed with encephalitis and encephalopathy was not
performed.” Pet’r’s Ex. 18, Tab G (1994 IOM report), at 144; see also Pet’r’s Ex,
18, Tab I (1998 Weibel study), at 384 (the authors noted that the 1981 NCES
study did not separate convulsions from cases of acute encephalopathy).

26
 The 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 recoveries; the outcome
for those subjects was materially different from S.S.’s.

5. The 2001 Holmes article

The authors of the 2001 Holmes study discussed the long-term
consequences of seizures in the developing versus the mature brain. Pet’r’s Ex.
18, Tab C (2001 Holmes study), 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 that
significant deficits can occur as a result of seizure activity in 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 authors specifically identified “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 Holmes study, Tr. at 115-
23, Dr. McDonald stated that the findings of the “pretty convincing” animal model
study 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 seizure.” 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 2001 Holmes article, as discussed by Dr. MacDonald, helpfully
delineates those circumstances in which seizures could lead to the type of brain
damage petitioner claims that S.S. suffered. But such circumstances were absent
when S.S. first began seizing and thus, the 2001 Holmes article furnishes modest
support for petitioner’s claim that the received vaccine caused S.S.’s injuries.

27
 6. Conclusion Regarding the Filed Medical Literature

The medical literature submitted by petitioner provides little or no
evidentiary 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 acknowledged they could not establish a causal connection between
the measles vaccine and neurologic disorders, encephalopathy or encephalitis. See
Pet’r’s Ex. 18, Tab D (1973 Landrigan study), at 1642; Pet’r’s Ex. 18, Tab I (1998
Weibel study), at 386-87; Pet’r’s Ex. 18, Tab G (1994 IOM report) at 130. The
authors of the 2001 Holmes study concluded 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 study), at 322.

In the 1998 Weibel and 1981 NCES studies, the investigators considered
cases of seizure onset that was accompanied by fever or was more prolonged and
severe than the seizure events suffered by S.S. Pet’r’s Ex. 18, Tab I (1998 Weibel
study), at 385; Pet’r’s Ex. 18, Tab A (1981 NCES study), 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, the
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 the 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-Pronged Althen Test

To prove vaccine causation, petitioner must satisfy all three prongs of the
Althen test. Althen, 418 F.3d at 1278. Respondent does not dispute that petitioner
has established a temporal relationship between the administered MMR vaccine
and thus, has satisfied 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.” Resp’t’s Br. at 1.

28
 Even if the 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. Petitioner contends she has
established the first and second prongs of the Althen test. Pet’r’s Br. at 34; Pet’r’s
Reply to Resp’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.” Resp’t’s Br. at 24.

To evaluate petitioner’s claim properly, the undersigned turns now to
consider the first and second prongs of the Althen analysis.

1. Considering the First and Second Althen Prongs

The 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 93 v. Sec’y of Health & Human Servs., 98 Fed. Cl. 553,
567 (Fed. Cl. 2011). The first prong focuses on general causation, that is whether
the administered vaccine can cause the particular injury which the vaccinee
suffers26 and, the second prong focuses on specific causation, that is whether 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). Petitioners must show that it is
more likely than not that the received vaccine can cause the alleged injury.

The 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 Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009)
(biologically plausible). Petitioners must prove this prong by preponderant
evidence. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350
(Fed. Cir. 2010).

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).

29
 Dr. Kinsbourne offered a theory of causation, based on a few critical
components. First, he asserted that the measles vaccine can cause seizures during
the period of peak viremia which occurs two weeks after vaccination. Pet’r’s Ex.
18 at 3; Tr. at 19-20. Unable to identify the exact mechanism involved--and not
required to do so, see Knudsen, 35 F.3d at 549, Dr. Kinsbourne averred that the
measles vaccine could 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 could cause seizures under certain
circumstances--particularly those involving fever and gastrointestinal illness. Tr.
at 130.

When discussing the seizures that S.S. experienced during the period of
peak viremia after he received the measles vaccine, Dr. Kinsbourne posited that
S.S.’s initial seizure event could have caused sufficient brain damage to lower his
seizure threshold and make him more susceptible to future seizure events. See
Pet’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 emphasized such
seizures must be prolonged or repetitive to lower a seizure threshold. Tr. at 116-
17.

Finally, Dr. Kinsbourne maintained that epileptic seizures--such as those
S.S. experienced on December 9, 2007 and thereafter--could cause brain damage
and lead to developmental delay and hyperactivity. Pet’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 same underlying 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, the undersigned
finds that in rare circumstances, the measles vaccine can trigger--within fourteen
days of administration--seizures if accompanied by fever or in the context of a
gastrointestinal illness. A finding that prolonged or repetitive seizures can result
in the lowering of a seizure threshold and lead to additional seizures as well as
developmental delay is also supported by the expert testimony and filed literature
introduced here. Although the record contains some evidence that hyperactivity
can result from seizure medications, the undersigned is not persuaded on the
weight of this record that hyperactivity can result from MMR vaccine-induced
seizure activity.

30
 To prevail on her vaccine claim, however, petitioner also must prove that
the MMR vaccine S.S. received in October of 2007 caused his injuries in the
manner proposed by Dr. Kinsbourne.

3. Second 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 1278. In other words, petitioner must show
that it is more likely than not that the received vaccine caused the alleged 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.

Petitioner contends that she has “demonstrated that the MMR vaccine
caused [S.S.’s] epilepsy and subsequent developmental delay,” Pet’r’s Br. at 25,
that S.S.’s “injury occurred within a medically appropriate time frame after the
MMR vaccine” and that “no other likely cause of [S.S.’s] injury [has been]
identified.” Id. at 26.

Petitioner’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.,
Pet’r’s Ex. 8 at 5. S.S.’s treating physicians did not know the cause of S.S.’s
epilepsy. See, e.g., Pet’r’s Ex 14 at 17.

Moreover, the theory advanced by Dr. Kinsbourne is not supported by the
facts of this case.28 Even with the undersigned’s acceptance of Dr. Kinsbourne’s
theory that the measles vaccine can cause seizures in rare circumstances involving
fever on gastrointestinal illness and that prolonged or repetitive seizures 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. experienced on October
15, 2007, consisted of several “staring spells, each lasting for less than a minute”

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.
31
and a seizure that lasted a few minutes. Tr. at 37. Moreover, Dr. Kinsbourne
acknowledged that S.S. was “behaving normally and had no neurological
symptoms the day after his hospital admission, and that this EEG was consistent
with a postictal state and showed 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
113.

Other than the temporal relationship, 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 agreed that fever and rash are the two most common symptoms of
measles viremia. Tr. at 61. However, S.S.’s fever occurred and abated seven days
prior to his October 15, 2007 seizures. The studies relied upon by Dr. Kinsbourne
mentioned fever occurring a few days prior to and usually continuing during the
time of the seizure. See Pet’r’s Ex. 18, Tab I (1998 Weibel study), at 4; Tab A
(1981 NCES study), at 63. And as previously mentioned, none of S.S.’s treating
physicians causally associated the measles vaccine with S.S.’s seizures.

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 alternative 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 alternate explanation exists for S.S.’s injury. Yet, as
reflected in his medical records, S.S. had a maternal great aunt with epilepsy, see
supra note 11, and thus, a likely genetic predisposition to have a seizure condition.

While petitioner has proposed a theory by which the MMR vaccine could
cause injuries such as those suffered by S.S., petitioner has failed to establish a
logical sequence of cause and effect--consistent with her proposed theory--proving
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

32
dubious claim that no other potential cause for S.S.’s injuries existed. For the
reasons more fully detailed above, the undersigned is persuaded that petitioner has
satisfied the first and third prongs 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. Because petitioner cannot establish a logical causal sequence,
petitioner’s claim must be denied.

Petitioner has failed to prove that she is entitled to compensation under the
Vaccine Program. 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.
33