# CATONE v. SECRETARY OF HEALTH AND HUMAN SERVICES

> United States Court of Federal Claims · September 19, 2025

URL: https://www.frixlaw.com/law-library/cases/11141103

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** September 19, 2025
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Daniel T. Horner
- **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/11141103

## How later opinions describe it (automated extraction)

- holding the special master did not err in resolving the case pursuant to Prong Two when respondent conceded that petitioner met Prong Three
- holding that “the special master did not commit legal error in considering evidence of SIDS, an allegedly alternative cause. Nothing in the Vaccine Act prohibits the government from presenting evidence that the petitioner's injury was due to “factors unrelated” to the vaccine …

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 19-690V
Filed: August 8, 2025

Special Master Horner
NICHOLAS CATONE and MARJORIE
CATONE, parents of N.C., deceased,

Petitioners,
v.

SECRETARY OF HEALTH AND
HUMAN SERVICES,

Respondent.

Jessica Wallace, Siri & Glimstad, LLP, Aventura, FL, for petitioners.
Catherine Elizabeth Stolar, U.S. Department of Justice, Washington, DC, for
respondent.

DECISION1

On May 9, 2019, petitioners filed a petition under the National Childhood Vaccine
Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 on behalf of their son, N.C. (ECF No.
1.) Petitioners allege that N.C.’s death on May 12, 2017, determined upon autopsy to
be a sudden unexplained death, was caused by his diphtheria-tetanus-acellular-
pertussis (“DTaP”) vaccination administered on April 25, 2017. (Id.)

On November 30, 2023, petitioners filed a motion for a ruling on the written
record finding them entitled to compensation for N.C.’s death. (ECF No. 85.)
Petitioners contend that N.C.’s April 25, 2017 DTaP vaccine caused him to suffer from a
witnessed seizure on May 7, 2017, and then an unwitnessed terminal seizure late on
1
Because this document contains a reasoned explanation for the action taken in this case, it must be
made publicly accessible and will be posted 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 document 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, I agree that the identified material fits within this definition, I will redact such material from
public access.
2
All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-
10-34.

1
May 11 or early on May 12, 2017. (ECF No. 85, pp. 25-26.) They theorize that N.C.’s
vaccination “initiated a hyperimmune reaction that eventually led to a terminal seizure in
N.C., a susceptible host.” (Id. at 29.) Respondent opposes the motion, contending that
the case should instead be dismissed for insufficient proof and stressing that N.C.’s
death was appropriately categorized as a sudden unexplained death. (ECF No. 92.)

When sudden deaths remain unexplained after examination and investigation,
such deaths are deemed either “SIDS” (Sudden Infant Death Syndrome) or “SUDC”
(Sudden Unexplained Death in Childhood). (Ex. 13, p. 9.) The term SIDS is applied to
infants under one year of age and the term SUDC is applied to children over the age of
one, usually affecting children between ages one and three. (Id.) Some additional
cases of sudden unexplained death are categorized as “SUDEP” (Sudden Unexpected
Death in Epilepsy) when the decedent had a history of epilepsy. (Ex. 18, p. 21.)
Because N.C. was over one year of age at the time of his death and with no prior history
of epilepsy, his death would be termed SUDC based on his autopsy and the
investigation into his death. (Ex. 18, pp. 8-9; Ex. 19, p. 10.) SIDS and SUDC are
“diagnoses” of exclusion in that they by definition require that the death remain
otherwise unexplained. (Ex. 13, p. 9.) Both phenomena usually occur during sleep and
affect boys more often than girls. (Id.) Safe sleeping campaigns have been effective in
reducing the rate of SIDS. (Id.) However, SIDS is the leading cause of infant mortality
in the U.S., affecting 0.53 per 1,000 infants. (Id.) SUDC is rarer than SIDS, affecting
1.3 per 100,000 children (ages 1-4). However, it still accounts for 10% of unexpected
deaths in childhood. (Id.)

Petitioners clearly suffered a profound loss, and I offer my sincerest
condolences. However, for all of the reasons discussed below, there is not
preponderant evidence that N.C.’s death was caused by his vaccination. Instead, the
evidence preponderates in favor of a finding that N.C.’s death remains unexplained and
therefore constitutes a SUDC. Thus, petitioners are not entitled to an award of
compensation.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury or death; and
has received no previous award or settlement on account of the injury. Finally – and the
key question in most cases under the Program – the petitioner must also establish a
causal link between the vaccination and the injury. § 300aa-11(c)(1); § 300aa-
13(a)(1)(A)-(B).

In some cases, the petitioner may simply demonstrate the occurrence of what
has been called a “Table Injury.” That is, it may be shown that the vaccine recipient
suffered an injury of the type enumerated in the “Vaccine Injury Table,” corresponding to

2
the vaccination in question, within an applicable time period following the vaccination
also specified in the Table. If so, the Table Injury is presumed to have been caused by
the vaccination unless it is affirmatively shown that the injury was caused by some
factor other than the vaccination. § 300aa-13(a)(1)(A)-(B); § 300aa-11(c)(1)(C)(i);
§ 300aa-14(a). In many cases, however, the vaccine recipient may have suffered an
injury not of the type covered in the Vaccine Injury Table. In such instances, an
alternative means exists to demonstrate entitlement to a Program award. That is, the
petitioner may gain an award by showing that the recipient’s injury was “caused-in-fact”
by the vaccination in question. § 300aa-11(c)(1)(C)(ii). In such a situation, the
presumptions available under the Vaccine Injury Table are inoperative. The burden is
on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines ex rel. Sevier v. Sec’y of Health & Human Servs.,
940 F.2d 1518, 1525 (Fed. Cir. 1991).

In this case, petitioners have not alleged that the vaccination at issue caused any
injury or condition listed on the Vaccine Injury Table. Therefore, petitioners must meet
the burden of proof for establishing causation-in-fact. (E.g., ECF No. 85, p. 56 (stating
that “[p]etitioners are aware that they have a heavy burden to carry in order to prove an
off-table claim”).)

The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation.
§ 300aa-13(a)(1)(A); see also Althen, 418 F.3d at 1278-79; Hines, 940 F.2d at 1525.
Under that standard, petitioners must show that it is “more probable than not” that the
vaccination was the cause of the injury, in this case N.C.’s death. Althen, 418 F.3d at
1279. They need not show that the vaccination was the sole cause but must
demonstrate that the vaccination was at least a “substantial factor” in causing the
condition at issue and was a “but for” cause. Shyface v. Sec’y of Health & Human
Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Thus, petitioners must supply “proof of a
logical sequence of cause and effect showing that the vaccination was the reason for
the injury[.]” Althen, 418 F.3d at 1278 (quoting Grant v. Sec’y of Health & Human
Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992)). Ultimately, petitioners must satisfy what
has come to be known as the Althen test, which requires: (1) a medical theory causally
connecting the vaccination and the injury; (2) a logical sequence of cause and effect
showing that the vaccination was the reason for the injury; and (3) a showing of
proximate temporal relationship between vaccination and injury. Id.

A petitioner may not receive a Vaccine Program award based solely on his or her
assertions; rather, the petition must be supported by either medical records or by the
opinion of a competent physician. § 300aa-13(a)(1). Medical records are generally
viewed as particularly trustworthy evidence because they are created
contemporaneously with the treatment of the patient. Cucuras v. Sec’y of Health &
Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, medical records and/or
statements of a treating physician’s views do not per se bind the special master to adopt
the conclusions of such an individual, even if they must be considered and carefully

3
evaluated. § 300aa-13(b)(1). A petitioner may rely upon circumstantial evidence. See
Althen, 418 F.3d at 1280. The Althen court noted that a petitioner need not necessarily
supply evidence from medical literature supporting petitioner’s causation contention, so
long as the petitioner supplies the medical opinion of an expert. Id. at 1279-80. While
scientific certainty is not required, that expert’s opinion must be based on “sound and
reliable” medical or scientific explanation. Boatmon v. Sec’y of Health & Human Servs.,
941 F.3d 1351, 1359 (Fed. Cir. 2019).

Cases in the Vaccine Program are assigned to special masters who are
responsible for “conducting all proceedings, including taking such evidence as may be
appropriate, making the requisite findings of fact and conclusions of law, preparing a
decision, and determining the amount of compensation, if any, to be awarded.” Vaccine
Rule 3(b)(1). Special masters must ensure each party has had a “full and fair
opportunity” to develop the record but are empowered to determine the format for taking
evidence based on the circumstances of each case, including having the discretion to
decide cases without an evidentiary hearing. Vaccine Rule 3(b)(2); Vaccine Rule 8(a);
Vaccine Rule 8(d). Special masters are not bound by common law or statutory rules of
evidence but must consider all relevant and reliable evidence in keeping with
fundamental fairness to both parties. Vaccine Rule 8(b)(1). The special master is
required to consider “all [] relevant medical and scientific evidence contained in the
record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s
report which is contained in the record regarding the nature, causation, and aggravation
of the petitioner’s illness, disability, injury, condition, or death,” as well as the “results of
any diagnostic or evaluative test which are contained in the record and the summaries
and conclusions.” § 300aa-13(b)(1). The special master is required to consider the
entirety of the evidentiary record, draw plausible inferences, and articulate a rational
basis for the decision. Winkler v. Sec’y of Health & Human Servs., 88 F.4th 958, 963
(Fed. Cir. 2023) (citing Hines, 940 F.2d at 1528).

II. Procedural History

This case was initially assigned to another special master. (ECF No. 6.)
Accompanying the petition, petitioners filed affidavits (Exs. 1-2) as well as N.C.’s
pediatric care records (Ex. 3). Shortly thereafter, they filed N.C.’s death certificate.
(ECF No. 8; Ex. 4.) In July of 2019 they filed autopsy and police reports (ECF No. 13;
Exs. 5-6), and in August of 2019 they filed additional medical records, including the
EMS report relating to N.C.’s death (ECF No. 15; Exs. 7-10) as well as scene and
autopsy photographs related to the investigation of N.C.’s death (ECF Nos. 16-17; Exs.
11-12).

Petitioners were then given the opportunity to submit an expert opinion. In July
of 2020 they filed a report and supporting literature by immunologist Omid Akbari, Ph.D.
(ECF No. 28; Exs. 13-14.) In August of 2020 they filed a case review from the
SUDCRRC (ECF No. 31; Ex. 15) and a nanodiagnostic report (ECF No. 31; Ex. 16).
And, in September of 2020, they filed a report and supporting literature by pathologist
Steven Rostad, M.D. (ECF Nos. 32-33; Exs. 17-18). Thereafter, respondent filed his

4
Rule 4 report recommending against compensation (ECF No. 41), along with
responsive expert reports by pediatric immunologist Christine McCusker, M.D. (ECF No.
38; Exs. A-B), pediatric neurologist Gregory L. Holmes, M.D. (ECF No. 39; Exs. C-D),
and pathologist Brent Harris, M.D., Ph.D. (ECF No. 40; Exs. E-F).

After the filing of respondent’s report, the special master assigned to the case
held a Rule 5 status conference to provide the parties preliminary guidance. (ECF No.
43.) The special master cautioned that, based on his review of the expert opinions, it
would be difficult for petitioners to establish entitlement to compensation, especially in
light of the Boatmon v. Secretary of Health & Human Services, 941 F.3d 1351 (Fed. Cir.
2019), a decision in which the Federal Circuit rejected the allegation that vaccination
had contributed to a death categorized as SIDS. (ECF No. 43.) Nonetheless, he
permitted petitioners an opportunity to have their experts respond to respondent’s
expert submissions. (Id. at 4.) Petitioners then filed supplemental expert reports by
Drs. Akbari and Rostad in August of 2021. (ECF Nos. 45-46; Exs. 19-20.) In January
of 2022, respondent filed further responsive reports from Drs. McCusker and Harris.
(ECF Nos. 53-54; Exs. G-H.) Petitioner filed additional reports by Drs. Akbari and
Rostad in February of 2022. (ECF No. 55; Exs. 21-22.)

The case was subsequently reassigned to the undersigned in March of 2022.
(ECF Nos. 58-59.) Petitioners filed autopsy photos annotated by Dr. Rostad (ECF No.
60; Ex. 23) and requested a status conference, which was held in April of 2022. (ECF
No. 62.) During the status conference, I advised that I felt this case may be appropriate
for resolution on the written record; however, respondent was permitted an opportunity
to determine if his expert(s) needed to respond to the annotated autopsy photos. (Id.)
Respondent then filed an additional expert report by Dr. McCusker in September of
2022 (ECF No. 67; Ex. I), but no report responding to the photos.

During a follow up status conference in December of 2022, petitioners initially
indicated they anticipated filing further expert reports (ECF No. 68); however, they
instead advised in a status report filed February 27, 2023, that they wished to secure
testimony from Dr. Ian Hood, the medical examiner that performed N.C.’s autopsy.
(ECF No. 72.) Petitioners filed a motion seeking to stay or extend their deadlines so
that they could pursue a deposition of Dr. Hood. (ECF No. 73.) During a follow up
status conference, I granted petitioners’ request in part and deferred in part. (ECF No.
74.) Specifically, I suspended petitioners’ pending expert report deadline but required
an offer of proof regarding the nature of Dr. Hood’s opinion, and whether he intended to
amend his official report. (Id.)

On June 12, 2023, petitioners filed an “addendum” to N.C.’s autopsy report (ECF
No. 77; Ex. 24), and I directed the parties to file status reports indicating their respective
positions regarding how to proceed (Non-PDF Scheduling Order, filed June 12, 2023).
Petitioners argued that Dr. Hood’s addendum rebutted points made by respondent’s
experts and that a deposition was therefore necessary for a fair and well-informed
ruling. (ECF No. 79.) Respondent argued that a deposition was not reasonably
necessary because Dr. Hood explicitly disclaimed having the knowledge necessary to

5
opine regarding petitioners’ experts’ theory of causation. (ECF No. 82.) I denied
petitioner’s request and instructed the parties to brief the case pursuant to Vaccine Rule
8(d). (ECF No. 83.) However, I allowed the parties to accompany their briefs with
expert reports commenting on Dr. Hood’s addendum to his report.3 (Id. at 3.)

Petitioner filed a motion for a ruling on the written record on November 30, 2023.
(ECF No. 85.) Petitioners did not include any expert report with their motion; however,
they subsequently filed a motion for leave to file newly published literature and a brief
expert report. (ECF No. 87.) They filed a study regarding video analysis of sudden
unexplained death in toddlers accompanied by a report by Dr. Rostad commenting on
the study. (ECF No. 90; Ex. 25.) Petitioner’s filing was permitted, and respondent was
directed to file his response to petitioner’s motion, accompanied by any expert response
to petitioner’s filing. (ECF No. 89.) Respondent filed his response to petitioner’s motion
on June 3, 2024 (ECF No. 92), along with a supplemental report by Dr. Holmes (ECF
No. 91; Ex. J). Petitioners filed their reply brief on August 31, 2024. (ECF No. 96.)

In light of the above, I have concluded that the parties have had a full and fair
opportunity to develop the record and that it is appropriate to resolve this case without
an entitlement hearing.4 See Kreizenbeck v. Sec’y of Health & Human Servs., 945 F.3d
1362, 1366 (Fed. Cir. 2020) (citing Simanski v. Sec’y of Health & Human Servs., 671
F.3d 1368, 1385 (Fed. Cir. 2012)); see also Vaccine Rule 8(d); Vaccine Rule 3(b)(2). In
total, the parties filed 314 exhibits, most of which are medical literature articles cited in
the numerous expert reports submitted in this case. Although this decision discusses
some but not all the literature in detail, the undersigned reviewed and considered all of
the medical records and literature submitted in this matter. Accord Moriarty v. Sec’y of
Health & Human Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume
that a special master considered the relevant record evidence even though he does not
explicitly reference such evidence in his decision.”); Simanski v. Sec’y of Health &
Human Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master is ‘not required to

3
Specifically, I concluded that a deposition of Dr. Hood was not reasonably necessary for two reasons.
First, I explained that “Dr. Hood’s amendment to his report offers several specific statements with respect
to N.C.’s autopsy findings. (ECF No. 83.) However, petitioner’s status report cites these statements for
the effect they contend the statements should have on interpreting the experts’ reports rather than the
autopsy report itself.” (Id. at 2 (emphasis original) (internal citation omitted).) Second, “Dr. Hood further
states that ‘the most I can opine is that if [N.C.] had a terminal seizure his autopsy findings would be just
as were present in this case. Whether his immunizations contributed in some way to causing such a
postulated terminal seizure is beyond my area of expertise.’ This strongly suggests that Dr. Hood has
provided as much information as he believes he can.” (Id. at 2-3 (quoting Ex. 24, p. 5).)
4
In this case, I advised the parties that I was “inclined to rule on the written record, potentially even over
petitioners’ objection, given that the issues presented are familiar within the program.” (ECF No. 68, p.
1.) However, I instructed that “[t]o the extent that petitioners’ object to proceeding with a ruling on the
written record, petitioners may address such arguments in their brief. If I were to ultimately agree to hold
a hearing in light of petitioners’ arguments, then petitioners’ brief would serve as a prehearing brief.” (Id.
at 2.) In their subsequent briefing, petitioners did not argue that they had been denied a full and fair
opportunity to develop the record, request or argue in favor of an entitlement hearing, or object to
proceeding on the written record pursuant to Vaccine Rule 8(d). (See ECF Nos. 85, 96.)

6
discuss every piece of evidence or testimony in [his or] her decision.’” (citation omitted)),
aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

III. Factual History

N.C. was born on September 8, 2015, after an uncomplicated pregnancy. (Ex. 1,
¶ 3; Ex. 3, p. 7; Ex. 8, pp. 43-44.) His newborn screening labs were normal. (Ex. 7, p.
12.) N.C. initially had neonatal jaundice, abnormal weight loss, and umbilical
granuloma; however, by the time of his one month well visit, he had a normal
examination. (Ex. 3, pp. 7-10, 34-35.) Thereafter, N.C. had routine health encounters
and received his routine vaccinations. (Ex. 10, pp. 17-63.) He also had some sick
visits. (Ex. 10, p. 19 (November 16, 2015 encounter for rash); Ex. 3, pp. 17-19 (April
27, 2016 encounter for upper respiratory infection); Ex. 3, pp. 20-21 (June 11, 2016
encounter for upper respiratory infection); Ex. 3, pp. 23-24 (July 26, 2016 encounter for
upper respiratory infection); Ex. 3, pp. 26-28 (January 3, 2017, encounter for bronchitis);
Ex. 3, pp. 29-31 (February 3, 2017 encounter for bronchiolitis, upper respiratory
infection, and left ear infection).) In her affidavit, Mrs. Catone, a registered nurse,
recalled that

N.C. was a healthy baby but in the winter of 2016 when he was just over a
year old, I noticed that N.C. always seemed to be sick with a cold and
occasional fevers but these symptoms almost always came shortly after
visiting the pediatrician for a well visit and vaccinations.

(Ex. 1, ¶ 7.) Mr. Catone echoed this observation.5 (Ex. 2, ¶ 5.)

On November 9, 2015, N.C. received a Pentacel vaccination, which includes
DTaP as well as polio and Hib. (Ex. 3, pp. 36-37, 55.) One week later, on November
16, 2015, he presented to his pediatrician with a 3-to-5-day history of a rash over his
face, back, chest, and abdomen, which was diagnosed as a “[r]ash and other
nonspecific skin eruption.” (Id. at 11-12.) The parties disagree as to whether N.C.’s
presentation was an adverse reaction to the Pentacel vaccination. (Compare ECF No.
85, p. 42 (petitioners citing Dr. Rostad as opining an adverse reaction occurred), with
ECF No. 92, pp. 2-3, 26-27 (respondent citing the medical record as containing no
suspicion of a vaccine reaction).) N.C. received the vaccination at issue in this case,
which was his fourth dose of DTaP, on April 25, 2017, during a well exam occurring at
about nineteen and a half months of age. (Ex. 3, pp. 54-56.) At that time there were no
complaints and N.C.’s physical exam was normal. (Id.)

Seventeen days following his DTaP vaccination, on the morning of May 12, 2017,
police and emergency medical services responded to the Catone home at 8:46 AM
regarding a report of a “20 month old baby who was reportedly unconscious and not
breathing.” (Ex. 6, p. 11; Ex. 9, p. 9.) Upon arrival, it was noted that N.C. was “not

5
Notably, this specific statement and several other observations are included in both affidavits verbatim.
(See Exs. 1-2.) While this fact alone does not lead me to conclude that these statements are untruthful, it
does significantly undercut any notion that that these affidavits present two independent recollections.

7
breathing, was cold to the touch, and was clearly deceased.” (Ex. 6, p. 11.) His skin
was observed to be cyanotic. (Ex. 9, p. 9.) At that time, Mrs. Catone was holding N.C.
in the living room; however, the police secured N.C.’s bedroom pending investigation.
(Id.; Ex. 6, p. 11.) Police scene photographs show that N.C. slept in a crib. (Ex. 11.)
Mr. and Mrs. Catone provided accounts indicating that N.C. had been placed in his crib
at around 7:30 PM or 8:30 PM. (Ex. 6, p. 11; Ex. 9, p. 9.) Mr. Catone recalled hearing
N.C. fussing (sneezing and coughing) between 11:00 PM and 11:30 PM, which was the
last activity heard. (Id.) The next morning, Mrs. Catone discovered N.C. lying face
down in his crib, not breathing, and cold to the touch, and immediately called 911. (Ex.
6, p. 11.) The family reported that N.C. “had a normal day the previous day” and that
“they did not notice anything suspicious or out of the ordinary.” (Ex. 9, p. 9.) N.C. was
officially pronounced dead as of 9:08 AM based on the medic’s consultation with Dr.
Azubuine of Newark Beth Isreal Hospital. (Id.; Ex. 6, p. 11.)

Later in the day on May 12, Mrs. Catone spoke with N.C.’s pediatrician. (Ex. 10,
p. 69.) The pediatrician recorded the following history as provided by Mrs. Catone:

She said that [N.C.] has been running fever with no other s/sx, since the
weekend (May 5/6? around 102 temp- no ER visits/office visits or phone
calls done)) and she was about to bring him in last Monday (5/8) if it persists.
Monday came and [N.C.] was doing well and was afebrile and so no visit
was done . . . Today she discovered him in his crib around 8:30 not
breathing, stiff and purplish (on prone).

(Id.)

However, in her affidavit prepared for this case in May of 2019, Mrs. Catone
indicated that N.C. developed a rash and cold symptoms within 24 hours of his April 25,
2017 vaccination, noting it to be “probably the worst cold I had seen him have.” (Ex. 1,
¶ 8.) She recalled he was “coughing and had an on and off runny nose but there was a
lot of nasal discharge.” (Id.) Mrs. Catone did not indicate when these symptoms
resolved. (See id.) However, she further recalled, consistent with the
contemporaneous account above, that on Sunday, May 7, 2017, N.C. was lethargic and
ran a fever of up to 103.9 Fahrenheit. (Id. ¶ 9.) She indicated that “he had never before
seemed this lethargic.” (Id.) While it is unclear from the affidavits alone whether N.C.’s
symptoms occurring 24 hours post-vaccination and his symptoms occurring on May 7
were one continuous illness or two distinct events, the more contemporaneous account
to N.C.’s pediatrician clearly indicates that N.C. had been sick “since” the weekend prior
to his death and that his febrile illness did not include any other significant symptoms.
(Ex. 10, p. 69.) Moreover, although Mrs. Catone did not specify when any of the earlier
symptoms resolved, Mr. Catone did specifically recall that the rash lasted only “a day or
so.” (Ex. 2, ¶ 7.) Thus, the record as a whole favors the conclusion that the symptoms
N.C. reportedly experienced post-vaccination resolved and did not persist up to the time
of his later May 7 illness.

8
Mrs. Catone recalled being out running errands on May 7, 2017. (Ex. 1, ¶ 10.)
Accordingly, Mr. Catone was with N.C. that afternoon. Mr. Catone recalled in his May
2019 affidavit that

N.C. napped that day and when he woke up from his nap he was still
feverish. After his nap I was playing quietly with him on the bed and reading
him a book. As I was reading to him, N.C. rolled over, closed his eyes and
fell asleep in an unusual manner.

(Ex. 2, ¶ 10.) Both Mr. and Mrs. Catone recalled that he called her, and they agreed it
was not normal. (Id.; Ex. 1, ¶ 10.) Mrs. Catone told Mr. Catone to wake N.C. up (Ex. 1,
¶ 10), following which Mr. Catone recalled

I tried to wake N.C. I shook his arm for a few seconds calling his name
trying to wake him and he wasn’t waking up. I remember feeling like my
heart stopped in my chest and then a few seconds later he finally opened
his eyes. It really scared me.

(Ex. 2, ¶ 10.) Thereafter, Mrs. Catone recalled giving N.C. Tylenol when she returned
home, which broke his fever, and both Mr. and Mrs. Catone recalled that he seemed
“fine and well” by the next day, though Mrs. Catone additionally recalled that he threw
up during the morning. (Id. ¶ 11; Ex. 1, ¶¶ 11-12.)

N.C.’s autopsy was performed by Dr. Ian C. Hood on May 12, 2017. (Ex. 5.) Dr.
Hood’s summary indicated that N.C. “had experienced 24 hours of a mild febrile illness
a few days before his death, but had been in his vigorous normal state of health
thereafter and was throughout the day he was last known alive.” (Id. at 16.) He noted
that N.C. was found “obviously deceased with the early onset of rigor mortis in his crib
with his buttocks raised and his head turned to one side and no evidence of obstruction
of the airway although two blankets and three stuffed toys were found in the crib with
him.” (Id.) Dr. Hood explained:

Autopsy disclosed a robust and apparently well nourished and well cared
for male child of at least 50th percentile development in all his growth
categories; no significant injuries, skin lesions or anomalies; visceral
congestion and mild pulmonary edema; a mildly swollen and somewhat
“dusky” brain, but no intracranial hemorrhage. No other significant trauma
or pathology was noted in or about the body and there were no significant
findings on toxicologic, histologic, metabolic or microbiologic studies and
death is attributed to sudden unexplained death, presumably from some
mechanism such as a sudden cardiac dysrhythmia on the basis of a
congenital conduction defect or “channelopathy” as is responsible for long
QT syndrome.

(Id.) The official cause of death was listed as “sudden unexplained death” and the
manner of death “natural.” (Id. at 16, 36.) A Sudden Unexplained Infant Death

9
Investigation (“SUIDI”) Reporting Form was completed. (Id. at 26-33.) It indicates that
Mrs. Catone noted that in the 72 hours prior to death, N.C. had a fever but marked “no”
for “lethargy or sleeping more than usual.” (Id. at 29.)

The autopsy originally resulted in the creation of three glass slides of stained
tissue in May of 2017. (Ex. 18, p. 2.) However, an additional 19 slides were later
created in April of 2019. (Id.) Further, four additional paraffin blocks of brain tissue
were preserved. (Id.) Five cassettes of brain tissue fixed in formalin were also created.
(Id.) Both parties’ pathology experts have confirmed that they reviewed all of this
material.6 (Id.; Ex. E, p. 2.)

N.C. was enrolled in a study by the SUDC Registry and Research Collaborative
(“SUDCRRC”).7 (Ex. 5, pp. 85-88; Ex. 15.) As part of the SUDCRRC study, whole
exome sequencing determined that N.C. did not have any genetic variants clinically
significant to SUDC. (Ex. 5, p. 85.) Additionally, a family interview was conducted on
October 12, 2017. (Ex. 15, p. 3.) In that interview, Mrs. Catone explained that in the
“two weeks to 72 hours” prior to death, N.C.

experienced a fever, cold symptoms, and took medications, which included
one dose of Tylenol and one dose of Motrin. [N.C.] reportedly had no
symptoms in his last 72 hours. [Mrs. Catone] described [N.C.’s] overall
health and demeanor during his last 48 hours as: “He was fine with not one
problem. Happy, healthy, and eating well. Normal self. Playful in the nice
weather at the boardwalk.”

(Id.)

In September of 2019, the Catones commissioned an analysis of N.C.’s
postmortem tissue samples by “Nanodiagnostics srl,” a consulting firm. (Ex. 16.) A
report was authored by Dr. Antonietta M. Gatti and Dr. Stefano Montanari. (Id. at 1.)
Nanodiagnostics srl indicates that “[i]ts main activity is detecting inorganic micro- and
nano-particles in any medium (biological tissues, food, drugs, cosmetics, environmental
samples, garments, etc.), through an innovative system of environmental scanning-
electron microscopy.” (Id. at 3.) Neither the authors’ credentials, nor the literature cited

6
However, the parties’ experts have raised a question as to how many slides the SUDCRRC, discussed
below, had reviewed. (E.g., Ex. E, p. 4; Ex. 19, p. 3.) Additionally, petitioners’ pathology expert raised an
issue as to the failure of SUDCRRC and respondent’s expert, Dr. Harris, to review gross autopsy photos.
(Ex. 19, p. 3.) However, Dr. Harris asserted that gross autopsy photos would not have changed his
opinion. (Ex. 15, p. 5; Ex. H, p. 2.)
7
SUDCRRC analyzes cases of sudden unexpected death in children to identify and understand risk
factors and causes, and to develop preventative measures. (Ex. 15, p. 1.) SUDCRRC reviews available
records, conducts a family interview, reviews the death investigation, and performs genetic analyses and
special studies. (Id.) The purpose of SUDCRRC is “to increase the understanding of the characteristics,
circumstances, medical histories, and pathologies of children who have died suddenly and unexpectedly,
and in some instances, without explanation.” (Id.)

10
in the report, have been introduced into the record of this case.8 The Catones provided
Nanodiagnostics srl three tissue samples preserved in paraffin by the medical examiner,
though only two were examined, one sample of brain tissue and one sample of brain
tissue with pancreatic tissue. (Id. at 4, 82, 86.)

After examining the tissue samples using an electron microscope,
Nanodiagnostics srl concluded that the tissue

revealed the presence of numerous foreign bodies of obvious exogenous
origin. A few of them had a micrometric size, others a sub-micrometric (in
the size range of nanoparticles). Some debris were trapped in a reaction
biological tissue that contains only Carbon, Oxygen Sodium, Phosphorus
and Sulfur. Other elements do not belong to the human organism and are,
therefore, exogenous.

(Ex. 16, p. 86.) They further remarked that “[w]hat was rather unexpected was finding
such a great quantity of foreign bodies in the brain and in the pancreas.”9 (Id. at 87.)

8
The report includes a reference list of 49 publications. (Ex. 16, pp. 90-94.) A single publication from
that bibliography by Gatti and Montanari was filed in connection with Dr. Rostad’s first supplemental
report. (Antonietta M. Gatti & Stefano Montanari, New Quality-Control Investigations on Vaccines: Micro-
and Nanocontamination, 4 INT’L J. VACCINES & VACCINATION 72 (2017) (Ex. 19, Tab J).) However, as was
noted by another special master in a prior case, this particular paper “just provided a hypothesis with no
evidentiary support.” C.N. ex rel. Dinh v. Sec’y of Health & Human Servs., No. 16-171V, 2022 WL
730258, at *4, *8 (Fed. Cl. Spec. Mstr. Feb. 14, 2022).
9
It should also be noted that the report authors do purport to reach the conclusion that N.C.’s death was
caused by his vaccination. The authors indicate that their finding “needs an explanation.” (Ex. 16, p. 88.)
Although inhalation and absorption through the lungs would be the “usual” explanation for such findings,
the authors hypothesize without any supporting citation that injection is a more likely explanation given
N.C.’s age and, further, that N.C. had only had vaccine injections throughout his life. (Id. at 87-88.) The
authors then suggest that vaccines are known to contain contaminants, though, again, the accompanying
citations have not been submitted into evidence. (Id. at 88.) Citing statistics relative to payments made
by the UK Vaccine Damage Payment Act of 1979 as well as following the introduction of the DPT vaccine
to Guinea-Bissau in 1981, the authors infer an increased risk of death following these vaccinations. (Id.
at 89.) Accordingly, they conclude that “[t]he pieces of evidence described in this pathological case are a
proof of a brain contamination and that that is incompatible with life and that the phenomenon is not rare.”
(Id.) This explanation is not persuasive on its face and, especially given the lack of evidence regarding
the authors’ credentials and the unavailability of the supporting citations, I do not have sufficient evidence
to conclude that the scientific/medical opinion rendered in this report was sound and reliable. Of
particular note, this opinion cites the safety profile of the earlier whole cell pertussis vaccine (“DPT”) as
evidence regarding the later acellular pertussis vaccine (“DTaP”), which is what is at issue in this case. In
the Althen prong one analysis below, I explain that this is not sound and reliable. After respondent’s
expert (Dr. McCusker) criticized the nanodiagnostics srl report, petitioner’s expert (Dr. Rostad) conceded
that “I am limited in my responses to Dr. McCusker’s concerns, since I have no special expertise in this
area, nor the research performed by Nanodiagnostics.” (Ex. 19, p. 24.) Dr. Rostad stated that “I cannot
begin to completely defend the analysis” of the nanodiagnostics report and that “[w]ith regards to potential
damage of these proposed contaminants to the CNS in N.C., no one knows this answer.” (Id.)
Accordingly, the nanodiagnostics srl report need not be discussed further.

11
On June 1, 2020, SUDCRRC produced a case review report for N.C. (Ex. 15.) It
indicated that:

Based on their review of the available information, the forensic pathologists
consider the significant findings in [N.C.’s] investigation to be: 1) No
significant anatomic abnormalities, 2) history of recent illness[,] 3) pattern
of facial pallor suggestive of face-down position, and 4) presence of only
alpha-hemolytic Streptococcus pneumoniae in both blood and lung cultures
(not mixed flora). While these could both be postmortem contaminants, a
possible underlying bacterial infection (S. pneumoniae) is possible.

(Id. at 6.) Thus, they indicate that “[i]t is the opinion of the reviewers that these findings
– inclusive of the genetic analysis performed by SUDCRRC, the complete case
information, and medical records made available to the reviewers – do not identify a
specific cause of death with a high level of probability.” (Id.)

Much later, in a May 20, 2023 “supplement” to his original report, Dr. Hood added
the following:

Since this autopsy nearly 6 years ago the case has been reviewed as a
possible vaccine related injury and several expert reports have been
provided to me as well as neuropathology review of the brain histology
slides and the further information that the child may have had an “absence”
attack or minor seizure in the presence of his father a few days before his
death. All lung lobes were histologically sampled with no pneumonitis
identified and staphylococcus is a common postmortem contaminant.
Neuropathological examination found no encephalitis but some histological
changes in the hippocampus of not yet established significance and they
may have made the child’s brain more susceptible to exhibiting seizure
activity. The brain was swollen and “dusky” in appearance which is not a
postmortem phenomenon and would be in keeping with a terminal seizure
but can result from almost any form of terminal hypoxia and the most I can
opine is that if [N.C.] had a terminal seizure his autopsy findings would be
just as were present in this case. Whether his immunizations contributed in
some way to causing such a postulated terminal seizure is beyond my area
of expertise.

(Ex. 24, p. 5.)

There are reports of a family history of febrile seizures, experienced by N.C.’s
older sister. (Ex. 3, p. 1; Ex. 15, p. 3; Ex. 19, p. 11, n.1.)

12
IV. Summary of Expert Opinions

a. Petitioners’ experts

i. Pathologist Steven Rostad, M.D.10

Dr. Rostad submitted four reports on petitioners’ behalf along with a set of
annotated autopsy photos.11 (Exs. 18, 19, 22-23, 25.) In his first report, Dr. Rostad
indicated he is satisfied that N.C.’s autopsy was of “adequate quality” and after review
of the investigative materials, autopsy slides, and test results, he agreed with the
medical examiner’s conclusion that the best classification for N.C.’s death would be
“sudden unexplained death,” specifically SUDC. (Ex. 18, p. 8.) However, he does raise
some differences from Dr. Hood in his own interpretation of the evidence.12 (Id. at 8-
13.)

10
Dr. Rostad earned his medical degree from the University of Washington in Seattle in 1983. (Ex. 17, p.
1.) He completed his internship in pathology at the University of Colorado in Denver in 1984. (Id.) After
the conclusion of his internship, Dr. Rostad returned to the University of Washington in Seattle, where he
completed a fellowship in neuropathology in 1986. (Id.) Thereafter, Dr. Rostad completed a residency in
anatomic pathology and served a term as chief resident from 1987 through 1988. (Id.) Dr. Rostad
became board-certified in anatomic pathology and neuropathology in 1988 and maintained his license to
practice medicine in Washington. (Id. at 3.) From 1988 to 2017, Dr. Rostad was employed as a staff
pathologist at CellNetix Pathology PLLC and as an attending pathologist and neuropathologist at Swedish
Medical Center in Seattle. (Id. at 1.) In addition, Dr. Rostad served as a clinical associate professor of
pathology at the University of Washington School of Medicine from 1990 to 2015. (Id.) During his thirty
years of practice, Dr. Rostad reviewed more than 70,000 cases microscopically representing surgical,
autopsy, cytologic, forensic, medical-legal, and pediatric specialties. (Ex. 18, p. 1.) He has published
over thirty peer-reviewed journal articles, including articles on topics relating to adult epilepsy. (Id.; Ex.
17, pp. 3-6.)
11
Dr. Rostad’s reports are very long, including lengthy rebuttal to respondent’s experts. His first report
was 36 pages. (See Ex. 18.) His second report was 43 pages. (See Ex. 19.) And his third report was
27 pages. (See Ex. 22.) Because the length of these reports leaves a complete summary impractical,
this summary emphasizes Dr. Rostad’s primary contentions in preference to his rebuttal, though I have
reviewed and considered each report in full. Exhibit 23 additionally includes five photographs of N.C.’s
brain, both within the skull and after being sectioned. Although I have reviewed the annotated photos, it
is not practical to attempt to describe the photographs and the many notations added by Dr. Rostad. (Ex.
23.) Suffice it to say that Dr. Rostad views the photographs as supportive of his interpretation of the
pathology as otherwise explained in his reports.
12
Additionally, Dr. Rostad was critical of the SUDCRRC report. (Ex. 18, p. 14; Ex. 19, p. 4; Ex. 22.)
These critiques make up a significant portion of Dr. Rostad’s reports. In discussing the SUDCRRC
findings, Dr. Rostad raised several questions with respect to what evidence was reviewed before
concluding that “the SUDCRRC pathology panel review was incomplete and therefore irrelevant for
consideration in this matter. I suspect that upon review of these materials, as well as more detailed
analysis of the information provided above, their conclusions would have been more coincident with
mine.” (Ex. 18, p. 14.) However, the SUDCRRC’s ultimate conclusion was that N.C.’s death was an
unexplained sudden death, and that the manner of death was undetermined. (Ex. 15, p. 6.) Even after
accounting for Dr. Rostad’s specific criticisms, it is difficult to see how he can reasonably fault the
SUDCRRC report for reaching the same ultimate view that he did. As noted above, Dr. Rostad stated
that “[a]fter review of the investigative scene report, scene photos and the autopsy slides supplementary
tests, I agree with Dr. Hood that the best initial classification of N.C.’s death would be sudden
unexplained death.” (Ex. 18, p. 8 (citing Ex. 5, p. 37).) Moreover, while Dr. Rostad also proposed a

13
In summary, Dr. Rostad listed twelve anatomic diagnoses based on his review:

1. Cerebral edema with tonsillar and uncal herniation.
2. Hippocampal formation abnormalities (dentate gyrus (“DG”)
malformations) including focal bilamination of DG, ectopic DG cells,
irregular thickening, hyperconvolution of DG[.]
3. Heavy lungs with diffuse pulmonary edema and vascular congestion.
a. [P]atchy mild infiltrates of lymphocytes and histiocytes involving
interstitium and terminal bronchioles.
4. Splenomegaly.
5. Hepatomegaly.
6. Diffuse vascular congestion, most organs, including brain and spinal
cord[.]
7. Focal mild dropout of Purkinje cells, cerebellum.
8. Foci of acute hemorrhage, dura.
9. Increased weight of thymus.
10. Focal lymphohistiocytic infiltrates of prostate.
11. Petechiae on the inferior surface of thymus.
12. Toxicology, metabolic screen, microbiologic cultures, whole exome
sequencing for 200 genes associated with sudden and unexpected
death show no significant findings.

(Id. at 12-13.)

Based on these findings, Dr. Rostad opined that the cause of N.C.’s death was
cerebral edema with tonsillar and uncal herniation resulting from a suspected seizure,
with a hippocampal malformation also significantly contributing. (Ex. 18, p. 13.) In his
second and third reports, Dr. Rostad addressed at length his disagreements with Dr.

specific cause of death, it is apparent that he does not view his own explanation of N.C.’s death as being
mutually exclusive of the SUDC categorization. In fact, Dr. Rostad stated that “N.C.’s death overlaps with
the description of sudden unexpected death in epilepsy (SUDEP), except N.C. had no history of epilepsy-
like symptoms and no evidence of genetic abnormalities related to epilepsy.” (Id. at 21.) Accordingly,
while all competing evidence must be weighed, Dr. Rostad is not persuasive in contending that the
SUDCRRC report is either suspect or irrelevant. Dr. Rostad has no personal knowledge regarding the
details of the SUDCRRC investigation and his assertion that, had the SUDCRRC conducted a different
investigation, they would have reached a conclusion similar to his, is speculative. Accord Anklam v.
Sec’y of Health & Human Servs., No.17-2061V, 2023 WL 8890662, at *17 (Fed. Cl. Spec. Mstr. Nov. 29,
2023) (petitioner’s pathology expert acknowledging that he cannot explain how the SUDCRRC reached
their findings without knowing the neuropathologist and what he reviewed.) Indeed, some of Dr. Rostad’s
specific criticisms fail to raise any reasonable point of disagreement. For example, in his third report, Dr.
Rostad criticized the SUDCRRC pathologist for relying on Dr. Hood’s autopsy report for the conclusion
that there was facial pallor suggestive of a face-down position, regarding this to be “poor practice of
pathology.” (Ex. 22, p. 14 (citing Ex. 15, p. 6).) Yet in the same report, Dr. Rostad acknowledged that the
SUDCRRC report reasonably explained that the “sheriff’s office refused the release of their death scene
investigations report and photos for our review.” (Id. at 14-15 (quoting Ex. 15, p. 5).) But, in any event,
despite stressing this limitation, Dr. Rostad never disputed the finding that N.C. had been in a face-down
position.

14
Harris, respondent’s pathology expert, regarding the presence of cerebral edema and
herniation. (Ex. 19, pp. 6-9; Ex. 22, pp. 7-12.) In his autopsy photo annotations, he
further drew attention to his findings relating to the flattening of the gyri, compression of
cerebral sulci due to edema, and herniation of the cerebellar tonsils and unci. (Ex. 23.)

Dr. Rostad explained:

The swelling and herniation of N.C.’s brain would be expected to contribute
to dysfunction of the heart and lungs with resultant cardiopulmonary arrest.
The documentation for these pathologic processes is challenging given the
absence of a witness and N.C.’s inability to express detailed clinical
symptoms. Several studies have raised whether febrile seizures may be
associated with some cases of SUDC and SIDS. A recent report of a 20-
month-old with prior febrile status epilepticus who died 2 days after her
seizure with diffuse cerebral suppressions and severe bradycardia, suggest
a mechanism of death like SUDEP. Another child with a history of febrile
seizures, died suddenly and unexpectedly after a suspected seizure. As for
N.C., although one could implicate the [hippocampal formation]
malformation or febrile seizure as the cause of a fatal seizure (and death),
as has been suggested by other studies, I argue that DTaP vaccination N.C.
received on April 25, 2017, initiated the chain of events that led directly and
inevitably to his untimely death.

(Ex. 18, p. 21 (internal citations omitted) (citing 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) (Ex. 18, Tab DDD);
Hannah C. Kinney et al., Witnessed Sleep-Related Seizure and Sudden Unexpected
Death in Infancy: A Case Report, 9 FORENSIC SCI., MED., & PATHOLOGY 418 (2013) (Ex.
18, Tab EEE); Kenneth A. Myers et al., Sudden Death After Febrile Seizure Case
Report: Cerebral Suppression Precedes Severe Bradycardia, 140 PEDIATRICS 1 (2017)
(Ex. 18, Tab FFF); 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) (Ex. 18, Tab GGG)).)

Dr. Rostad opined that the hippocampal formation maldevelopment he identified
would have lowered N.C.’s seizure threshold. (Ex. 18, pp. 24-25.) Citing studies by
Kinney et al. and Hefti et al., he opined that

[t]hese studies suggested that [hippocampal formation] malformation
represented a marker of an impaired forebrain/limbic network that increases
the risk of sudden death due to potential brainstem cardiorespiratory related
circuits nuclei, or to a subclinical seizure in an infant predisposed to
epilepsy. The association of epilepsy-related pathology (such as
[hippocampal formation] maldevelopment) with SIDS, SUDEP and SUDC
leads to possible epilepsy-related mechanisms in sudden death.

15
(Id. at 25 (citing Hannah C. Kinney et al., Hippocampal Formation Maldevelopment and
Sudden Unexpected Death Across the Pediatric Age Spectrum, 75 J. NEUROPATHOLOGY
& EXPERIMENTAL NEUROLOGY 981 (2016) (Ex. 18, Tab XXX); Marco M. Hefti et al.,
Hippocampal Malformation Associated with Sudden Death in Early Childhood: A
Neuropathologic Study, 12 FORENSIC SCI., MED. & PATHOLOGY 14 (2016) (Ex. 13, Tab S)
(see also Ex. C, Tab 2)).) Further to this, Dr. Rostad opined that N.C. was in a critical
period of development wherein the maturing brain is more vulnerable to seizures. (Id. at
25-26 (citing Sanjay N. Rakhade & Frances E. Jensen, Epileptogenesis in the Immature
Brain: Emerging Mechanisms, 5 NATURE REVS. NEUROLOGY 380 (2009) (Ex. 18, Tab
V)).) Significantly, however, Dr. Rostad acknowledged that “only a subset of SIDS and
SUDC show these pathologic changes [of hippocampal malformation], so that not all
individuals would be affected. In other words, these population groups are not
homogeneous. In addition, individuals who are outside these groups, including
‘controls’ also may show these hippocampal changes.” (Ex. 19, p. 31.) Thus, while
positing that these findings counsel “less distinction between SIDS and SUDC, and
even SUDEP,” he agreed that present data does not allow for “adoption of a unified
hypothesis.” (Id.)

Notably, however, Dr. Rostad confirmed that he agrees that N.C. did not suffer
SUDEP as he did not have a history of epilepsy, even if he did have a witnessed
seizure. (Ex. 19, p. 10.) Although respondent’s experts stressed the absence of
evidence that a terminal seizure occurred, Dr. Rostad opined that specific signs of a
seizure may be absent or nonspecific. (Id. at 11.) In his final report, Dr. Rostad further
opined regarding a study in the journal Neurology by Gould et al. (Ex. 25 (discussing
Laura Gould et al., Video Analyses of Sudden Unexplained Death in Toddlers, 102
NEUROLOGY e208038 (2024) (Ex. 25, Tab 1) (see also Ex. J, Tab 1)).) In this final
report, Dr. Rostad firmly placed petitioners’ theory of causation within the SIDS/SUDC
context. (Id.) Discussing the risk factors that have been identified in SIDS/SUDC, he
explained that

a history of febrile seizures is noted in 30% of the children who suffered
from an unexplained death, a significant increase over the controls in the
studies. Another identified risk factor identified through these studies
includes children who have malformations in the hippocampi in the brain.
These risk factors can lower a child’s threshold for suffering a seizure. When
a child has these risk factors and another internal or external stimulus is
applied, a terminal seizure can result.

(Id. at 1.)

According to Dr. Rostad, the study by Gould et al. adds “strong evidence” that
convulsive seizures are a cause of deaths in infants and toddlers that may otherwise be
considered either unexplained or sleep-related deaths. (Ex. 25, p. 1.) The Gould et al.
study reviewed crib camera footage that was available for seven out of 301 children that
had been enrolled in the SUDCRRC. (Ex. 25, p. 2 (discussing Gould et al., supra, at
Ex. 25, Tab 1).) The study found that six cases had suggestive or definite convulsive

16
movements before death, suggesting that terminal seizures may be much more
common than previously believed. (Id. at 2-3 (citing Gould et al., supra, at Ex. 25, Tab
1, p. 6).) He explained that “[t]his article is extremely relevant to the instant case as it is
directly on point with Petitioner’s proposed medical theory that N.C. more likely than not
suffered from a terminal seizure and therefore, his death is not unexplained. The
question turns on whether the DTaP vaccine N.C. received caused or contributed to this
terminal seizure.” (Id. at 3.)

Given the likelihood of contamination and a lack of a substantial acute
inflammatory response as expected in pneumonia, Dr. Rostad opined that S.
pneumoniae infection is “highly unlikely.” (Ex. 18, p. 14.) However, he did otherwise
opine that N.C. was suffering a viral upper respiratory infection in the several days prior
to his death, beginning on May 7, 2017. (Id. at 16-17.) Dr. Rostad opined that onset of
an upper respiratory infection “amplified” N.C.’s ongoing cytokine response to his prior
vaccination. (Id. at 16.) He proposed that the episode described by Mr. Catone
occurring on May 7 likely represented an atonic seizure, which he attributed to either
N.C.’s high fever or the cytokine elevation initially due to the DTaP vaccination.13 (Id. at
16-17.) Thus, he hypothesized that “[t]his same phenomenon of cytokine elevation and
neuronal excitation is the most likely trigger for the final proposed seizure which likely
occurred on May 12, 2017.” (Id. at 17.) Dr. Rostad cited a number of papers14 for the
13
Dr. Rostad acknowledged that febrile seizures are typically tonic-clonic but suggested that atonic
seizures have also been reported. (Ex. 18, p. 16 (citing Alexander K.C. Leung et al., Febrile Seizures:
An Overview, 7 DRUGS CONTEXT 1 (2018) (Ex. 18, Tab L)).)
14
Specifically: Nina Dupuis & Stéphane Auvin, Inflammation and Epilepsy in the Developing Brain:
Clinical and Experimental Evidence, 21 CNS NEUROSCIENCE & THERAPEUTICS 141 (2015) (Ex. 18, Tab R);
Luca Bartolini et al., Viral Triggers and Inflammatory Mechanisms in Pedatric Epilepsy, 56 MOLECULAR
NEUROBIOLOGY 1897 (2019) (Ex. 18, Tab S); Karen S. Wilcox & Annamaria Vezzani, Does Brain
Inflammation Mediate Pathological Outcomes in Epilepsy?, 813 ADVANCES EXPERIMENTAL MED. & BIOLOGY
169 (2014) (Ex. 18, Tab T); Amna Rana & Alberto E. Musto, The Role of Inflammation in the
Development of Epilepsy, 15 J. NEUROINFLAMMATION 144 (2018) (Ex. 18, Tab U); Sanjay N. Rakhade &
Frances E. Jensen, Epileptogeneis in the Immature Brain: Emerging Mechanisms, 5 NATURE REVS.
NEUROLOGY 380 (2009) (Ex. 18, Tab V); Giovanna Vitaliti et al., Molecular Mechanisms Involved in the
Pathogenesis of Early Onset Epileptic Encephalopathy, 12 FRONTIERS MOLECULAR NEUROSCIENCE 1
(2019) (Ex. 18, Tab W); Pavanish Kumar et al., Proinflammatory IL-17 Pathways Dominate the
Architecture of the Immunome in Pediatric Refractory Epilepsy, 4 JCI INSIGHT 1 (2019) (Ex. 18, Tab Y);
R.S. Rao et al., Role of Different Cytokines and Seizure Susceptibility: A New Dimension Towards
Epilepsy Research, 47 INDIAN J. EXPERIMENTAL BIOLOGY 625 (2009) (Ex. 18, Tab Z); Fatma Mujgan
Sonmez et al., Blood Levels of Cytokines in Children with Idiopathic Partial and Generalized Epilepsy, 22
SEIZURE 517 (2013) (Ex. 18, Tab AA); Kavitha Kothur et al., Etiology is the Key Determinant of
Neuroinflammation in Epilepsy: Elevation of Cerebrospinal Fluid Cytokines and Chemokines in Febrile
Infection-Related Epilepsy Syndrome and Febrile Status Epilepticus, 60 EPILEPSIA 1678 (2019) (Ex. 18,
Tab BB); James G. Heida et al., The Role of Interleukin-1β in Febrile Seizures, 31 BRAIN DEV. 388 (2009)
(Ex. 18, Tab CC); James G. Heida & Quentin J. Pittman, Causal Links Between Brain Cytokines and
Experimental Febrile Convulsions in the Rat, 46 EPILEPSIA 1906 (2005) (Ex. 18, Tab DD); Bo Feng et al.,
Transient Increase of Interleukin-1β After Prolonged Febrile Seizures Promotes Adult Epileptogenesis
Through Long-Lasting Upregulating Endocannabinoid Signaling, 6 SCI. REPS. 1 (2016) (Ex. 18, Tab EE);
Adam L. Numis et al., Early Changes in Pro-Inflammatory Cytokine Levels in Neonates with
Encephalopathy are Associated with Remote Epilepsy, 86 PEDIATRIC RSCH. 616 (2019) (Ex. 18, Tab FF);
Aram Kwon et al., Cytokine Levels in Febrile Seizure Patients: A Systematic Review and Meta-Analysis,
59 SEIZURE 5 (2018) (Ex. 18, Tab GG); Hong-Mei Yu et al., IL-1β: An Important Cytokine Associated with

17
proposition that inflammatory mediators, including pro-inflammatory cytokines, can
incite seizures. (Id. at 17-20.) He also includes several citations for the proposition that
vaccines, and in particular whole cell pertussis vaccines, are known to cause seizures
and encephalopathy. 15 (Id. at 22.)

Dr. Rostad also, like Dr. Akbari (as discussed further below), cited cytokine
storms as evidence that uncontrolled cytokine responses can occur and can lead to
death. (Ex. 18, pp. 20-21.) He opined that the acute respiratory distress that
significantly contributed to mortality from Covid-19 may have been due to cytokine
storm and that “it is worth noting that the histopathologic findings are like those seen
with N.C.” (Id. (citing Farinaz Safavi & Avindra Nath, Silencing of Immune Activation
with Methotrexate in Patients with COVID-19, J. NEUROLOGICAL SCIS. 116942 (2020)
(Ex. 18, Tab SS); Yu-Ting Yen et al., Modeling the Early Events of Severe Acute
Respiratory Syndrome Coronavirus Infection In Vitro, 80 J. VIROLOGY 2684 (2006) (Ex.
18, Tab CCC)).) Dr. Rostad stressed that, whereas Dr. Harris appeared unconcerned
regarding findings relative to the thymus, liver, and spleen, Dr. Rostad felt the liver and
spleen were heavy and congested, qualifying as hepatomegaly and splenomegaly,
which he viewed as “a likely sign of a generalized reaction, perhaps to a seizure or
inflammation.” (Ex. 19, pp. 2-3.) Dr. Rostad confirmed that he viewed increased weight
of the liver, spleen, and thymus, as evidence of a generalized inflammatory reaction
consistent with a cytokine storm. (Ex. 22, p. 2.)

Febrile Seizures?, 28 NEUROSCIENCE BULL. 301 (2012) (Ex. 18, Tab HH); Kyungmin Kim et al., Analysis of
Plasma Multiplex Cytokines and Increased Level of IL-10 and Il-1Ra Cytokines in Febrile Seizures, 14 J.
NEUROINFLAMMATION 1 (2017) (Ex. 18, Tab II); Anne A. Kan et al., Prolonged Increase in Rat
Hippocampal Chemokine Signalling After Status Epilepticus, 245 J. NEUROIMMUNOLOGY 15 (2012) (Ex. 18,
Tab JJ); Jieun Choi et al., Increase Levels of HMGB1 and Pro-Inflammatory Cytokines in Children with
Febrile Seizures, 8 J. NEUROINFLAMMATION 1 (2011) (Ex. 18, Tab KK); Miia Virta et al., Increased Plasma
Levels of Pro- and Anti-inflammatory Cytokines in Patients with Febrile Seizures, 43 EPILEPSIA 920 (2002)
(Ex. 18, Tab LL); Nikola Šutulović et al., Glial Cells, Blood Brain Barrier and Cytokines in Seizures:
Implications for Therapeutic Modalities, 69 MEDICINSKI PODMLADAK 33 (208) (Ex. 18, Tab MM); Bridgette
D. Semple et al., Immune Challenges and Seizures: How Do Early Life Insults Influence
Epileptogenesis?, 11 FRONTIERS PHARMACOLOGY 1 (2020) (Ex. 18, Tab NN); Narges Karimi et al.,
Frequent Convulsive Seizures in an Adult Patient with COVID-19: A Case Report, 22 IRANIAN RED
CRESCENT MED. J. 1 (2020) (Ex. 18, Tab OO); Dominik Kobylarek et al., Advances in the Potential
Biomarkers of Epilepsy, 10 FRONTIERS NEUROLOGY 1 (2019) (Ex. 18, Tab PP).
15
Specifically: Jennifer Tam et al., Review of Pediatric Encephalitis and Encephalopathy Cases
Following Immunization Reported to the Canadian Immunization Monitoring Program Active (IMPACT)
from 1992 to 2012, 38 VACCINE 4457 (2020) (Ex. 18, Tab JJJ); Marie R. Griffin et al., Risk of Seizure and
Encephalopathy After Immunization with the Diphtheria-Tetanus-Pertussis Vaccine, 263 JAMA 1641
(1990) (Ex. 18, Tab KKK); CTRS. FOR DISEASE CONTROL & PREVENTION, Prevention of Pertussis, Tetanus,
and Diphtheria with Vaccines in the United States: Recommendations of the Advisory Committee on
Immunization Practices (ACIP), 67 MORBIDITY & MORTALITY WEEKLY REP. 1 (2018) (Ex. 18, Tab LLL)
[hereinafter CDC Report]; Yuelian Sun et al., Risk of Febrile Seizures and Epilepsy After Vaccination with
Diphtheria, Tetanus, Acellular Pertussis, Inactivated Poliovirus, and Haemophilus Influenzae Type B, 307
JAMA 823 (2012) (Ex. 18, Tab MMM) (see also Ex. C, Tab 14); Pedro L. Moro et al., Safety Surveillance
of Diphtheria and Tetanus Toxoids and Acellular Pertussis (DTaP) Vaccines, 142 PEDIATRICS 1 (2018)
(Ex. 18, Tab NNN); Prescribing Information, DAPTACEL (Diphtheria and Tetanus Toxoids and Acellular
Pertussis Vaccine Adsorbed): Suspension for Intramuscular Injection [DAPTACEL Package Insert] (Ex.
18, Tab OOO).

18
Dr. Rostad also invoked the immune stimulant effect of aluminum containing
adjuvants. (Ex. 18, pp. 23-24.) He further discussed the nanodiagnostics srl findings of
multiple metals, including aluminum and silicon, as strengthening “[t]he linkage of
aluminum to N.C.’s potential seizure and ultimate death.” (Id. at 24.) However, he
ultimately concluded that any potential role for aluminum in the hypothesized seizures
“is not clear.” (Id.) Dr. Rostad purported to rebut Dr. McCusker’s opinion (discussed
below) as well as her criticisms of the nanodiagnostics srl report; however, he
acknowledged that “I am limited in my responses to Dr. McCusker’s concerns, since I
have no special expertise in this area, nor the research performed by Nanodiagnostics.”
(Ex. 19, p. 24.) Dr. Rostad stated that “I cannot begin to completely defend the
analysis” of the nanodiagnostics report and that “[w]ith regards to potential damage of
these proposed contaminants to the CNS in N.C., no one knows this answer.” (Id.)

ii. Immunologist Omid Akbari, Ph.D.16

Dr. Akbari presented three reports in this case. (Ex. 1317, Ex. 20, Ex. 21.) He
observed that cytokines are “key regulators of the inflammatory and immune
responses,” explaining that “the immune cells involved in the body’s immune response
need to communicate with each other. They do this by releasing a set of proteins that
serve as chemical messengers. These proteins, called cytokines, tell immune cells
what to do and also tell the body to produce more if needed.” (Ex. 13, p. 7.) Cytokines
can be blamed for triggering symptoms associated with inflammation, such as fever,
aches, or runny nose. (Id.) In some “severe cases,” the cytokine response can “grow
out of control.” (Id.) In such instances, chemokines, a subset of cytokines that recruit
immune cells to sites of inflammation, create a positive feedback loop called a “cytokine
storm.” (Id.) Cytokine storms begin locally but spread throughout the body, causing

16
Dr. Akbari earned his Ph.D. in cellular and molecular immunology in 1998 from the National Institute for
Medical Research in London. (ECF No. 28-48, p. 1.) Thereafter, he completed a postdoctoral fellowship
at Standford University in 2001. (Id.) Currently, Dr. Akbari serves as a Professor of Medicine and
Professor of Allergy and Immunology at the University of Southern California Keck School of Medicine.
(Id. at 2.) Additionally, he holds adjunct professorships at the University of California, Los Angeles David
Geffen School of Medicine’s Department of Pediatrics and Chiba University’s Department of Immunology
in Japan. (Id.; Ex. 13, p. 1.) Dr. Akbari’s research focuses on the role that immune cells play in inducing
autoimmune and allergic diseases. (Ex. 13, p. 1.) He serves as an associate editor and as a reviewer on
various journals. (Id. at 2.) He has authored or co-authored over eighty publications. (ECF No. 28-48,
pp. 9-15.)
17
Petitioners filed a medical journal article marked Exhibit 13, Tab O with Dr. Akbari’s initial report at
Exhibit 13. (ECF No. 28.) Petitioners’ exhibit list and Dr. Akbari’s bibliography identified the exhibit as the
following article: K. Helweg-Larsen & E. Garde, Sudden Natural Death in Childhood. A Review of
Forensic Autopsy Protocols in Cases of Sudden Death Between the Ages of One and Five Years, 1982-
1991, with a Special View to Sudden Unexplained Death, 82 ACTA PAEDIATRICA 975 (1993). (See Ex. 13,
p. 16; ECF No. 98-2, p. 3.) However, the medical literature actually filed by petitioners as Ex. 13, Tab O
is the following article: Ali Riza Tϋmer et al., Sudden Unexpected Child Deaths: Forensic Autopsy
Results in Cases of Sudden Deaths During a 5-Year Period, 51 J. TROPICAL PEDIATRICS 131 (2005). (See
Ex. 13, Tab O.) Within the copy of this article by Tϋmer et al., petitioners highlighted the text relevant to
Dr. Akbari’s report. (See id.) Accordingly, use of the Tϋmer article does not appear to have been
inadvertent and all citations to Exhibit 13, Tab O within this decision refer to the article by Tϋmer et al.

19
redness, swelling, edema, heat, pain, and loss of function. (Id.) Cytokine storms can
lead to organ damage, especially affecting the lungs and central nervous system, and
can be fatal. (Id.)

Cytokines can be activated by either infection or vaccination. (Ex. 13, p. 7.)
Citing a study by Kashiwagi et al., Dr. Akbari indicated that vaccination has been shown
to increase the following cytokines: IL-1β, IL-6, G-CSF, and TNF-α. (Id. at 12 (citing
Yasuyo Kashiwagi et al., Production of Inflammatory Cytokines in Response to
Diphtheria-Pertussis-Tetanus (DPT), Haemophilus Influenzae Type b (Hib), and 7-
Valent Pneumococcal (PCV7) Vaccines, 10 HUM. VACCINES & IMMUNOTHERAPEUTICS 677
(2014) (Ex. 13, Tab OO) (see also Ex. A, Tab 10)).) However, he indicated that “the
presence of antigen stimulation alone is not sufficient to trigger cytokine storm.” (Id.)
Instead, “activation of the innate immune system by adjuvants or microbial products is
necessary to break self-tolerance and cause reactions including autoimmunity.” (Id.
(citing Chiaki Fujimoto et al., Pertussis Toxin is Superior to TLR Ligands in Enhancing
Pathogenic Autoimmunity, Targeted at a Neo-Self Antigen, by Triggering Robust
Expansion of Th1 Cells and their Cytokine Production, 177 J. IMMUNOLOGY 6896 (2006)
(Ex. 13, Tab PP); Hanspeter Waldner et al., Activation of Antigen-Presenting Cells by
Microbial Products Breaks Self Tolerance and Induces Autoimmune Disease, 113 J.
CLINICAL INVESTIGATION 990 (2004) (Ex. 13, Tab QQ)).) Dr. Akbari posits that the initial
innate immune reaction led to the production of autoreactive T cells that “initiated an
adverse reaction that ultimately led to his untimely death.” (Id. at 10; Ex. 20, pp. 4-5.)
In particular, Dr. Akbari suggests that there is “sequence homology between
components of the DTaP vaccine and key biological proteins involved in regulating the
immune response” and that N.C.’s death resulted from an autoimmune reaction. (Ex.
20, pp. 4-5.) He also suggested that tetanus toxoid is known to bind to gangliosides
and neuronal cells. (Id. at 4.) Dr. Akbari opined that

it is more likely than not as well as biologically possible that N.C.’s immune
system produced autoreactive T cells or antibodies in response to the
administration of the DTaP vaccine he received on April 25, 2017 and that
these autoreactive immune cells initiated an adverse reaction that ultimately
lead to his untimely death on May 12, 2017.

(Id. at 5; Ex. 13, p. 10.) However, he is no more specific than to endorse Dr. Rostad’s
suggestion of a terminal seizure and state that cytokines trafficked across the blood
brain barrier had “neuropathological effects.” (Ex. 20, p. 5.)

Yet, despite invoking an autoimmune process to explain the 17-day latency in
this case, Dr. Akbari stressed that “[o]ne very important aspect of this case is the
evidence which supports the presence of febrile seizure in N.C.” (Ex. 20, p. 5.) He
explained that

[t]he role of cytokines in the induction of fever is very relevant to this case
and it is important to point out that although, in many cases innate cytokines

20
are able to cause fever and high temperature, recent data suggest that
these cytokines play an important but not obligatory role in fever induction.

(Ex. 21, p. 6 (citing Katarina Alheim et al., Hyperresponsive Febrile Reactions to
Interleukin (IL) 1α and IL-1β, and Altered Brain Cytokine mRNA and Serum Cytokine
Levels, in IL-1β-Deficient Mice, 94 PROCS. NAT’L ACAD. SCIS. 2681 (1997) (Ex. 21, Tab
10)).) In that regard, Dr. Akbari opined that N.C. had likely suffered a seizure on May 7,
2017. (Id. at 9.)

In addition to noting the tetanus toxoid molecules to be “antigenically complex
and capable of cross-reactivity,” Dr. Akbari implicated the aluminum adjuvant included
in the DTaP vaccine. (Ex. 13, pp. 10-12.) “Aluminum stimulates the innate immune
system at the site of injection by directly recruiting naïve immune cells to the site and
indirectly by activating the tissue resident macrophages to rapidly produce cytokines
and chemokines, also attracting other immune cells of the innate system to the area.”
(Id. at 11.) Additionally, he contended that aluminum adjuvants induce dendritic cells to
secrete IL-1β, which he asserted to be a “potent inflammatory cytokine” associated with
acute and chronic inflammatory disorders. (Id. (citing Mirjam Kool et al., Cutting Edge:
Alum Adjuvant Stimulates Inflammatory Dendritic Cells Through Activation of the
NALP3 Inflammasome, 181 J. IMMUNOLOGY 3755 (2008) (Ex. 13, Tab JJ)).)

Regarding the details of this case, Dr. Akbari opined as follows:

When N.C. received the DTaP vaccination on April 25, 2017, the vaccine
components, including the aluminum adjuvant, stimulated his immune
system and a local inflammatory immune reaction ensued. This is
evidenced by statements in the mother’s and father’s affidavits that “[w]ithin
24 hours of receiving this vaccine, N.C. developed a rash and symptoms of
another cold. This was a very bad cold, probably the worst cold I had seen
him have. N.C. was coughing and had an on and off runny nose but there
was a lot of nasal discharge” and “[w]ithin 24-48 hours after receiving the
vaccine, N.C. developed a rash that lasted for a day or so. He also
developed symptoms of a very bad cold. He was coughing and had an on
and off runny nose with lots of nasal discharge.” Initially a nonspecific
innate response would have been employed. This nonspecific response
has only recently become recognized for its role in initiation of inflammation.
Only recently has understanding of immune response by adjuvant been
advanced and there is no consensus regarding how aluminum-containing
adjuvants potentiate the immune system. However, recent research shows
that peripherally injected aluminum adjuvant nanoparticles engulfed by
macrophages actively spread throughout the body eventually crossing the
blood-brain-barrier (BBB) and blood-CSF barrier. Once in the CNS,
aluminum adjuvant nanoparticles incite deleterious inflammatory
responses, resulting in a range of neuropathological effects. It should be
noted that aluminum on its own can alter the properties of BBB, making the
brain more accessible to inflammatory and immune mediators. Aluminum

21
also increases endothelial adhesion of activated monocytes, which, in the
case of aluminum penetration in the CNS can likewise facilitate the entry of
immune-competent cells into the CNS and lead to adverse manifestations.

(Ex. 13, p. 11 (internal citations omitted) (citing Sunita Awate et al., Mechanisms of
Action of Adjuvants, 4 Frontiers Immunology 1 (2013) (Ex. 13, Tab CC); Zakir Khan et
al., Slow CCL2-Dependent Translocation of Biopersistent Particles from Muscle to
Brain, 11 BMC MED. 1 (2013) (Ex. 13, Tab DD); Michael S. Petrik et al., Aluminum
Adjuvant Linked to Gulf War Illness Induces Motor Neuron Death in Mice, 9
NEUROMOLECULAR MED. 83 (2007) (Ex. 13, Tab EE); Christopher A. Shaw & Michael S.
Petrik, Aluminum Hydroxide Injections Lead to Motor Deficits and Motor Neuron
Degeneration, 103 J. INORGANIC BIOCHEMISTRY 1 (2009) (Ex. 13, Tab FF); William A.
Banks & Abba J. Kastin, Aluminum-Induced Neurotoxicity: Alterations in Membrane
Function at the Blood-Brain Barrier, 13 NEUROSCIENCE & BIOBEHAVIORAL REVS. 47 (1989)
(Ex.13, Tab GG); Robert A. Yokel, Blood-Brain Barrier Flux of Aluminum Manganese,
Iron and Other Metals Suspected to Contribute to Metal-Induced Neurodegeneration, 10
J. ALZHEIMER’S DISEASE 223 (2006) (Ex. 13, Tab HH); Elizabeth Oesterling et al.,
Alumina Nanoparticles Induce Expression of Endothelial Cell Adhesion Molecules, 178
TOXICOLOGY LETTERS 160 (2008) (Ex. 13, Tab II)).)

Dr. Abkari suggested that generally “cytokine storm after initial immunization
reaches to the highest levels in 1-3 days.” (Ex. 13, p. 13.) However, he asserted that
“large quantities of cytokine[s]” sufficient to cause death in individuals susceptible to
febrile seizure, can be detected “for many weeks” after a booster vaccination. (Id.) In
particular, Dr. Akbari indicated that pro-inflammatory cytokines, specifically IFN-γ and
IL-13, are “strongly upregulated” for as much as two weeks following a DTaP booster
vaccination. (Id. (citing Saskia van der Lee et al., Robust Humoral & Cellular Immune
Responses to Pertussis in Adults After a First Acellular Booster Vaccination, 9
FRONTIERS IMMUNOLOGY 1 (2018) (Ex. 13, Tab RR)).) Moreover, he asserted that a
mouse model study by Bairwa et al. demonstrated that proinflammatory cytokines,
including IL-6 and TNF-α, can cross the blood brain barrier to affect central nervous
system function. (Ex. 21, pp. 3-4 (discussing S.C. Bairwa et al., Cytokines Profile in
Neonatal and Adult Wild-Type Mice Post-Injection of U.S. Pediatric Vaccination
Schedule, 15 BRAIN, BEHAV., & IMMUNITY - HEALTH 1 (2021) (Ex. 21, Tab 2)).)

In his initial conclusion, Dr. Akbari described three potential explanations for
N.C.’s death, all three of which are cytokine-mediated: (1) “cytokines stimulated by mild
infection and subsequent immunization accompanied with abnormal development of
[the] ventral medulla fits well with occurrence of SUDC in minor N.C.”; or (2) in a
susceptible person, such as N.C., having “received several doses of aluminum based
adjuvants, immune responses are more likely triggered to produce higher amounts of
cytokines capable of causing cytokine storm and eventually caused death”; or (3)
“cytokines as [a] result of immunization, in a susceptible host such as N.C. with
abnormal development of the ventral medulla and family history of febrile seizures, may
directly suppress the medullary system, leading to death.” (Ex. 13, p. 14.) However,
after Dr. McCusker challenged Dr. Akbari regarding the nature of cytokine storms, he

22
disclaimed per se reliance on the concept in his second report. (Ex. 20, pp. 2-3.) He
suggested that Dr. McCusker’s view of cytokine storms is “myopic” and indicated that

I am not suggesting that N.C. succumbed to a cytokine storm following a
massive and systemic infection, rather, I am positing that N.C. suffered from
an initial reaction to the DTaP immunization wherein cytokines were
induced . . . The cytokines circulated throughout N.C.’s body, damaging
local tissue structures. Over the next two weeks, active and passive
regulatory systems in N.C.’s body worked to try and heal his body from the
stimulation of these cytokines, however, due to his dysregulated immune
system he was not able to overcome the damage to his tissues and organs.

(Id. at 3.)

b. Respondent’s experts

i. Pathologist Brent Harris, M.D., Ph.D.18

Dr. Harris submitted two reports on respondent’s behalf. (Exs. E, H.) He
concluded that “I mostly concur with [the] medical examiner and SUDCRRC
neuropathologist reviewer that found no significant structural abnormalities in the brain.
My opinion would differ only [in] that I recognize some mild, subtle changes in the
hippocampus, changes that have been reported in the SUDC literature.” (Ex. E, p. 5
(citing 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)
(Ex. E, Tab 2) (see also Ex. 18, Tab F)).) However, Dr. Harris stressed that this
literature indicates that about half of SUDC cases remain unexplained even after taking
hippocampal malformation into account. (Id. at 6.) Thus, he characterized the evidence
regarding presumed seizures to be “limited” and the issue in need of further
investigation. (Id. at 5-6.)

Although he acknowledged a heavy brain weight, Dr. Harris observed that there
were “[n]o hemorrhages within the brainstem or neuronal hypoxia-ischemia change to
the neurons was seen, so I do not believe the swelling was enough to cause a lethal

18
Dr. Harris earned his Ph.D. in pharmacology and his medical degree from Georgetown University in
1995. (Ex. F, p. 1.) He completed his internship and residency in pathology at Stanford University in
1996 and 1998 respectively. (Id.) After finishing his residency, Dr. Harris went on to complete a
fellowship in neuropathology at Stanford University in 1999. (Id.) From 1999 to 2002, he completed a
postdoctoral fellowship at Stanford University Department of Neurobiology. (Id. at 1-2.) He is board-
certified in anatomic pathology and neuropathology. (Id. at 3.) Dr. Harris has held various academic
appointments, including professorships at Stanford University Medical center, Dartmouth Medical School,
Howard University Medical School, and Georgetown University School of Medicine. (Id. at 1.) Currently,
Dr. Harris serves as an Associate Professor for the Departments of Neurology and Pathology, staff
neuropathologist, Director of Neuropathology, and Director of the Brain Bank at Georgetown University.
(Id. at 1-2.) He has reviewed over 10,000 surgical pathology and autopsy cases throughout the course of
his career. (Ex. E, p. 1.) Dr. Harris has published over 200 peer-review articles, book chapters, and
meeting abstracts. (Id.; Ex. F, pp. 4-18.)

23
herniation.” 19 (Ex. E, p. 6.) He further concluded that “[t]he neuropathological
examination was not sufficient to rule in or out a seizure related incident,” additionally
noting that no astro- or microgliosis was seen, which would be expected with multiple
prior seizures. (Id. at 5-6.) Dr. Harris observed that the lungs were congested, but with
no evidence of pneumonia. (Id. at 5.) However, due to the limitations of the tissue
samples, and given culture findings of streptococcus in the blood and lung tissue, a
bacterial infection remains possible. (Id.)

Dr. Harris characterized his observations regarding the autopsy as being “very
similar” to those of Dr. Rostad, stressing, in particular, that both experts agree with the
medical examiner’s classification of N.C.’s death as a natural death and as a sudden
unexplained death. (Ex. E, p. 6.) However, he does not agree that the medical
literature supports the causal link to vaccination that Drs. Rostad and Akbari seek to
draw. (Id.) Further, he is “not aware of medical literature describing this type of delay
between receiving a medication such as vaccination and seizure related side effects.”
(Id.)

Dr. Harris agreed that the thymus, liver, and spleen had increased weight;
however, he stressed that neither he, nor Dr. Rostad, nor Dr. Hood, observed significant
inflammation in these organs on slide review. (Ex. H, p. 2.) Instead, he explained that
these are non-specific findings often seen in autopsies as a result of ante- or
perimortem congestion and edema. (Id.) Dr. Harris acknowledged that Dr. Hood had
noted a few petechiae on the inner surface of the thymus but noted that this does not
change his overall opinion. (Id. at 1.) Dr. Harris noted that much of Dr. Rostad’s
rebuttal was devoted to Dr. Rostad’s strong disagreement with Dr. Harris’s observation
that there was not enough swelling to result in herniation. (Id. at 2.) In that regard, Dr.
Harris stressed that N.C. was not in any distress when he was put down to sleep prior to
his death and that this “is not the behavior you would see with an emerging herniation.”
(Id.)

19
Additionally, Dr. Harris noted that “Hefti and colleagues found no excess brain weight in their series of
cases form children with explained, seizure-related, undetermined, or SUDC groups. (Ex. E, p. 6 (citing
Hefti et al., supra, at Ex. E, Tab 2).) However, Drs. Rostad and Harris disagree as to the correct
interpretation of the data from this study. (Ex. 19, pp. 5-6; Ex. H, p. 2; Ex. 22, p. 7.)

24
ii. Pediatric Neurologist Gregory Holmes, M.D.20

Dr. Holmes presented two reports in this case. (Exs. C, J.) Dr. Holmes agreed
with the aspect of Dr. Rostad’s opinion that classified N.C.’s death as a SUDC. (Ex. C,
p. 7.) He disagreed with Dr. Rostad’s further opinion that N.C. experienced a DTaP
vaccine-related seizure that resulted in cerebral edema and fatal herniation. (Id. at 7-9.)

Dr. Holmes indicated that tonsillar and uncal herniation is very rare in children
under two and that, while cerebral herniation has rarely been reported following
infection, “Dr. Rostad provides no supporting evidence that cerebral edema following a
seizure results in herniation and death in a 15 months-old[21] child.” (Ex. C, p. 7.) Dr.
Holmes acknowledged that edema can occur with status epilepticus, but explained that
status epilepticus involves either a single epileptic seizure of greater than 30 minutes or
a series of epileptic seizures from which function is not regained between seizures. (Id.
(citing Eugen Trinka et al., A Definition and Classification of Status Epilepticus – Report
of the ILAE Task Force on Classification of Status Epilepticus, 56 EPILEPSIA 1515 (2015)
(Ex. C, Tab 22) (see also Ex. J, Tab 4)).) Dr. Holmes explained:

Cerebral edema is associated with vascular congestion, swelling and
degenerative features in astrocytes, distention of perivascular spaces and
pallor of myelin staining, with eosinophilic, PAS-positive exudate, none of
which were reported in the pathological report. Dr. Hood’s report showed
no histological evidence of either cytotoxic or vasogenic edema. Dr. Rostad
states “No definite ischemic neuronal injury is seen, particularly in the CA1
region of both hippocampi although there appears to be shrinkage of the
neurons and increased basophilia of the nuclei in these areas. I believe
these hippocampal abnormalities are identical to those described by Hefti
and other researchers and associated with SUDC.” While Dr. Rostad
agrees with the diagnosis of SUDC and cites Hefti et al., these authors do
not describe cerebral edema in the patients with SUDC. Hefti et al. also
described hyper-eosinophilic neurons in the cerebral cortex and/or other
vulnerable regions, consistent with agonal hypoxia–ischemia. It is not clear
whether these are the cells Dr. Rostad refers to in his report. While there

20
Dr. Holmes earned his medical degree from the University of Virginia School of Medicine in 1974. (Ex.
D, p. 1.) He completed his internship and residency in pediatrics at Yale University School of Medicine in
1976. (Id.) Thereafter, Dr. Holmes returned to the University of Virginia School of Medicine where he
completed a second residency in pediatric neurology in 1979. (Id.) He is board-certified in pediatrics,
psychiatry and neurology with special qualification in child neurology, and clinical neurophysiology. (Id.)
Dr. Holmes has held various academic appointments, including professorships at the University of
Connecticut Health Center, the Medical College of Georgia, Harvard Medical School, Dartmouth Medical
School, and the University of Vermont College of Medicine. (Id. at 2.) Currently, Dr. Holmes serves as a
Professor of Neurological Sciences and Pediatrics and the Chair of the Department of Neurological
Sciences at the University of Vermont College of Medicine. (Id.; Ex. C, p. 1.) Dr. Holmes serves as a
reviewer and on the editorial board for various journals and has published over 200 articles. (Ex. D, pp.
6-7, 38-62.) Dr. Holmes has published and lectured on a wide range of topics in pediatric neurology with
an emphasis on pediatric epilepsy. (Ex. C, p. 1.)
21
In fact, N.C. was 20 months old.

25
may have been some mild cerebral edema, there is lack of histological
evidence for either cytotoxic or vasogenic edema.

(Id. at 8 (internal citations omitted) (citing Hefti et al., supra, at Ex. C, Tab 2; Herbert J.
Manz, The Pathology of Cerebral Edema, 5 HUM. PATHOLOGY 291 (1974) (Ex. C, Tab
28)).)

Dr. Holmes further stressed that the timing of N.C.’s death is not compatible with
Dr. Rostad’s theory, because even where children have been shown to suffer cerebral
edema following status epilepticus, the development of the cerebral edema is not
instantaneous. (Ex. C, pp. 8-9 (citing Shih-Yun Lan et al., Analysis of Fulminant
Cerebral Edema in Acute Pediatric Encephalitis, 57 PEDIATRICS & NEONATOLOGY 402
(2016) (Ex. C, Tab 32); Kenneth A. Myers et al., Fatal Cerebral Edema with Status
Epilepticus in Children with Dravet Syndrome: Report of 5 Cases, 139 PEDIATRICS e1
(2017) (Ex. C, Tab 33); Setsuri Yokoi et al., Hippocampal Diffusion After Febrile Status
Epilepticus is Related to Subsequent Epilepsy, 60 EPILEPSIA 1306 (2019) (Ex. C, Tab
30)).) In contrast, “a heavy brain may be the result of simple brain swelling due to blood
congestion in the terminal phase.” (Id. at 7 (citing Johanna Marie Lundesgaard Eidahl
et al., Postmortem Evaluation of Brain Edema: An Attempt with Measurements of
Water Content and Brain-Weight-to-Inner-Skull-Circumference Ratio, 64 J. FORENSIC &
LEGAL MED. 1 (2019) (Ex. C, Tab 20)).) In that regard, Dr. Holmes noted that Dr. Hood
observed only “mild bilateral uncal impressions and a modest cerebellar ‘cone,’ but no
other herniation of any of its parts.” (Id. (quoting Ex. 5, p. 19).)

Dr. Holmes agreed that the Gould et al. study cited by Dr. Rostad in his final
report “provides some limited support for the idea that seizures may be involved in
sudden, unexpected death in children.” (Ex. J, p. 1 (discussing Gould et al., supra, at
Ex. J, Tab 1).) However, he disagreed that the study supports the specific argument
advanced in this case that the DTaP vaccine contributed to N.C.’s death. (Id.) In
particular, Dr. Holmes explained that the study found the children experienced
convulsive seizures of between 8-50 seconds whereas “[m]ost convulsive seizures,
whether occurring during the awake or sleep states, febrile or afebrile, last longer than
five minutes, and rarely, if ever, cause death.” (Id. (internal citations omitted) (citing
Dale C. Hesdorffer et al., Distribution of Febrile Seizure Duration and Associations with
Development, 70 ANNALS NEUROLOGY 93 (2011) (Ex J, Tab 3); Trinka et al., supra, at
Ex. J, Tab 4; Shlomo Shinnar et al., How Long Do New-Onset Seizures in Children
Last?, 49 ANNALS NEUROLOGY 659 (2001) (Ex. J, Tab 5); Manoj Chungath & Simon
Shorvon, The Mortality and Morbidity of Febrile Seizures, 4 NATURE CLINICAL PRAC.
NEUROLOGY 610 (2008) (Ex. J, Tab 6); Victoria Nesbitt et al., Risk and Causes of Death
in Children with a Seizure Disorder, 54 DEVELOPMENTAL MED. & CHILD NEUROLOGY 612
(2012) (Ex. J, Tab 7)).)

Dr. Holmes noted that “the [Gould et al.] authors do not conjecture on how such
short seizures could cause death nor whether the seizures could have been secondary
to cerebral hypoxia-ischemia complicating a cardiorespiratory disorder of unknown
etiology.” (Ex. J, p. 1 (citing Gould et al., supra, at Ex. J, Tab 1).) Moreover, while Dr.

26
Rostad had hypothesized that N.C.’s death resulted from cerebral edema leading to
herniation and death, he has not explained how such pathology could result from an 8-
50 second seizure. (Id.) By contrast, Dr. Holmes explained that, while the DTaP
vaccine is associated with a slight increased risk of febrile seizures within 1-2 days of
immunization, the DTaP vaccine is not associated with afebrile seizures. (Ex. C, p. 7
(citing John Hansen et al., Safety of DTaP-IPV/Hib Vaccine Administered Routinely to
Infants and Toddlers, 34 VACCINE 4172 (2016) (Ex. C, Tab 13); Sun et al., supra, at Ex.
C, Tab 14; Jennifer C. Nelson et al., Adapting Group Sequential Methods to
Observational Postlicensure Vaccine Safety Surveillance: Results of a Pentavalent
Combination DTaP-IPV-Hib Vaccine Safety Study, 177 Am. J. Epidemiology 131 (2013)
(Ex. C, Tab 15); INSTITUTE OF MED., ADVERSE EFFECTS OF VACCINES: EVIDENCE AND
CAUSALITY 539-44 (Kathleen Stratton eds., 2012) (Ex. C, Tab 16)).) Nor would a fever
occurring 17 days post-vaccination be attributable to a DTaP vaccine.22 (Id. (citing Sun
et al., supra, at Ex. C, Tab 14; Emmanuel B. Walter et al., Fever After Influenza,
Diphtheria-Tetanus-Acellular Pertussis, and Pneumococcal Vaccinations, 145
PEDIATRICS 1 (2020) (Ex. C, Tab 17); Lisa A. Jackson et al., Retrospective Population-
Based Assessment of Medically Attended Injection Site Reactions, Seizures, Allergic
Responses and Febrile Episodes After Acellular Pertussis Vaccine Combined with
Diphtheria and Tetanus Toxoids, 21 PEDIATRIC INFECTIOUS DISEASE J. 781 (2002) (Ex. C,
Tab 18); Deborah G Hirtz et al., Seizures Following Childhood Immunizations, 102 J.
PEDIATRICS 14 (1983) (Ex. C, Tab 19)).)

iii. Immunologist Christine McCusker, M.D.23

Dr. McCusker presented three reports in this case. (Exs. A, G, I.) She opined
that N.C. suffered a SUDC and that his prior vaccination was unrelated and non-
contributory. (Ex. A, p. 14.) She agreed that vaccinations produce cytokines, often
resulting in symptoms such as pain and redness at the injection site, fever, or malaise.
(Id. at 4.) However, the effects are limited and resolve once the pathogen is

22
Dr. Holmes further opined that Dr. Akbari’s initial report “adds little useful information to this case.” (Ex.
C, p. 9.) While Dr. Akbari addressed the role of cytokines and immune dysregulation broadly, he
provided no explanation of a mechanism by which a DTaP vaccine would be related to N.C.’s death
occurring 17 days later. (Id.)
23
Dr. McCusker earned her medical degree in 1993 from McMaster University Medical School in
Hamilton, Ontario, Canada. (Ex. B, p. 1.) In 1996, she completed her residency in pediatrics at McGill
University, training at Montreal Children’s Hospital. (Id. at 2.) Thereafter, Dr. McCusker completed a
clinical fellowship in allergy and immunology in 1999 at McGill University in Montreal, Quebec, Canada.
(Id.) She board-certified in pediatrics by the American Board of Pediatrics and is certified by the Royal
College of Physicians and Surgeons of Canada and by the College des Medecins du Quebec in both
pediatrics and allergy and clinical immunology. (Id.; Ex. A, p. 1.) Since completing her fellowship, Dr.
McCusker has held various academic appointments at McGill University and clinical appointments at
Montreal Children’s Hospital. (Ex. B, p. 3.) Currently, Dr. McCusker serves as an Associate Professor of
Pediatrics at McGill University and as Division Director of Pediatric Allergy, Immunology and Dermatology
at Montreal Children’s Hospital. (Id.) Additionally, Dr. McCusker is a research director at Meakins-
Christie Laboratories of McGill University Health Centre Research Institute where her research focus is
the regulation of the immune response. (Ex. A, p. 1; Ex. B, p. 3.) She has published over fifty peer-
reviewed articles. (Ex. B, pp. 33-39.)

27
neutralized. (Id.) The release of cytokines happens immediately as part of the first
phase of the immune response, intended to fight the pathogen locally while activating
the adaptive immune response. (Id.) In the context of repeat exposure, “the presence
of immunological memory, for example in the form of antibodies, results in rapid
clearance of the pathogen from the system, with only limited activation of the innate,
pro-inflammatory pathways.” (Id. at 4-5.) She opined that “[t]here is no evidence in the
extant literature of prolonged subclinical inflammation post vaccination” as proposed by
petitioners. (Id. at 5 (discussing Claire-Anne Siegrist, Vaccine Immunology, in
PLOTKIN’S VACCINES 16 (2015) (Ex. 13, Tab A)).)

The studies cited by Dr. Akbari do not support the idea of a sustained or delayed
cytokine storm. (Ex. A, pp. 5-6 (discussing Rui Huang et al., Profiles of Acute Cytokine
and Antibody Responses in Patients Infected with Avian Influenza A H7N9, 9 PLOS ONE
1 (2014) (Ex. 13, Tab G); Lee et al., supra, at Ex. 13, Tab RR).) Instead, citing a clinical
trial of a monoclonal antibody, Dr. McCusker explained the course of a cytokine storm
as follows:

Within 60 minutes of the intravenous injection, the patients developed
headache and myalgias followed by high fever. All patients had notable
rash and rigors. Respiratory distress and nausea, vomiting and diarrhea
also developed followed by low blood pressure. Over the course of the next
few days patients developed multi-organ failure. Fortunately, due to the
rapid response of the critical care teams, all patients recovered with
resolution of most symptoms within 30 days. Serum cytokine levels were
measured (Figure 3) and there were significant cytokine elevations within 4
hours of injection of the trial drug, including TNFα (levels between 4000-
5000pg/ml), interferon-γ (5000pg/ml), IL6 (range 2000-5000pg/ml) and IL1β
(5000pg/ml). Of note, despite the extreme levels of peripheral cytokines
released during this event, no patient developed clinical signs of significant
brain edema. Neurologic sequelae included delirium associated with the
high fever, partial amnesia, localized numbness, difficulty concentrating,
and headaches (see Table 3).

(Id. at 6-7 (discussing Ganesh Suntharalingam et al., Cytokine Storm in a Phase 1 Trial
of the Anti-CD28 Monoclonal Antibody TGN1412, 355 NEJM 1018 (2006) (Ex. A, Tab
8)).)

By contrast, this was not N.C.’s presentation and the study by Kashiwagi et al.,
(also cited by petitioners), found post-vaccination cytokines were produced at much
lower levels. (Ex. A, p. 7 (Kashiwagi et al., supra, at Ex. A, Tab 10).) Dr. McCusker
explained that “while peripheral cytokines are released by vaccination, the levels are
extremely low, even in the case of booster vaccination.” (Id. at 13 (citing Kashiwagi et
al., supra, at Ex. A, Tab 10).) According to Dr. McCusker, the cytokine levels
demonstrated in the Kashiwagi et al. study are lower than would be expected to affect
the seizure threshold as hypothesized by petitioners’ experts. (Id.; see also Id. at 14
(citing Wen-Hsuan W. Lin et al., Plasma Cytokines and Chemokines in Zambian

28
Children with Measles: Innate Responses and Association with HIV-1 Coinfection and
In-Hospital Mortality, 215 J. INFECTIOUS DISEASES 830 (2017) (Ex. A, Tab 33)); Celine
Dubé et al., Interleukin-1β Contributes to the Generation of Experimental Febrile
Seizures, 57 ANNALS NEUROLOGY 152 (2005) (Ex. A, Tab 26)).) Here, “there were no
significant clinical signs or symptoms in N.C. consistent with chronic cytokine activation
sufficient to cause [central nervous system] damage. Indeed, he was in a good state of
health from May 8-11, 2017, when he was put to bed on the evening of his death.” (Ex.
G, p. 3 (citing Ex. 1, p. 3).) Moreover, Talaat et al. shows that post-vaccination
proinflammatory cytokines peak after 16-24 hours and return to baseline by 44 hours.
(Ex. I, p. 3 (citing Kawsar R. Talaat et al., Rapid Changes in Serum Cytokines and
Chemokines in Response to Inactivated Influenza Vaccination, 12 INFLUENZA & OTHER
RESPIRATORY VIRUSES 202 (2018) (Ex. I, Tab 2)).) In mice, cytokine levels have been
shown to peak at 48 hours post-vaccination and return to baseline within 7 days. (Id. at
3-4 (citing Tetsuo Nakayama et al., Long-term Regulation of Local Cytokine Production
Following Immunization in Mice, 62 MICROBIOLOGY & IMMUNOLOGY 124 (2018) (Ex. I, Tab
3)).) Talaat et al. showed that patients experiencing systemic side effects after
vaccination (specifically the flu vaccine) had elevated cytokine levels for only 1-2 days
post-vaccination. (Ex. I, p. 4 (citing Talaat et al, supra, at Ex. I, Tab 2).)

Contrary to Dr. Rostad’s suggestion that the cytokine response to vaccination
may have acted in concert with N.C.’s May 7 infection, Dr. McCusker explained that
prior studies have shown that vaccinations do not worsen viral illness or inflammatory
autoimmune disease. (Ex. A, pp. 7-8 (discussing Thomas G. Boyce et al., Pertussis
Vaccination and the Risk of Respiratory Syncytial Virus-Associated Hospitalization, 23
PEDIATRIC INFECTIOUS DISEASE J. 897 (2004) (Ex. A, Tab 11); Johanna Westra et al.,
Vaccination of Patients with Autoimmune Inflammatory Rheumatic Diseases, 11 NATURE
REVS. RHEUMATOLOGY 135 (2015) (Ex. A, Tab 12)).) After reviewing Dr. Akbari’s
supporting citations, she further concluded that Dr. Akbari has not presented literature
that would support the hypothesis that the vaccine components N.C. received “induced
a catastrophic autoimmune response either T cell or cytokine mediated.” (Id. at 10.)

Regarding the relationship between cytokines and seizures, Dr. McCusker
explained that certain cytokines, namely IL-1β and IL-6, act as neurotransmitters and so
it is not surprising that they would be increased in epilepsy or following a seizure. (Ex.
A, p. 10.) Cytokine upregulation is a consequence of seizure activity rather than an
etiologic factor. (Id. at 10-11 (citing Gang Li et al., Cytokines and Epilepsy, 20 SEIZURE
249 (2011) (Ex. A, Tab 22); A. Vezzani et al., Powerful Anticonvulsant Action of IL-1
Receptor Antagonist on Intracerebral Injection and Astrocytic Overexpression in Mice,
97 PROCS. NAT’L ACAD. SCIS. 11534 (2000) (Ex. A, Tab 23); Annamaria Vezzani & Tallie
Z. Baram, New Roles for Interleukin-1 Beta in the Mechanisms of Epilepsy, 7 EPILEPSY
CURRENTS 45 (2007) (Ex. A, Tab 24)).) A study by Li et al. examined the role of
proinflammatory cytokines in causing seizures and determined based on an animal
model that, while super-physiological levels of IL-1β had epileptogenic potential, levels
comparable to what occurs in vaccination appeared to have an anti-epileptic effect. (Id.
(Li et al., supra, at Ex. A, Tab 22).) Moreover, IL-1β has a very short half-life, with
clearance occurring within 19 minutes of release. (Id. at 13 (citing Shoji Kudo et al.,

29
Clearance and Tissue Distribution of Recombinant Human Interleukin 1β in Rats, 50
CANCER RSCH. 5751 (1990) (Ex. A, Tab 28)).) While cytokines can cross the blood brain
barrier, the pathways for this to occur regulate both the location and amount of
cytokines expressed. (Id. at 9.) “Local production of cytokines by the [central nervous
system] parenchymal cells are more likely to mediate any neuroimmune communication
compared with those produced in the periphery.” (Id. (citing Ning Quan, In-Depth
Conversation: Spectrum and Kinetics of Neuroimmune Afferent Pathways, 40 BRAIN,
BEHAVIOR, & IMMUNITY 1 (2014) (Ex. A, Tab 18)).) In fact, Dr. McCusker opined that
“[t]here is no evidence submitted that low levels of peripheral cytokines released during
vaccination result in pathological increases in [central nervous system] cytokines.” (Id.
at 13.)

Dr. McCusker does not agree that the hippocampal changes discussed by Dr.
Rostad have been clearly implicated as a cause of seizures or a contributor to SUDC.
(Ex. I, p. 5 (citing 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, 48 NEUROPATHOLOGY &
APPLIED NEUROBIOLOGY 1 (2021) (Ex. I, Tab 5); Declan McGuone et al., Neuropathologic
Changes in Sudden Unexplained Death in Childhood, 79 J. NEUROPATHOLOGY &
EXPERIMENTAL NEUROLOGY 336 (2020) (Ex. I, Tab 6)).) In any event, while Dr. Rostad
cited work by Kinney et al. to support a role for seizures in SUDC, Dr. McCusker
stressed that the cited study does not identify vaccination as a risk factor. (Ex. A, p. 12
(discussing Kinney et al., supra, at Ex. 18, Tab DDD).) By contrast, she cited several
studies24 that she indicated constitute evidence against a causal relationship between
vaccines and SIDS. (Ex. G, pp. 8-9.) Moreover, while the Kinney et al. study
hypothesized an association between febrile seizures and SUDC, the study results were
not necessarily clear in distinguishing either hippocampal anomalies or family history of
febrile seizures from controls. (Ex. A, p. 12 (citing Kinney et al., supra, at Ex. 18, Tab
DDD).) Additional studies by Hesdorffer et al. and Hefti et al. did not find that a family
history of febrile seizures was significantly associated with SUDC. (Id. (discussing Dale
C. Hesdorffer et al., Sudden Unexplained Death in Childhood: A Comparison of Cases
with and Without a Febrile Seizure History, 58 EPILEPSIA 1294 (2015) (Ex. A, Tab 25)
(see also Ex. 13, Tab R); and Hefti et al., supra, at Ex. 13, Tab S).) In any event, Dr.
McCusker cited a number of studies25 for the proposition that the DTaP vaccine has not

24
Specifically: Pedro L. Moro et al., Deaths Reported to the Vaccine Adverse Event Reporting System
(VAERS), United States, 1997-2013, 61 CLINICAL INFECTIOUS DISEASES 980 (2015) (Ex. G, Tab 3) (see
also Ex. 21, Tab 13); Richard D. Goldstein et al., Overall Postneonatal Mortality and Rates of SIDS, 137
PEDIATRICS 1 (2016) (Ex. G, Tab 4); Ronny Kuhnert et al., Reanalyses of Case-Control Studies Examining
the Temporal Association Between Sudden Infant Death Syndrome and Vaccination, 30 VACCINE 2349
(2012) (Ex. G, Tab 5) (see also Ex. 21, Tab 14); Jacqueline Mϋller-Nordhorn et al., State-Level Trends in
Sudden Unexpected Infant Death and Immunization in the United States: An Ecological Study, 21 BMC
PEDIATRICS 1 (2021) (Ex. G, Tab 6) (see also Ex. 21, Tab 16)).
25
Specifically: Sarah von Spiczak et al., A Retrospective Population-Based Study on Seizures Related to
Childhood Vaccination, 52 EPILEPSIA 1506 (2011) (Ex. A, Tab 29); Nienke E. Verbeek et al., Etiologies for
Seizures Around the Time of Vaccination, 134 PEDIATRICS 658 (2014) (Ex. A, Tab 30); Wan-Ting Huang
et al., Lack of Association Between Acellular Pertussis Vaccine and Seizures in Early Childhood, 126
PEDIATRICS e263 (2010) (Ex. A, Tab 31); Jo M. Wilmshurst et al., Summary of Recommendations for the

30
been shown to be a cause of seizures. (Id. at 13-14.) She further suggested that the
literature cited by petitioners’ experts likewise do not support a causal relationship
between the DTaP vaccine and seizures and further disputing that evidence related to
the whole cell DPT vaccine is relevant. (Ex. A, p. 14 (citing at CDC Report, supra, at
Ex. 18, Tab LLL; Sun et al., supra, at Ex. 18, Tab MMM; Paolo Bellavite, Causality
Assessment of Adverse Events Following Immunization: The Problem of Multifactorial
Pathology, 9 F1000 RSCH. 1 (2020) (Ex. 18, Tab VVV)); Ex. G, pp. 3-4 (citing Paddy
Farrington et al., A New Method for Active Surveillance of Adverse Events from
Diphtheria/Tetanus/Pertussis and Measles/Mumps/Rubella Vaccines, 345 LANCET 567
(1995) (Ex. 19, Tab N); Moro et al., supra, at Ex. 13, Tab NNN).)

V. Analysis

a. Medical theory of causation (Althen prong one)

Under Althen prong one, petitioners must provide a “reputable medical theory,”
demonstrating that the vaccine received can cause the type of injury alleged. Pafford v.
Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (quoting
Pafford v. Sec’y of Health & Human Servs., No. 01-0165V, 2004 WL 1717359, at *4
(Fed. Cl. Spec. Mstr. July 16, 2004)). Such a theory must only be “legally probable, not
medically or scientifically certain.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d
543, 548-49 (Fed. Cir. 1994). Petitioners may satisfy the first Althen prong without
resort to medical literature, epidemiological studies, demonstration of a specific
mechanism, or a generally accepted medical theory. See Andreu v. Sec’y of Health &
Human Servs., 569 F.3d 1367, 1378 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of
Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). However, “[a]
petitioner must provide a ‘reputable medical or scientific explanation’ for [their] theory.”
Boatmon, 941 F.3d at 1359 (quoting Moberly v. Sec’y of Health & Human Servs., 592
F.3d 1315, 1322 (Fed. Cir. 2010)). “While it does not require medical or scientific
certainty, it must still be ‘sound and reliable.’” Id. (quoting Knudsen, 35 F.3d at 548-49).

There have been a significant number of prior cases in this Program that have
addressed allegations that one or more childhood vaccines caused or contributed to a
SIDS or SUDC-labeled death. However, given that these deaths have necessarily been
deemed “unexplained,” prior petitioners have, unsurprisingly, failed to come forward
with sound and reliable evidence that suggests a more likely than not cause of the
death. See, e.g., Anklam v. Sec’y of Health & Human Servs., No. 17-2061V, 2023 WL
8890662 (Fed. Cl. Spec. Mstr. Nov. 29, 2023) (SUDC); Whitesell v. Sec’y of Health &
Human Servs., No. 17-1557V, 2022 WL 3081327 (Fed. Cl. Spec. Mstr. July 12, 2022)
(SUDC); Bohn v. Sec’y of Health & Human Servs., No. 16-0265V, 2021 WL 4302367
(Fed. Cl. Spec. Mstr. Aug. 23, 2021) (SIDS); Wunderler v. Sec’y of Health & Human
Servs., No. 19-1468V, 2020 WL 4346694 (Fed. Cl. Spec. Mstr. July 7, 2020) (sudden
unexplained death (“SUDS”)); Martin v. Sec’y of Health & Human Servs., No. 15-789V,

Management of Infantile Seizures: Task Force Report for the ILAE Commission of Pediatrics, 56
EPILEPSIA 1185 (2015) (Ex. A, Tab 32)); see also Ex. G, pp. 3-4 (citing Dana Craiu et al., Vaccination and
Childhood Epilepsies, 36 EUR. J. PAEDIATRIC NEUROLOGY 57 (2022) (Ex. G, Tab 1)).

31
2020 WL 4197748 (Fed. Cl. Spec. Mstr. May 8, 2020) (SUDC), mot. rev. den’d, 158
Fed. Cl. 459 (2020); Olsavicky v. Sec’y of Health & Human Servs., No. 17-1806, 2019
WL 2881009 (Fed. Cl. Spec. Mstr. June 4, 2019) (SIDS); Nunez v. Sec’y of Health &
Human Servs., No. 14-863V, 2019 WL 2462667 (Fed. Cl. Spec. Mstr. Mar. 29, 2019)
(SIDS), mot. rev. den’d, 144 Fed. Cl. 540 (2019), aff’d, 825 F. App’x 816 (Fed. Cir.
2020); Frady v. Sec’y of Health & Human Servs., No. 16-148V, 2017 WL 5379391 (Fed.
Cl. Spec. Mstr. Sept. 20, 2017) (SIDS); Pelton v. Sec’y of Health & Human Servs., No.
14-674V, 2017 WL 1101767 (Fed. Cl. Spec. Mstr. Feb. 27, 2017) (SIDS); Jewell v.
Sec'y of Health & Human Servs., No. 11-138V, 2016 WL 5404165 (Fed. Cl. Spec. Mstr.
Aug. 29, 2016) (SIDS); Copenhaver v. Sec'y of Health & Human Servs., No. 13-1002V,
2016 WL 3456436 (Fed. Cl. Spec. Mstr. May 31, 2016) (SIDS), mot. rev. den’d, 129
Fed. Cl. 176 (2016); Lord v. Sec'y of Health & Human Servs., No. 12-255V, 2016 WL
806818 (Fed. Cl. Spec. Mstr. Feb. 9, 2016) (SIDS); Cozart v. Sec'y of Health & Human
Servs., No. 00-590V, 2015 WL 6746616 (Fed. Cl. Spec. Mstr. Oct. 15, 2015) (SIDS),
mot. rev. den’d, 126 Fed. Cl. 488 (2016); Waterman v. Sec’y of Health & Human Servs.,
No. 13-960V, 2015 WL 4481244 (Fed. Cl. Spec. Mstr. June 30, 2015) (SIDS), mot. rev.
den’d, 123 Fed. Cl. 564 (2015); Sanchez v. Sec’y of Health & Human Servs., No. 11-
651V, 2013 WL 4476750 (Fed. Cl. Spec. Mstr. July 26, 2013) (SIDS); Bigbee v. Sec’y of
Health & Human Servs., No. 06-663V, 2012 WL 1237759 (Fed. Cl. Spec. Mstr. Mar. 22,
2012) (SIDS); Heller v. Sec’y of Health & Human Servs., No. 96-0797V, 1998 WL
408612 (Fed. Cl. Spec. Mstr. June 22, 1998) (SIDS).26

In some instances, the parties have litigated whether SIDS presents an
alternative explanation to what petitioners otherwise alleged to have been a vaccine-
caused death. See, e.g., Doe 11 v. Sec’y of Health & Human Servs., 601 F.3d 1349,
1351 (Fed. Cir. 2010) (holding that “the special master did not commit legal error in
considering evidence of SIDS, an allegedly alternative cause. Nothing in the Vaccine
Act prohibits the government from presenting evidence that the petitioner's injury was
due to ‘factors unrelated’ to the vaccine (here, SIDS)”); Bigbee, 2012 WL 1237759, at
*47-49. However, many of these prior cases have directly addressed at length
allegations that one or more vaccines directly caused or contributed to a child’s death
within a framework of SIDS or SUDC itself. For example, it has been repeatedly found
that attempts to establish vaccination as an exogenous stressor under the accepted
Triple Risk Model of SIDS were unpersuasive. See, e.g., Jewell, 2016 WL 5404165, at
*13; Copenhaver, 2016 WL 3456436, at *12-13; Lord, 2016 WL 806818, at *14; Cozart,
2015 WL 6746616, at *13. One such case, Boatmon v. Secretary of Health and Human
Services, was reviewed by the Federal Circuit. 941 F.3d 1351 (Fed. Cir. 2019).27

26
Special masters reasonably draw upon their experience in resolving Vaccine Act claims. Doe v. Sec’y
of Health & Human Servs., 76 Fed. Cl. 328, 338–39 (2007) (“[o]ne reason that proceedings are more
expeditious in the hands of special masters is that the special masters have the expertise and experience
to know the type of information that is most probative of a claim”). Nonetheless, special masters are not
bound by the prior decisions of other special masters or of the Court of Federal Claims. Hanlon v. Sec’y
of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). Thus, these cases do not dictate the outcome in
this case.
27
In Boatmon, the special master initially found petitioners entitled to compensation before being
overturned by the Court of Federal Claims. 941 F.3d. at 1353. The Court of Federal Claims was then

32
Although there are fewer prior SUDC cases, petitioners have not fared any better when
seeking to assert vaccine causation within the research framework associated with
SUDC. E.g., Anklam, 2023 WL 8890662, at *40 (rejecting petitioners’ theory in part
because “the idea that hippocampal abnormalities cause children to be vulnerable and
at risk of sudden death is likewise not sound and reliable”); Martin, 2020 WL 4197748,
at *27 (distinguishing a case of SUDC from prior SIDS precedent, but explaining that
“this claim, like the prior SIDS cases, relies on the theory that vaccine-induced cytokine
interference with the brain in some way has pathologic, and ultimately fatal, outcomes
under circumstances involving very young children that otherwise remain mysterious to
medical science”).

In Boatmon, the petitioners’ expert (Dr. Miller) had theorized that post-vaccination
cytokines “can inhibit the activity of 5-hydroxytryptamine (‘5-HT’ or serotonin) neurons in
the medulla, causing prolonged apnea and interference with autoresuscitation.” 941
F.3d at 1356. This was presented as an application of the so-called “Triple Risk Model”
of SIDS by Kinney et al., which suggested that (1) a vulnerable infant, i.e. one having a
defect of the medulla, may (2) experience an exogenous stressor, during (3) a critical
developmental period, and thereby experience a sudden unexplained death. Id. at
1355-56. However, the Federal Circuit explained that “[i]t would be an extension of the
Triple Risk Model to include vaccination-induced cytokine activity in the list of
exogenous stressors as Dr. Miller proposes. Dr. Miller himself concedes that, outside of
Vaccine Act litigation, vaccinations have not been identified as an exogenous stressor
for SIDS.” Id. at 1360. They further stressed that, petitioners were unable to move
beyond asserting the presence of cytokines in the brain to explain how cytokine function
in the brain supported their theory. Id. at 1361. Accordingly, the Circuit concluded that,
whereas they were obligated to present “sound and reliable” scientific opinion, the
petitioners had presented a merely “plausible” or “possible” theory that was insufficient
to meet their burden of proof under Althen prong one.28 Id. at 1361-62.

In this case, petitioners theorize that “the DTaP vaccine initiated a hyperimmune
reaction that eventually led to a terminal seizure in N.C., a susceptible host.” (ECF No.

affirmed by the Court of Appeals for the Federal Circuit, though with differences in reasoning. Id. The
instant petition was filed between the time the Court of Federal Claims reversed the special master’s
ruling and the time when the Federal Circuit affirmed the Court of Federal Claims.
28
Federal Circuit rulings concerning legal issues are binding on special masters. Guillory v. Sec’y of
Health & Human Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also
Spooner v. Sec’y of Health & Human Servs., No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec.
Mstr. Jan. 16, 2014). However, the Federal Circuit has also stressed that “[c]ausation in fact under the
Vaccine Act is ... based on the circumstances of the particular case.” Boatmon, 941 F.3d at 1358-59
(quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cr. 1994). Thus, Federal
Circuit precedents do not automatically control the outcome of subsequent cases even when they involve
the same injury. See, e.g., Sanchez v. Sec’y of Health & Human Servs., 809 Fed. Appx. 843, 851-52
(Fed. Cir. 2020) (citing back to a prior Federal Circuit holding in Paluck v. Secretary of Health & Human
Services involving the same injury and noting that “while there are substantial parallels between this case
and Paluck, the differences between the two cases are such that the outcome of this case is not dictated
by Paluck.”).

33
85, p. 29.) This theory encompasses several underlying assertions. First, petitioners
explain that the DTaP vaccine produces an innate immune response that includes the
production of cytokines. (Id. at 30-31.) This is the only aspect of petitioner’s theory that
is not controverted. Second, petitioners argue that immune dysregulation can result in a
positive feedback loop that causes the cytokine response from vaccination to become a
“cytokine storm,” a damaging and potentially fatal overproduction of cytokines. (Id. at
31.) Third, petitioners argue that, concomitantly, there are several pathways by which
the DTaP vaccine can dysregulate the adaptive immune response to result in
autoimmunity. (Id. at 32-33.) Most significantly, aluminum within the DTaP vaccine can
damage the blood brain barrier, opening up the central nervous system to an
inflammatory reaction. (Id.) Fourth, once the blood brain barrier has been made “more
accessible,” the further inflammatory response from a subsequent upper respiratory
infection can further inflame the brain. (Id. at 34.) And, fifth, where a subject is
susceptible to seizures due to a hippocampal malformation, cytokine damage within the
brain can decrease the seizure threshold and hyper-excite the neuronal network,
resulting in a terminal seizure as evidenced in the SUDC literature. (Id. at 35-37.)
Specifically, they assert that a seizure can result in cerebral edema and fatal brain
herniation. (Id. at 38.)

Although petitioners’ theory invokes several different concepts and includes
multiple steps, it is important to note that it remains firmly grounded in the idea that a
vaccination can initiate a process that ultimately results in a terminal seizure consistent
with what they assert is hypothesized as the cause of at least a subset of SUDC cases.
Indeed, petitioners have filed some 32 publications, either introduced or discussed by
their experts,29 having the primary purpose of exploring the potential cause of SIDS,
SUDC, and/or SUDEP, representing a body of literature current up to 2024, and their
experts have affirmatively relied on concepts and data derived from this body of
literature. Moreover, Dr. Rostad, petitioner’s pathology expert, agreed that N.C.’s
autopsy was correct in initially classifying N.C.’s death as a sudden unexplained death.
(Ex. 18, p. 8 (citing Ex. 5, p. 37).) Citing studies by Kinney et al. and Hefti et al., he
opined that

[t]hese studies suggested that hippocampal formation] malformation
represented a marker of an impaired forebrain/limbic network that increases
the risk of sudden death due to potential brainstem cardiorespiratory related
circuits nuclei, or to a subclinical seizure in an infant predisposed to
epilepsy. The association of epilepsy-related pathology (such as HF
maldevelopment) with SIDS, SUDEP and SUDC leads to possible epilepsy-
related mechanisms in sudden death.

(Id. at 25 (citing Kinney et al., supra, at Ex. 18, Tab XXX; Hefti et al., supra, at Ex. 13,
S).) Thus, despite the preceding steps of petitioners’ theory, this case still ultimately
falls squarely within the prior line of cases, including Boatmon, in which petitioners have

29
Some of these 32 filings are instances where petitioners’ experts resubmitted papers originally cited by
respondent’s experts for purposes of highlighting counterpoints.

34
attempted to leverage research into the phenomena of SIDS and SUDC as evidence
supporting a theory of vaccine causation within that framework. That is, rather than
seeking to wholly supplant the SUDC concept, petitioners purport to have presented a
theory that explains how the leading hypotheses of SUDC could actually support
vaccination as a trigger. However, similar to what was explained by the Federal Circuit
in Boatmon, this effort fundamentally lacks support in the relevant body of literature.

Petitioners’ pathology expert has sought to distinguish this case from Boatmon
based on differences between the leading hypotheses of SIDS and SUDC. (Ex. 19, pp.
30-32.) To that point, prior decisions have noted that SIDS and SUDC are not
interchangeable. Martin, 2020 WL 4197748, at *27 (noting that “[a]ll of the experts
testifying in this case agreed that SIDS and SUDC are not congruent, and that the ‘triple
risk’ model employed in SIDS circumstances has no direct application here”). In
particular, Dr. Rostad has explained that petitioners’ theory of causation in this case is
premised on a hippocampal abnormality leading to a terminal seizure rather than being
premised on a medullary defect leading to arrested breathing as was at issue in
Boatmon.30 (Ex. 19, pp. 30-32.) Yet, Dr. Rostad conceded that “[d]espite the robust
SUID/SIDS literature, research about the relationship of immunization and SUID/SIDS is
scant. The papers evaluating vaccine as a risk factor in SUDC are even more rare.”
(Ex. 19, p. 37.) “Furthermore, there is a considerable gap in knowledge with regards to
SUDC pathobiology.” (Id.) Given these concessions, if it was unreliable to extend the
hypotheses underlying SIDS to vaccination as was done in Boatmon, then it is a fortiori
unreliable to do the same in the context of SUDC, which petitioners’ experts explain to
be even less well understood. Accord Martin, 2020 WL 4197748, at *27; Anklam, 2023
WL 8890662, at *39-40.

Indeed, of the 32 publications petitioners’ experts have discussed regarding the
potential cause(s) of SIDS, SUDC, and/or SUDEP, 20 include no mention of
vaccinations whatsoever, even where other risk factors for these phenomenon are
discussed.31 Of the remaining twelve, five (mostly case reports) reference a history of

30
However, while Dr. Rostad explicitly disclaimed reliance on the Triple Risk Model, he nonetheless cited
approvingly to a paper by Kinney, et al., for the proposition that “SIDS, SUDC, and SUDEP cases
represent a spectrum of serotonopathy that affects the caudal and rostral 5-HT domains in the brainstem
and their preferential targets, including the hippocampus.” (Ex. 19, p. 32 (citing Hannah C. Kinney et al.,
Sudden and Unexpected Death in Early Life: Proceedings of a Symposium in Honor of Dr. Henry F.
Krous, 8 FORENSIC SCI., MED. & PATHOLOGY 414 (2012) (Ex. 19, Tab R)); see also Kinney et al., supra, at
Ex. 18, Tab XXX, p. 1 (suggesting hippocampal abnormalities may represent “a common vulnerability that
defies the 1-year age cutoff between SIDS and SUDC”).) Moreover, both of petitioners’ experts explicitly
rely in part on papers and data pertaining to SIDS. (E.g., Ex. 13, pp. 13-14 (citing W.G. Guntheroth,
Interleukin-1 as Intermediary Causing Prolonged Sleep Apnea and SIDS During Respiratory Infections,
28 MED. HYPOTHESES 121 (1989) (Ex. 13, Tab TT) (see also Ex. 20, Tab Q)); Ex. 20, p. 3 (citing Walker,
supra, at Ex. 20, Tab C); Ex. 18, pp. 24-25 (cit

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11141103. Public record. Not legal advice.