CATONE v. SECRETARY OF HEALTH AND HUMAN SERVICES

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

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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.

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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 (citing Hannah C. Kinney et al., Dentate Gyrus Abnormalities

in Sudden Unexplained Death in Infants: Morphological Marker of Underlying Brain Vulnerability, 129

ACTA NEUROPATHOLOGICA 65 (2015) (Ex. 18, Tab ZZZ)).) In that regard, Dr. Akbari did initially invoke the

idea that his theory was compatible with the idea that SUDC is partly explained by a medullary defect.

(Ex. 13, p. 14.)

31

Specifically: Hannah C Kinney & Bradley T. Thach, The Sudden Infant Death Syndrome, 361 NEJM

795 (2009) (Ex. 13, Tab M); Felicia L. Trachtenberg et al., Risk Factor Changes for Sudden Infant Death

35

vaccination among subjects but without suggesting any causal role32 and five actually

indicate that vaccines are exonerated as a cause of sudden unexplained deaths.33

Importantly, among these 32 publications, eight specifically acknowledge concepts

pertaining to petitioners’ theory of causation – hippocampal abnormalities leading to

seizure – as a mechanism of sudden death, but include no discussion of vaccination as

a potential trigger.34 By contrast, petitioners’ experts have presented only two articles

purporting to implicate vaccination as a cause of sudden death. (Ex. 20, p. 3 (citing to

Alexander M. Walker et al., Diphtheria-Tetanus-Pertussis Immunization and Sudden

Infant Death Syndrome, 77 AM. J. PUB. HEALTH 945 (1987) (Ex. 20, Tab C)35; Neil Z.

Syndrome After Initiation of Back-to-Sleep Campaign, 129 Pediatrics 630 (2012) (Ex. 13, Tab N); 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) (Ex. 13, Tab O); Henry F. Krous et al.,

Sudden Unexpected Death in Childhood: A Report of 50 Cases, 8 PEDIATRIC & DEVELOPMENTAL

PATHOLOGY 307 (2005) (Ex. 13, Tab Q); Hefti et al., supra, at Ex. 13, Tab S; Guntheroth, supra, at Ex. 13,

Tab TT; Hefti et al., supra, at Ex. 18, Tab F; James J. Filiano & Hannah C. Kinney, Arcuate Nucleus

Hypoplasia in the Sudden Infant Death Syndrome, 51 J. NEUROPATHOLOGY & EXPERIMENTAL NEUROLOGY

394 (1992) (Ex. 18, Tab G); H.C. Kinney et al., Subtle Developmental Abnormalities in the Inferior Olive:

An Indicator of Prenatal Brainstem Injury in the Sudden Infant Death Syndrome, 61 J. NEUROPATHOLOGY

& EXPERIMENTAL NEUROLOGY 427 (2002) (Ex. 18, Tab H); Kinney et al., supra, at Ex. 18, Tab DDD; Myers

et al., supra, at Ex. 18, Tab FFF; Dlouhy et al., supra, at Ex. 18, Tab GGG; Kinney et al., supra, at Ex. 18,

Tab XXX; Hannah C. Kinney et al., Abnormalities of the Hippocampus in Sudden and Unexpected Death

in Early Life, in SIDS – SUDDEN INFANT AND EARLY CHILDHOOD DEATH 661 (Jhodie R. Duncan & Roger W.

Byard eds., 2018) (Ex. 18, Tab YYY); Kinney et al., supra, at Ex. 18, Tab ZZZ; Maxine Dibué et al.,

Sudden Death in Epilepsy: There is Room for Intracranial Pressure, 10 BRAIN & BEHAVIOR 1 (2020) (Ex.

19, Tab I); Laura Crandall & Orrin Devinsky, Sudden Unexplained Death in Children, 1 LANCET 8 (2017)

(Ex. 19, Tab S); Matthew Halvorsen et al., De Novo Mutations in Childhood Cases of Sudden

Unexplained Death that Disrupt Intracellular Ca2+ Regulation, 118 PROCS. NAT’L ACAD. SCIS. 1 (2021) (Ex.

21, Tab 12); Orrin Devinsky et al., Underestimation of Sudden Deaths Among Patients with Seizures and

Epilepsy, 89 NEUROLOGY 886 (2017) (Ex. 22, Tab 9); Gould et al., supra, at Ex. 25, Tab 1.

32

Specifically: D.P. Southall et al., Sudden and Unexpected Death Between 1 and 5 Years, 62 J.

ARCHIVES DISEASE CHILDHOOD 700 (1987) (Ex. 13, Tab P); Hesdorffer et al., supra, at Ex. 13, Tab R;

Laura Gould Crandall et al., Potential Role of Febrile Seizures and Other Risk Factors Associated with

Sudden Death in Children, 2 JAMA 1 (2019) (Ex. 13, Tab V); Kinney et al., supra, at Ex. 18, Tab EEE;

Hannah C. Kinney et al., Sudden Death in Toddlers Associated with Developmental Abnormalities of the

Hippocampus: A Report of Five Cases, 10 PEDIATRIC & DEVELOPMENTAL PATHOLOGY 208 (2007) (Ex. 18,

Tab WWW).

33

Specifically: JHODIE R. DUNCAN & ROGER W. BYARD, SIDS SUDDEN INFANT AND EARLY CHILDHOOD DEATH:

THE PAST, THE PRESENT AND THE FUTURE (2018) (Ex. 13, Tab J, pp. 46, 351, 479); Stephen M. Adams et

al., Sudden Infant Death Syndrome, 79 AM. FAM. PHYSICIAN 870 (2009) (Ex. 13, Tab K, p. 3); Moro et al.,

supra, at Ex. 21, Tab 13, pp. 2, 5-6; Kuhnert et al., supra, at Ex. 21, Tab 14, pp. 7-8; Mϋller-Nordhorn et

al., supra, Ex. 21, Tab 16, pp. 6-8.

34

Specifically: Hefti et al., supra, at Ex. 13, Tab S; Crandall et al., supra, at Ex. 13, Tab V; Hefti et al.,

supra, at Ex. 18, Tab F; Kinney et al., supra, at Ex. 18, Tab DDD; Kinney et al., supra, at Ex. 18, Tab

XXX; Kinney et al., supra, at Ex. 18, Tab YYY; Crandall et al., supra, at Ex. 19, Tab S; Devinsky et al.,

supra, at Ex. 22, Tab 9.

35

In fact, although Dr. Akbari cites this paper by Walker et al., his report includes a quotation that he

attributes to a presentation by William Torch. (Ex. 20, p. 3.) A paper by Dr. Torch is among the

references listed in the Walker paper. (Walker et al., supra, at Ex. 20, Tab C, p. 6.) However, the

quotation included within Dr. Akbari’s report is not included in the paper and no paper by Dr. Torch has

36

Miller, Vaccines and Sudden Infant Death: An Analysis of the VAERS Database 1990-

2019 and Review of the Medical Literature, 8 TOXICOLOGY REPS. 1324 (2021) (Ex. 26)).)

However, these studies are unpersuasive.

Walker et al. is a study from 1987 that examined medical records for a population

of 26,500 infants to determine immunizations status and mortality between 1972 and

1983. (Ex. 20, Tab C, p. 1.) The authors identified 29 instances of SIDS based on their

definition (i.e. any death for which no cause could be discerned among infants of normal

birth weight with no predisposing medical conditions). (Id.) Of that group, six were

never immunized. (Id. at 2.) Of the remaining 23 subjects, there were increased

incidences of death within three days of a DPT vaccine followed by decreased

incidences between 4-29 days post-DPT vaccination. (Id. at 2, 4.) There are several

reasons why this finding is not significant evidence in this case. First, despite the size

of the population from which the study was drawn, the finding of elevated instances of

SIDS in the three days post-vaccination was based on only four deaths, followed by a

noted decrease in mortality wherein the confidence interval extended to into mortality

deficit. (Id. at 2.) The authors suggest the subsequent decrease below typical mortality

rates could be a “compensatory decline,” but also specifically caution that “[t]he

relatively small number of SIDS cases in the present study also admits the possibility of

substantial random error.” (Id. at 2, 4.) Second, based on the finding that six of the 29

SIDS subjects were not vaccinated, the authors found overall that the resulting mortality

rate among the unvaccinated infants was 6.5 times higher than among vaccinated

infants. (Id. at 1-2.) And third, this study predates the introduction of the acellular

pertussis vaccine and assesses the earlier whole cell pertussis vaccine. Special

masters have repeatedly found that the safety profile of the whole cell pertussis vaccine

cannot be imputed to the acellular pertussis vaccine. See, e.g., Bangerter v. Sec’y of

Health & Human Servs., No. 15-1186V, 2022 WL 439535, at *21 (Fed. Cl. Spec. Mstr.

Jan. 18, 2022); Martin v. Sec’y of Health & Human Servs., No. 13-486V, 2020 WL

6865931, at *30 (Fed. Cl. Spec. Mstr. Oct. 27, 2020); Kottenstette v. Sec’y of Health &

Human Servs., No. 15-1016V, 2020 WL 4197301, at *8-9 (Fed. Cl. Spec. Mstr. June 2,

2020) (Horner), rev’d on other grounds, 861 F. App’x 433 (Fed. Cir. 2021); Sharpe v.

Sec’y of Health & Human Servs., No. 14-65V, 2018 WL 7625360, at *31-32 (Fed. Cl.

Spec. Mstr. Nov. 5, 2018); Taylor v. Sec'y of Health & Human Servs., No. 05-1133V,

2012 WL 4829293, at *30 (Fed. Cl. Spec. Mstr. Sept. 20, 2012); Holmes v. Sec'y of

Health & Human Servs., No. 08-185V, 2011 WL 2600612, at *20 (Fed. Cl. Spec. Mstr.

Apr. 26, 2011); Simon v. Sec'y of Health & Human Servs., No. 05-941V, 2007 WL

1772062, at *7 (Fed. Cl. Spec. Mstr. June 1, 2007); Grace v. Sec'y of Health & Human

Servs., No. 04-[redacted], 2006 WL 3499511, at *9 (Fed. Cl. Spec. Mstr. Nov. 30,

2006); but see Kottenstette v. Sec’y of Health & Human Servs., 2017 WL 6601878 (Fed.

Cl. Spec. Mstr. Dec. 12, 2017) (Millman), aff’d 861 F. App’x 433 (Fed. Cir. 2021).

Indeed, Dr. Rostad effectively conceded this point in his final report. (Ex. 25, p. 3

(contending that the DTaP vaccine is not risk free for seizures but acknowledging the

risk to at least be “dramatically” reduced).)

been filed by petitioners. However, Dr. McCusker nonetheless explained that the Torch presentation was

a case series only, with no examination of background incidences of SIDS. (Ex. G, p. 8.)

37

The Miller study similarly purported to find that instances of SIDS are clustered

within three or seven days post-vaccination. (Miller, supra, at Ex. 26, p. 3.) That study

examined reports of infant deaths to VAERS36 between 1990 to 2019, identifying 2,605

reported deaths occurring within 60 days of vaccination, 1,048 of which were classified

as SIDS. (Id.) Among the SIDS cases, 51% occurred within 3 days of vaccination and

75.5% occurred within 7 days of vaccination. (Id.) The author suggests that this finding

accords with a cytokine-based theory of vaccination causation of SIDS (Id. at 9-10);

however, as Dr. McCusker observed, this study had no control population or

comparison to background rates (Ex. G, p. 8). Moreover, as the author himself notes,

the fact that this data was drawn from a system for collecting voluntary reports of

vaccine adverse events introduced an inherent selection bias. (Miller, supra, Ex. 26, p.

9.) He explains that “[t]he main weakness of this study is the potential for reporting

bias. Doctors and parents may have been more likely to report a sudden death to

VAERS when it occurred in close temporal proximity to vaccination than if it had

happened several days or weeks later.” (Id. at 9.) By contrast, Dr. McCusker cited

another study of VAERS data that concluded that “[n]o concerning pattern was noted

among deaths submitted to VAERS during 1997-2013. The main causes of death were

consistent with the most common causes of death in the U.S. population.” (Moro et al.,

supra, at Ex. G, Tab 3, p. 2 (see also Ex. 21, Tab 13, p. 1).)

Thus, as in Boatmon, petitioners’ experts are attempting to extend the leading

hypotheses for SUDC to encompass a purported risk relative to vaccination based

largely on their own ipse dixit. However, nothing requires the acceptance of an expert's

conclusion “connected to existing data only by the ipse dixit of the expert,” especially if

“there is simply too great an analytical gap between the data and the opinion proffered.”

Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen.

Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec'y of Health &

Human Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30,

2012), aff’d, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013).

Moreover, petitioners’ theory of causation is also unreliable in its attempt to

conflate SUDC and SUDEP. Respondent persuasively argues that the hippocampal

abnormalities that petitioners’ experts incorporate into the causal chain they theorize are

not actually predictive of SUDC. (ECF No. 92, p. 25.) In particular, respondent cites

studies by Leitner et al. and McGuone et al. as undermining petitioners’ assertion that

hippocampal malformation leaves an individual more susceptible to seizures. (Id. (citing

36

The Vaccine Adverse Event Reporting System (VAERS) is a national safety surveillance program

created by the National Childhood Vaccine Injury Act of 1986 that collects information about possible

adverse reactions to vaccines that are administered in the U.S. (Miller, supra, at Ex. 26, pp. 1, 3.)

VAERS collects and analyzes reports adverse events following the administration of a vaccination in the

U.S., and each report includes information concerning the patient, the vaccine(s) administered, and the

symptoms the patient experienced after vaccination. (Id. at 3.) Since the program’s creation in 1990,

VAERS has received over 700,000 reports which describe adverse events ranging from mild sild events

to serious life-threatening conditions, including death. (Id.) The VAERS database is available to and

relied upon by both government and independent researchers. (Id.) VAERS allows for identification and

detection of unusual patterns and important safety concerns regarding vaccines administered in the U.S.

(Id.)

38

Leitner et al., supra, at Ex. I, Tab 5; McGuone et al., supra, at Ex. I, Tab 6; Dominique

F. Leitner et al., Proteomic Differences in Hippocampus and Cortex of Sudden

Unexplained Death in Childhood, 143 ACTA NEUROPATHOLOGICA 585 (2022) (Ex. I, Tab

7)).) Thus, Dr. McCusker opined that the data from these studies “shows that changes

in the hippocampus are not predictive of cause of death and do not differentiate patients

with known causes of death from those that fall into the SUDC group such as N.C.” (Ex.

I, p. 6.) Although Dr. Rostad did cite papers hypothesizing that SIDS, SUDC, and

SUDEP may exist as a spectrum (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));

Kinney et al., supra, at Ex. 18, Tab XXX)), he 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.” (Id. at 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.) Prior petitioners have likewise been unpersuasive under Althen

prong one where they “have extrapolated information taken from studies that relate to

children with epilepsy (SUDEP) and applied it to children who do not have epilepsy or a

history of prior seizures.” Anklam, 2023 WL 8890662, at *40. In this case, despite

relying on the idea of “epilepsy-related mechanisms in sudden death” (Ex. 18, p. 25),

Dr. Rostad conceded 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).

In his final report, Dr. Rostad introduced a study by Gould et al. for the

proposition that terminal seizures may be an underrecognized cause of SUDC. (Ex. 25;

Gould et al., supra, at Ex. 25, Tab 1.) He asserted 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.” (Ex. 25, p. 3.) However, while that Gould et al. study

observed convulsive events among seven cases otherwise determined to represent

SUDC, the authors acknowledged that hippocampal findings did not correlate with

febrile seizure history, that this was a small study that lacked physiologic monitoring to

distinguish abnormal movements, and, importantly, that “[t]he cause of the convulsive

events in our cases are unknown.” (Gould et al., supra, at Ex. 25, Tab 1, pp. 6-7.)

Thus, Dr. Holmes observed of the Gould et al. study that “the authors do not conjecture

on how such short seizures could cause death” and further noted that neither the Gould

et al. study, nor Dr. Rostad, have explained how a short seizure of 8-50 seconds (as

reported by Gould et al.) could result in cerebral edema, herniation, and death,

especially given that convulsive seizures usually last much longer and yet still do not

generally result in death. (Ex. J, p. 1.) The SIDS, SUDC, and SUDEP literature does

explore the possibility that the mechanism of death in some sudden death cases may

be a terminal seizure; however, contrary to what Dr. Rostad asserts, this literature does

not suggest that such a hypothesis renders these deaths “explained” and Gould et al. is

not to the contrary. As noted above, Gould et al. explicitly stated that the cause of the

39

convulsive events they observed remains unknown. (Gould et al., supra, at Ex. 25, Tab

1, pp. 6-7.)

Of further note, while the concept of a cytokine storm is indisputably a part of

petitioners’ theory, as repeatedly cited by their experts (e.g., Ex. 13, pp. 7-9, 12-14; Ex.

18, pp. 20-21; Ex. 19, p. 3; Ex. 20, pp. 2-3.) and as explained in their initial brief (e.g.,

ECF No. 85, p. 39 (heading titled “In summary, the combination of a DTaP booster

vaccine, subsequent cytokine storm, aluminum adjuvant, subsequent infection, and host

susceptibility creates a perfect storm for a catastrophic event”), petitioners have

ultimately disclaimed any allegation that N.C. suffered a cytokine storm. (ECF No. 96,

p. 2.) This issue is further discussed under Althen prong two. However, for purposes of

Althen prong one, it is also important to note that petitioners in this program “must

provide a reputable medical or scientific explanation that pertains specifically to the

petitioner’s case.” Brokelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339,

1345 (Fed. Cir. 2020). Given that petitioners’ experts repeatedly invoked a cytokine

storm to explain how a post-vaccination cytokine response -- which is itself otherwise an

expected, and indeed intended, immune response -- could become fatally uncontrolled,

petitioners’ concession that N.C. did not suffer a cytokine storm dramatically undercuts

the reliability of their experts’ theory as it would apply in this case. These petitioners are

not the first to seek unsuccessfully to use the “cytokine storm” concept in a SUDC case

to bolster their cytokine-based theory despite its lack of applicability. E.g., Martin, 2020

WL 4197748, at *28 n.37 (noting in dismissal of a SUDC case that “[c]ircumstances

might be different if the record supported the conclusion that a ‘cytokine storm’ had

occurred, but Petitioner’s experts plainly stated they did not believe this to have

occurred herein”); Whitesell, 2022 WL 3081327, at *6 (rejecting cytokine storm theory to

explain SUDC); see also Bohn, 2021 WL 4302367, at *21 (explaining in a SIDS case

that, notwithstanding petitioner’s assertions, her pathologist expert “agrees on

petitioner’s behalf that a cytokine storm is not a useful concept in this case. He notes

that ‘[t]his is not a prototypical case of “cytokine storm,” a term used to describe fatal or

near-fatal events in the setting of severe infection with, usually, septicemia, which is

clearly not the case here’”).

In addition to the above, respondent argues that petitioners’ theory of causation

fails for numerous other reasons. He contends that there is no evidence that the DTaP

vaccine can cause a cytokine storm. (ECF No. 92, pp. 16-17.) Moreover, transient

elevations in cytokine levels as would be seen post vaccination have not been shown to

trigger seizures. (Id. at 17-18.) Petitioners have not demonstrated how peripheral

cytokines would affect the central nervous system. (Id. at 19.) Dr. Akbari’s invocation

of autoreactive T cells is entirely unsupported. (Id. at 19-20.) Neither the fact that

N.C.’s DTaP vaccination was a booster, nor the fact that it contained multiple antigens,

indicates that it would be more likely to produce pathogenic levels of cytokines. (Id. at

20-21.) Petitioners have not put forward reliable or persuasive evidence regarding any

pathologic role for aluminum adjuvant and have not demonstrated that nanoparticles

play any obvious role in disease development. (Id. at 22-23.) And, finally, petitioners

overstate the ability of the DTaP vaccine to cause any type of seizure. The evidence

favors only a finding that there is an increased risk of febrile seizure within 1-2 days of

40

DTaP vaccination. (Id. at 23-24.) However, because petitioners’ inability to meet their

burden of proof is otherwise clear from the analysis herein, and especially the analysis

under Althen prong two, I do not find it necessary to separately address each of these

points as a matter of general causation. Nonetheless, all of these points raised by

respondent are well taken and further demonstrate the shortcomings of petitioners’

theory of causation.

In light of all of the above, and considering the record as a whole, petitioners

have not met their burden of proof under Althen prong one.

b. Logical sequence of cause and effect (Althen prong two)

The second Althen prong requires proof of a logical sequence of cause and

effect, usually supported by facts derived from a petitioner’s medical records. Althen,

418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326-27;

Grant, 956 F.2d at 1147-48. Medical records are generally viewed as particularly

trustworthy evidence. Cucuras, 993 F.2d at 1528. However, medical records and/or

statements of a treating physician’s views do not per se bind the special master. See

§ 300aa-13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment, test result,

report, or summary shall not be binding on the special master or court”); Snyder, 88

Fed. Cl. at 745 n.67 (“[T]here is nothing . . . that mandates that the testimony of a

treating physician is sacrosanct—that it must be accepted in its entirety and cannot be

rebutted.”). A petitioner may support a cause-in-fact claim through either medical

records or expert medical opinion. § 300aa-13(a). The special master is required to

consider all the relevant evidence of record, draw plausible inferences, and articulate a

rational basis for the decision. Winkler, 88 F.4th at 963 (citing Hines, 940 F.2d at 1528).

In this case, the available medical opinion strongly favors the conclusion that

N.C.’s death is unexplained. N.C.’s case has undergone four different pathology

reviews – by the medical examiner, the SUDCRRC, and the two pathology experts

opining in this case – and all four reviews resulted in the conclusion that no cause for

N.C.’s death is evident. First, as part of the initial investigation, the medical examiner,

Dr. Hood, concluded that N.C. died a natural death and concluded that the cause of

death was “sudden unexplained death.” (Ex. 6, p. 16.) Later, a secondary analysis was

conducted by the SUDCRRC. (Ex. 15.) Following an independent pathology review, as

well as additional family interviews and genetic screening, the SUDCCRC also came to

the conclusion that N.C.’s death was an unexplained sudden death. (Id. at 6.) Although

Dr. Rostad criticized the SUDCCRC review, the SUDCCRC report simply characterized

their review as “in agreement with the pathologist of record.” (Id.) In that regard, Dr.

Rostad acknowledged that Dr. Hood’s autopsy was adequate and opined that he was

correct in classifying N.C.’s death as SUDC. (Ex. 18, p. 8.) Additionally, despite

seeking to otherwise explain N.C.’s death, Dr. Rostad at a minimum agreed that N.C.’s

death “overlapped” with sudden unexplained death (Id. at 21 (characterizing N.C.’s

death as similar to SUDEP, but without epilepsy)) and placed his findings within that

context. Thus, even setting aside his explicit endorsement of Dr. Hood’s conclusion, Dr.

Rostad’s own explanation for N.C.’s death is still firmly grounded in the SUDC literature

41

as explained under Althen prong one. (Id. at 24 (indicating that “[t]he autopsy findings,

favor that N.C.’s seizure threshold was lowered by hippocampal formation (HF)

maldevelopment. Recent evidence has emphasized the importance of the HF

maldevelopment in unexplained deaths in the pediatric age group”).) As respondent’s

pathology expert, Dr. Harris, summarized:

This tragic child’s death does not have a clear cause, an opinion shared by

the multiple physicians evaluating it during the autopsy process and now in

retrospect by our evaluations. I also have this opinion and believe this was

correctly stated at autopsy and by the body of physicians of the SUDCRRC

who evaluated this and many such cases.

(Ex. E, p. 7.) Moreover, after developing their theory of causation, petitioners sought to

have the medical examiner revisit his initial conclusions. However, even after being

apprised of petitioners’ theory, Dr. Hood did not change his conclusion as to the cause

of N.C.’s death and explicitly declined to comment on whether N.C.’s vaccination

contributed to his death.37 (Ex. 24, pp. 1, 5.)

Although rebuttable, the “medical records and medical opinion testimony” of

treating physicians can be “quite probative,” because “treating physicians are likely to

be in the best position to determine whether ‘a logical sequence of cause and effect

show[s] that the vaccination was the reason for the injury.’” Capizzano, 440 F.3d at

1326 (quoting Althen, 418 F.3d at 1280); accord Andreu, 569 F.3d at 1376. This

principle has also been applied in the context postmortem conclusions because,

although not strictly speaking “treating” physicians, the opinions of coroners and

medical examiners are based on their direct autopsy examinations and role in

investigating the cause of death. Nordwall ex rel. Tori v. Sec’y of Health & Human

Servs., 83 Fed Cl. 477, 488 (2008) (explaining that “[a]n autopsy report by a medical

examiner is without question a contemporaneous medical record” and that “[w]hile such

records may not have been created in the context of diagnosis and treating a patient,

they are contemporaneous records made by a health professional outside the context of

litigation, and should be given the same probative weight as other medical records”);

Pelton v. Sec’y of Health & Human Servs., No. 14-674V, 2017 WL 1101767, at *13

(Fed. Cl. Spec. Mstr. Feb. 27, 2017) (indicating that “[a]lthough neither Dr. Eisenstat nor

the coroner are treating physicians, it remains the case that they were better positioned

than [petitioner’s expert] to evaluate the cause and effect based on in-person inspection

37

Both parties raise competing arguments with respect to Dr. Hood’s report and addendum to his report.

(ECF No. 92, pp. 30-32; ECF No. 96, pp. 6-10.) Of particular note, petitioner questions the reliability of

Dr. Hood’s initial report because he presumed that N.C.’s SUDC was related to cardiac dysthymia related

to long QT syndrome whereas the SUDCRRC report subsequently cast doubt on that presumption by

ruling out long QT syndrome. (ECF No. 96, pp. 6-7, 9.) However, this is not very significant. Dr. Hood’s

conclusion, in both his initial report and, by extension, his addendum, was that N.C.’s death was

unexplained. The fact that Dr. Hood’s speculation regarding one potential mechanism of SUDC did not

withstand further investigation does not undermine the conclusion that N.C.’s death remains unexplained

or in any way suggest any other cause. In contrast, respondent argues that Dr. Hood’s addendum to his

report should be given less weight given that it was not produced in the context of his initial evaluation.

(ECF No. 92, pp. 31-32.) However, because I have not identified any manner in which Dr. Hood’s

addendum meaningfully supports petitioners’ allegations, this issue is moot.

42

of the scene and physical examination of the body.”); Bohn, 2021 WL 4302367, at *11;

Gaskin v. Sec’y of Health & Human Servs., No. 21-835V, 2025 WL 786306, at *13 (Fed.

Cl. Spec. Mstr. Feb. 11, 2025). Indeed, the Vaccine Act specifies that the special

master “shall consider” any “autopsy or coroner’s report which is contained in the

record” with respect to the nature or cause of a vaccinee’s death. § 300aa-13(b)(1)(A).

Here, I have considered petitioners’ challenges to the medical examiner’s conclusion

that N.C.’s death was a sudden unexplained death. However, despite having compiled

an extensive record reviewing those findings, they have not presented any significant

cause to doubt that conclusion. Accordingly, the medical opinion in this case

preponderates in favor of a finding that N.C.’s death remains unexplained.

Dr. Rostad has not preponderantly established that N.C. suffered fatal cerebellar

edema and brainstem herniation. Although Dr. Harris did not engage in great detail with

Dr. Rostad’s observations, and in fact declined to respond to Dr. Rostad’s annotated

autopsy photos, he was clear in asserting 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 herniation.” (Ex. E, p. 6.) This is

consistent with Dr. Hood’s autopsy report. (Ex. 5, p. 19; Ex. 24, p. 4 (noting brain

swelling “as evidenced by some effacement of sulci” and with “mild bilateral uncal

impressions” and a modest cerebellar ‘cone,’ but no other herniation of any of its

parts.”).) In that regard, Dr. Holmes further explained that a fatal cerebral edema is

unlikely given N.C.’s own history. (Ex. C, pp. 7-9.) Whereas cerebral edema can be

associated with status epilepticus, that is a more severe presentation than the two

seizures alleged by petitioners. (Ex. C, p. 7 (citing Trinka et al., supra, at Ex. C, Tab

22)).) Moreover, Dr. Holmes opines that cerebral edema does not develop

instantaneously following a seizure, meaning that Dr. Rostad’s implication that a

terminal seizure resulted in a fatal degree of cerebral edema is unlikely. (Ex. C, pp. 8-9

(citing Lan et al., supra, at Ex. C, Tab 32; Myers et al., supra, at Ex. C, Tab 33).) In that

regard, Dr. Harris noted that N.C.’s last known presentation was not consistent with a

developing brain herniation. (Ex. H, p. 2.)

Despite this, Dr. Rostad effectively contends that he completed the most detailed

pathology review and therefore his opinion should carry the most weight. (See, e.g., Ex.

19, pp. 3-8; Ex. 22, pp. 2-8 (arguing that the reviews completed by Dr. Harris and

SUDCRRC were not complete or comprehensive, notably for their failure to review the

scene and gross autopsy photographs).) However, this is not persuasive. Dr. Harris,

Dr. Hood, and the SUDCRRC, each separately concluded that there were insufficient

abnormalities to set aside the SUDC designation and Dr. Rostad at a minimum

acknowledged Dr. Hood’s autopsy to be adequate. (Ex. 18, p. 8.) Criticism of Dr

Harris’s decision not to explicitly rebut Dr. Rostad’s annotated autopsy photos is

misdirected given that Dr. Hood – the only pathologist to have completed an in person

gross autopsy examination and who created the photographs at issue – was likewise

explicit in noting the absence of any herniation despite also acknowledging some

degree of swelling. And, as explained above, he did not revisit this finding even after

being prompted by petitioners to address Dr. Rostad’s reports and provide a

supplement to his original report. (Ex. 24, pp. 4-5.) Without entirely discounting Dr.

43

Rostad’s competing medical judgment, preferring his review would effectively mean

accepting that cerebral swelling significant enough to cause death could occur while

leaving signs so subtle that only one out of four pathologists would note them and

conclude they were significant. Even accounting for Dr. Rostad’s criticisms of the

completeness of the other reviews, and especially given the overall record, this seems

less likely. To the extent this issue of clinical judgment may boil down to a difference of

degrees, both Dr. Harris and Dr. Holmes confirmed that some degree of excessive brain

weight and congestion remains consistent with a sudden unexplained death. (Ex. C, p.

7; Ex. E, p. 6.)

In any event, there is also not preponderant evidence that N.C. suffered a

terminal seizure as has been proposed by petitioners. In his supplement to the autopsy

report, Dr. Hood stated that N.C. had findings consistent with a terminal seizure, but he

cautioned that the same findings “can result from almost any form of terminal hypoxia.”

(Ex. 24, p. 5.) Dr. Hood stated that “the most I can opine is that if [N.C.] had a terminal

seizure his autopsy finding would be just as were present in this case.” (Id.) This is not

significant evidence supportive of petitioners’ claim. Dr. Harris had similarly explained

that “[t]he neuropathological examination was not sufficient to rule in or out a seizure

related incident.” (Ex. E, p. 6.) In response, Dr. Rostad stressed that “[f]requently there

is scant evidence at autopsy to determine when a seizure has occurred and or that it

was the cause of death in an unwitnessed case.” (Ex. 19, p. 10.) He relied on the idea

that specific features of a terminal seizure “may be absent or nonspecific.” (Id. at 11.)

Without more, the fact that the autopsy findings do not “rule out” a terminal seizure is

not tantamount to preponderant evidence that such a seizure occurred.38

Petitioners have suggested the undersigned’s prior ruling in Rodela v. Secretary

of Health & Human Services, No. 17-236V, 2024 WL 2034220 (Fed. Cl. Spec. Mstr.

Apr. 5, 2024), supports the proposition that prior petitioners were “found to be entitled to

compensation for an unwitnessed seizure in a toddler that resulted in the toddler’s death

following administration of multiple vaccinations.” (ECF No. 96, p. 7.) However, the

Rodela case is not informative, because it was not an unexplained death case. 2024

WL 20344220, at *28 (explaining that “I have concluded that this is not an instance of

unexplained death consistent with any of the categorizations of sudden unexplained

deaths in either infancy or childhood (i.e., SUDC, SUDEP, SIDS, or SUID).”) Rather,

the Rodela ruling addressed a claim of a Table Injury of encephalitis, which was entitled

to a presumption of vaccine causation, and the seizures at issue in that case were

attributable to the encephalitis. Id. at 24-25, 29. Here, however, the medical examiner

has confirmed that “[neuropathological examination found no encephalitis.” (Ex. 24, p.

5.) Absent the presence of an encephalitis, and more similar to this case, prior

petitioners were unable to reliably hypothesize that an unwitnessed seizure explained

how vaccination could result in SUDC. Anklam, 2023 WL 8890662, at *38-41.

38

Additionally, to the extent respondent’s experts acknowledged that the DTaP vaccine can cause febrile

seizures (albeit only 1-2 days post-vaccination), it is also worth noting that there is no evidence that N.C.

was suffering a fever around the time of his death. Instead, the contemporaneous accounts are explicit in

indicating that he had seemingly recovered from his prior febrile illness days prior to his death. (See, e.g.,

Ex. 1, ¶ 12; Ex. 2, ¶ 11; Ex. 9, p. 9; Ex. 10, p. 69.)

44

Moreover, the specific finding in Rodela that a terminal seizure had likely occurred was

base

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