# ANKLAM v. SECRETARY OF HEALTH AND HUMAN SERVICES

> United States Court of Federal Claims · December 26, 2023

URL: https://www.frixlaw.com/law-library/cases/10736662

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** December 26, 2023
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Nora Beth Dorsey
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10736662

## How later opinions describe it (automated extraction)

- rejecting a theory based on a “bare statistical fact”
- noting that “close calls” are resolved in a petitioner’s favor
- noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”

## Opinion text

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 entangle

[Text truncated at 120,000 characters. The full text is on the page linked above.]

---

Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10736662. Public record. Not legal advice.