In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 09-0585V

(Filed: June 5, 2013)

(Reissued for Case Caption: June 21, 2013)

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

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.

DECISION1

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

petition 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 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 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 other substantive changes have been made.

on 
2

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 measlesmumps-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. 

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 

 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.
3

(“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.

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. 
4

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

 4 Kathleen R. Stratton, et al., Adverse Events Associated With Childhood 

Vaccines: Evidence Bearing on Causality, Institute of Medicine 1-464 (1994).

 Both his hearing and 

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, 

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 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. 

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,

 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. 
6

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 antiseizure 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 

 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.
7

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

 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. 

 Pet’r’s Exs. 3 at 281; 16 at 2. 

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 
8

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 Sows’ impression that the

prescribed anti-epileptic medication had exacerbated S.S.’s seizures. Id.

Similarly, he 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 antiseizure 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. 

 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.) 
9

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 antiepileptic 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 

special education placement at school and was encouraged to repeat prekindergarten. 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. 
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 

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 

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.
11

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 

peak incidence [occurs] within the second week after vaccination.”13

 12 Dr. Kinsbourne testified that “[i]t’s not believed that the measles virus 

actually invades the brain.” Tr. at 25.

 Pet’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 Live 
12

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 

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

 

Measles-Virus Vaccination, 223(13) JAMA 1459-62 (1973). 

--which reaches 

its peak two weeks after a measles infection. Tr. at 61. He further acknowledged

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). 

15 Viremia is “the presence of viruses in the blood.” Dorland’s at 2058. 
13

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 measlesinduced 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 

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.

 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.
14

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 

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 Childhoodonset 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).

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 
15

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.

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. 

 

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. 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. 

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. 
17

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 

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. 

 19 Holmes, supra note 17, at 320-25.
18

McDonald explained that a lowered seizure threshold can result from seizureinduced 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. 

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 
19

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 

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 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).
20

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. 

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

 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

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 vaccinerelated. 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 

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 

 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 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.

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

 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. Pet’r’s Ex. 
23

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 

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

 

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. 
24

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 

(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 
25

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 

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 
26

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). 

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 
27

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.

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 
28

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. 

 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, 
29

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).

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

 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

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. 

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 
31

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” 

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. 

 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 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 

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.