ANKLAM v. SECRETARY OF HEALTH AND HUMAN SERVICES

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: November 29, 2023

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

BRIAN ANKLAM and KAREN ANKLAM, *

as the legal representatives of the estate of *

their daughter, N.A., deceased, * PUBLISHED

*

Petitioners, * No. 17-2061V

*

v. * Special Master Nora Beth Dorsey

*

SECRETARY OF HEALTH * Dismissal; Measles, Mumps, Rubella,

AND HUMAN SERVICES, * Varicella (“MMRV”) Vaccine; Seizure;

* Death.

Respondent. *

*

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

Curtis R. Webb, Monmouth, OR, for Petitioners.

Katherine Carr Esposito, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

I. INTRODUCTION

On December 29, 2017, Brian Anklam and Karen Anklam (“Petitioners”), as legal

representatives of the estate of their daughter, N.A., deceased, filed a petition for compensation

under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42

1

Because this Decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it on the United States Court of Federal Claims’ website and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc in accordance with the E-

Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of

Electronic Government Services). This means the Decision will be available to anyone with

access to the Internet. In accordance with Vaccine Rule 18(b), Petitioners have 14 days to

identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. If, upon review, the undersigned agrees that the

identified material fits within this definition, the undersigned will redact such material from

public access.

U.S.C. § 300aa-10 et seq. (2018). 2 Petitioners alleged that as a result of a Measles, Mumps,

Rubella, Varicella (“MMRV”) vaccine N.A. received on June 23, 2016, N.A. developed a fever,

which triggered a seizure that caused her death. 3 Petition at 2-3 (ECF No. 1). Respondent

argued against compensation, stating that “this case is not appropriate for compensation under

the terms of the [Vaccine] Act.” Respondent’s Report (“Resp. Rept.”) at 2 (ECF No. 9).

After carefully analyzing and weighing the evidence presented in this case in accordance

with the applicable legal standards, the undersigned finds that Petitioners have failed to provide

preponderant evidence that N.A.’s MMRV vaccine caused her death. Thus, Petitioners have

failed to satisfy their burden of proof under Althen v. Secretary of Health & Human Services,

418 F.3d 1274, 1280 (Fed. Cir. 2005). Accordingly, the petition must be dismissed.

II. ISSUES TO BE DECIDED

There are two factual disputes. Joint Prehearing Submission, filed June 3, 2022, at 4

(ECF No. 72). The parties dispute whether N.A. suffered a seizure during the night of June 30,

2016 or the morning of July 1, 2016. Id. The parties also dispute whether N.A.’s autopsy slides

show abnormalities in the hippocampus, 4 specifically granule cell dispersion and/or bilamination

of the dentate gyrus. 5 Id.

Regarding causation, the parties agree the Court should apply Althen but disagree as to

whether Petitioners have provided preponderant evidence of the Althen prongs. Joint Prehearing

Submission at 4-5. The parties agree the MMRV vaccine can cause febrile seizures and that

2

The National Vaccine Injury Compensation Program is set forth in 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. §§ 300aa-10 to -34 (2018) (“Vaccine Act” or “the Act”). All citations in this Decision

to individual sections of the Vaccine Act are to 42 U.S.C.A. § 300aa.

3

N.A. also received Haemophilus influenzae type B (“Hib”), pneumococcal conjugate

(“Prevnar”), and Hepatitis A vaccines on June 23, 2016; however, Petitioners allege only the

MMRV vaccine caused N.A.’s death. Petition at 2-3; Joint Prehearing Submission, filed June 3,

2022, at 4 (ECF No. 72).

4

The hippocampus is “a convoluted elevation of gray matter extending the entire length of the

floor of the temporal horn of the lateral ventricle; it is part of the limbic system and plays major

roles in short-term memory and spatial navigation.” Hippocampus, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=22696 (last visited Nov. 13,

2023). Hippocampus is used “to denote the entire structure, including the hippocampus proper

(Ammon’s horn), the dentate gyrus, and the subicular complex (presubiculum, parasubiculum,

and subiculum), but it can also be used more restrictively, most often denoting the hippocampus

proper, in which case the entire structure may be called the hippocampal formation.” Id.

5

Although not mentioned in the Joint Prehearing Submission, Petitioners’ expert, Dr. Miller,

also opined that there was an abnormality in the medulla. See Petitioners’ Exhibit (“Pet. Ex.”)

22 at 5, 8; Pet. Ex. 65 at 3; Transcript (“Tr.”) 23, 46-49.

2

most of these seizures occur between seven to 10 days after MMRV vaccination. Id. at 4.

However, they disagree as to (1) whether the MMRV vaccination administered to N.A. on June

23, 2016 caused her to have a vaccine-related seizure that led to her death, (2) whether an

unobserved febrile seizure can cause a child to die, and (3) whether an unobserved febrile seizure

did cause N.A. to die. Id.

III. BACKGROUND

A. Procedural History

Petitioners filed a petition along with medical records on December 29, 2017. Petition;

Petitioners’ Exhibits (“Pet. Exs.”) 1-8. Petitioners filed medical literature on March 29, 2018.

Pet. Exs. 9-12. Respondent filed his Rule 4(c) Report on May 25, 2018, arguing against

compensation. Resp. Rept. at 2.

Petitioners filed an expert report from Dr. Marcel Kinsbourne on November 13, 2018 and

an expert report from Dr. Douglas C. Miller on January 14, 2019. Pet. Exs. 13, 22. On May 30,

2019, Respondent filed expert reports from Dr. Christine McCusker, Dr. Sara O. Vargas, and Dr.

Hart G.W. Lidov. Resp. Exs. A, C, E. Petitioners filed supplemental expert reports from Dr.

Kinsbourne and Dr. Miller and photomicrographs of autopsy slides on November 4, 2019. Pet.

Exs. 61, 65-66. From February to June 2020, Respondent filed supplemental expert reports from

Dr. McCusker, Dr. Lidov, and Dr. Vargas. Resp. Exs. H-J.

The undersigned held a Rule 5 conference on August 18, 2020. Rule 5 Order dated Aug.

19, 2020 (ECF No. 53). Prior to the conference, the parties filed briefs. Resp. Pre-Rule 5

Conference Brief, filed Aug. 7, 2020 (ECF No. 51); Pet. Memorandum in Support of Rule 5

Ruling Favoring the Petitioners, filed Aug. 7, 2020 (ECF No. 52). The undersigned

preliminarily found Petitioners’ theory under Althen prong one may not be sound and reliable.

Rule 5 Order at 1-2. The undersigned also preliminarily found no evidence that N.A. more likely

than not suffered a seizure, and thus, given the lack of factual evidence and competing expert

opinions, the undersigned was unable to conclude by preponderant evidence that N.A.’s

hippocampus was pathologically abnormal. Id. at 2. As for the third Althen prong, the

undersigned preliminarily found there was a temporal association but stressed that a temporal

association alone is insufficient to prove causation. Id. Petitioners indicated their preference for

an entitlement hearing, and one was set for January 2022. Id. at 2; Pre-Hearing Order dated

Sept. 18, 2020 (ECF No. 55).

On September 20, 2021, Respondent filed additional medical literature. Resp. Exs. K-L.

On November 24, 2021, Petitioners filed their pre-hearing submissions along with an expert

report and medical literature from Dr. Miller and a case review report from Sudden Unexplained

Death in Childhood (“SUDC”) Registry and Research Collaborative (“SUDCRRC”). Pet.

Prehearing Brief, filed Nov. 24, 2021 (ECF No. 58); Pet. Exs. 69-77. The undersigned held a

status conference on December 9, 2021, on Respondent’s request, due to Petitioners’ recently

filed expert report. Order dated Dec. 10, 2021 (ECF No. 64). Because Respondent’s experts

were unable to prepare responsive expert reports prior to the hearing, and because Petitioners

3

preferred to receive these reports prior to the hearing, the entitlement hearing was moved to July

2022. Id. at 1-2; Order dated Dec. 16, 2021 (ECF No. 66).

Respondent filed supplemental expert reports from Dr. Lidov and Dr. Vargas on February

28, 2022. Resp. Exs. M-N. Petitioners filed the parties’ joint submission on June 3, 2022, and

Respondent filed his pre-hearing submission on June 7, 2022. Joint Prehearing Submission;

Resp. Pre-Hearing Submission, filed June 7, 2022 (ECF No. 73).

An entitlement hearing was held on July 12 and 13, 2022. Order dated July 14, 2022

(ECF No. 75); Transcript (“Tr.”) 1, 219. Karen Anklam (N.A.’s mother), Dr. Miller, Dr.

Kinsbourne, Dr. Lidov, Dr. Vargas, and Dr. McCusker testified. Tr. 3. Thereafter, additional

medical literature and medical records were filed by the parties. Resp. Exs. U-Y; Pet. Exs. 78-

80. In December 2022, Petitioners filed a post-hearing brief along with an affidavit from Mrs.

Anklam, N.A.’s mother. Pet. Post-Hearing Brief, filed Dec. 13, 2022 (ECF No. 88); Pet. Ex. 81.

On February 8, 2023, Respondent filed his post-hearing brief. Resp. Post-Hearing Brief, filed

Feb. 8, 2023 (ECF No. 90). Petitioners filed a reply on March 13, 2023, and Respondent filed a

sur-reply on April 4, 2023. Pet. Reply Brief, filed Mar. 13, 2023 (ECF No. 93); Resp. Sur-

Reply, filed Apr. 4, 2023 (ECF No. 95).

This matter is now ripe for adjudication.

B. Factual History

1. Stipulated Facts

The parties agreed to the following stipulated facts as set forth in their Joint Prehearing

Submission. See Joint Prehearing Submission at 1-4.

N.A. was born on June 18, 2015 in Saginaw, Michigan. Pet. Ex. 2 at 3. She was noted to

be doing well with appropriate growth and development at her one-year well-child visit on June

23, 2016. Pet. Ex. 4 at 33. N.A. received Haemophilus influenzae type B (“Hib”),

pneumococcal conjugate (“Prevnar”), Hepatitis A, and MMRV vaccinations on June 23, 2016 at

the office of her pediatrician in Croswell, Michigan. Pet. Ex. 4 at 34.

N.A.’s parents took N.A. and her three siblings to a splash park for about two hours

during the afternoon of June 30, 2016. Pet. Ex. 1 at 2; Pet. Ex. 5 at 5. N.A.’s mother thought

that N.A. had developed a fever at about 6:00 p.m. on the evening of June 30, 2016. Pet. Ex. 1 at

3; Pet. Ex. 5 at 5. N.A.’s mother gave N.A. a 3.75 ml dose of Motrin and a tepid bath at about

6:00 p.m. Pet. Ex. 1 at 3; Pet. Ex. 5 at 5. N.A.’s mother put N.A. in her crib for the night at

between 6:30 p.m. and 7:00 p.m. on June 30, 2016. Pet. Ex. 1 at 3; Pet. Ex. 5 at 5.

N.A. was found dead, face down in her crib, by her father, at about 9:00 a.m. on July 1,

2016. Pet. Ex. 1 at 3; Pet. Ex. 5 at 2, 5; Pet. Ex. 6 at 1. He reported that he first saw N.A.’s feet

sticking out of the crib slats. Pet. Ex. 1 at 3; Pet. Ex. 5 at 3. He said that N.A.’s feet were

purple, her arms were straight out at her elbows at her sides (like a star), and her face was

4

straight down to the mattress. Pet. Ex. 1 at 3; Pet. Ex. 5 at 3-5. He did not see anything coming

out of N.A.’s mouth. Pet. Ex. 1 at 3.

N.A.’s father is an experienced paramedic. He immediately knew that N.A. was dead

and had died some time before. Pet. Ex. 1 at 3; Pet. Ex. 5 at 5.

An autopsy of N.A. was done on July 3, 2016. Dr. Kanu Virani, M.D., the Forensic

Pathologist who performed the autopsy, opined

[N.A.] died of asphyxia. She was found dead face down in a crib. The

entire autopsy failed to identify any natural disease. Children at age of one year

and older should be able to turn side way or face up at the time of possible

breathing difficulties during sleep. The entire autopsy and investigation

surrounding her death[] failed to identify [a] possible factor for asphyxia. There

are no physical injuries. The manner of death is undeterminable.

Pet. Ex. 6 at 1.

Other potentially relevant notations in the autopsy report include Dr. Virani’s

observations of a “[s]mall amount of mucus [] present in nostrils,” that the “[t]he respiratory

mucosa [was] mildly congested,” a “[s]mall amount of mucus [] present in the trachea and

bronchi,” and that “[t]here [was] no laryngeal edema or upper airway obstruction.” Pet. Ex. 6 at

2-3. Microscopic examination of the lungs showed congested septa and minimal chronic

inflammation of the submucosa of the epiglottis. Id. at 4.

N.A.’s twin sister, L.A., slept in a separate crib in the same room as her sister. She also

received an MMRV vaccination on June 23, 2016. During the evening of July 1, 2016, Mrs.

Anklam noted that L.A. had a rash on her back and felt a little warm. She had an elevated

temperature, less than 100°F. Pet. Ex. 1 at 4. Petitioners brought L.A. to the emergency room

(“ER”) at the local hospital on July 1, 2016. She had a temperature of 100.2°F (rectal) at the

hospital. Pet. Ex. 1 at 4; Pet. Ex. 7 at 3.

N.A.’s older brother, L.B.A. (DOB: 04/25/2012), experienced febrile seizures on March

16, 2015, and August 28, 2016, and was seen in the hospital on July 17, 2016, for fever,

vomiting, and being “somewhat dazed and not acting quite right.” Pet. Ex. 1 at 4; Pet. Ex. 7 at 4-

6, 9-14, 24-27.

2. Summary of Medical Records

In addition to the facts stipulated to by the parties, the following summary of facts

provides additional relevant information.

N.A. was born on June 18, 2015, along with her twin sister, L.A., without complications.

Pet. Ex. 2 at 3. N.A. had a heart murmur that was resolved by discharge on June 21, 2015. Pet.

Ex. 3 at 6-8; Pet. Ex. 4 at 2. At discharge, N.A. had a normal examination and appeared healthy.

Pet. Ex. 3 at 6-8.

5

N.A. visited her pediatrician, Dr. Matthew Gormley, regularly for well-child visits from

June 2015 to March 2016. Pet. Ex. 4 at 2-17, 20-27. N.A. was noted to be doing well and had

appropriate growth and development. Id. at 3, 7, 12, 15-16, 21-22, 26. At visits in September

2015 and November 2015, N.A. received Pediatrix (diphtheria-tetanus-acellular pertussis

(“DTaP”), hepatitis B, and Polio), Hib, Rotarix (Rotavirus), and Prevnar vaccinations. Id. at 12,

16. N.A. received the third doses of Pediatrix and Prevnar at a visit in December 2015. Id. at 22.

No adverse reactions were noted following these vaccinations. See id. at 12, 16, 22.

On November 23, 2015, N.A. presented to Dr. Gormley with “nasal congestion and

cough/wheezing for the last [three] weeks.” Pet. Ex. 4 at 18. She had no fever or chills. Id.

Assessment was an upper respiratory infection. Id. Dr. Gormley noted it was likely a viral

illness and recommended follow-up if no improvement. Id.

N.A. presented to Dr. Gormley’s office on May 13, 2016. Pet. Ex. 4 at 28. N.A. had

some congestion, slight swelling near the right eye, and some eye drainage the day prior. Id. By

that morning, the right eye was red and swollen shut. Id. No fever was noted. Id. Assessment

was cellulitis. Id. N.A. was prescribed Cephalexin and was directed to return in one week. Id.

On May 18, 2015, N.A. returned for a follow-up examination. Pet. Ex. 4 at 30. N.A.’s

father reported her “eye [was] no longer red or swollen and [there was] no further drainage.” Id.

N.A. was tolerating the antibiotics well. Id. Physical examination was normal. Id. N.A. was

noted to have a body mass index in the “5th percentile to less than 85th percentile for age.” Id.

Notes indicated N.A.’s cellulitis was “resolved.” Id. N.A.’s parents were instructed to continue

giving her Cephalexin twice daily. Id.

N.A. presented to Dr. Gormley for her one-year well-child visit on June 23, 2016. Pet.

Ex. 4 at 32. She was not currently on any medications. Id. N.A. did not have a fever, cough, or

breathing issues. Id. Physical examination was normal. Id. at 33. Dr. Gormley noted N.A. was

“[d]oing well” and had “appropriate growth and development.” Id. At this visit, N.A. received

her third Hib, fourth Prevnar, first hepatitis A, and first MMRV vaccinations. Id. at 34. No

adverse reactions were noted. See id. at 32-35.

On the morning of July 1, 2016, shortly after 9:00 a.m., N.A. was found unresponsive in

her crib. Pet. Ex. 5 at 3. N.A. “had obvious rigor mortis and was cold to the touch.” Id. at 3.

She “also had pooling on her skin that indicated that she had been deceased for some time.” Id.

Time of death was placed between 9:00 p.m. and 10:00 p.m. on June 30, 2016. Id. at 6.

3. Sheriff’s Records

The Sheriff’s records indicated Officer Robby Joe Wendling arrived on scene at

approximately 9:35 a.m. on July 1, 2016. Pet. Ex. 5 at 3. He entered N.A.’s room and noted she

was face up, “had obvious rigor mortis[,] and was cold to the touch.” Id. She “also had pooling

on her skin that indicated that she had been deceased for some time.” Id.

6

Detective Mark Ruggles and Sergeant Shelly Park arrived on the scene shortly thereafter.

Pet. Ex. 5 at 4. Detective Ruggles noted rigor mortis was fixed, livor mortis was consistent with

Mr. Anklam’s description that N.A. was found face down in a blanket, and N.A. was cold to the

touch. Id. Detective Ruggles examined N.A. and found no injuries. Id.

The Incident Report documented that Petitioners took their children, including N.A., to

the Splash Pond until 5:15 p.m. on June 30, 2016. Pet. Ex. 5 at 5. Once the family arrived

home, the children were fed chicken noodle soup for dinner and then given a bath. Id. Mrs.

Anklam stated N.A. was running a low-grade fever and given Motrin around 6:00 p.m. Id.

Around 6:30 p.m., the children were put to bed. Id. Petitioners reported they did not hear

anything from L.A. and N.A.’s room during the night. Id.

Mrs. Anklam stated she woke up around 6:30 a.m. and did not check on N.A. prior to

leaving for work. Pet. Ex. 5 at 5. Mr. Anklam stated he went into L.A. and N.A.’s room around

9:00 a.m., when he found L.A. awake. Id. While changing L.A.’s diaper, he noticed N.A.’s

“feet were just outside the rails of the crib.” Id. He noticed “some discoloring to [N.A.’s] feet”

and felt they were cold. Id. He turned her over and saw “she was ‘pooling.’” Id. “[Mr.

Anklam] stated that he knew right away that she was dead.” Id.

Petitioners reported that N.A. “ha[d] been running a low grade fever, sometimes up to

100.5 since [June 19, 2016].” Pet. Ex. 5 at 5. The fever would fluctuate and sometimes

dissipate. Id. Other than that, N.A.’s only other issue since birth was right eye swelling in May

2016. Id.

Time of death was placed between 9:00 p.m. and 10:00 p.m. on June 30, 2016. Pet. Ex. 5

at 6.

4. Autopsy 6

An autopsy was conducted by Dr. Virani on July 3, 2016. Pet. Ex. 6 at 1. Autopsy

findings indicated asphyxia with pulmonary edema and blanching on face. Id. Dr. Virani opined

[N.A.] died of asphyxia. She was found dead face down in a crib. The

entire autopsy failed to identify any natural disease. Children at age of one year

and older should be able to turn side way or face up at the time of possible

breathing difficulties during sleep. The entire autopsy and investigation

surrounding her death[] failed to identify [a] possible factor for asphyxia. There

are no physical injuries. The manner of death is undeterminable.

Id.

External examination noted “[b]lanching . . . in central portion of the face” and “[s]mall

amount of mucus present in nostrils.” Pet. Ex. 6 at 2. Internal examination revealed the

“hippocampi [were] without abnormality.” Id. There was no abnormality of the head or brain.

6

For additional facts and findings found during the autopsy, see Pet. Ex. 6.

7

Id. “There [was] no laryngeal edema or upper airway obstruction.” Id. at 3. Examination of the

respiratory system revealed “[p]ulmonary edema and congestion,” “[s]mall amount of mucus . . .

in trachea and bronchi,” and “mildly congested” respiratory mucosa. Id.

Microscopic examination of the lungs revealed “edema fluid and scatter macrophages[7]

in alveoli,” 8 congested septa, 9 and “[m]inimal chronic inflammation . . . in the submucosa of

epiglottis.” Pet. Ex. 6 at 4. There was no acute or chronic inflammation in the trachea or

bronchi and no evidence of aspirated foreign material and inflammation in airways or alveoli.

Id.

Dr. Virani examined sections of the brain and did not find any abnormality. Pet. Ex. 6 at

4. He also reviewed “[s]ections of brain, heart, liver, spleen, thymus, kidneys, thyroid, adrenals,

pituitary, stomach, intestines, appendix, pancreas, lymph nodes, bone marrow[,] and urinary

bladder” and reported that they were all “unremarkable.” Id. Additionally, toxicology testing

did not reveal any positive findings. Id. at 5-6.

Dr. Virani documented the date of death to be “June 30, 2016, unknown PM.” Pet. Ex. 6

at 1.

7

A macrophage is a “form[] of mononuclear phagocytes found in tissues” that “arise from

hematopoietic stem cells in the bone marrow.” Macrophage, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=29296 (last visited Nov. 13, 2023).

Macrophages engage in “[p]hagocytic activity” and are also “involved in cell-mediated immune

responses.” Stedman’s Medical Dictionary 1141 (28th ed. 2006). Phagocytosis is the process by

which “particulate material, such as microorganisms or cell fragments[,] . . . is taken into the cell

in membrane-bound vesicles (phagosomes) that originate as pinched-off invaginations of the

plasma membrane. Phagosomes fuse with lysosomes, forming phagolysosomes in which the

engulfed material is killed and digested.” Phagocytosis, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=38307 (last visited Nov. 13, 2023).

8

An alveolar macrophage is “a rounded granular type, found within the alveoli of the lungs and

serv[es] to ingest inhaled particulate matter.” Alveolar Macrophage, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=87677 (last visited Nov. 13,

2023). Alveolus is “a small saclike structure” found in the lungs. Alveolus, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=2006 (last visited

Nov. 13, 2023).

9

Septum is “a dividing wall or partition.” Septum, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=45434 (last visited Nov. 13, 2023).

Septa can “separate adjacent pulmonary alveoli, containing connective tissue constituents of the

respiratory tissue and the capillary network of the blood supply of the lung.” Interalveolar

Septum, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?

id=105585 (last visited Nov. 13, 2023).

8

5. SUDC Registry and Research Collaborative Case Review Report

Petitioners participated in the SUDCRRC, consenting to have N.A.’s case reviewed. This

collaborative “analyzes cases of sudden unexpected deaths in children to understand risk factors

and causes and to develop preventative measures by studying available records . . . and

performing genetic analyses and special studies.” Pet. Ex. 77 at 3.

As part of the case review, N.A.’s parents were interviewed. In the interview on

September 1, 2016, N.A.’s parents (Petitioners) reported no concerns about N.A.’s development.

Pet. Ex. 77 at 5. During her life, N.A. had “no known seizures.” Id. During the last 48 hours of

her life, N.A. was “[c]ongested occasionally, but otherwise fine.” Id. In her last 24 hours, N.A.

“had a minor cold and [] appeared ‘worn out, but not lethargic.’” Id. She also had a low-grade

fever. Id. She was given one dose of Motrin after her dinner at 6:00 p.m. Id. at 5, 8.

Autopsy tissue of the brain (3 slides) was reviewed by the SUDCRRC neuropathologist

who found no significant histopathology. Pet. Ex. 77 at 8. Further, “[t]he SUDCRRC Forensic

Pathology reviewers were in complete agreement with the reviews of the study’s . . .

neuropathologist.” Id. Based on their review, the “forensic pathologist consider[ed] the

significant findings . . . to be: 1) [s]ibling with genetic syndrome associated with slightly

prolonged QT,[10] 2) [s]ibling with febrile seizures, 3) [f]ound prone with face pressed into

mattress with blanching lividity on face.” Id. at 8-9. Under cause of death, the report concluded

N.A.’s death was an “[u]nexplained sudden death,” with intrinsic factors including “[f]ebrile at

time of death and evidence of immune activation” and extrinsic factors including “[f]ound prone

with face down with blanching.” Id. at 9. The manner of death was “[u]ndetermined.” Id. The

report was signed by Dr. Orrin Devinsky, Principle Investigator. Id. at 10.

A SUDCRRC genetic panel was also performed for N.A. and “[n]o clinically significant

variants [were] identified.” Pet. Ex. 80 at 2.

6. Mrs. Anklam’s Affidavit & Hearing Testimony

Mrs. Anklam is N.A.’s mother. Tr. 6; Pet. Ex. 1 at ¶ 1. She works as a nurse anesthetist,

and her husband, Mr. Anklam, is a paramedic. Tr. 225; Pet. Ex. 1 at ¶¶ 19, 33.

N.A. was born on June 18, 2015. Pet. Ex. 1 at ¶ 2. She had a heart murmur that resolved

prior to discharge. Id. “[N.A.] was healthy and developing normally until her sudden death on

June 30, 2016.” Id. at ¶ 3. Her “development was normal” and she was “always fed well.” Id.

at ¶¶ 4-5.

10

“A prolonged QT interval is an irregular heart rhythm that can be seen on an

electrocardiogram. It reflects a disturbance in how the heart’s bottom chambers (ventricles) send

signals. In a prolonged QT interval, it takes longer than usual for the heart to recharge between

beats.” Prolonged QT Interval, Mayo Clinic, https://www.mayoclinic.org/diseases-

conditions/long-qt-syndrome/multimedia/prolonged-q-t-interval/img-20007972 (last visited Nov.

13, 2023).

9

On June 23, 2016, N.A. received her third Hib, fourth Prevnar, first hepatitis A, and first

MMRV vaccinations at the office of her pediatrician, Dr. Gromley. Pet. Ex. 1 at ¶ 6. Although

she cried after receiving the vaccinations, her “behavior was pretty normal.” Id. at ¶¶ 7-8. For

the first two days following the vaccinations, Mrs. Anklam gave N.A. Motrin. Id. at ¶ 8.

Because she was getting her first molars, “she was a little more cranky and drooling more than

usual.” Id. “[N.A’s] behavior was unremarkable from June 23 to June 29.” Id. at ¶ 9.

On the morning of June 30, 2016, N.A. was well. Tr. 6. That afternoon, around 3:00

p.m., Petitioners took their children, including N.A., to a splash park. Tr. 6-7; Pet. Ex. 1 at ¶ 10.

“[N.A.] was a bit crankier than usual, but it was a warm day, and [Mrs. Anklam] attributed it to

that.” Pet. Ex. 1 at ¶ 10. They arrived home around 5:00 p.m. and had chicken noodle soup for

dinner, which ended sometime between 5:30 p.m. and 5:45 p.m. Tr. 7, 14; Pet. Ex. 1 at ¶ 11.

“N.A. was very sleepy.” Tr. 8; see also Pet. Ex. 1 at ¶ 11.

Following dinner, both N.A. and her twin sister, L.A., felt warm. Tr. 8; Pet. Ex. 1 at ¶ 12.

Because of her experience as a mother and a nurse, Mrs. Anklam did not take their temperatures.

Tr. 8; Pet. Ex. 1 at ¶ 13. She bathed both N.A. and L.A. together and noted they were both fine

at the time. Tr. 9. Following the bath, Mrs. Anklam gave both N.A. and L.A. Motrin around

6:30 p.m., before putting them to bed in the same room in separate cribs sometime between 7:00

p.m. and 7:30 p.m. Tr. 9-10, 14; Pet. Ex. 1 at ¶ 14.

During the night, Petitioners did not hear anything from N.A.’s room. Pet. Ex. 1 at ¶ 15.

N.A. and L.A. had been sleeping longer, and Petitioners attributed it to a growth spurt. Id. at ¶

16.

The following morning, July 1, 2016, Mrs. Anklam left home at 6:30 a.m. to go to work.

Tr. 10. She did not check on N.A. and L.A. prior to leaving for work. Tr. 10-11. Mr. Anklam

went into N.A. and L.A.’s room around 9:00 a.m. that morning. Pet. Ex. 1 at ¶ 17. “When he

glanced at [N.A.’s] crib, he knew something was wrong. Her feet were sticking out of the crib

slats and her arms were straight at the elbows and out to her sides (like a little star).” Id. at ¶ 18.

He saw N.A.’s feet were purple, she was face down, and “[t]here was nothing coming out of her

mouth.” Id. at ¶ 19. “He picked [N.A.] up and knew she was dead and had been for a while.”

Id. at ¶ 20. He then called 911 and Mrs. Anklam. Id.

Mrs. Anklam testified that she never saw N.A. have a seizure or knew her to have a fever

in excess of 100°F. Tr. 15.

Mrs. Anklam testified the none of the three other children were ill on June 30, 2016, or

showed symptoms of infection on July 1, 2016. Tr. 12. However, during the evening of July 1,

2016, around 7:00 p.m., Petitioners took N.A.’s twin sister L.A. to the ER because she had a

slightly elevated fever and a rash on her back. Tr. 11; Pet. Ex. 1 at ¶¶ 21, 24. Mrs. Anklam

averred that she was terrified to put her to bed because Petitioners did not know what led to

N.A.’s death. Pet. Ex. 1 at ¶¶ 21-22. A thorough work up was completed and L.A. was

discharged shortly after 9:00 p.m. Id. at ¶ 24.

10

After N.A. passed, Petitioners enrolled their family in a study of SUDC. Pet. Ex. 1 at ¶

26. “Throughout [their] participation in that study []and [Mrs. Anklam’s] own efforts to

understand [N.A.’s] death[], [she] [] learned medical literature links [SUDC] to unobserved

febrile seizures,” which she averred “seem[s] especially relevant to [N.A.’s] death because

MMRV vaccinations cause fevers and febrile seizures in the second week after vaccinations.”

Id. at ¶¶ 27-28.

Additionally, Mrs. Anklam explained that one of her sons had suffered three febrile

seizures, and “[she] learned that children who die unexpectedly often have a history of febrile

seizures or a family history of febrile seizures.” Pet. Ex. 1 at ¶¶ 28, 41. His first seizure

occurred on March 16, 2015. Id. at ¶ 30; Tr. 14-15, 224. On that day, he complained of ear pain

and he had a “high normal” temperature below 100°F. Tr. 224; Pet. Ex. 1 at ¶ 30. He was given

Motrin. Tr. 224; Pet. Ex. 1 at ¶ 30. While at the park over one hour later, he began seizing. Tr.

224-25; Pet. Ex. 1 at ¶¶ 31-32. When they arrived at the ER, his temperature was between 103°F

and 104°F. Tr. 225; Pet. Ex. 1 at ¶ 35. He had two subsequent febrile seizures in July and

August 2016. Pet. Ex. 1 at ¶¶ 36-40. He had genetic testing done that showed he had a 3q26

microdeletion, which Mrs. Anklam testified is not associated with seizures. Tr. 16, 223.

Additionally, following N.A.’s passing, the other three children received cardiac evaluations, and

all three were cleared. Tr. 15.

C. Expert Reports

1. Petitioners’ Expert, Dr. Douglas C. Miller, M.D., Ph.D. 11

a. Background and Qualifications

Dr. Miller is an anatomic pathologist and a neuropathologist. Tr. 18. He received his

B.A. in biology from Williams College in Massachusetts and his M.D. and Ph.D. in physiology

and biophysics from the University of Miami in Florida. Pet. Ex. 23 at 1. Thereafter, he

completed an anatomic pathology residency and a neuropathology residency at Massachusetts

General Hospital. Id. Dr. Miller has held various teaching and consulting positions throughout

his career. Id. at 3-4. He currently works as a Professor in the Department of Pathology and

Anatomical Sciences at the University of Missouri Medical Center, is the Chair of the

Department of Pathology, and is the Director of the Pathology Residency Program. Tr. 18-19.

He has authored or co-authored almost 300 publications. Pet. Ex. 23 at 7-27. Dr. Miller has

served as a neuropathology consultant for medical examiners for over 30 years and he has

“extensive experience with the neuropathology of sudden infant death.” Pet. Ex. 22 at 2-3.

11

Dr. Miller testified at the hearing and submitted three expert reports. Tr. 3; Pet. Exs. 22, 65,

69. Some of Petitioners’ medical literature contains pagination that begins at page one, and

others begin at varying page numbers. To avoid confusion, the undersigned used pagination

consistent with the ECF pagination for the medical literature that did not begin at page one.

11

b. Opinion 12

Dr. Miller opined that the MMRV vaccination administered to N.A. on June 23, 2016 led

to a fever on June 30, that provoked a seizure that night, which caused N.A.’s death. Tr. 21-22,

25, 34-35.

i. Background

Dr. Miller discussed the relevant syndromes, including sudden unexplained death in

children (“SUDC”), sudden infant death syndrome (“SIDS”), and sudden unexplained death in

epilepsy (“SUDEP”), and briefly explained their relevance to this case. He classified N.A.’s case

as SUDC, or sudden unexplained death in a young child over the age of one year when “there is

no identified underlying disease or cause of death, including after a thorough autopsy, to which

death can be attributed, plus a detailed scene investigation which confirms that the environment .

. . cannot be blamed for [the child’s] death.” Pet. Ex. 22 at 5; see also Tr. 42.

He did not classify N.A.’s case as SIDS given her age at death 13 because SIDS “is

defined as the sudden unexpected death of a child older than [one] month of age and no older

than one year of age, for which no anatomic or toxicological cause of death can be found after a

thorough scene investigation and thorough complete autopsy.” Pet. Ex. 22 at 5; see also Tr. 41-

42. Dr. Miller noted, however, “such arbitrary limits” between SUDC and SIDS “have little

scientific basis.” Pet. Ex. 22 at 5. Although N.A.’s autopsy did not conclude that she had SUDC

or SIDS, he found these terms have bearing on N.A.’s cause of death because their risk factors,

including sleeping position and fever, 14 are relevant to this case. Id. at 4; Tr. 42-43.

Lastly, Dr. Miller did not classify N.A.’s case as SUDEP because she did not have

epilepsy, which by definition, requires two unprovoked seizures separated in time. Tr. 45, 67.

12

At the hearing, Dr. Miller testified that his opinions in his first expert report regarding

“vaccine adjuvants and cytokines . . . [are] not relevant to this case.” Tr. 61; see Pet. Ex. 22 at 9-

12. He also retracted his opinions related to “the hypercarbia theory where there was a build-up

of carbon dioxide.” Tr. 61; see Pet. Ex. 22 at 6-12. As such, the undersigned will not address

these opinions.

13

At the hearing, and in his expert reports, Dr. Miller argued that N.A. was born slightly early at

36 weeks and 3 days, and thus, her actual age at death could be calculated to be less than one

year, which would make this a SIDS case. Pet. Ex. 22 at 5; Tr. 41-42. The undersigned does not

find this opinion affects her opinions or is determinative, and therefore, she will not address it.

14

Dr. Miller acknowledged that vaccination is not a risk factor but noted that fever is a risk

factor, and fevers are associated with vaccinations, including MMRV. Tr. 43. Dr. Miller was an

expert in the Boatmon case, where the Federal Circuit held that mere evidence that it was

“medically plausible” that the premature infant’s death was caused by vaccinations failed to

demonstrate a causal connection required for compensation under the Vaccine Act. Boatmon v.

Sec’y of Health & Hum. Servs., 941 F.3d 1351 (Fed. Cir. 2019). In this case, Dr. Miller testified

that he did not “plan on relitigating Boatmon . . . . That’s not what this case is about.” Tr. 43.

12

Dr. Miller agreed that there was no evidence that N.A. ever had another seizure, which he opined

is common in SUDC cases. Tr. 43.

ii. Althen Prong One

Dr. Miller opined the MMRV vaccine can lead to fever and febrile seizure, and a seizure

can lead to death. Pet. Ex. 22 at 8. As an overview, Dr. Miller opined that a child who receives

an MMRV vaccine has “a significant risk of fever and febrile seizures,” and “[s]uch seizures,

occurring unwitnessed in sleep, would present a significant risk of death in a child with a

dysplastic dentate gyrus (the hippocampal abnormality associated with SUDC), with or without

defects in the medullary 5HT system (such as the abnormality in the accurate nuclei associated

with SIDS).” Id. He further opined that the risk of death is greater in a child with both defects.

Id. He opined that “[t]his chain of events represents a highly plausible, scientifically valid,

hypothesis.” Id. at 13.

He explained that the MMRV vaccine can lead to fevers and seizures seven to 10 days

after vaccination. Pet. Ex. 22 at 8, 12; see Tr. 34, 39; Pet. Ex. 19 at 2; 15 Pet. Ex. 21 at 2, 4-5. 16

“Fever is one of the consequences of the vaccination,” explained Dr. Miller, “and fever can

predispose to seizures.” Tr. 34. He testified that “[a]ll people . . . have some risk . . . of having a

febrile reaction to a vaccine.” Id. For the MMRV vaccine in particular, Dr. Miller noted there is

a “significantly greater risk of febrile seizures with a peak period of around seven to 10 days

after the vaccination.” Id. He acknowledged that such an event is “rare” but maintained that

there is a “significantly increased risk” of fever and febrile seizures following the MMRV

vaccine. Tr. 23-24, 58, 60.

Dr. Miller then explained that febrile seizures “certainly can lead to death in a vulnerable

patient.” Tr. 37. “Seizures represent an electrical storm . . . that affects the brain and leads to a

number of other things that can happen.” Id. For example, “electrical impulses from the

cerebral hemispheres where the seizures occur[] can be transmitted down into the brainstem and

the brainstem controls both respiratory effort and heart rate.” Id. Thus, “a sudden electrical

discharge can shut down the medulla and cause cessation of breathing and/or cardiac

arrhythmia.” Id. This “electrical activity may also stimulate an outpouring of autonomic

nervous system activity,” which can lead to “a discharge of sympathetic [] neurons [that] can

also lead to cardiac arrhythmia and death.” Tr. 37-38.

15

Nicola P. Klein et al., Safety of Measles-Containing Vaccines in 1-Year-Old Children, 135

Pediatrics e321 (2015).

16

Shannon E. MacDonald et al., Risk of Febrile Seizures After First Dose of Measles-Mumps-

Rubella-Varicella Vaccine: A Population-Based Cohort Study, 186 Canadian Med. Ass’n J. 824

(2014).

13

Next, he discussed the significance of abnormalities in the hippocampal and medullary

brain tissue in sudden and unexpected deaths of children. 17 Pet. Ex. 22 at 5-9. He stated that the

literature shows “a significant association between finding [] dentate gyrus abnormalities in

children who have died in sleep and found dead, usually in a prone position, and with no

anatomic cause of the death.” Tr. 24-25. Literature has also “made an explicit connection []

suggest[ing] these children died in sleep or emerging from sleep at a time when the brain is more

vulnerable to epileptogenesis, especially when the dentate gyrus, which normally acts as a sort of

electrical gate to tamp down neuronal activity in the hippocampus, is defective.” Pet. Ex. 65 at

2. Additionally, children with “hippocampal abnormalities at autopsy either themselves had a

previous febrile seizure or had a first- or second-degree relative who had a febrile seizure

history,” and thus, Dr. Miller opined there is “an increased risk for this kind of sudden

unexplained death when there’s a family history of febrile seizures.” Tr. 26, 33.

He testified that the hippocampus is located in the temporal lobe, with one on each side

or hemisphere of the brain. Tr. 22. “[I]t is a very important structure in formation and

consolidation of memories, other kinds of structures which are generally referred to as part of the

limbic system, . . . and is frequently associated with temporal lobe seizures.” Tr. 22-23; see, e.g.,

Pet. Ex. 28 at 9, 11. 18

Dr. Miller opined that a “finding frequently found in autopsies of children whose death is

classified as SUDC, SIDS[,] and [SUDEP]” is “dentate gyrus dysplasia, with what is termed

granule cell dispersion including bilamination.” Pet. Ex. 22 at 4-5 (internal quotations omitted)

17

At the hearing, Dr. Miller also maintained febrile seizures can be fatal, even without

hippocampal abnormalities. Tr. 51, 54.

18

Marco M. Hefti et al., Hippocampal Malformation Associated with Sudden Death in Early

Childhood: A Neuropathologic Study, 12 Forensic Sci. Med. & Pathology 14 (2016).

14

(citing Pet. Ex. 18; 19 Pet. Ex. 25; 20 Pet. Ex. 26; 21 Pet. Ex. 27; 22 Pet. Ex. 28; Pet. Ex. 29) 23 (noting

this abnormality on autopsy “is believed to be related to an increased risk of seizures and sudden

death related to seizures”); see also Tr. 69. The dentate gyrus is thought to govern nerve

impulses in the hippocampus, and when it is dysplastic or abnormal, seizures may be generated.

Pet. Ex. 69 at 2. Granule cell dispersion is an “abnormality of the gyrus in which some cells are

located beyond the normal boundaries of that narrow line.” Pet. Ex. 65 at 1. Bilamination, a

form of dispersion, “describes lines of such granular cells outside the normal boundaries of the

gyrus parallel to the direction of the gyrus.” 24 Id. at 2.

Also, according to Dr. Miller, a brain abnormality in the medullas of infants is seen in

over 70% of SIDS cases. Pet. Ex. 22 at 5, 8; Pet. Ex. 65 at 3. These abnormalities “involv[e]

one or more parts of a network of neurons utilizing serotonin (5HT) as a neurotransmitter.” Pet.

Ex. 65 at 3 (citing, e.g., Pet. Ex. 67; 25 Pet. Ex. 68); 26 see also Pet. Ex. 22 at 5, 8. Dr. Miller

explained that “[t]he neurons of this network have their developmental origins in cells from the

embryonic rhombic lip, and so other abnormalities of rhombic-lip derived structures may suggest

that there are abnormalities of the 5HT system, even though those specific abnormalities may not

be detectable at autopsy except by special research techniques” not routinely availability in

forensic autopsies. Pet. Ex. 65 at 3; see also Pet. Ex. 22 at 5, 8. “The inferior olivary nuclei are

19

Hannah C. Kinney et al., Sudden Death, Febrile Seizures, and Hippocampal and Temporal

Lobe Maldevelopment in Toddlers: A New Entity, 12 Pediatric & Developmental Pathology 455

(2009).

20

Michael L. Rodriguez et al., Hippocampal Asymmetry and Sudden Unexpected Death in

Infancy: A Case Report, 8 Forensic Sci. Med. & Pathology 441 (2012).

21

Hannah C. Kinney et al., Dentate Gyrus Abnormalities in Sudden Unexplained Death in

Infants: Morphological Marker of Underlying Brain Vulnerability, 129 Acta Neuropathologica

65 (2015).

22

Marco M. Hefti et al., Sudden Unexpected Death in Early Childhood: General Observations in

a Series of 151 Cases, 12 Forensic Sci. Med. & Pathology 4 (2016).

23

Hannah C. Kinney et al., Hippocampal Formation Maldevelopment and Sudden Unexpected

Death Across the Pediatric Age Spectrum, 75 J. Neuropathology & Experimental Neurology 981

(2016).

24

Citing an article from Dr. Kinney, Dr. Miller noted “the minimum number of cells to qualify

for bilamination would be eight.” Tr. 31; see also Pet. Ex. 65 at 2. It is not clear from the record

which article Dr. Miller was referring to.

25

Y. Ozawa & N. Okado, Alteration of Serotonergic Receptors in the Brain Stems of Hyman

Patients with Respiratory Disorders, 33 Neuropediatrics 142 (2002).

26

Y. Ozawa & S. Takashima, Developmental Neurotransmitter Pathology in the Brainstem of

Sudden Infant Death Syndrome: A Review and Sleep Position, 130S Forensic Sci. Int’l S53

(2002).

15

also rhombic lip derivatives,” and thus, “the presence of the gaps in neuronal populations . . . are

evidence of such medullary abnormalities.” Pet. Ex. 65 at 3.

Dr. Miller testified that the mechanism at play in a SUDC case “may be similar or

identical” to the mechanism purported in SUDEP, described in more detail below. Tr. 67-68.

He also explained that the literature has reported three main commonalities in SUDC cases: (1)

“the deceased young child[] ha[s] a high frequency of a family history of febrile seizures;” (2)

the child is “almost always found dead in bed, in a prone position;” and (3) the autopsy discloses

hippocampal dysplasia. Pet. Ex. 22 at 5; see also Pet. Ex. 65 at 2; Pet. Ex. 74. 27 For support, Dr.

Miller discussed various articles from Kinney et al. and others who described abnormalities in

the hippocampus that they associated with sudden unexpected death, fever, and a family history

of febrile seizures. Pet. Ex. 65 at 2.

In 2009, Kinney et al. examined 64 cases of sudden death in children aged one to 5.9

years to determine whether SUDC “is characterized by hippocampal and temporal lobe

maldevelopment and an individual and/or family history of simple febrile seizures.” Pet. Ex. 18

at 1. In the 49 SUDC cases, 28% had a familial history of febrile seizures, 98% were found

during sleep, and 79% were found in the prone sleep position. Id. at 1, 10 tbl.1. Twenty-six of

the 49 SUDC cases had hippocampal sections available for examination, and 16 of these cases

(16/26 or 62%) had hippocampal abnormalities. Id. at 5, 10 tbl.1. When compared to non-

SUDC cases, Kinney et al. found SUDC cases had more hippocampal abnormalities (62% versus

22%). Id. at 5.

Kinney et al. separated their data into three groups—SUDC with a personal history of

febrile seizures, SUDC with a family history of febrile seizure, and SUDC with no personal or

family history of seizures. Pet. Ex. 18 at 11 tbl.2. Seven SUDC cases had a family history of

febrile seizures. Id. In this group, three children had hippocampal areas available for

examination, and two of these three exhibited hippocampal abnormalities, specifically in the

dentate gyrus. Id. at 5, 11 tbl.2, 12 tbl.3. Additionally, four of the seven (57%) had fever and all

seven (100%) were found in their sleep in the prone position. Id. at 11 tbl.2.

Based on this study, Kinney et al. stated “that a subset of SUDC cases is characterized by

an individual and/or family history of febrile seizures and hippocampal maldevelopment.” Pet.

Ex. 18 at 5. They hypothesized a new entity of SUDC cases “defined by unwitnessed sleep-

related, sudden death and hippocampal/temporal lobe maldevelopment and characterized by an

individual and/or family history of febrile seizures and prone sleep position, often face-down, at

discovery.” Id. They stressed the “defining feature[s]” of this entity are abnormalities in the

hippocampus and temporal lobe and “individual and/or family histories of febrile seizures are

important risk factors for sudden death in association with this [] pathology.” Id. at 5-6.

Kinney et al. further stated that the abnormalities seen in the temporal lobe, in

conjunction with SUDEP cases, “suggests the possibility that affected toddlers experience an

unwitnessed, sleep-related seizure that originates in the anomalous epileptogenetic focus in the

27

Jenna Harowitz et al., Seizure-Related Deaths in Children: The Expanding Spectrum, 62

Epilepsia 570 (2021).

16

hippocampus, resulting in upper airway occlusion/cardia arrythmia/hypotension, and fetal

cardiopulmonary arrest.” Pet. Ex. 18 at 6. They “speculate[d]” that in this entity of SUDC

cases, “a terminal and fatal seizure leads to death . . . due to seizure-induced upper airway

occlusion, augmented by airway compression in the prone (face-down) position.” Id.

Respiratory tract infections were noted as a “potential triggering factor.” Id.

In 2014, Kinney et al. examined 153 autopsies of infants with sudden and unexpected

death and found hippocampal pathology—bilamination and granule cell dispersion—present in

47 of 114 (41.2%) of the unexplained death group and 3 of the 39 (7.7%) of the explained death

group. Pet. Ex. 26 at 2, 6. A 2016 article authored by Kinney et al. stated that hippocampal

abnormalities in the dentate gyrus were associated with sudden death in children regardless of

age. Pet. Ex. 29 at 3. Kinney et al. examined 32 cases with hippocampal abnormalities, 17 of

which were over the age of one. Id. at 4. Of those 17 cases, 16 were sleep-related deaths and 13

were found in the prone position. Id. at 4 tbl.1. Dentate bilamination was found in 31 of the 32

cases, or 18 of the 19 children over one year of age. Id. at 5. Additionally, nine cases had a

family history of seizures and 22 had a family history of febrile seizures and/or epilepsy. Id.

Kinney et al. stated that “[t]he neuropathological findings . . . provide[d] a plausible mechanism

for sudden and unexpected death via an epilepsy-like mechanism.” Id. at 13. Specifically they

stated seizures “may be generated in the abnormal [hippocampus]” and “triggered by stress (e.g.

asphyxia or fever).” Id. None of the Kinney et al. articles discussed vaccinations, or any

potential role of vaccinations.

Similar findings were reported by Hefti et al. 28 in 2016. Pet. Ex. 28. Hefti et al.

examined 83 cases with at least one hippocampal section for microscopic review. Id. at 5. They

classified these 83 cases into subgroups, including a subgroup of SUDC without hippocampal

pathology or febrile seizure phenotype (22/83) and a subgroup termed “hippocampal

maldevelopment associated with sudden death,” or HMASD (40/83). Id. at 2. For the HMASD

cases, 95% died during sleep and 85% were discovered in the prone position. Id. at 5. Twenty-

five of the 40 (62.5%) had a personal and/or family history of febrile seizures, and 15 of the 40

(37.5%) had only a family history of febrile seizures. Id. Additionally, 20 had a fever within 48

hours of death. Id. at 6 tbl.2. For the 22 SUDC cases without hippocampal pathology or febrile

seizure phenotype, 13 (59.1%) had a fever within 48 hours of death, 21 (95.5%) died during

sleep, and 13 (61.9%) were found in the prone position. Id.

Hefti et al. hypothesized that the death in the HMASD cases “may be related to an

unwitnessed seizure during sleep that originates in the malformed hippocampus,” which they

noted “is supported by the reported association of hippocampal malformations in [SUDEP] [and]

those in HMASD.” Pet. Ex. 28 at 9. They also hypothesized that “potential triggering events are

sleep itself, fever, unwitnessed febrile seizure, and/or prone sleep.” Id. Because none of the

deaths in the HMSAD cases were witnessed, Hefti et al. concluded that “the direct relationship

of febrile seizures (or hippocampal maldevelopment) to death is unknown.” Id. at 11.

28

Dr. Kinney is also an author on this publication.

17

Kon et al. (2020) 29 reviewed cases of SIDS (358), SUDC (48), and SUDEP (18) to

determine the prevalence of hippocampal abnormalities, history of seizures, and demographic

features. Pet. Ex. 73 at 2. Their findings revealed hippocampal abnormalities 30 associated with

temporal lobe epilepsy in 16 of 36 31 (44.4%) of SUDC cases. Id. at 2, 5 tbl.2. Five of 11 SUDC

cases with a history of afebrile seizures demonstrated hippocampal abnormalities, and none of

the four SUDC cases with a history of febrile seizures displayed abnormalities in their

hippocampus. 32 Id. at 2, 10. Most SUDC cases (27) were found in the prone position and half

(24) experienced illness 33 within their last 72 hours. Id. at 5 tbl.2.

The authors noted that “[a]s hippocampal abnormalities are strongly associated with

epilepsy, . . . researchers [have] hypothesize[d] that SUDC is ‘epilepsy in situ.’” Pet. Ex. 73 at

10. Although none of their SUDC cases with a febrile seizure history had hippocampal

abnormalities, the authors noted such link is well-documented and analogous to SUDEP, opining

“[h]ippocampal abnormalities could predispose certain individuals to seizures in the event of a

precipitating event such as infection.” Id. Because hippocampal abnormalities were more likely

to be seen in SUDC and SUDEP cases, the authors “suggest[ed] that the hippocampus likely

plays a major role in SUDC and SUDEP.” Id. at 11. Additionally, because an association

between a history of seizures and prone sleeping position has been suggested, the authors noted a

“possible explanation . . . is that these children may had experienced an unwitnessed seizure

whilst in a prone position and being unable to free themselves from this position, asphyxiate,

resulting in death.” Id. at 10.

Dr. Miller acknowledged that a more recent article from 2021, authored by Leitner et

34

al., reported “the lack of association of hippocampal findings in SUDC in controls as well as

inconsistency of observations by multiple blinded reviewers indicates discrepancy with previous

studies.” Tr. 53-54 (citing Resp. Ex. K at 2); see also Pet. Ex. 69 at 3. In Leitner et al.,

hippocampal specimens from 19 SUDC and 26 sudden explained deaths in children (“SEDC”)

control cases were reviewed by nine different reviewers from three types of pathologists

(forensic pathologists, neuropathologists, and dual-certified neuropathologists/forensic

pathologists). Resp. Ex. K at 1, 3. The reviewers reported a similar frequency of findings

29

Fu Chuen Kon et al., Hippocampal Abnormalities and Seizures: A 16-Year Single Center

Review of Sudden Unexpected Death in Childhood, Sudden Unexpected Death in Epilepsy and

SIDS, 16 Forensic Sci. Med. & Pathology 423 (2020).

30

For the specific hippocampal abnormalities seen, see Pet. Ex. 73 at 8 tbl.6.

31

Only 36 of the 48 SUDC cases had this information available. Pet. Ex. 73 at 5 tbl.2, 7.

32

Family history of seizures was not documented. See Pet. Ex. 73.

33

Fever was not included in this category. Pet. Ex. 73 at 4 tbl.1.

34

Dominique F. Leitner et al., Blinded Review of Hippocampal Neuropathology in Sudden

Unexplained Death in Childhood Reveals Inconsistent Observations and Similarities to

Explained Paediatric Deaths, 2021 Neuropathology & Applied Neurobiology 1.

18

relative to the hippocampal slides from the SUDC and control cases. Id. at 9. Also, the

reviewers were in agreement about hippocampal findings in SUDC cases with or without a

history of febrile seizure. Id. However, “half of the slides were reported as abnormal (SUDC

52.5%, control 53.0%), indicating a potential range in as yet unidentified normal variation,

undiagnosed pathology[,] or phenomena unrelated to SUDC or febrile seizures.” Id. The

authors concluded that the “discordance among reviewer groups indicates a discrepancy with

previous studies and a need for larger consensus studies to standardise hippocampal findings to

identify both the range of normal variation and pathology or phenomenon unrelated to SUDC or

febrile seizures.” Id. at 11.

Dr. Miller argued the study “ha[d] multiple flaws,” including a lack of critical analysis as

to whether the cause of death was correctly determined by the original pathology, which “could

have [] tainted” the control group with cases that should have been classified as SUDC and were

not. Pet. Ex. 69 at 3.

Dr. Miller also discussed an unpublished study he worked on that found dentate gyrus

dysplasia “is very common in the general autopsy population at all ages and with [various]

causes of death.” Pet. Ex. 22 at 6; see also Pet. Ex. 69 at 3-4. The study was a retrospective

review of autopsies with neuropathology examinations from 2008 through 2016. Tr. 41; Pet. Ex.

69 at 3. In total, 962 autopsies were examined, including all age ranges. Tr. 41; Pet. Ex. 69 at 3.

Dr. Miller explained that 201 of the 962 displayed “at least one dentate gyrus with dysplasia,

whether granule cell dispersion with or without bilamination, duplications, or hyperconvolutions

(or combinations thereof).” Pet. Ex. 69 at 3. He concluded that “in the general autopsy

population, including cases of SIDS, SUDC, and SUDEP, there were dentate gyrus abnormalities

in 20.8% of the cases.” Id. The study population had 11 cases of SUDC, seven (63.6%) of

which had definite dentate gyrus abnormalities. Id. at 4. Given this data, Dr. Miller asserted

“the incidence of dentate gyrus dysplasia in SUDC cases . . . is at least [three] times that in the

general population (63% to 21%).” Id. He acknowledged, however, that he did not have

statistical testing completed on this data. Id. As of July 2022, his study was not yet peer-

reviewed or sent for publication. Tr. 40. Nor was the study filed in this case.

Two case reports were filed by Petitioners. Dlouhy et al., 35 in 2017, described a child

with a history of two witnessed complex febrile seizures who died suddenly and unexpectedly

following a suspected unwitnessed seizure during sleep; the death was classified as a SUDEP.

Pet. Ex. 70 at 2. The authors wrote, “[a]lthough some cases of [SUDC] have a history of febrile

seizures, no documented case of febrile seizure-induced death has been reported.” Id. They

suggested that “febrile seizures can lead to sudden unexpected death in children through

mechanisms similar to those involved in SUDEP.” Id. at 4. However, Dlouhy et al.

acknowledged that a seizure may not have occurred. Id. The authors did not discuss vaccines.

35

Brian J. Dlouhy et al., Unexpected Death of a Child with Complex Febrile Seizures—

Pathophysiology Similar to Sudden Unexpected Death in Epilepsy?, 8 Frontiers Neurology 1

(2017).

19

Similarly, Myers et al. (2017) 36 reported the case of a 20-month-old girl with a complex

chromosomal disorder and episode of febrile status epilepticus, 37 who died suddenly and

unexpectedly during a video electroencephalogram (“EEG”). Pet. Ex. 71 at 2. The “sequence of

physiologic changes leading up to death suggest[ed] a pathophysiology similar to [SUDEP].” Id.

The child did not meet the criteria for an epilepsy diagnosis, and thus the death was classified as

a SUDC. Id. at 4. However, the authors suggested that the mechanism of her death was

“SUDEP-like” following febrile seizure. Id. at 5. Vaccinations were not at issue.

Dr. Miller acknowledged that epidemiological studies have conflicting findings regarding

a connection with vaccination and sudden unexpected deaths. Pet. Ex. 22 at 9. He cited various

studies that found no causal relationship between vaccinations 38 and sudden unexpected deaths.

See, e.g., Pet. Ex. 40 at 2; 39 Pet. Ex. 41 at 3 (finding “no way to prove that the[ir] infant deaths

[were] caused by vaccination”); 40 Pet. Ex. 44 at 18 (concluding “[t]he evidence does not indicate

a causal relation between [diphtheria-pertussis-tetanus (“DPT”)] vaccine and SIDS”). 41 He also

cited studies on SIDS. See, e.g., Pet. Ex. 45; 42 Pet. Ex. 46 at 2 (“There is no increased or

reduced risk of sudden infant death during the period after the vaccination.”). 43 He argued that

there are various flaws in these studies, and in his view, epidemiology “does not provide any

answer to the question of a possible causal relationship between vaccinations and SIDS.” Pet.

Ex. 22 at 9. However, Dr. Miller maintained “there is a scientifically and medically plausible

means to connect these events.” Id.

36

Kenneth A. Myers et al., Sudden Death After Febrile Seizure Case Report: Cerebral

Suppression Precedes Severe Bradycardia, 140 Pediatrics 1 (2017).

37

Status epilepticus is “a prolonged series of seizures without return to full consciousness

between them.” Status Epilepticus, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=108327 (last visited Nov. 13, 2023).

38

MMRV and MMR vaccinations were not included in these studies.

39

Rüdiger von Kries et al., Sudden and Unexpected Deaths After the Administration of

Hexavalent Vaccines (Diphtheria, Tetanus, Pertussis, Poliomyelitis, Hepatitis B, Haemophilius

Influenzae Type B): Is There a Signal?, 164 Eur. J. Pediatrics 61 (2005).

40

B. Zinka et al., Unexplained Cases of Sudden Infant Death Shortly After Hexavalent

Vaccination, 24 Vaccine 5779 (2006).

41

Inst. of Med., Evidence Concerning Pertussis Vaccines and Deaths Classified as Sudden Infant

Death Syndrome, in Adverse Effects of Pertussis and Rubella Vaccines 125 (Christopher P.

Howson et al. eds., 1991).

42

M.M.T. Vennemann et al., Do Immunizations Reduce the Risk for SIDS? A Meta-Analysis, 25

Vaccine 4875 (2007).

43

Ronny Kuhnert et al., Reanalyses of Case-Control Studies Examining the Temporal

Association Between Sudden Infant Death Syndrome and Vaccination, 30 Vaccine 2349 (2012).

20

Dr. Miller concluded that his theory, or “chain of events[,] represents a highly plausible,

scientifically valid, hypothesis.” Pet. Ex. 22 at 13. He acknowledged “[t]here are no

experimental or clinical studies possible to fully prove [his] hypothesis” in this case. Id.

iii. Althen Prongs Two and Three

Dr. Miller opined the MMRV vaccination administered to N.A. on June 23, 2016 caused

N.A. to develop a fever, and this vaccine-induced fever provoked a seizure on June 30 that

resulted in N.A.’s death due to her unknown vulnerability. Tr. 21-22, 25, 34-35; Pet. Ex. 69 at 1-

2.

First, he noted there is evidence N.A. had a fever on the night of June 30, 2016, within

the risk period following MMRV vaccines. Pet. Ex. 22 at 4, 12. He explained Petitioners

reported on the morning of July 1, 2016 that N.A. “had been having episodic low grade fever, up

to 100.5°F, since [June 13],” although “[t]his [was] not mentioned in the pediatrician’s records

for the [June 23] visit.” Id.; see also Tr. 34.

Dr. Miller opined that the fact that N.A. received Motrin around 7:00 p.m. on June 30

does not suggest N.A. did not suffer a fever or febrile seizure. Tr. 234. He found this argument

“speculative” and he argued that “Motrin is not 100[%] effective in reducing or preventing

fever” and “Motrin won’t affect the development of fever.” Tr. 234-35. But see Pet. Ex. 21 at 7

(“If MMRV continues to be offered for first-dose administration, it might be advisable to counsel

parents regarding antipyretic use if children experience a fever within the peak risk period.”). 44

Dr. Miller next opined N.A. suffered a seizure during the night of June 30, 2016 and cited

four reasons for support: (1) N.A.’s family history of seizures; (2) N.A. received an MMRV

vaccination within the appropriate time period; (3) N.A. was found dead in the prone position;

and (4) N.A.’s autopsy abnormalities. Tr. 25-26.

First, he noted N.A. had a positive family history of seizures (her brother), which he

opined was evidence in favor of a finding that N.A. suffered a seizure on the night of June 30,

2016. Tr. 25-26. Dr. Miller noted N.A.’s brother’s 3q29 microdeletion syndrome is separate

from his history of febrile seizures because seizures have not been found to be related to a 3q29

microdeletion syndrome. Tr. 231-32, 248; see also Pet. Ex. 79 at 8 (finding “seizures are not a

significant part of the 3q29 deletion phenotype,” and thus, “the neurodevelopmental pathway

affected by 3q29 deletion is . . . not [relevant to] epilepsy or seizure”). 45

44

Dr. Miller agreed this happened here. Tr. 248-49. An antipyretic is “an agent that relieves

fever.” Antipyretic, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=3479 (last visited Nov. 13, 2023).

45

Megan R. Glassford et al., Novel Features of 3q29 Deletion Syndrome: Results from the 3q29

Registry, 170 Am. J. Med. Genetics 999 (2016).

21

Second, he noted N.A. received an MMRV vaccination seven to 10 days prior to her

development of a fever and her death, which is within the risk period for seizures post-MMRV

vaccination. Tr. 25, 34. Third, N.A. was found dead in a prone position, which he explained “is

a common position for those with SUDEP, . . . [SUDC], and [] in SIDS.” Tr. 25.

And fourth, he opined N.A.’s autopsy supports a finding that N.A. suffered a seizure the

night of June 30 because (1) no definite cause of death was found on autopsy and (2) N.A.’s

brain slides showed abnormalities consistent with SUDC. Tr. 25-26. Specifically, the autopsy

and police investigation showed no evidence of trauma, no toxins, no anatomical cause of death

(no infectious process), no developmental abnormality, and “no specific finding” as to what

caused N.A.’s death. Tr. 22, 25-26; Pet. Ex. 22 at 4. Additionally, Dr. Miller examined the

autopsy slides and found most showed “no significant abnormality of any kind, no infectious

process, no developmental abnormality, [and] no signs of trauma.” Tr. 22. However, he

observed two significant abnormalities on the brain slides that he explained were commonly seen

in SUDC cases in association with febrile seizures. Tr. 25-26, 35; Pet. Ex. 22 at 12.

According to Dr. Miller, the first abnormality was in N.A.’s hippocampus, which he

explained exhibited a dysplastic, or abnormally formed, dentate gyrus. Tr. 23, 28-29 (citing Pet.

Ex. 66 at 3); see also Pet. Ex. 22 at 4-6. Specifically, he found granule cell dispersion including

bilamination. 46 Tr. 23, 28-29 (citing Pet. Ex. 66 at 3, 7); see also Pet. Ex. 22 at 4-6.

The second brain abnormality Dr. Miller found on the autopsy slides dealt with the

medulla. Tr. 23. He opined “the slide of the medulla showed some patches in the medulla which

were lacking neurons[] [and] lacking nerve cells, suggestive of a developmental abnormality or

perhaps other unappreciated episodes of anoxia in the medulla, although there were no other

signs of anoxia anywhere else in the brain.” Id. Specifically, he found a “subtle depletion of

large neurons from each inferior olivary nucleus along with a mild gliosis” and he opined this

finding has been reported in autopsies of SIDS cases. Pet. Ex. 22 at 5, 8; see also Tr. 46-49; Pet.

Ex. 65 at 2-3; Pet. Ex. 66 at 9. This abnormality is “thought to indicate either a developmental

abnormality in medullary structures derived from the embryonic rhombic lip, or prior

unrecognized episodes [] from which there had been spontaneous recovery.” Pet. Ex. 22 at 5, 8;

see also Pet. Ex. 65 at 3. Dr. Miller opined that if N.A.’s case was viewed as a SIDS case,

instead of SUDC, “the olivary abnormalities” would be “evidence of a rhombic lip problem that

likely also affected some parts of the medullary 5HT system and predisposed [N.A.] to sudden

death with exposure to additional risk factors,” or fever. Pet. Ex. 65 at 3.

Because of the abnormalities identified by Dr. Miller in the brain autopsy slides, he

opined N.A.’s MMRV vaccine put her at “greater risk.” Tr. 25. He opined that “more likely

than not[,] these abnormalities represent the underlying vulnerability that made [N.A.’s] death

possible.” Pet. Ex. 22 at 7. He found it “likely that both abnormalities played a role in [N.A.’s]

death” because there are “connections between the medullary systems governing respiration and

the cerebral hemispheric limbic system, notably the hippocampi.” Id. During the hearing, Dr.

Miller testified that the abnormality in N.A.’s hippocampus would be sufficient to have caused

46

For a further discussion of Dr. Miller’s opinions on bilamination, in general and in N.A.’s

case, see Tr. 226-31, 235-37; Pet. Ex. 65 at 1-2; Pet. Ex. 26 at 8; Pet. Ex. 28 at 4.

22

her death. Tr. 50. He explained that “for those cases where there’s been an autopsy with a

neuropathology examination, there’s a very strong indication that the hippocampal abnormalities

are associated with a vastly increased risk, more than three times [the] risk, over the general

population.” Tr. 51-52; see also Pet. Ex. 69 at 4.

If, however, there were no abnormalities in the brain at autopsy, Dr. Miller concluded it

would be “unknown” as to whether the vaccine was involved in N.A.’s death. Tr. 51 (stating

“presumably” febrile seizures can be fatal in the absence of hippocampal abnormalities).

During the hearing, Dr. Miller was questioned about the report from SUDCRRC,

specifically the fact that the neuropathologist and forensic pathologist who reviewed the brain

slides did not report any abnormalities, which he did not review prior to or during the hearing.

Tr. 237-38. He could not account for why he found abnormalities in the hippocampus when the

SUDCRRC noted no abnormalities. Tr. 238-41. Dr. Miller testified that he was unable to

comment without knowing the neuropathologist that examined the hippocampus or what slides

of the hippocampus were examined. Id.

Next, Dr. Miller compared the facts in N.A.’s case to those deaths that occur in those

with epilepsy. Tr. 35-36. He explained “[it is] very well documented that patients who have a

known history of epilepsy have an increased risk for sudden unexpected death, those deaths

almost always [] com[e] out of sleep or during sleep, [and they are] almost always found in bed

face down.” Tr. 36. Such cases are referred to as SUDEP, although he agreed that N.A.’s case

was not SUDEP. Tr. 36, 42, 45.

On cross-examination, Dr. Miller maintained that the “terminal event” in N.A.’s case was

a febrile seizure that led to apnea or cardiac arrhythmia and cardiac arrest. Tr. 62. He

acknowledged that his theory is “not very well understood because it’s such a rare event and

[there have] been no animal model or human studies which have fully documented in a large

enough number of cases to have some certainty about the actual mechanism.” Id. He opined

there was a “very small” likelihood that N.A. could suffer from apnea or cardia arrhythmia and

cardiac arrest without the MMRV vaccination. Id. But he emphasized that “SUDC is a very rare

event[,] . . . far less common than SIDS.” Id.

Dr. Miller had no opinion on how long N.A.’s seizure lasted. Tr. 44-45. Given his

experience in forensic pathology and as a medical examiner, he opined that the time of death is

“highly subjective” and “subject to many variables.” Tr. 246. Time of death is “an

approximation” that “could be off by several hours in either direction.” Id.

Regarding Dr. Vargas’ opinion that N.A. had a viral infection at the time of death, Dr.

Miller responded by opining that it was “implausible” without better evidence. Tr. 58-59. But

see Pet. Ex. 22 at 8 (noting N.A. “did not clearly have an upper respiratory infection prior to her

death, although the intermittent low grade fever . . . might represent such condition”). Dr. Miller

was also not persuaded by Dr. Vargas’ opinion that N.A. had a chronic respiratory viral

infection. Pet. Ex. 65 at 3-4.

23

On July 1, 2016, N.A.’s sister, L.A., had “yellow nasal crusting.” Tr. 59. Dr. Miller

agreed this would indicate an infection, which he called a “common cold.” Id. He opined that a

cold is not usually associated with a fever. Tr. 59-60. Even if N.A.’s twin sister L.A. had a viral

infection on July 1, Dr. Miller maintained that N.A.’s fever would still be caused by her MMRV

based on “statistics.” Tr. 60. His reliance on statistics is that “children get colds, and they don’t

generally die of them. . . . There is a described increased risk for both fever and febrile seizures

in children who got the MMRV vaccine . . . . It’s still a very rare event, but it’s a definite

increased incidence.” Id.

Further, Dr. Miller was not persuaded by Dr. McCusker’s arguments that N.A.’s mucus

in her airways led to her death. Pet. Ex. 65 at 3. Dr. Miller argued Dr. McCusker misstated the

autopsy findings because only a “[s]mall amount of mucus” was present. Id. (quoting Pet. Ex. 6

at 2). He asserted that Dr. McCusker’s theory, which is based on the belief that infants only

breathe out of their nose and cannot switch to breathing out of their mouth, is without

foundation. Id.

He concluded that the combination of factors here, including N.A.’s fever on the night of

June 30, 2016, N.A.’s receipt of MMRV vaccination seven days prior, N.A.’s family history of

seizures, N.A.’s prone position on death, and N.A.’s autopsy findings, constitutes compelling

evidence that N.A.’s MMRV vaccination triggered a fever that led to a seizure that subsequently

caused her death. Tr. 34-36, 69; Pet. Ex. 69 at 2.

2. Petitioners’ Expert, Marcel Kinsbourne, M.D. 47

a. Background and Qualifications

Dr. Kinsbourne is a neurologist and pediatric neurologist. Tr. 88-89. In 1955, he

obtained his B.M., B.Ch. from Oxford University Medical School, and he completed

postdoctoral training through 1964 in the United Kingdom. Pet. Ex. 14 at 1. Thereafter, he

obtained board certification and licensing in the United States and Canada and worked as a

professor at various teaching institutions. Id. at 1-2. Dr. Kinsbourne has served and is currently

serving on a number of editorial boards. Id. at 3-4. He has authored or co-authored more than

400 publications. Id. at 5-39. Dr. Kinsbourne is no longer a practicing physician and no longer

works as a professor at the New School University in New York. Tr. 90. He has not practiced

clinical medicine or worked in a hospital since 1981. Id.

b. Opinion

Dr. Kinsbourne opined that “more likely than not[,] [] the fever and seizure generated by

the MMRV [vaccination] was . . . the cause of [N.A.’s] death.” Tr. 78; see also Pet. Ex. 13 at 4;

Pet. Ex. 61 at 3.

47

Dr. Kinsbourne provided two expert reports and testified at the hearing. Pet. Exs. 13, 61; Tr.

3. Dr. Kinsbourne cited and discussed some of the same literature as Dr. Miller. For sake of

brevity, the undersigned will not repeat those studies.

24

i. Althen Prong One

Dr. Kinsbourne opined that the MMRV vaccine can trigger an unwitnessed seizure that

can cause death. Pet. Ex. 13 at 3-4; Pet. Ex. 61 at 2-3.

Dr. Kinsbourne began by explaining that is it well-known that the MMRV vaccine can

cause fevers and febrile seizures between seven to 10 days post vaccination. Tr. 76; see also Pet.

Ex. 19 at 2; Pet. Ex. 21 at 2; Pet. Ex. 61 at 1. He testified that “the MMRV vaccination is . . . the

most prone to cause the adverse effects of fever and seizure, in other words, febrile seizure,

within an appropriate time frame.” Tr. 78-79. According to Dr. Kinsbourne, a child who

receives an MMRV vaccination is seven times more likely to have a seizure seven to 10 days

following administration. Tr. 79, 105. He also opined that a fever increases the risk of a seizure,

especially in children between the ages of six months and six years, with a peak at year two. Tr.

80. At the hearing, Dr. Kinsbourne did not indicate which studies support these statistics. In his

expert reports, he cited studies that compared the risk of seizures between the MMRV vaccine

and the MMR and separate varicella (“MMR+V”) vaccines. See Pet. Exs. 19, 21. MacDonald et

al. showed that the risk of seizures was higher after MMRV as compared to MMR+V; however

Klein et al. did not find a significantly increased risk with the MMRV vaccine. Pet. Ex. 19 at 2,

8; Pet. Ex. 21 at 2. Both studies showed that both MMRV and MMR+V “are associated with

fever and seizure [seven] to 10 days after vaccination,” but neither reported increase of seven

fold, as testified to by Dr. Kinsbourne. Pet. Ex. 19 at 8; see also Pet. Ex. 21 at 2. When asked to

identify the study that reported a seven-fold increase in seizures following the MMRV

vaccination, Dr. Kinsbourne was unable to remember the name of the article. Tr. 105-07.

Next, Dr. Kinsbourne opined febrile seizures can lead to death in certain circumstances

depending on the seizure threshold of the individual and risk factors. Tr. 84, 251; Pet. Ex. 13 at

3; Pet. Ex. 61 at 2-3. He explained that febrile seizures are “really common” and occur in two to

five percent “of all children.” Tr. 85. He testified that most are short and benign, but some

(30%) may be prolonged, and thus, dangerous. Id. “In a healthy child and an uncomplicated

setting[,] a simple febrile seizure would indeed not be considered potentially fatal.” Pet. Ex. 61

at 3.

He testified that unobserved seizures “undoubtedly” occur and can cause death. Tr. 84-

85; see, e.g., Pet. Ex. 18. He added that the risk of impaired respiration is less likely in a

witnessed febrile seizure than in an unwitnessed seizure because interventions can occur when a

seizure is witnessed. Pet. Ex. 61 at 3. Such lack of intervention “is especially true of

unwitnessed seizures that occur during sleep.” Id.; see also Tr. 80-81 (opining sleep increases

the risk of seizures); Pet. Ex. 18 at 6. Dr. Kinsbourne maintained that “[t]he rarity of death due

to a witnessed febrile seizure does not suggest that unwitnessed febrile seizures don’t cause

death.” Pet. Ex. 61 at 3.

Dr. Kinsbourne explained that a family history of febrile seizures is “a risk factor for

febrile seizures in a member of that family.” Tr. 78. He added that “[a] family history makes it

more likely that the seizure occurs in a given child.” Tr. 103. Additionally, “[a] family history

of febrile seizures is found in a disproportionate percentage of infants who die in a sudden

unexpected death.” Pet. Ex. 13 at 3.

25

For support, he cited Hesdorffer et al. 48 and argued they “proposed that children with

[SUDC] who had a family history of febrile seizures had an increased risk of dying in a terminal

seizure.” Pet. Ex. 13 at 2 (citing Pet. Ex. 16 at 2). They examined 123 SUDC cases and found

31.7% had a personal history of febrile seizures, 18.7% had a first-degree family history of

febrile seizures, 96.8% died during sleep and the death was unwitnessed, 73.9% were found in

the prone position at death, and 75.6% had a terminal fever or illness symptoms within 48 hours

before death. Pet. Ex. 16 at 5, 4-5 tbl.1. Of the 84 SUDC cases without a personal history of

febrile seizure, 75.9% had a terminal fever or illness symptoms within 48 hours of death, 70.1%

were found in the prone position at death, and 14.3% had a first-degree family history of febrile

seizures. Id. at 6, 4-5 tbl.1. Hesdorffer et al. found that “[i]n children with SUDC and a history

of [febrile seizure], terminal fever may increase the risk for an unwitnessed terminal seizure.”

Id. at 2. Dr. Kinsbourne acknowledged that this finding relates to a personal history of febrile

seizures, and not a family history of febrile seizures. Tr. 103. Hesdorffer et al. could not

“exclude the possibility in these unwitnessed deaths that among the 75.9% of children with

terminal fever or illness symptoms but without a prior [febrile seizure], their first [febrile

seizure] might have been a terminal event.” Pet. Ex. 16 at 7.

Another article cited by Dr. Kinsbourne reported a similar conclusion related to children

who had a history of febrile seizures. Crandall et al. 49 determined “[p]atients with febrile

seizures are at [an] increased risk for sudden death.” Pet. Ex. 72 at 2. The authors examined and

interviewed 391 families where a child aged one to six died, and 264 were classified as SUDC.

Id. at 4. Of these 264 cases, 181 did not have any seizure history, 76 had a febrile seizure

history, and seven had an afebrile seizure history. Id. First- and second-degree family history of

febrile seizures was found in 45 of 160 cases of SUDC without a personal seizure history. Id. at

5 tbl.1. Crandall et al. found SUDC cases with a personal history of febrile seizures were more

likely to have a family history of seizures, both febrile and afebrile. Id. at 6. Additionally, 253

of 264 (95.8%) SUDC cases were found unresponsive during a sleep period and 173 of 211

(82%) were discovered in the prone position. Id. at 5. In 112 of 245 SUDC cases (45.7%), a

terminal fever was reported. Id. Crandall et al. concluded their “findings implicate [febrile

seizure] as a contributing factor or cause of death via a SUDEP-like process in some SUDC

cases.” Id. at 6. The authors, however, “speculate[d] that [febrile seizures] occur in some

children without a known [febrile seizure] history.” Id. at 7. They added, “[p]ostmortem

evidence of terminal seizures is often absent or nonspecific . . . . Explained deaths attributed to

asphyxia could include [febrile seizure] cases where the child remained prone . . . .” Id.

Dr. Kinsbourne also cited medical literature relating to SUDEP and found this literature

can relate to SUDC, explaining “[SUDEP] literature suggests indirectly, not with certainty, that

in SUDC, there is, indeed, a tendency for the child to have had a history of febrile seizures, . . .

48

Dale C. Hesdorffer et al., Sudden Unexplained Death in Childhood: A Comparison of Cases

with and Without a Febrile Seizure History, 56 Epilepsia 1294 (2015).

49

Laura Gould Crandall et al., Potential Role of Febrile Seizures and Other Risk Factors

Associated with Sudden Deaths in Children, 2 JAMA e192739 (2019).

26

either a personal history or family history of febrile seizures.” Tr. 82-83, 256. Dr. Kinsbourne

cited Devinsky, 50 who suggested that cases of SUDEP may occur after a seizure, usually a tonic-

clonic seizure. Pet. Ex. 15 at 3. Findings that may be seen include bitten tongue or cheek and

pulmonary edema. Id. at 2, 9 tbl.3. The finding of pulmonary edema was not explained.

Devinsky also suggested that there may be impaired respiration following a seizure, which may

be lethal and involve pulmonary dysfunction. Id. at 5, 6 tbl.2.

Kloster and Engelskjøn 51 examined risk factors and their role in SUDEP. Pet. Ex. 20 at

2. Of the 42 cases classified as SUDEP with no verified cause of death, 62% had pulmonary

edema, 67% showed signs of a preceding seizure, 71% were found in the prone position at death,

and 60% were found in bed “presumably dying before, during, or after sleep.” Id. at 2, 4-5. The

authors noted signs of seizures immediately before death included fresh bites, blood on the

pillow, cyanosis, 52 and sounds associated with ongoing seizures. Id. at 3. “The prone position

may cause obstruction of the nose and mouth due to pressure against the bed clothing.” Id. at 5.

The authors hypothesized that those who were found dead in bed may have died due to their

positioning or due to sleep itself, which would implicated the respiration. 53 Id. at 6. Kloster and

Engelskjøn noted, “[c]learly[] seizures play an important part in SUDEP, but some patients die

without visible seizures,” and thus, there is a “possibility that some of these deaths are unrelated

or only indirectly related to epilepsy.” Id. at 5.

Dr. Kinsbourne also cited Kinney et al. (2009) and Hefti et al., discussed in more detail

above, which reported an association of sudden death, febrile seizures, hippocampal

abnormalities, and sleep. Pet. Ex. 13 at 2 (citing Pet. Ex. 18); Pet. Ex. 61 at 3 (citing Pet. Exs.

27-28). Kinney et al. “suggest[ed] that simple febrile seizures may not be totally benign,” and

found a group of deaths characterized by sleep-related unwitnessed sudden death in the toddler in

the prone position, individual/family history of febrile seizures, and hippocampal anomalies.”

Pet. Ex. 18 at 7. Based on the medical literature, Dr. Kinsbourne opined febrile seizures can be

lethal in certain circumstances. Pet. Ex. 61 at 3.

50

Orrin Devinsky, Sudden, Unexpected Death in Epilepsy, 365 New Eng. J. Med. 1801 (2011).

51

Robert Kloster & Torstein Engelskjøn, Sudden Unexpected Death in Epilepsy (SUDEP): A

Clinical Perspective and a Search for Risk Factors, 67 J. Neurology Neurosurgery & Psychiatry

439 (1999).

52

Cyanosis is “a bluish discoloration, especially of the skin and mucous membranes due to

excessive concentration of deoxyhemoglobin in the blood.” Cyanosis, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=12098 (last visited

Nov. 13, 2023).

53

See also Pet. Ex. 17 (John Hewertson et al., Epileptic Seizure-Induced Hypoxia in Infants with

Apparent Life-Threatening Events, 94 Pediatrics 148 (1994)) (explaining how epileptic seizures

can be accompanied by episodes of hypoxia and apnea).

27

ii. Althen Prongs Two and Three

Dr. Kinsbourne opined the MMRV vaccine N.A. received on June 23, 2016 triggered a

fever and an unobserved seizure that caused her death on June 30, 2016. Tr. 76-78; Pet. Ex. 13

at 3-4; Pet. Ex. 61 at 2-3. He summarized that N.A. was at an increased risk for sudden

unexplained death because her family history of febrile seizures put her at risk for a febrile

seizure, her hippocampal abnormalities made her more susceptible to seizure generation, and

sleep lowered her seizure threshold. Pet. Ex. 61 at 2. Because of this triad of risk factors, she

was “vulnerable to the febrile seizure risk inherent in MMRV, to which she succumbed.” Id.

He explained N.A. received her MMRV vaccine on June 23, and seven days later, on

June 30, she developed a fever. Tr. 79-80; Pet. Ex. 13 at 1-3. Because N.A.’s fever was within

the risk interval following an MMRV vaccination, he opined “the presumption is that [the fever]

was an MMRV fever.” Tr. 77; see also Pet. Ex. 61 at 3. Dr. Kinsbourne acknowledged that

N.A.’s fever was a low-grade fever, and that Mrs. Anklam did not take N.A.’s temperature. Tr.

92-93. He agreed that that literature associates febrile seizures with a certain threshold of

temperature (about 102°F), but he opined that a temperature under 100°F can trigger a seizure

depending on the individual’s seizure threshold. Tr. 107-08. However, he agreed that a

temperature of less than a 100°F “would not be sufficient” to cause a seizure in most people. Tr.

107. There would have to be “some genetic trait” to cause “relatively low seizure threshold.” Id.

He also agreed that N.A.’s seizure threshold was unknown. Tr. 108.

He “assume[ed] that when [N.A.] had the seizure . . . , her temperature had gone

considerably higher.” Tr. 94. “In other words, it was the beginning of a fever engendered by the

vaccination.” Id.

Dr. Kinsbourne next opined that this fever caused by her MMRV vaccination led to an

unobserved seizure that caused N.A.’s death due to her family history of seizures, prone position

on death, and evidence of pulmonary edema and hippocampal abnormality on autopsy. Tr. 76-

78; Pet. Ex. 13 at 3-4.

As noted above, one of N.A.’s brother has a history of febrile seizures. Tr. 78, 98; Pet.

Ex. 13 at 1-3. Dr. Kinsbourne opined “[a] family history of febrile seizure is found in a

disproportionate percentage of infants who die a sudden unexpected death.” Pet. Ex. 13 at 3.

Second, N.A. was found in the prone position on death, and Dr. Kinsbourne believed she

was likely already unconscious when she got into this position. Tr. 86; Pet. Ex. 61 at 2. He

added that this position would make it hard for her to breathe. Tr. 85-86. The medical examiner

“could not explain why [N.A.] remained face down” and “cautioned that a one-year-old who is

lying face down is capable of turning to the side if she becomes short of breath.” Pet. Ex. 13 at 2

(citing Pet. Ex. 6 at 1); see also Pet. Ex. 61 at 2; Tr. 96. Dr. Kinsbourne agreed that children at

one year of age “are well able to move their head sideways if the circumstances require it, which

she clearly didn’t have that ability.” Tr. 86.

Additionally, Dr. Kinsbourne opined this position at death was “suggestive of terminal

seizure activity;” “the configuration of the body in rigor mortis was unusual, less like an infant

28

death by asphyxia than death during a seizure.” Pet. Ex. 13 at 2-3. He noted that although the

medical examiner diagnosed death by asphyxia, the manner of death was undeterminable. Id. at

2; see Pet. Ex. 6 at 1 (“[N.A.] died of asphyxia. . . . The manner of death is undeterminable.”).

And third, because pulmonary edema was found on autopsy, Dr. Kinsbourne opined that

N.A.’s respiratory system likely was unable to maintain normal functioning for long enough for

N.A. to survive, and lying on her face would have made it difficult to breathe. Tr. 85-86; Pet.

Ex. 13 at 2. However, medical literature referenced by Dr. Kinsbourne does not show that the

finding of pulmonary edema is specific to a seizure or evidence of a seizure. Although Devinsky

noted “[s]eizure can cause pulmonary edema” and that “[p]ulmonary edema is the most common

autopsy finding,” Devinsky failed to explain how a finding of pulmonary edema is specific to a

seizure. Pet. Ex. 15 at 5, 6 tbl.2. Kloster and Engelskjøn observed the incidence of pulmonary

edema in SUDEP cases, but they did not state that it was a sign of seizure. Pet. Ex. 20 at 3. And

they did not attribute pulmonary edema specifically to seizures. Id. Harowitz et al. described

pulmonary edema as a non-specific finding. Pet. Ex. 74 at 5.

At the hearing, Dr. Kinsbourne testified that his findings regarding N.A.’s hippocampal

abnormalities are based on Dr. Miller’s opinions, and he acknowledged the medical examiner

who conducted the autopsy found no abnormalities. Tr. 91-92; see also Pet. Ex. 13 at 2. Dr.

Kinsbourne opined the hippocampal abnormality Dr. Miller described would double N.A.’s risk

of seizure. Tr. 83. If N.A. did not have the hippocampal abnormality, Dr. Kinsbourne “would

regard the evidence [in favor of a seizure the night of June 30, 2016] as less strong, but still

easily strong enough.” Id. He maintained “that more likely than not, N.A. did die because of the

MMRV [vaccine] causing a febrile seizure which then precipitated her death as described” even

without a hippocampal abnormality. Tr. 83, 102.

Overall, Dr. Kinsbourne found “the presumption that there was a seizure [was] strong.”

Tr. 84. “[A]nd if she had a seizure the possibility or the probability that it cause[d] her death

[was] also strong, considering [] that there [were] no other factors in evidence that could have

caused her death.” Id. He opined it was “impossible” to know how long N.A.’s inferred seizure

lasted. Tr. 85. He also acknowledged that N.A. had no history of seizure but hypothesized that

“if N.A. had survived, she might have had the seizures subsequently or not.” Tr. 103.

In response to Dr. Lidov’s arguments that N.A.’s absence of tongue biting was evidence

against the existence of an unwitnessed seizure, Dr. Kinsbourne explained “[t]he absence of a

lacerated tongue at [N.A.’s] autopsy is not useful criterion of whether a seizure occurred.” Pet.

Ex. 61 at 2 (citing Pet. Ex. 28 at 6 tbl.2). Compare Pet. Ex. 20 at 3 (noting “fresh bites” to be a

sign of a seizure), and Pet. Ex. 15 at 2, 9 tbl.3 (finding evidence of a seizure to include bitten

tongue or cheek), with Pet. Ex. 72 at 7 (indicating tongue biting is an “infrequent” finding), and

Pet. Ex. 74 at 5 (“In young children, seizures may lack classic signs (e.g., . . . tongue-biting),

making diagnosis more difficult.”). He agreed with Dr. Lidov that “there is no direct scientific

proof” a seizure occurred; however, he stressed that “there is ample circumstantial evidence

[N.A.] died in a seizure.” Pet. Ex. 61 at 2.

Regarding the length of N.A.’s seizure, Dr. Kinsbourne agreed that most febrile seizures

are short and benign, but he explained if they are prolonged, they are more dangerous. Tr. 85.

29

Dr. Kinsbourne testified that it is “impossible to say how long N.A.’s inferred seizure was, but

unfortunately, she died, and there was no other imaginable reason why she might have died.” Id.

Dr. Kinsbourne maintained there was no evidence of alternative causation. Pet. Ex. 13 at

3; Pet. Ex. 61 at 3. In response to Dr. McCusker’s argument that N.A. had a viral respiratory

infection that would have explained N.A.’s fever and blocked N.A.’s airway, Dr. Kinsbourne

opined that no infection was diagnosed and the autopsy did not reveal an obstructed airway. Pet.

Ex. 61 at 3. He added that any fever N.A. may have had in the week leading up to her MMRV

vaccination “was evidently insufficient to provoke a seizure[] because it did not in fact do so.”

Id. Lastly, he opined “[t]he fever at the time of [N.A.’s] death can more directly be attributed to

the MMRV vaccination.” Id.

As for the temporal association between vaccination and seizure, Dr. Kinsbourne

emphasized that N.A. had an elevated risk of seizure because she received her MMRV

vaccination seven days prior to her death. Pet. Ex. 61 at 1-2.

3. Respondent’s Expert, Dr. Hart G.W. Lidov, M.D., Ph.D. 54

a. Background and Qualifications

Dr. Lidov is a board-certified neuropathologist and pediatric neurologist, licensed in

Massachusetts. Resp. Ex. E at 1-2; Resp. Ex. P at 6. He obtained his B.A. in Biophysics, Ph.D.

in Anatomy, and M.D. from Johns Hopkins before completing a pediatric internship at

Massachusetts General Hospital and residencies in pediatrics, neurology, neuropathology, and

anatomic pathology at Massachusetts General Hospital, National Hospital Queens Square in

London, UK, and Brigham and Women’s Hospital. Resp. Ex. P at 1. He held clinical

fellowships in pediatrics, neurology, and pathology and neurology at Harvard Medical School

and has been a Professor in pathology and neurology at Harvard Medical School for almost 20

years. Id. at 1-2. Since 1991, he has been a staff Neuropathologist at Boston Children’s Hospital

and Brigham and Women’s Hospital. Id. at 2. He “routinely see[s] surgical neuropathology

cases from these hospitals, and autopsy examinations of the [central nervous system], as well as

consultations.” Resp. Ex. E at 2. Dr. Lidov has authored or co-authored over 100 publications.

Resp. Ex. P at 8-16.

b. Opinion

i. Althen Prong One

Dr. Lidov opined that Petitioners’ theory that N.A.’s MMRV vaccination caused a fatal

unwitnessed seizure was unlikely. Tr. 141-43. He explained that febrile seizures are uncommon

and rare, and “a febrile seizure following a vaccination by itself is an extremely unlikely event.”

Tr. 116-17 (citing Pet. Ex. 19). He did agree that the MMRV vaccine increases the risk of fevers

and seizures in the period of seven to 10 days post-vaccination. Tr. 148. However, based on his

personal experience and review the literature, Dr. Lidov opined that a first febrile seizure is not

54

Dr. Lidov submitted three expert reports and testified at the hearing. Resp. Exs. E, I, M; Tr. 3.

30

known to be fatal. Tr. 118-23; Resp. Ex. E at 4-5; Resp. Ex. M at 1. Further, since febrile

seizures are the most common form of seizures in children, he expected that if there was an

increase in mortality associated with an initial febrile seizure, it would probably be reported in

the literature. Resp. Ex. E at 5; see also Resp. Ex. I at 13 (“If simple febrile seizures had the

potential to be fatal, there should be reports, likely many reports . . . .”).

For support, he cited Byard, 55 who stated that death during febrile seizures was rare.

Resp. Ex. E at 5 (citing Resp. Ex. E, Tab 1 at 2). Shinnar and O’Dell 56 stated “[t]he morbidity

and mortality associated with febrile seizures is extremely low,” and “[e]ven cases of febrile

status epilepticus have shown almost zero mortality.” Id. (quoting Resp. Ex. E, Tab 3 at 5); see

also Resp. Ex. E, Tab 7 at 3 (“The mortality of febrile status epilepticus in recent series is

extremely low.”); 57 Resp. Ex. U at 3 (“The mortality associated with febrile seizures is extremely

low.”); 58 Resp. Ex. L at 2 (noting “the absolute risk of death [from febrile seizure] [is] [] very

low”). 59 Dr. Lidov also cited Leung and Robson, 60 who similarly reported “[c]hildren with

febrile seizures have no increased risk of mortality.” Resp. Ex. E at 5 (quoting Resp. Ex. E, Tab

4 at 4 (internal citations omitted)).

Dr. Lidov was not persuaded by Petitioners’ literature. Tr. 119-20 (citing Pet. Exs. 70-

71); see also Resp. Ex. E at 5 (citing Pet. Ex. 70). Dlouhy et al., for example, noted “no

documented case of febrile seizure-induced death has been reported” in SUDC, “[a]lthough some

cases of [SUDC] cases have a history of febrile seizures.” Pet. Ex. 70 at 2. Dr. Lidov also

explained that the Dlouhy et al. case report involved a child with a prior history of multiple

complex seizures prior to the terminal event. Tr. 119 (citing Pet. Ex. 70 at 2). Based on this

history, she would not be classified as SUDC, but as SUDEP. Id. (citing Pet. Ex. 70 at 2).

Further, Dr. Lidov opined that since N.A. did not have a history of prior seizures, and her

“death [was] unwitnessed, [] the occurrence during a febrile seizure [was] only a supposition.”

Resp. Ex. E at 5 (citing Pet. Ex. 70 at 2).

Dr. Lidov also disagreed that the case report by Myers et al. was relevant, opining that

the child’s death described in Myers et al. was not caused by a fatal febrile seizure but instead

55

Roger W. Byard, Sudden Death in the Young (3d ed. 2010). Three non-consecutive pages

from this textbook were filed.

56

Shlomo Shinnar & Christine O’Dell, Febrile Seizures, 33 Pediatric Annals 395 (2004).

57

Shlomo Shinnar & Tracy A. Glauser, Febrile Seizures, 17 J. Child Neurology S44 (2002).

58

1 Shlomo Shinnar, Febrile Seizures, in Swaiman’s Pediatric Neurology 790 (Kenneth F.

Swaiman et al. eds., 5th ed. 2012).

59

Maitreyi Mazumdar, Febrile Seizures and Risk of Death, 372 Lancet 429 (2008).

60

Alexander K.C. Leung & W. Lane M. Robson, Febrile Seizures, 21 J. Pediatric Health Care

250 (2007).

31

reflected the child’s complex chromosomal abnormality. Tr. 119-20 (citing Pet. Ex. 71 at 1).

The child had a chromosomal disorder with “dysmorphic features, bilateral cleft palate, short

webbed neck, congenital heart disease . . . , and severe bilateral bronchomalacia.” Pet. Ex. 71 at

3. Brain magnetic resonance imaging (“MRI”) was abnormal. Id. She had “hypotonia from

birth and global developmental delay.” Id. Although the child presented to the hospital after

febrile status epilepticus, she did not experience sudden death until two days later, during video

EEG monitoring. Id. The authors suggested that the physiologic changes prior to death may be

similar to “some rare cases of adults who have experienced [SUDEP].” Id. at 2. N.A. did not

have epilepsy.

Dr. Lidov was also not persuaded by Petitioners’ reliance on Crandall et al. Tr. 120

(citing Pet. Ex. 72). There, the researchers collected interviews of family members who had

voluntarily registered with the SUDC Foundation. 61 Pet. Ex. 72 at 2. In the SUDC group, 87 of

241 (36.1%) reported a family history of febrile seizures, and 41 of 241 (17%) reported both a

case and family history. Id. at 5. Information was obtained from “[d]etailed demographic and

interview histories.” Id. at 4. “No independent medical record or autopsy review was

performed.” Id. at 3. Due to the lack of such more specific information, Dr. Lidov did not find

the study persuasive. Tr. 120.

On cross-examination, Dr. Lidov agreed that not all seizures are witnessed and some

occur during sleep. Tr. 146-47. He also agreed that seizures can cause death, specifically

generalized tonic-clonic seizures and focal seizures. Tr. 147, 156. He opined that the literature,

specifically articles authored or co-authored by Dr. Kinney, hypothesizes that an unwitnessed

seizure can cause SUDC. Id. But he opined that articles related to SUDEP have only raised the

possibility, which is “unproven,” that unwitnessed seizures can lead to death. Tr. 147-48.

Regarding Petitioners’ assertion that the presence of hippocampal abnormalities is

evidence that supports Petitioners’ theory, Dr. Lidov disagreed. Resp. Ex. E at 5-7; Resp. Ex. I

at 13. Any association between febrile seizures and hippocampal abnormalities, according to Dr.

Lidov, is not evidence of a causal mechanism. Resp. Ex. E at 4-5; Resp. Ex. I at 13. He

explained that the literature noted an association, but never showed causality, despite Dr.

Miller’s assertions. Resp. Ex. E at 5-7 (citing, e.g., Pet. Exs. 18, 26-29). Dr. Lidov contended

that Petitioners are proposing a theory that “is at most ‘conceivable,’ or ‘cannot be proven to be

utterly impossible.’” Resp. Ex. I at 13. Dr. Lidov found Dr. Kinney’s hypothesis that the

mechanism in SUDC cases is an epilepsy-like mechanism may be plausible, but it is unproven.

Tr. 157; see Pet. Ex. 29 at 13.

Dr. Lidov agreed that a family history of febrile seizures is a risk factor for febrile

seizures, but noted it is because of a genetic component. Tr. 139-40; see also Resp. Ex. E, Tab 7

at 2 tbl.1 (noting first-degree relative with history of febrile seizures as a risk factor for first

febrile seizure); Resp. Ex. E, Tab 4 at 2 (same). Even though a family history of febrile seizures

increases the risk of having a febrile seizure, Dr. Lidov maintained “it [does not] make it a likely

event.” Tr. 140; see also Resp. Ex. I at 13 (explaining “all children are at some risk,” but “this

does not prove that [a seizure] occurred”).

61

Of note, Dr. Orrin Devinsky was a named author on this paper.

32

He opined that Petitioners suggest that a febrile seizure can cause death and relied upon

literature noting an association of a family or personal history of febrile seizures with SUDC. Tr.

144-45. He concluded that any association is not causal and in fact, a history of febrile seizure is

a marker for a genetic abnormality. Tr. 145. And these genetic abnormalities can explain SUDC

via a different mechanism. Id.

ii. Althen Prongs Two and Three

Dr. Lidov opined Petitioners’ theory was weak and unlikely here. Tr. 141; Resp. Ex. E at

8-9. He found that more likely than not, N.A.’s vaccination was unrelated to her death. Resp.

Ex. E at 9. Additionally, he found no evidence to support the assertion that more likely than not,

N.A. died of a fatal first febrile seizure. Resp. Ex. I at 12.

Dr. Lidov concluded there was “no evidence of a seizure, febrile or otherwise,” no

evidence N.A. was febrile, and even if she was febrile, there was evidence that it was antecedent

to her vaccination. Tr. 141-42. Next, he explained there is no literature to support a finding of a

first fatal febrile seizure. Id.; see also Resp. Ex. I at 12. Moreover, the literature reports

hippocampal abnormalities in children without a history of seizures. Tr. 142. He opined the

probability of this factor of Petitioners’ theory was “more reasonable,” however, he found it was

a “low probability of indicating seizures.” Id. Lastly, he opined the MMRV vaccine “was not in

any way responsible for [N.A.’s] death.” Tr. 144.

Dr. Lidov opined there was no evidence that N.A. had a seizure at the time of her death

for numerous reasons. Resp. Ex. E at 4; see also Tr. 117; Resp. Ex. I at 12-14; Resp. Ex. M at 1.

First, N.A. had no history of seizures or any history of febrile responses following any previous

vaccinations. Resp. Ex. E at 4. Second, there was no report of tongue biting on autopsy, despite

evidence of deciduous dentition. Id. He noted the lack of physical evidence (tongue biting,

disrupted bed clothing) does not prove N.A. did not have a seizure, but would be strong evidence

in favor of a seizure if this evidence was present. Tr. 117.

Third, N.A. only had “a very low fever,” which “argues [] against the idea of [N.A.]

having had a febrile seizure” because her temperature did not reach the threshold seen in fever-

induced seizures. Tr. 117-18; see also Resp. Ex. E at 8 (noting a fever-induced seizure typically

requires a significant fever of around 103°F); Resp. Ex. E, Tab 4 at 2 (“The most significant risk

factor for the development of a first febrile seizure is the height of the temperature; the higher the

temperature, the higher the likelihood of a febrile seizure.”). Because N.A. had experienced low-

grade fevers prior to the night of June 30 but had never had a seizure, Dr. Lidov argued that it is

“less likely” that N.A.’s response to the low-grade fever on June 30 would be a seizure. Tr. 140-

41; see also Resp. Ex. E at 8. Additionally, because N.A. had low-grade fevers since June 19,

prior to her MMRV vaccination, Dr. Lidov found “no basis for presuming her vaccination[]

[was] a necessary cause.” Resp. Ex. E at 8.

Fourth, Dr. Lidov did not find N.A.’s family history of febrile seizures in her brother to

be persuasive evidence that she had a seizure. Tr. 118. Lastly, Dr. Lidov did not find the fact

that N.A. was found in the prone position to be evidence that she died of a seizure. Tr. 138-39.

33

He found it indicated that N.A. was unconscious at the time of her death but did not provide

evidence of the cause of death. Tr. 138-39, 156. Additionally, he asserted it could indicate other

processes that result in the prone position. Tr. 155. Given Dr. Lidov’s experience, and his

review of the literature, he found no evidence of a first febrile seizure being fatal. Tr. 123, 137,

141-42.

Dr. Lidov disagreed with Dr. Miller’s brain abnormality findings and opined “the autopsy

brain slides were completely [] normal for her age.” Tr. 125; see also Resp. Ex. E at 3 (noting

“the brain regions sampled show[ed] no definite or diagnostic abnormalities”); Resp. Ex. I at 2-

12 (detailing his disagreements with Dr. Miller over the brain slides and findings); Resp. Ex. M

at 1-2 (maintaining bilamination and dispersion were not present on N.A.’s slides). He found the

photomicrographs “simply [did] not show bilamination at all and that there [were] no other

abnormalities in the hippocampus.” Tr. 136; see also Resp. Ex. E at 8. He also found it

“unclear” how cell loss in the inferior olivary bears on this case as it is not a source of seizures.

Tr. 136.

Specifically, Dr. Lidov found no evidence of a subtle depletion of the large neurons from

each inferior olivary nucleus and no evidence of bilamination. Tr. 125; Resp. Ex. E at 3, 8. In

his expert reports and during the hearing, Dr. Lidov detailed what a normal dentate gyrus and

bilamination look like, relying on photographs from the literature, and using those, he explained

why N.A. exhibited no hippocampal abnormalities. See Tr. 126-34; Resp. Ex. E at 3, 8; Resp.

Ex. I at 5-9 (citing Pet. Exs. 26, 29; Resp. Ex. I, Tab 2; 62 Resp. Ex. I, Tab 5; 63 Resp. Ex. I, Tab

8). 64 Dr. Lidov also detailed his findings as to the inferior olivary. See Tr. 136-37; Resp. Ex. I

at 9-12.

He opined that Dr. Miller’s photomicrographs of N.A.’s dentate gyrus were at a higher

magnification and not the same magnification as the photographs in the literature. Tr. 134. By

using a higher magnification, Dr. Lidov testified, “you can find areas like this in normal dentate

gyruses and in dentate gyruses of children who’ve died of lots of different diseases.” Id. He

further explained that a close up, cropped photograph does not show the entire field. Tr. 135.

Overall, he found Dr. Miller’s photomicrographs “not convincing for bilamination.” Id.; see also

Resp. Ex. I at 12

Further, in a supplemental report, Dr. Lidov noted “the significance attributed to the

presence of hippocampal malformations may be moot” as recent studies have suggested such

findings occur more frequently in the general population. Resp. Ex. M at 2; see, e.g., Resp. Ex.

62

Ingmar Blümcke et al., Towards a Clinico-Pathological Classification of Granule Cell

Dispersion in Human Mesial Temporal Lobe Epilepsies, 117 Acta Neuropathology 535 (2009).

63

Carolyn R. Houser, Granule Cell Dispersion in the Dentate Gyrus of Humans with Temporal

Lobe Epilepsy, 535 Brain Rsch. 195 (1990).

64

Alexandre Valoota da Silva et al., Dysmorphic Neurons in Patients with Temporal Lobe

Epilepsy, 1072 Brain Rsch. 200 (2006).

34

K at 2; Resp. Ex. I, Tab 1 at 18. 65 Thus, “their presence or absence is of no established

significance.” Resp. Ex. M at 2. He cited Dr. Miller’s first expert report, which stated,

[f]or completeness I must point out that I and some colleagues here at the

University of Missouri School of Medicine have been studying this very issue of

dentate gyrus dysplasia, and we have found that it is very common in the general

autopsy population at all ages and with all sorts of causes of death [].

Pet. Ex. 22 at 7.

Additionally, Dr. Lidov referenced the SUDCRRC investigation and the fact that they did

not find any brain abnormality confirmed his opinions that N.A. did not have any brain

abnormalities. Tr. 144. Dr. Lidov explained that the SUDCRRC neuropathologist would have

focused on brain abnormalities, a focus of interest in their group. Tr. 154. Additionally, he

testified that Dr. Devinsky, the principal investigator of the SUDCRRC report, is also an author

in many of the articles filed herein on the subject of brain abnormalities in children. Tr. 153-55;

see, e.g., Pet. Exs. 15, 72, 74.

In summary, Dr. Lidov agreed that N.A. fell into the SUDC category. Tr. 138; Resp. Ex.

E at 4. He opined that her death was unexplained, stating “[w]e do not understand why” N.A.

died. Tr. 138. Speculative causes include genetic abnormalities and cardiac arrhythmia. Id.; see

also Resp. Ex. I at 15. However, Dr. Lidov concluded that it is “very unlikely” that N.A. had a

febrile seizure. Tr. 137. He disagreed that N.A. had any brain abnormalities. Id. And he opined

the literature does not support Petitioners’ theory that N.A. had a fatal febrile seizure. Id. Lastly,

Dr. Lidov opined that more likely than not, N.A.’s vaccination was unrelated to her death. Resp.

Ex. E at 9.

4. Respondent’s Expert, Dr. Sara O. Vargas, M.D. 66

a. Background and Qualifications

Dr. Vargas is a pathologist with board certifications in anatomic pathology, clinical

pathology, and pediatric pathology. Resp. Ex. C at 2. She received her A.B. from Harvard

University and an M.D. from the University of Vermont College of Medicine. Resp. Ex. Q at 1.

She then completed a residency in anatomic and clinical pathology and fellowship in pulmonary

pathology at Brigham and Women’s Hospital and a pediatric pathology fellowship at Children’s

Hospital in Boston, Massachusetts. Id.; Tr. 161. Dr. Vargas is an associate professor at Harvard

Medical School and a staff pathologist at Children’s Hospital and Brigham and Women’s

Hospital. Resp. Ex. Q at 1-2; Resp. Ex. C at 2. As a pathologist, she “practice[s] surgical

pathology, cytopathology, postmortem examinations, and consultative diagnostic services.”

65

Achira Roy et al., Hippocampal Granule Cell Dispersion: A Non-Specific Finding in Pediatric

Patients with No History of Seizures, 8 Acta Neuropathologica Commc’ns 1 (2020).

66

Dr. Vargas submitted three expert reports and testified at the hearing. Resp. Exs. C, J, N; Tr.

3.

35

Resp. Ex. C at 2. She also reviews autopsies for Robert’s Program, “a multidisciplinary group

that investigates sudden unexpected death in infancy and in childhood,” similar to SUDCRRC.

Tr. 164-65, 167. Dr. Vargas has authored or co-authored over 200 publications. Resp. Ex. Q at

18-41.

b. Opinion

Dr. Vargas opined N.A. “died of [SUDC] in the setting of a viral respiratory tract

infection,” with “no evidence that immunizations caused, or contributed in any way to [] [N.A.’s]

death.” Resp. Ex. C at 8; see also Resp. Ex. J at 1, 4.

i. Althen Prong One

Dr. Vargas opined there is no evidence that vaccination can cause SUDC via a seizure.

Tr. 168; Resp. Ex. J at 1-2 (finding “no evidence that vaccinations are associated with any

increased risk of SIDS/SUDC or that they ‘potentiate’ SIDS/SUDC”). Dr. Vargas testified that

certain vaccinations protect against forms of sudden death. Tr. 168. Varicella, for example,

“protects against varicella and therefore protects against the fatal complication of that which can

include fatal pneumonia, fatal superimposed bacterial pneumonia on a viral pneumonia, or

sometimes from the skin lesions[] you can get a superimposed bacterial infection[] [] that can

enter the bloodstream and cause death.” Tr. 168-69.

Dr. Vargas also “disagree[d] strongly with [Petitioners’] theory that the large majority of

SIDS and SUDC are caused by a seizure,” regardless of the presence of a hippocampal

abnormality. Tr. 179. She opined that the hippocampal abnormality described in cases of SIDS,

SUDC, and SUDEP “is a nonspecific finding” seen in many cases. Resp. Ex. J at 3; see also Tr.

178-79. “Although it is present at increased rates in patients with epilepsy history, it is unclear

whether the hippocampal malformation might be a cause of seizure, a consequence of seizure,

two separate consequences of another abnormality (e.g., genetic), or other.” Resp. Ex. J at 3

(citing Resp. Ex. J, Tab 5 at 8-9). 67 Additionally, she noted there is no evidence that such

malformations “cause death, no evidence that fever induces them to cause death, nor any

evidence that vaccination induces them to cause death.” Id. Thus, Dr. Vargas argued the

presence of a hippocampal abnormality does not automatically classify a case as SUDC without

a cause or explanation. Tr. 178.

In support of her opinions, Dr. Vargas cited several papers. McGuone et al. examined 20

SUDC cases and found 12 had a history of febrile seizures, 85% died during apparent sleep, and

80% were in the prone position. Resp. Ex. J, Tab 5 at 1. The authors concluded that any

“significance and specificity of hippocampal findings [was] unclear” because abnormalities in

the dentate gyrus were found in unexplained and explained deaths. Id. at 1, 8-9. Thus, the

“hippocampal findings may be a result of seizures, a contributor to seizures, an unrelated

phenomenon, or a normal anatomic variant in children.” Id. at 9.

67

Declan McGuone et al., Neuropathologic Changes in Sudden Unexplained Death in

Childhood, 79 J. Neuropathology & Experimental Neurology 336 (2020).

36

Abdel-Mannan et al. 68 defined a definite case of SUDEP as “[s]udden, unexpected,

witnessed or unwitnessed, non-traumatic and non-drowning death, occurring in benign

circumstances, in an individual with epilepsy, with or without evidence for a seizure and

excluding documented status epilepticus in which postmortem examination does not reveal a

cause of death.” Resp. Ex. J, Tab 1 at 2. Dr. Vargas explained the mechanism of death in

SUDEP is unknown. Resp. Ex. J at 3 (citing Resp. Ex. J, Tab 1 at 1). There is also no evidence

that fevers can trigger SUDEP. Id. Dr. Vargas explained that for SUDEP, it is postulated that

abnormalities of ion channels in the brain and heart may render individuals predisposed to

seizures and sudden cardiac arrest. Id. (citing Resp. Ex. J, Tab 1 at 7).

Dr. Vargas agreed the MMRV vaccination causes fevers and sometimes causes seizures,

and this risk of seizure peaks at seven to 10 days post-vaccination. Tr. 181-82. When asked

whether death could occur when “a child [] sleeping on the[ir] stomach [] [loses] consciousness

due to a seizure,” Dr. Vargas testified “[p]robably.” Tr. 185. She explained, however, that death

from a first febrile seizure is rare. Tr. 180.

She also noted fevers caused by viral infections can trigger seizures. Tr. 184. And

seizures can lead to injuries, such as tongue biting, falls, and a compromised respiratory tract due

to aspiration of material. Tr. 184-85.

ii. Althen Prongs Two and Three

Dr. Vargas agreed N.A.’s death is best classified as SUDC. Resp. Ex. C at 5; Resp. Ex. J

at 4; Tr. 169. Although there are aspects of N.A.’s death that resemble SIDS, Dr. Vargas opined

N.A.’s death does not qualify as SIDS. Resp. Ex. C at 5; see also Tr. 163-64 (testifying there is a

“strict age cut-off” at “one year of age”). She also opined that N.A. did not have epilepsy or

SUDEP, and even if she had a history of epilepsy, Dr. Vargas found no evidence that a vaccine-

induced fever could have caused death in such scenario. Resp. Ex. J at 3.

Next, Dr. Vargas opined that there is no evidence that N.A. had a febrile seizure. Resp.

Ex. C at 6-7; Tr. 175. She noted N.A. had no history of seizures and no seizure was observed on

the night of her death. Resp. Ex. C at 6. N.A.’s fevers around the time of her death were only

“low-grade, lower than characteristically observed with febrile seizures.” Id.; see also Tr. 175-

76. Additionally, Dr. Vargas found N.A.’s autopsy showed no evidence of seizure activity.

Resp. Ex. C at 6. For example, there was no evidence of tongue-biting, which is a finding Dr.

Vargas found typical with a suspected seizure. Id. at 7. Dr. Vargas found “[t]he fact that the

medical examiner did not describe or sample [N.A.’s] tongue may reflect a lack of any

substantial degree of suspicion for seizure on the part of the medical examiner.” Id.

She disagreed with Petitioners’ experts’ arguments that a history of seizures in N.A.’s

brother was evidence that N.A. had a seizure. Resp. Ex. C at 7. While Dr. Vargas agreed that

“[s]eizures can be familial,” she disagreed that “[h]aving a single family member with seizures . .

68

Omar Abdel-Mannan et al., A Systematic Review of Sudden Unexpected Death in Epilepsy

(SUDEP) in Childhood, 90 Epilepsy & Behavior 99 (2019).

37

. automatically confer[s] seizure susceptibility.” Tr. 176; Resp. Ex. C at 7. Additionally, N.A.

did not exhibit a history of seizures or developmental issues that were seen in her brother. Resp.

Ex. J at 2; Tr. 176-77. Thus, Dr. Vargas opined any link between N.A.’s death and her brother’s

seizures “[was] tenuous at best” and “probably negligible.” Resp. Ex. J at 2; Tr. 177.

Dr. Vargas questioned Dr. Kinsbourne’s opinions that “the configuration of the body in

rigor mortis was unusual, less like an infant death by asphyxia than death during a seizure.”

Resp. Ex. C at 7 (quoting Pet. Ex. 13 at 2). She responded that Dr. Kinsbourne “provide[d] no

explanation for what was ‘unusual’ about the rigor mortis, or why the configuration would

indicate death due to seizure.” Id. Additionally, the autopsy did not mention a particular body

configuration that was “unusual” and rigor mortis, as Dr. Vargas explained, “is a natural and

expected phase of postmortem change, and it is not in any way an indication of seizure.” Id.

With regard to the prone position on death, Dr. Vargas agreed this position is a common

position in patients with SIDS or SIDS-like death and “it supports some of the mechanisms . . .

proposed in SIDS.” Tr. 176. And for the disagreement as to the presence of a hippocampal

abnormality in N.A., Dr. Vargas noted the presence of such abnormality “[was] not critical to

[her] opinion that [N.A.’s] death was not caused by vaccination nor by fever.” Resp. Ex. J at 3.

Dr. Vargas reviewed the report from SUDCRRC. Resp. Ex. N at 1-2. She noted the

SUDCRRC did not find vaccination, fever, or seizure to be a cause of N.A.’s death. Id. The

report concluded cause of death was unexplained sudden death with an undetermined manner of

death. Id. at 2 (citing Pet. Ex. 77 at 9). Additionally, SUDCRRC conducted a genetic analysis

and identified no known or expected pathogenic variants. 69 Id. (citing Pet. Ex. 77 at 8); see also

Pet. Ex. 80 (genetics report). Based on the lack of any genetic abnormalities, Dr. Vargas opined

that N.A. “had a little low risk” of seizures given the fact that the SUDCRRC did not identify

genetic susceptibility to seizures. Tr. 177.

Regarding the autopsy, Dr. Vargas reviewed the 12 autopsy slides and had several

opinions. 70 Resp. Ex. C at 3-6; Tr. 171-72. First, she opined that there were no pathologic

features shown in the heart tissue. Resp. Ex. C at 4.

Second, Dr. Vargas found some of N.A.’s organs weighed more than what would be

expected in a child N.A.’s age. Resp. Ex. C at 3 (citing Resp. Ex. C, Tab 1). 71 She noted that

the lungs stood out as heavy compared to other organs. Id. at 5-6; Tr. 172. Dr. Vargas agreed

69

Dr. Vargas hypothesized the role of genetics in N.A.’s death in an expert report, prior to the

filing of the genetic testing results from SUDCRRC. See Resp. Ex. J at 1-2.

70

For Dr. Vargas’ findings on the microscopic slides, see Resp. Ex. C at 4.

71

J.M. Coppoletta & S.B. Wolbach, Body Length and Organ Weights of Infants and Children: A

Study of the Body Length and Normal Weights of the More Important Vital Organs of the Body

Between Birth and Twelve Years of Age, 9 Am. J. Pathology 55 (1933). Only one chart from

the article was filed.

38

with the medical examiner that there was inflammation in the submucosa of the upper airway but

opined the inflammation chronic, not minimal, because it was well developed and lymphoid

follicles were seen. Tr. 171. She also testified there was inflammation in the lower respiratory

tract in the lungs with mild expanded lymphoid tissue. Tr. 172. Additionally, she agreed with

the medical examiner’s finding of scatter macrophages in the alveoli; however, she did not find

pulmonary edema present. Tr. 172, 188-89.

Based on the autopsy and other evidence, Dr. Vargas opined it was “unlikely that

‘asphyxia’ described the cause of death accurately or fully.” Resp. Ex. C at 5. She explained

“[a]sphyxia, by definition, indicated a lack of oxygen,” and “[w]hen death is attributed to

‘asphyxia’ it usually indicated a blockage of air [] by a physical object.” Id. “[N]atural diseases

[] may lead to a deficiency of oxygen as the mechanism of death,” but the term “asphyxia” is not

applied. Id. She opined N.A. “had no obvious entanglement in bedding, no unsafe co-sleeping

arrangement, and no apparent foul play to indicate asphyxiation as a sole cause of death.” Id.

She also agreed healthy one-year-olds “are expected to be able to turn their heads during periods

of sleep to avoid suffocation.” Id.

Regarding the cause of death, Dr. Vargas testified that there were many possible causes

of death, including occult infection, cardiac arrhythmia, and failure to autoresuscitate. Tr. 180.

On cross-examination, Dr. Vargas noted that these possible causes of N.A.’s death did not reach

the level of more likely than not. Tr. 182-83. However, she opined that each were more likely to

cause death than a febrile seizure. Tr. 185-86.

Dr. Vargas opined that “the most likely explanation for [N.A.’s] fevers was a virus.”

Resp. Ex. C at 5; see also Resp. Ex. J at 3. N.A. had low-grade fever beginning on June 19,

2016, which pre-dated her MMRV vaccination on June 23, 2016, and thus, it could not have

been caused by vaccination. Resp. Ex. C at 5 (citing Pet. Ex. 5 at 5); Tr. 174; Resp. Ex. J at 3.

Dr. Vargas opined N.A. had “chronic lymphoplasmacytic inflammation involving the respiratory

tract observed at autopsy.” Resp. Ex. C at 5; see also Resp. Ex. J at 3. She stressed that the

respiratory tract inflammation involved both the lower and upper respiratory tract. Resp. Ex. J at

4. Given these findings, Dr. Vargas opined N.A. had a respiratory tract viral infection. Id. at 3;

Resp. Ex. C at 5; Tr. 172-73. Additionally, N.A.’s twin sister, L.A., had a low-grade fever on

July 1, 2016, and a viral cause would be “a likely possibility.” Resp. Ex. C at 6 (citing Pet. Ex. 7

at 5 (noting “viral illness” as a differential diagnosis)). She opined that this “could indicate that

[L.A.] had whatever viral infection that N.A. had.” Tr. 175; see also Resp. Ex. J at 4.

Dr. Vargas explained “[v]iruses with a predilection for the pediatric respiratory tract

include rhinoviruses, respiratory syncytial virus, adenoviruses, influenza viruses, parainfluenza

viruses, human bocavirus, and human metapneumovirus” and “[i]nfection with respiratory

viruses is exceedingly common in children.” Resp. Ex. C at 5. Although there were “no reports

39

of any viral testing conducted as a part of [N.A.’s] autopsy, nor of any bacterial testing,” 72 Dr.

Vargas opined “[i]t is expected that had comprehensive testing for viral respiratory pathogens

been conducted, it would have likely confirmed viral infection.” Id. at 5-6. She added that a

virus would explain the chronic inflammation seen in N.A.’s upper and lower respiratory tract

and could have caused concomitant chronic inflammation in other organs. Id. at 6. She

concluded that such respiratory tract inflammation could not be explained by a vaccination. Id.

at 6. During the hearing, Dr. Vargas testified that a viral cause of N.A.’s death remained a

“possibility.” Tr. 183.

Dr. Vargas also posited that there could have been a bacterial cause of N.A.’s death.

Resp. Ex. C at 6; Tr. 186. N.A. had cellulitis in her eye six weeks prior to her death. Resp. Ex.

C at 6. Dr. Vargas noted various causes of cellulitis and opined that “these bacteria can spread

through the body hematogenously and seed other sites.” Id. Additionally, “[o]ccult abscesses

and other bacterial infections can be associated with intermittent and persistent fevers, such as

was observed in [N.A.].” Id. Dr. Vargas opined it was “possible that the bacterial infection was

not fully cured and seated somewhere or had a pocket left and could have been a source of

infection . . . rather than the respiratory tract.” Tr. 186. Dr. Vargas acknowledged no anatomic

sources of infection were identified during autopsy but explained that only a small proportion of

N.A.’s tissue was sampled, making it difficult to rule out infection in other unsampled areas.

Resp. Ex. C at 6; Tr. 183-84. Here, the cellulitis predated N.A.’s MMRV vaccination, and thus,

it would preclude causation. Resp. Ex. C at 6. At the hearing, Dr. Vargas agreed that cellulitis

or bacterial infection as a cause of death was only a “possibility.” Tr. 182-84, 186.

5. Respondent’s Expert, Dr. Christine McCusker, M.D. 73

a. Background and Qualifications

Dr. McCusker received a B.Sc. in microbiology and immunology, M.Sc. in molecular

biology, and M.D. in Ontario, Canada. Resp. Ex. A at 1; Resp. Ex. O at 1. She then completed a

pediatric residency, fellowship in immunology, and a fellowship in allergy and immunology.

Resp. Ex. O at 2. She obtained board certification from the American Board of Pediatrics and is

certified in pediatrics and allergy and clinical immunology in Canada. Id.; Resp. Ex. A at 1. Dr.

McCusker’s “research focus is the regulation of the immune responses.” Resp. Ex. A at 1. She

treats an average of 50-120 children per week in allergy and clinical immunology as well as

urgent care general pediatrics. Id. at 2. Throughout her career, she has held various university

72

Dr. Vargas noted “[a] typical autopsy workup in unexpected death includes postmortem

microbiologic culture for bacteria.” Resp. Ex. C at 6 (citing Resp. Ex. C, Tab 2 (Johan J.

Dempers et al., The Institution of a Standardized Investigation Protocol for Sudden Infant Death

in the Eastern Metropole, Cape Town, South Africa, 61 J. Forensic Scis. 1508 (2016))). She

found it “striking . . . that there [was] no record of any postmortem microbiologic testing.” Id.

73

Dr. McCusker submitted two expert reports and testified at the hearing. Resp. Exs. A, H; Tr.

3. Dr. McCusker’s expert reports address theories from Dr. Miller that he abandoned at the

hearing, and thus, the undersigned addresses only those opinions from Dr. McCusker that are

relevant to this case and Petitioners’ theory.

40

and hospital appointments and she has authored or co-authored over 100 publications. Resp. Ex.

O at 3-4, 33-46.

b. Opinion

i. Althen Prong One

Dr. McCusker addressed Petitioners’ theory that N.A. suffered her first febrile seizure on

the night of her death and this seizure was vaccine-induced. Resp. Ex. A at 9. Dr. McCusker

noted Petitioners relied upon Kinney et al. (2009), which found 19 of the 49 SUDC cases had a

family or personal history of febrile seizures. Id. (citing Pet. Ex. 18 at 10 tbl.1). She explained

that the incidence of febrile seizure or family history of febrile seizures “was not significantly

different from controls in this study.” Id. (citing Pet. Ex. 18 at 10 tbl.1). Additionally, Kinney et

al. studied the frequency of hippocampal and temporal lobe abnormalities; however, only a small

number amount of children’s hippocampus and temporal lobes were available for examination

and some “frequencies were not statistically different.” Id. Lastly, Dr. McCusker noted

vaccination was not listed as a risk factor in Kinney et al. Id.

Dr. McCusker testified that “there is an increased risk of febrile seizures in family

members of those who’ve had febrile seizures,” although the literature is “not particularly

strong.” Tr. 210. She briefly discussed Hesdorffer et al. and Hefti et al., articles relied upon by

Petitioners, and argued that these articles did not find a family history of febrile seizures was

significantly increased in SUDC cases, with or without hippocampal abnormalities. Resp. Ex. A

at 10 (citing Pet. Exs. 16, 27-28). She determined that an increased risk of febrile seizures in

family members “would imply that there are genetic causes of the febrile seizures.” Tr. 210.

Next, she explained that there are many similarities in the risk factors for death in SIDS

and SUDC cases, including the prone sleeping position and infection or illness, although “an

upper respiratory tract infection is considered a risk factor for [SIDS]” and “less so” for SUDC.

Tr. 196; see also Resp. Ex. H at 1; Resp. Ex. A, Tab 27 at 3, 3 tbl.1 (noting prone position and

mild infections as risk factors for SIDS); 74 Pet. Ex. 18 at 7, 10 tbl.1 (analyzing similarities in

SUDC and non-SUDC cases); Pet. Ex. 16 at 7 tbl.2 (listing risk factors for SIDS, SUDC, febrile

seizures, and SUDEP); Pet. Ex. 34 at 14 (“Mild infection around the time of death is present in

approximately one-half of SIDS infants.”). 75 Kinney et al. explained that because these risk

factors are not found in all cases, they “are not causative.” Resp. Ex. A, Tab 27 at 3.

Vaccination was not listed as a risk factor. Resp. Ex. H at 2; see, e.g., Pet. Exs. 16, 18; Resp. Ex.

A, Tab 27.

74

Hannah C. Kinney & Bradley T. Thach et al., Sudden Infant Death Syndrome, 361 New Eng.

J. Med. 795 (2009).

75

Hannah C. Kinney et al., The Serotonergic Anatomy of the Developing Human Medulla

Oblongata: Implications for Pediatric Disorders of Homeostasis, 41 J. Chem. Neuroanatomy 182

(2011).

41

At the hearing, Dr. McCusker explained that theoretically the prone position is a risk

factor due to an infant’s inability to lift and turn their head, which can lead to an obstructed

airway in the bedding or other item in the crib. Tr. 197-98; see also Resp. Ex. A at 13; Resp. Ex.

A, Tab 27 at 4, 7. A child (over the age of one) engages in “resistive breathing,” where

abdominal muscles are used to breathe and the stomach pushes out while breathing. Tr. 198.

Thus, when a child is in the prone position, there is more effort engaged to breathe. Id. Dr.

McCusker contended that if a child has an upper respiratory infection with an obstructed airway,

the prone position can result in a child that is unable to breathe. Tr. 199.

Dr. McCusker cited various articles discussing airway obstruction in SIDS/SUDC and in

the presence of upper respiratory infections. Resp. Ex. A at 13-15. She opined that upper

respiratory tract infections in infants can cause upper airway obstructions, compromising airway

function. Id. at 15; Resp. Ex. H at 2. And unlike vaccination, an upper respiratory tract

infections “is a defined risk factor for SIDS, SUDC[,] and SUDEP.” Resp. Ex. H at 2.

Bollag 76 explained “[i]nfants and small children have narrow airways,” and thus,

“[i]nflammation and congestion of the mucosa can result in obstruction very rapidly.” Resp. Ex.

A, Tab 37 at 1. Children up to the age of two have difficulty when both breathing and feeding

through the mouth. Id. Infants breathe through their nose and learn to breathe through their

mouth during their first year of life. Resp. Ex. H at 2; see also Resp. Ex. A, Tab 33 at 4; 77 Resp.

Ex. A, Tab 38 at 1. 78 Moschino et al. suggested that mucus in upper airways can affect

respiratory functions. Resp. Ex. A, Tab 38 at 1. deAlmeida et al. 79 noted “[t]he switch to oral

breathing in response to a nasal obstruction is crucial for survival, and has been put forward as an

important mechanism in preventing [SIDS].” Resp. Ex. A, Tab 36 at 1; see also, e.g., Resp. Ex.

G, Tab 1 at 1 (“It has [] been suggested that blockage of the nasal passages of infants who are

obligate nose breathers could result in asphyxia and SIDS. In some infants, nasal obstruction

may lead to pharyngeal closure, which may prolong an apnoeic period and exacerbate associated

hypoxaemia.” (internal citations omitted)). 80

76

Ueli Bollag, Acute Respiration Infections in Childhood: Tackling the Problem at the Level of

the Nose, 35 J. Tropical Pediatrics 140 (1989).

77

W.J. Kleemann et al., Infections of the Upper Respiratory Tract in Cases of Sudden Infant

Death, 108 Int’l J. Legal Med. 85 (1995).

78

L. Moschino et al., Is Nasal Suctioning Warranted Before Measuring 02 Saturation in Infants

with Bronchiolitis?, 101 Archives Disease Childhood 114 (2016).

79

Victor L. deAlmeida et al., The Effect of Nasal Occlusion on the Initiation of Oral Breathing

in Preterm Infants, 18 Pediatric Pulmonology 374 (1994).

80

Richard Harding et al., Postnatal Development of Responses to Airflow Obstruction, 22

Clinical & Experimental Pharmacology & Physiology 537 (1995).

42

Ralston et al., 81 a clinical practice guideline from the American Academy of Pediatrics,

discussed frequent respiratory infections in children and recognized that an upper airway

obstruction due to infection can increase the effort of breathing. Resp. Ex. A, Tab 31 at 6.

Kleemann et al. compared nasal cavities in SIDS cases to control cases, all under the age of one,

and determined rhinitis 82 “seem[ed] to be merely a result of the high incidence of upper

respiratory tract infections in this age group.” Resp. Ex. A, Tab 33 at 1. The authors

“speculate[d] [] that infections of the nose combined with other factors could play a role in []

[SIDS].” Id. at 4. The authors concluded that since infants breathe through their nose and learn

to breathe through their mouth during their first year, “even small infections of the nose can

cause obstruction of the airway.” Id.

ii. Althen Prongs Two and Three

Dr. McCusker found Petitioners’ theory “exceedingly unlikely.” Tr. 213. Dr. McCusker

could not discern how N.A. died. Id. But she found it “highly unlikely that the MMR[V]

vaccine played a role in [N.A.’s] death.” Id. She explained that even if seizures post-MMRV

vaccine occur, “there is no increased frequency of infant death or SUDC in children who receive

their MMRV.” Tr. 213-14. This “sequence of events” from Petitioners “simply doesn’t occur in

the children who are at risk for febrile seizures who develop febrile seizures post-MMRV.” Tr.

214.

Dr. McCusker classified N.A.’s case as SUDC. Tr. 195. N.A. was described as having

her feet sticking through the slacks of the crib upon discovery, which Dr. McCusker believed

made it difficult for her to roll over. Tr. 200. She found this prone position increased the

possibility of SUDC. Resp. Ex. A at 16; Resp. Ex. H at 3.

Dr. McCusker acknowledged that N.A. was on day seven post-vaccination and was

therefore within the risk period of febrile seizures post-MMRV vaccine. Resp. Ex. A at 9, 15;

Resp. Ex. H at 3. She noted, however, that even though Petitioners’ studies showed febrile

seizures occur at an increased frequency seven to 10 days following MMRV vaccination, these

studied failed to mention an increased frequency of death (or SUDEP) during this time period.

Resp. Ex. A at 9, 15; Resp. Ex. H at 3.

Given the time of death from the medical examiner (between 9:00 p.m. and 10:00 p.m. on

the night of June 30, 2016), and N.A.’s receipt of Motrin around 7:00 p.m. the night of June 30,

2016, Dr. McCusker testified that the Motrin “would have been working” at the time of death

since it is effective for eight hours. Tr. 211-12. Thus, she opined that N.A. would not have had a

fever during this time. Tr. 213. And “any fever she had at that time prior to the [Motrin] would

81

Shawn L. Ralston et al., Clinical Practice Guideline: The Diagnosis, Management, and

Prevention of Bronchiolitis, 134 Pediatrics e1474 (2014).

82

Rhinitis is “inflammation of the mucous membrane of the nose.” Rhinitis, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=43725 (last visited

Nov. 13, 2023).

43

have been controlled during the time of her demise, suggesting . . . [a] fever-inducing seizure

would be unlikely.” Tr. 211.

With regard to the significance of family history of febrile seizures, Dr. McCusker opined

that N.A.’s brother with a history of febrile seizures also has a genetic abnormality, a

microdeletion in an area associated with neurodevelopmental delays. Tr. 210-11. Based on this,

Dr. McCusker opined N.A.’s brother is not at the same “genetic standpoint” as N.A. Tr. 211.

She explained that “the familial febrile seizures would not be predicted to be the same risks if the

microdeletion is responsible for his . . . susceptibility to febrile seizures.” Id.

Dr. McCusker opined N.A. had a viral respiratory infection, which is a risk factor for

SIDS and SUDC, for the following reasons. Tr. 200; Resp. Ex. A at 15; Resp. Ex. H at 2-3.

First, N.A.’s autopsy revealed small amount of mucous in her nares, trachea, and bronchi and the

respiratory mucosa was mildly congested. Tr. 200; Resp. Ex. A at 15 (citing Pet. Ex. 6 at 4). Dr.

McCusker also relied upon Dr. Vargas’ findings here as it relates to the pathology. Tr. 200. She

noted N.A. had a runny nose on the day she died. Id. Although N.A. was noted to be feeling

warm on the night of her death, Dr. McCusker found no evidence N.A. had a fever. Resp. Ex. H

at 2. She maintained N.A.’s autopsy findings can be “reasonably [] attributed” to an upper

respiratory tract infection. Id. And at the hearing, she noted that there are explanations other

than vaccination for why a child would develop a fever. Tr. 202-04 (citing Resp. Ex. V). 83

Additionally, N.A.’s twin sister, L.A., went to the hospital following N.A.’s passing and

“was diagnosed with crusting in the nose and what was felt to be a[n] acute viral infection.” Tr.

200; see also Resp. Ex. A at 15. N.A.’s brother was diagnosed with an infection 16 days after

N.A.’s death, which Dr. McCusker found suggested an acute viral illness was circulating in the

family on the night of N.A.’s death. Resp. Ex. A at 15. Given these facts, she concluded that

“[i]t [was] possible . . . that [N.A.] may also have had an undiagnosed upper respiratory tract

infection leading to airway occlusion in the prone position as suggested by Kinney et al.” Id.

(citing Pet. Ex. 18); see also Resp. Ex. H at 2.

Dr. McCusker opined that any congestion N.A. had would not have been caused by her

MMRV vaccination. Tr. 201. She agreed MMRV vaccination can trigger a fever but “runny

nose and crusting of the nose is not a feature of MMRV.” Id.

She acknowledged that a finding of an upper respiratory infection would be insufficient

to cause asphyxia, but argued that an upper respiratory tract infection can cause upper airway

obstruction and, unlike vaccination, an upper respiratory tract infection “is a defined risk factor

for SIDS, SUDC[,] and SUDEP.” Resp. Ex. H at 2.

Dr. McCusker concluded that N.A. likely had an acute infection at the time of death.

Resp. Ex. A at 16; Resp. Ex. H at 2-3. She found no evidence supporting a mechanistic role for

MMRV vaccination in N.A.’s death. Resp. Ex. A at 16; Resp. Ex. H at 3.

83

Caroline Hervé et al., The How’s and What’s of Vaccine Reactogenicity, 39 NPJ Vaccines 1

(2019).

44

IV. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as

a simple, fair and expeditious means for compensating vaccine-related injured persons. The

Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty

and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting

H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioners’ burden of proof is by a preponderance of the evidence. § 13(a)(1). The

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health

& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioners need not make a specific type of

evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic predisposition, or general acceptance in the scientific or medical communities

to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioners may satisfy their burden by

presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioners must prove that the vaccine was “not only [the] but-for cause of

the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321

(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));

see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The

received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d

at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent

can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors

unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to

establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum.

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the [R]espondent, the special master

may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner

has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,

162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.

2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors

unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine

was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.

Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted

to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite

element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of

multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the

vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated

contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

45

B. Factual Issues

Petitioners must prove, by a preponderance of the evidence, the factual circumstances

surrounding their claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh

the evidence presented, which may include contemporaneous medical records and testimony.

See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a

special master must decide what weight to give evidence including oral testimony and

contemporaneous medical records).

Medical records, specifically contemporaneous medical records, are presumed to be

accurate and generally “warrant consideration as trustworthy evidence.” Cucuras v. Sec’y of

Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health

& Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (rejecting the presumption that “medical

records are accurate and complete as to all the patient’s physical conditions”); Shapiro v. Sec’y

of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2011) (“[T]he absence of a reference to a

condition or circumstance is much less significant than a reference which negates the existence

of the condition or circumstance.” (quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct.

726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand,

105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013). The weight afforded to

contemporaneous records is due to the fact that they “contain information supplied to or by

health professionals to facilitate diagnosis and treatment of medical conditions. With proper

treatment hanging in the balance, accuracy has an extra premium.” Id. To overcome the

presumptive accuracy of medical records, a petitioner may present testimony which is

“consistent, clear, cogent, and compelling.” Sanchez v. Sec’y of Health & Hum. Servs., No. 11-

685V, 2013 WL 1880825, at *3 (Fed. Cl. Spec. Mstr. Apr. 10, 2013) (citing Blutstein v. Sec’y of

Health & Hum. Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30,

1998)), mot. for rev. denied, 142 Fed. Cl. 247 (2019), vacated on other grounds & remanded, 809

F. App’x 843 (Fed Cir. 2020).

There are situations in which compelling testimony may be more persuasive than written

records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of

Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the

factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.

Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)

(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than

those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733). Ultimately, a

determination regarding a witness’s credibility is needed when determining the weight that such

testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379

(Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded medical records, special masters are not bound rigidly by

those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &

Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see

also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.

46

Spec. Mstr. Feb. 18, 1994) (Section 13(b)(2) “must be construed so as to give effect also to §

13(b)(1) which directs the special master or court to consider the medical records (reports,

diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special

master or court to be bound by them”).

C. Causation

To receive compensation through the Program, Petitioners must prove either (1) that N.A.

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a

vaccine that she received, or (2) that N.A. suffered an injury that was actually caused by a

vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioners must

show that the vaccine was “not only a but-for cause of the injury but also a substantial factor in

bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioners do not allege N.A. suffered a Table Injury, they must prove a vaccine

N.A. received caused her injury. To do so, Petitioners must establish, by preponderant evidence:

“(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence

of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing

of a proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioners must provide a sound

and reliable medical or scientific explanation that pertains specifically to this case, although the

explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Hum. Servs., 35 F.3d. 543, 548-49 (Fed. Cir. 1994). Petitioners cannot

establish entitlement to compensation based solely on their assertions; rather, a vaccine claim

must be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1).

In determining whether a petitioner is entitled to compensation, the special master shall consider

all material in the record, including “any . . . conclusion, [or] medical judgment . . . which is

contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh

the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioners’

favor when the evidence weighs in their favor. See Moberly, 592 F.3d at 1325-26 (“Finders of

fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence

presented to them and, if appropriate, as to the credibility of the persons presenting that

evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in a petitioner’s

favor).

Testimony that merely expresses the possibility—not the probability—is insufficient, by

itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &

Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying a petitioner’s motion for review and

noting that a possible causal link was not sufficient to meet the preponderance standard). The

Federal Circuit has made clear that the mere possibility of a link between a vaccination and a

petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at

1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and

the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon

v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is

47

by no means required, a possible mechanism does not rise to the level of preponderance.

Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

V. FACTUAL ANALYSIS

As Federal Circuit precedent establishes, in certain cases it is appropriate to determine the

nature of an injury before engaging in the Althen analysis. Broekelschen v. Sec’y of Health &

Hum. Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). Since “each prong of the Althen test is

decided relative to the injury[,]” determining facts relating to the claimed injury can be

significant. Id. Here, the parties have identified two factual issues. First, they dispute whether

N.A. suffered a seizure during the night of June 30, 2016 or the morning of July 1, 2016. Joint

Prehearing Submission at 4. Next, they dispute whether N.A.’s autopsy slides show

abnormalities in the hippocampus, specifically granule cell dispersion and/or bilamination of the

dentate gyrus. Id. Additionally, Dr. Miller opines that N.A. had abnormalities in the medulla.

See Pet. Ex. 22 at 5, 8; Pet. Ex. 65 at 3; Tr. 23, 46-49.

A. There Is Not Preponderant Evidence That N.A. Suffered a Seizure

The undersigned finds that Petitioners did not prove by preponderant evidence that N.A.

suffered a seizure prior to her death.

The first reason for this finding is based on N.A.’s individual history. She did not have a

history of seizures, febrile, or otherwise. None of her medical records identify a history of any

prior seizures. During periods of prior illness, when N.A. had a fever, she did not experience a

seizure. Her parents were both health care providers, and they provided detailed histories during

N.A.’s medical appointments and during the investigation of N.A.’s demise. N.A. had previous

illnesses, including upper respiratory infections and cellulitis, but during these illnesses, she did

not experience a febrile seizure. She had also received routine childhood vaccinations prior to

the vaccination at issue, and she did not have a febrile seizure associated with her vaccinations.

On the evening prior to her demise, N.A.’s mother noted that she had a low-grade fever and

Motrin was administered. Her low-grade fever was not elevated to the level that is reportedly

associated with febrile seizures. See, e.g., Pet. Ex. 16 at 3 (“[Febrile seizures] were defined as a

seizure associated with illness or fever of ≥ 101°F . . . .”); Resp. Ex. E, Tab 4 at 2 (“The most

significant risk factor for the development of a first febrile seizure is the height of the

temperature; the higher the temperature, the higher the likelihood of a febrile seizure. . . . Most

children have a temperature of at least 39°C at the time of a seizure.”). 84

In summary, there is no evidence from N.A.’s history to suggest that she ever had a

seizure, or that illnesses or vaccinations which cause fever ever triggered a seizure.

N.A. did have a family history of febrile seizures; her brother had several febrile seizures.

The medical literature shows that this fact may have increased N.A.’s risk to have a febrile

seizure, but this increased risk does not equate to preponderant evidence. See Tr. 58, 60, 62 (Dr.

Miller testifying that this is a “rare event”).

84

39°C is 102.2°F.

48

Next, Dr. Virani, the pathologist who conducted the autopsy, did not opine or suggest that

a seizure was a contributing factor to the cause of death. Moreover, N.A.’s case was reviewed

by the SUDCRRC, and they conducted a thorough investigation, including a review of records,

histology tissue review by a cardiac pathologist and neuropathologist, and genetic analyses.

They did not conclude that N.A. had a seizure.

Further, there was no physical evidence to suggest that N.A. had a seizure. As explained

by Crandell et al., “[p]ostmortem evidence of [a] terminal seizure is often absent or nonspecific.”

Pet. Ex. 72 at 7. “Common stigma” may include tongue biting or urinary incontinence. Id. Due

to N.A.’s age, urinary incontinence could not be evaluated. But there is no sign or description in

the autopsy to suggest tongue biting. Thus, there is no physical evidence to support the

conclusion that that N.A. had a seizure.

Dr. Virani noted pulmonary edema in his autopsy, but he did not opine that the finding

suggested or supported febrile seizure as a cause of death. Dr. Kinbsourne mentioned pulmonary

edema as a finding in support of a seizure, but he did not provide supportive evidence for his

opinion. Devinsky did not explain why pulmonary edema would occur due to a seizure as

opposed to another cause of death. And Kloster and Engelskjøn described pulmonary edema as a

non-specific finding. Moreover, Dr. Miller did not opine that the presence of pulmonary edema

was significant to him. And none of the pathologists offered opinions about the finding of

pulmonary edema. The only pathologist with special expertise in pulmonary pathology is Dr.

Vargas, 85 and she did not see evidence of pulmonary edema in the lung tissue. Resp. Ex. C at 4.

The

This text is long and has been trimmed here. Open the source document for the complete record.