1

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: February 9, 2016

* * * * * * * * * * * * * PUBLISHED DECISION

LESLIE LORD and RANDALL *

MAGNUSKI, legal representatives of a * No. 12-255V

deceased minor child, C.L., *

* Chief Special Master Dorsey

Petitioners, *

* Denial of Entitlement; 

v. * Hepatitis B (Hep B) Vaccine;

* Inactivated Polio (IPV) Vaccine;

SECRETARY OF HEALTH * DTaP Vaccine; Haemophilus Influenza 

AND HUMAN SERVICES, * (Hib) Vaccine; Pneumococcal 

* Conjugate (PCV) Vaccine; Rotavirus

Respondent. * Vaccine; Sudden Infant Death 

* Syndrome (SIDS)

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

Ronald C. Homer, Conway, Homer & Chin-Caplan, P.C., Boston, MA, for petitioners.

Jennifer L. Reynaud, United States Department of Justice, Washington, DC, for respondent. 

DECISION1

Leslie Lord and Randall Magnuski (“petitioners”) filed a petition under the National 

Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”),242 U.S.C. § 300aa-10 

et seq. (2012), as the representatives of the estate of their deceased minor child, C.L. Petitioners 

alleged that C.L. died on May 13, 2011, as a result of receiving the hepatitis B (“Hep B”); 

Diphtheria-Tetanus-acellular-Pertussis (“DTaP”), inactivated polio (“IPV”), haemophilus influenza 

(“Hib”); Pneumococcal Conjugate (“PCV”); and Rotavirus vaccinations on May 11, 2011. See

Petition, filed Apr. 18, 2012, at 1 n.1, ¶ 8; Amended Petition, filed May 23, 2013, at 1. Respondent 

recommended against awarding compensation to petitioners. See Respondent’s Response (“Resp. 

Res.”), filed Aug. 8, 2013, at 1. 

 

1 Because this decision contains a reasoned explanation for the undersigned’s action in this case, the 

undersigned intends to post this ruling on the website of the United States Court of Federal Claims, in 

accordance with the E-Government Act of 2002, 44 U.S.C. § 3501 note (2012)(Federal Management and 

Promotion of Electronic Government Services). As provided by Vaccine Rule 18(b), each party has 14 days 

within which to request redaction “of any information furnished by that party: (1) that is a trade secret or 

commercial or financial in substance and is privileged or confidential; or (2) that includes medical files or 

similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine 

Rule 18(b). 

2 The National Vaccine Injury Compensation Program is set forth in Part 2 of the National Childhood 

Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended, 42 U.S.C. §§ 300aa10 to -34 (2012). All citations in this decision to individual sections of the Vaccine Act are to 42 U.S.C. § 

300aa.
2

After carefully analyzing and weighing all of the evidence and testimony presented in this 

case in accordance with the applicable legal standards, the undersigned finds that petitioners have

not met their legal burden. Petitioners have failed to provide preponderant evidence that the 

vaccinations C.L. received on May 11, 2011, caused his death. Accordingly, petitioners are not 

entitled to compensation. 

The undersigned notes that her decision in this case is consistent with those in other similar 

SIDS cases heard by special masters in the Vaccine Program (and upheld on review), in which 

petitioners have been denied entitlement because of the lack of sufficient proof of causation. See, 

e.g., Doe/11 v. Sec’y of Health & Human Servs., 601 F.3d 1349 (Fed. Cir. 2010) (upholding Special 

Master Campbell-Smith’s decision that a death labeled “SIDS” was not caused by a hepatitis B 

vaccine); Waterman v. Sec’y of Health & Human Servs., No. 13-960V, 2015 WL 4481244 (Fed. Cl. 

Spec. MsTr. at June 30, 2015) (aff’d 123 Fed. Cl. 564 (Fed. Cl. 2015) (Chief Judge CampbellSmith)) (Special Master Hamilton-Fieldman denied entitlement in a SIDS case finding that 

petitioners did not prove that their child suffered an encephalopathy prior to his death); Sanchez v. 

Sec'y of Health & Human Servs., No. 11-651V, 2013 WL 4476750 (Fed. Cl. Spec. MsTr. at July 

26, 2013 ) (Special Master Millman found that petitioner failed to prove that vaccinations caused 

SIDS death); Bigbee v. Sec'y of Health & Human Servs., No. 06-663V, 2012 WL 1237759 (Fed. 

Cl. Spec. MsTr. at Mar. 22, 2012) (Special Master Golkiewicz held that petitioners failed to 

produce preponderant evidence that the vaccines caused the child’s death); Nordwall v. Sec’y of 

Health & Human Servs., No. 05-0123V, 2008 WL 857661 (Fed. Cl. Spec. MsTr. at Feb. 19, 2008)

(Special Master Moran held that a SIDS death was not due to a vaccine but rather “positional 

asphyxia”) (mot. for review denied, 83 Fed. Cl. 477 (Fed. Cl. 2008)); and Heller v. Sec’y of Health 

& Human Servs., No. 96-797V, 1998 WL 408612 (Fed. Cl. Spec. MsTr. at June 22, 1998) (Special 

Master Millman found that studies did not show a causal link and that petitioner failed to 

demonstrate a causal relationship between DPT vaccine and SIDS).

I. BACKGROUND

A. Procedural History

On April 18, 2012, petitioners filed a petition for compensation on behalf of their deceased 

minor son, C.L., pursuant to the Vaccine Act. On May 23, 2013, petitioners filed an amended 

petition alleging that “as a result of receiving [the] vaccinations on May 11, 2011, [C.L.] died on 

May 13, 2011.” Amended Petition at 1. 

Petitioners filed the expert report of Dr. Douglas C. Miller, a neuropathologist, on February 

8, 2013, along with the medical literature referenced in Dr. Miller’s report. See Pet. Exs. 22-46. In

a status report filed March 28, 2013, respondent noted that petitioners had filed expert reports 

espousing the same theory of causation, with the same literature, and from the same expert, as

petitioners in Cozart, 00-590V, and Sexton, 99-453V. Resp. Status Rep., filed March 28, 2013. 

Because of this overlap, respondent requested that common testimony be taken for all three cases at 

one hearing. Id. Petitioners, however, opposed such a consolidation. Pet. Status Rep., file June 14, 

2013, at 2. After a status conference on July 9, 2013, the undersigned ordered the parties to proceed 

with proposing dates for a hearing in this case only, and the cases were not consolidated. See

Order, filed July 9, 2013. 
3

Respondent filed the expert report of Dr. Hart Lidov, a neuropathologist, on May 28, 2013, 

followed by the medical literature referenced in his report on June 4, 2013. See Resp. Ex. A.

3

 

Respondent also filed an expert report from Dr. Christine McCusker, an immunologist, on August 

8, 2013, followed by the medical literature referenced in her report on August 9, 2013. Resp. Ex. C. 

On August 8, 2013, respondent filed her Rule 4(c) report advising against compensation.

Petitioners filed an expert report from Dr. James Oleske, an immunologist, on December 11, 

2013, along with the medical literature referenced in his report. Pet. Ex. 50. Respondent filed a 

supplemental expert report from Dr. Christine McCusker on February 10, 2014. See Resp. Ex. E. 

Respondent filed two additional medical articles on July 17, 2015. Resp. Exs. F, G. 

At numerous stages of this case, the undersigned encouraged the parties to pursue the 

possibility of an informal resolution, and/or to consider mediation. See, e.g. Order, filed July 9,

2013; Order, filed October 29, 2013; Order, filed June 26, 2015. The parties made several attempts

but were ultimately unable to resolve the case informally before hearing. See, e.g. Joint Status 

Rep., filed March 28, 2014; Joint Status Rep., filed July 9, 2015.

An entitlement hearing was held on Wednesday, July 29, and Thursday, July 30, 2015, in 

Washington, D.C. Dr. Miller testified on behalf of petitioners, and Drs. McCusker and Lidov 

testified on behalf of respondent. Dr. Oleske did not testify. After the hearing, the parties filed 

additional medical literature referenced by their experts during the hearing. See Pet. Exs. 57-61; 

Resp. Exs. F-H.

4

 Petitioners filed a status report indicating that they did not intend to present 

additional expert testimony from Dr. Oleske. Pet. Status Rep., filed Aug. 31, 2015. Petitioners 

filed their post-hearing brief on October 26, 2015, and respondent filed her post-hearing brief on 

December 2, 2015. 

This matter is now ripe for adjudication. 

B. Summary of Relevant Facts

C.L. was born prematurely on November 6, 2010, at just under thirty-six weeks gestation. 

Pet. Ex. 1; Pet. Ex. 2 at 4. A few hours after birth, C.L. became hypothermic and was noted to show

decreased peripheral blood oxygen content (“desaturation”). See Pet. Ex. 22 at 4. However, he was 

subsequently observed to be growing and developing normally at his one, two, and four-month 

well-baby checkups. Pet. Ex. 4 at 4, 6, 13. At his one month checkup, the pediatrician noted that 

his father smoked outside of the family home. Id. at 3. In addition, the pediatrician noted that C.L. 

was “sleeping in rocker with pillow underneath and blanket tucked tightly in rocker. . . aware of 

increased risk of SIDS with pillows and blanket.” Id. On physical exam at his two-month visit, the 

pediatrician noted that C.L. was “not yet fixing and following” and had a “dysconjugate gaze.” Id.

at 6. At his four month checkup, however, he was noted to fix and follow. Id. at 12. C.L. received 

 

3 The medical records filed by petitioner included handwritten pagination, and citations to medical records in 

this decision are to the handwritten page number. The majority of the expert reports and medical literature 

filed by both parties, however, was not individually paginated, therefore citations in this decision are to the 

case management electronic case filing system (CM/ECF) pdf page number.

4 Respondent’s exhibits appear to be mislabeled, as she had already filed exhibits labeled F and G on July 17, 

2015.
4

DTaP, IPV, Hib, PCV and rotavirus vaccinations at his four-month well-baby checkup, and his 

mother noted that he “seemed a bit sleepier than usual, but otherwise [nothing] unusual.” Pet. Ex. 

10 at ¶ 4. 

On May 11, 2011, C.L. was seen for his six-month well-baby checkup and received DTaP,

IPV, Hib, PCV, rotavirus, and Hep B vaccines.5 Pet. Ex. 4 at 17. At this visit, the pediatrician 

described C.L. as “[a]lert, interactive, [and] [s]miling.” Id. at 16. The pediatrician also noted that 

C.L. had macrocephaly, which she thought was “likely benign and genetic,” but she nonetheless 

wanted to rule out underlying conditions of the brain. Id. at 17. 

C.L.’s mother, father, grandmother, and baby-sitter submitted affidavits in support of the 

petition. C.L.’s mother stated that receiving his vaccinations on May 11, 2011, C.L. “became very 

sleepy and fell asleep” in the car. Pet. Ex. 10 at ¶ 9. That afternoon and evening, C.L. was cranky, 

refused to eat dinner, and went to bed much earlier than usual. Id. at ¶¶ 11-13. C.L. spent the next 

day with his babysitter, “remained out of sorts,” and went to bed a little earlier than usual again. Id.

at ¶¶ 14-15. 

His parents attested that the following day, May 13, 2011, C.L. did not wake up on his own, 

which was unusual. Pet. Ex. 10 at ¶ 16; Pet. Ex. 11 at ¶ 9. That morning, C.L.’s father drove him to 

his grandmother, Suzanne Lord, who had agreed to watch him for the day. Pet. Ex. 11 at ¶ 10. 

C.L.’s grandmother attested that C.L. took a nap around 10:30 in the morning for about an hour, fell 

asleep again during a walk outside in a stroller, and remained asleep until about 1:45 pm. Pet. Ex. 

12 at ¶¶ 8-10. He was “extremely fussy and crying” when he awoke, and it was unusual for him to 

“sleep like this up to this point in the day.” Id. at ¶¶ 9, 10. Around 3:00 o’clock in the afternoon, 

C.L. became sleepy again, so she placed him face up in the crib for a nap. Id. at ¶ 12. When she 

returned to his room around 4:15 pm, she saw him lying in the crib face down. Id. at ¶ 13. Nothing 

was coming out of his mouth at that time. Id. C.L. was unresponsive when nudged, and when she 

turned him over on his back, she saw a bluish hue around his eyes and face. Id. at ¶ 14. She tried to 

perform chest compressions and blow into his mouth, whereupon a “white fluid that seemed like 

baby formula” came out of his mouth. Id. at ¶ 15.

The police incident report states that Suzanne Lord had been babysitting C.L. and laid him 

on his back for a nap around 3:00 o’clock in the afternoon. Pet. Ex. 8 at 5. “There was no blanket 

covering him and there was a small stuffed animal in the corner.” Id. at 5, 21. Upon returning to 

the room at around 3:55PM, she saw that he had “turned onto his stomach and had his arms out to 

the sides.” Id. Ms. Lord told the police that she had never seen C.L. sleep on his stomach. Id. 

When re-interviewed on May 14, 2014, Ms. Lord was again “adamant” about having placed C.L. in 

the crib on his back, and reiterated that she found him on his stomach. Id. at 6. He did not respond

when nudged, and when she picked him up his face was blue. Id. She said she immediately began 

doing chest compressions, placed him on the changing table, and dialed 911. Id. When the police 

arrived, C.L.’s grandmother “pointed out a wet spot where his face had been on the mattress” and 

said that “when she was blowing into his mouth he spit up some white liquid which she thought was 

formula.” Id. at 5. C.L.’s father stated that there had been several occasions where C.L. would spit 

up when placed on his stomach on the floor for play time. Id. at 6. 

 

5 He received the rotavirus vaccine orally, and the other vaccines in his thighs. See Pet. Ex. 4 at 17. 
5

C. L. was transported to Saint Anne’s Hospital by the Little Compton and Tiverton 

Fire/Rescue, and was admitted to the emergency department at 5:22PM on May 13, 2011. Pet. Ex. 

6; Pet. Ex. 7 at 1. Efforts to resuscitate him were unsuccessful, and C.L. was pronounced dead on 

May 13, 2011. Id. at 5; Pet. Ex. 14. The attending physician at Saint Anne’s reported finding 

lividity on C.L.’s back. See Pet. Ex. 7 at 4-5; Pet. Ex. 8 at 5. Dr. Zane, the medical examiner who 

performed the autopsy on May 15, 2011, also noted posterior lividity.6 Pet. Ex. 9 at 10. 

On autopsy, Dr. Zane ruled the cause of death “[s]udden unexpected infant death of 

uncertain etiology” and the manner “natural.” Pet. Ex. 9 at 9. The parties agree that the 

characterization of C.L.’s cause of death as sudden infant death syndrome (“SIDS”), is appropriate. 

Joint Prehearing Submission, filed June 16, 2015, at 1.

The parties’ experts in neuropathology, Dr. Miller and Dr. Lidov, reviewed slides of C.L.’s 

brain. Both experts agreed that the slides showed some nonspecific abnormalities in the frontal 

white matter, as well as a group of cells that appeared to belong to the inferior olivary nucleus (part 

of the medulla) located out of place, more dorsally in the brainstem. See Tr. at 11-12, 344-46. 

II. SUDDEN INFANT DEATH SYNDROME 

Sudden infant death syndrome is defined as “the sudden death of an infant less than [one]

year of age that remains unexplained after a complete autopsy, death scene investigation, and 

review of the clinical history.” Pet. Ex. 27 at 2.

7

 The majority of deaths occur during “a sleep 

period.” Resp. Ex. A-10 at 1.

8

 It is not clear “whether SIDS occurs during sleep itself or during the 

many transitions between sleep and arousal that occur . . . since [] deaths are typically not 

witnessed.” Id.

SIDS is the leading cause of infant mortality in the United States, with an incidence of about 

.53 per 1,000 infants. Resp. Ex. C-11 at 3.9 Research into the causes of SIDS has revealed that the 

risk of death is twofold in infants who are put to sleep in the prone, i.e. face down, position. Id. 

Sleeping in the prone position is thought to trigger infant death through “asphyxia due to airway 

compression or rebreathing of exhaled gases in the face-down position . . . . and compromised 

arousal in response to asphyxia generated in the prone position.” Resp. Ex. A-10 at 2. Other risk 

factors for SIDS related to the “sleeping environment” have been recognized, including “overbundling, bed sharing, face down position and soft bedding.” Pet. Ex. 27 at 3. 

 

6 According to the police report, when informed that C.L.’s grandmother reported finding C.L. lying on his 

stomach, Dr. Zane opined that her account was not inconsistent with the facts of the case. Pet. Ex. 8 at 9. 

Dr. Zane said that due to the time C.L. was placed in the crib and the time of the call to 911, lividity would 

have set in after C.L. was moved. Id. at 9.

7 Pet. Ex. 27, Hannah C. Kinney, Brainstem Mechanisms Underlying the Sudden Infant Death Syndrome: 

Evidence from Human Pathologic Studies, 51 DEV. PSYCHOBIOL. 223 (2009).

8 Resp. Ex. A-10, Hannah C. Kinney & Bradley T. Thach, The Sudden Infant Death Syndrome, 361(8) NEW 

ENG. J. MED. 795, 798 (2009) (quoting Daniel C. Shannon & Dorothy H. Kelly, SIDS and Near-SIDS, 306 

NEW ENG. J. MED. 959 (1982)).

9 Resp. Ex. C-11, Felicia L. Trachtenberg et al., Risk Factor Changes for Sudden Infant Death Syndrome 

After Initiation of Back-to-Sleep Campaign, 129 PEDIATRICS 630 (2012).
6

In 1994, Dr. Hannah C. Kinney and her colleagues proposed the Triple Risk Model as a way 

to conceptualize the “emerging multidisciplinary data.” Resp. Ex. A-10 at 2. According to this 

model, SIDS occurs when three factors are simultaneously present: an underlying vulnerability in 

the infant; a critical developmental period; and an exogenous stressor. Pet. Ex. 25/Resp. Ex. A-7 at 

3.10 The Venn diagram below illustrates the Triple Risk Model: 

 

Id. at 2, Figure 1.

The underlying vulnerability of an infant is affected by intrinsic risk factors, which may be 

either genetic or environmental. Resp. Ex. A-10 at 4; Resp. Ex. C-11 at 3-4. Intrinsic risk factors 

include “developmental factors, such as prematurity . . . genetic factors, such as familial SIDS (i.e., 

a recurrence of SIDS in subsequent siblings), male sex (by a 2:1 ratio), and race or ethnic group.” 

Resp. Ex. A-10 at 4. In addition, “environmental conditions extrinsic to the infant, such as poverty, 

adverse prenatal exposures to certain substances (e.g. cigarette smoke and alcohol or illicit drugs), 

and postnatal exposure to cigarette smoke.” Id. at 4-5. 

Exogenous, or “extrinsic” risk factors, on the other hand, are “physical stressors that [] place 

a vulnerable infant at risk for asphyxia or other homeostatic derangement.” Resp. Ex. A-10 at 4. 

These factors include “prone and side-sleeping positions, bedclothes that cover the head, sleeping 

on sofas or other soft furniture in which the infant could become wedged, a high ambient 

temperature in the sleeping environment, soft bedding, and bed sharing.” Id. The prone sleeping 

position is still associated with 30% to 50% of SIDS cases and another 50% occur where infants are 

“sharing a bed, sofa, or sofa chair with another person.” Id. Another extrinsic risk factor is mild 

infection, including colds or upper respiratory tract infections. Id.; Resp. Ex. C-11 at 4. 

“The occurrence of extrinsic risks in virtually all SIDS deaths implies that SIDS is 

precipitated by a ‘trigger’ at the time of death. These extrinsic risk factors are consistent with 

asphyxia-generating conditions, e[.]g[.], face-down position, prone position, and adult mattress.” 

Resp. Ex. C-11 at 5. Studies have shown that having multiple risk factors significantly increases the 

risk of SIDS. In a 2012 article by Trachtenberg, et al.,11 the authors studied 568 SIDS deaths from 

 

10 Pet. Ex. 25/Resp. Ex. A-7, Hannah C. Kinney et al., Medullary Serotonergic Network Deficiency in the 

Sudden Infant Death Syndrome: Review of a 15-Year Study of a Single Dataset, 60 J. NEUROPATHOLOGY 

AND EXPERIMENTAL NEUROLOGY 228 (2001). 

11 Resp. Ex. C-11, Trachtenberg, supra note 8 at 635. 
7

the San Diego Medical Examiner’s Office from 1991 to 2008 and found that the “majority of SIDS 

infants were subject to at least 2 extrinsic risk factors.” Resp. Ex. C-11 at 7.

The mechanism of death of SIDS has been thought to be related to a failure of the 

“autonomic regulation of cardiovascular or respiratory activity or both.” Resp. Ex. A-10 at 5. 

There is “compelling evidence for a respiratory pathway in the majority of SIDS deaths.” Id. The 

“respiratory pathway to SIDS” can be described in five steps. Id. The infant first has a “lifethreatening event,” which may occur in any infant during sleep, which causes “severe asphyxia, 

brain hypoperfusion, or both.” Id. Examples of life-threatening events include “rebreathing of 

exhaled gases in the face-down position . . . reflex apnea originating from the laryngeal 

chemoreflex, and obstructive apnea due to gastric regurgitation.” Id. Second, the “vulnerable 

infant does not wake up and turn his or her head in response to asphyxia . . . resulting in rebreathing 

or an inability to recover from apnea.” Id. “Third, progressive asphyxia leads to a loss of 

consciousness and areflexia, a so-called hypoxic coma.” Id. Fourth, the infant develops “extreme 

bradycardia and hypoxic gasping.” Id. Fifth and finally, there is a failure of autoresuscitation due 

to ineffective gasping that leads to “uninterrupted apnea and death.” Id. The increased risk of SIDS 

in infants younger than six months is probably due to “immature homeostatic systems” and 

“developmental motor mechanisms,” such as the inability of an infant to lift and turn his or her head 

in the prone position. Id. at 7-8. 

Research on the “underlying vulnerability” present in infants who die of SIDS has focused 

on the area of the brainstem responsible for autonomic function and respiration. Resp. Ex. A-10 at 

7. This research suggested that 50% to 75% of infants who die of SIDS may have a neurochemical 

abnormality in the “medullary 5-hydroxytryptamine system,” (“5-HT system”), which modulates 

and integrates many different homeostatic functions, including “ventilation and gasping . . . 

responses to carbon dioxide and oxygen, [and] arousal from sleep.” Id. This vulnerability has also 

been described as a “deficiency in the neurotransmitter serotonin [5-HT] in [the] brainstem regions

that help mediate protective responses to homeostatic stressors such as asphyxia...” Resp. Ex. C-11 

at 5. The area of defect is referred to as the “medullary 5-HT system,” which is comprised of “5-

HT neuronal cell bodies” located in the medulla. Pet. Ex. 27 at 4. Animal research indicated that 5-

HT “influences multiple homeostatic functions mediated by the medulla,” including “central 

chemoreception to carbon dioxide and/or oxygen . . . cardiovascular function . . . upper airway 

control . . . [and] respiratory rhythm generation.” Id. at 4-5. Kinney and her colleagues believed 

that there is a “subclinical autonomic dysfunction associated with SIDS” related to abnormalities of 

the “medullary 5-HT system,” which is seen on autopsy. Id. at 5. They hypothesized that the 

medullary 5-HT defect originates in utero during the period of development and differentiation of 

the brainstem. Id. at 7. They also believed that “sudden death in SIDS likely results from a 

complex interaction of several/multiple dysfunctional neurotransmitter systems in the brainstem, 

and that death is triggered by homeostatic stressors during sleep in a vulnerable developmental 

period.” Id. at 8.

III. STANDARDS FOR ADJUDICATION

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

300aa-10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system 

as a simple, fair and expeditious means for compensating vaccine-related injured persons. The 

Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty and 
8

generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7 (1996) (quoting H.R. 

Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioners’ burden of proof is by a preponderance of the evidence. § 300aa-13(a)(1). The 

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the 

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health & 

Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, petitioners must prove that that 

the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing 

about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 

165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 

1352, 1355 (Fed. Cir. 2006). A petitioner who satisfies this burden is entitled to compensation 

unless respondent can prove, by a preponderance of the evidence, that the vaccine’s injury is “due 

to factors unrelated to the administration of the vaccine.” § 300aa-13(a)(1)(B).

IV. EXPERT OPINIONS AND CAUSATION ANALYSIS

A. Issue

The parties agree that the sole issue to be resolved is “[w]hether the vaccines that C.L.

received on May 11, 2011, caused or substantially contributed to his death.” (citations omitted). 

See Joint Prehearing Submission, filed June 16, 2015, at 2.

B. Legal Framework

To receive compensation under the Program, petitioners must prove either: (1) that C.L. 

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table— corresponding to a 

vaccine that he received, or (2) that C.L. suffered an injury that was actually caused by a 

vaccination. See §§ 300aa-13(a)(1)(A) and 11(c)(1); Capizzano v. Sec’y of Health & Human Servs., 

440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Petitioners must show that the vaccine was “not only a 

but-for cause of the injury but also a substantial factor in bringing about the injury.” Moberly, 592 

F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because petitioners do not allege that C.L. suffered a Table injury, they must prove that the 

vaccines C.L. received caused his death. To do so, they must establish, by preponderant evidence: 

(1) a medical theory causally connecting the vaccine and his injury (“Althen Prong One”); (2) a 

logical sequence of cause and effect showing that the vaccine was the reason for his injury (“Althen

Prong Two”); and (3) a showing of a proximate temporal relationship between the vaccine and his 

injury (“Althen Prong Three”). § 300aa–13(a)(1); Althen v. Sec’y of Health & Human Servs., 418 

F.3d 1274, 1278 (Fed. Cir. 2005).

The causation theory must relate to the injury alleged. Thus, petitioners must provide a 

reputable medical or scientific explanation that pertains specifically to this case, although the 

explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Petitioners cannot 

establish entitlement to compensation based solely on their assertions. Rather, a vaccine claim must 

be supported either by medical records or by the opinion of a medical doctor. § 300aa-13(a)(1). In 

determining whether petitioners are entitled to compensation, the special master shall consider all 
9

material contained in the record, including “any . . . conclusion, [or] medical judgment . . . which is 

contained in the record regarding . . . causation.” § 300aa-13(b)(1)(A). The undersigned must 

weigh the submitted evidence and the testimony of the parties’ offered experts and rule in 

petitioners’ favor when the evidence weighs in their favor. See Moberly, 592 F.3d at 1325-26 

(“Finders of fact are entitled—indeed, expected—to make determinations as to the reliability of the 

evidence presented to them and, if appropriate, as to the credibility of the persons presenting that 

evidence”); Althen, 418 F.3d at 1280 (“close calls” are resolved in petitioner’s favor).

Another important aspect of the causation-in-fact case law under the Vaccine Act concerns 

the factors that a special master should consider in evaluating the reliability of expert testimony and 

other scientific evidence relating to causation issues. In Daubert v. Merrell Dow Pharm., Inc., 509 

U.S. 579 (1993), the United States Supreme Court listed certain factors that federal trial courts 

should utilize in evaluating proposed expert testimony concerning scientific issues. In Terran v. 

Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999), the Federal Circuit ruled 

that it is appropriate for special masters to utilize Daubert’s factors as a framework for evaluating 

the reliability of causation-in-fact theories actually presented in Program cases.

The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or 

technique can be (and has been) tested; (2) whether the theory or technique has been subjected to 

peer review and publication; (3) whether there is a known or potential rate of error and whether 

there are standards for controlling the error; and (4) whether the theory or technique enjoys general 

acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing Daubert, 

509 U.S. at 592-95). In addition, where both sides offer expert testimony, a special master’s 

decision may be “based on the credibility of the experts and the relative persuasiveness of their 

competing theories.” Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. 

Cir. 2010) (citing Lampe v. Sec'y of Health & Human Servs., 219 F.3d 1357, 1362 (Fed.Cir. 2000)). 

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 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)).

C. Althen Analysis

(1) Althen Prong One: Petitioners’ Medical Theory

Under Althen Prong One, petitioners must set forth a medical theory explaining how the 

vaccines could have caused C.L.’s death. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 

1367, 1375 (Fed. Cir. 2009); Pafford, 451 F.3d at 1355-56.

Petitioners’ theory of causation must be informed by a “sound and reliable medical or 

scientific explanation.” Knudsen, 35 F.3d at 548; see also Veryzer v. Sec’y of Health & Human 

Servs., 98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 300aa- 13(b)(1) 

and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If 

petitioners rely upon a medical opinion to support their theory, the basis for the opinion and the 

reliability of that basis must be considered in the determination of how much weight to afford the 

offered opinion. See Broekelschen, 618 F.3d at 1347 (Fed. Cir. 2010) (“The special master’s 

decision often times is based on the credibility of the experts and the relative persuasiveness of their 

competing theories.”); Perreira v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 n.6 (Fed. 
10

Cir. 1994) (stating that an “expert opinion is no better than the soundness of the reasons supporting 

it.”) (citing Fehrs v. United States, 620 F.2d 255, 265 (Ct. Cl. 1980)).

a. Petitioners’ Expert Dr. Douglas Miller

Dr. Douglas Miller earned his medical degree from the University of Miami School of

Medicine in 1978. Curriculum Vitae of Dr. Douglas C. Miller, Pet. Ex. 46 at 1. He received a 

Ph.D. in physiology and biophysics from the University of Miami in 1980. Id. Dr. Miller was a 

resident at Massachusetts General Hospital from 1980-1984, focusing in the areas of anatomic 

pathology and neuropathology. Id. Currently, he serves as a clinical professor of pathology and 

anatomical sciences at the University of Missouri School of Medicine, and is also the program 

director of pathology residency. Id. at 3. In addition, he is an associate medical examiner for 

Boone, Callaway, and Greene Counties in Missouri. Id.; Tr. at 6.

Dr. Miller used the Triple Risk Model for SIDS12 as a framework for his proposed theory of 

causation. Tr. at 17-21. He explained that in the Triple Risk Model, an infant in a critical stage of 

development (the first year of life), with an intrinsic vulnerability in the form of a brainstem 

abnormality affecting the serotonin network, encounters one or more extrinsic stressors, such as 

prone sleeping position, and an elevated level of carbon dioxide results. Id. at 18-20. An infant 

with a defective serotonin network then fails to sufficiently arouse themselves and breathe. Id. at 

20-21. 

Dr. Miller stated that infants may have an intrinsic vulnerability because of “brainstem 

abnormalities which lead to deficiencies in serotonin-mediated synaptic activity, from the arcuate 

nuclei or other brainstem serotoninergic nuclei.” Expert Peport of Dr. Douglas C. Miller, Pet. Ex. 

22 at 7. “A significant proportion of SIDS cases have histopathological or biochemical 

abnormalities in the medulla, the lowest part of the brainstem.” Id. at 6; Tr. at 16-17. The medulla 

is “responsible for the initiation and regulation of muscle efforts underlying breathing,” and 

regulation of heart rate. Pet. Ex. 22 at 6. The 5-HT system in the medulla is a network that uses 

serotonin as an excitatory neurotransmitter, and is linked to respiration, particularly arousal from 

sleep and sleep apnea through increased respiration. Tr. at 25. In tandem with the inhibitory 

network of GABAergic neurons, the medullary 5-HT serotonergic system works to keep 

homeostasis. Id. at 24-25. Dr. Miller opined that a deficiency in the medullary 5-HT system would 

affect an infant’s ability to arouse and breathe in response to elevated levels of carbon dioxide 

encountered due to an external stressor. Id. at 25-26.

In addition, Dr. Miller opined that prematurity would be an intrinsic risk factor, because “the 

presumption would be that the nervous system’s development in the medulla is even more immature 

because of prematurity than in an equivalent aged full-term baby. . . . So that there’s even less

ability to respond.” Tr. at 27-28 (stating that the articles filed as Pet. Exs. 55 and 5613 show that 

 

12 See Pet. Ex. 25/Resp. Ex. A-7, Kinney, supra note 9 at 228-247.

13 Pet. Ex. 55, Jackie Lee et al., Frequency of Apnea, Bradycardia, and Desaturations Following First 

Diphtheria-Tetanus-Pertussis-Inactivated Polio-Haemophilus Influenzae Type B Immunization in 

Hospitalized Preterm Infants, BMC PEDIATRICS (2006), available at http://www.biomedcentral.com/1471-

2431/6/20; Pet. Ex. 56, Sven Schulzke et al., Apnoea [sic] and Bradycardia in Preterm Infants Following 

Immunisation with Pentavalent or Hexavalent Vaccines, 164 EUR. J. PEDIATR. AT 432 (2005).
11

following vaccination, there was an increased incidence of nonfatal apnea and bradycardia in 

premature infants). 

One recognized extrinsic risk factor for SIDS is mild infection, such as an upper respiratory 

infection (“URI”) or gastrointestinal infection (“GI infection”). Tr. at 31. Dr. Miller opined that 

infection does not operate as a mechanical risk factor, but rather that the peripheral cytokines 

produced by the innate immune response to infection communicate with the nervous system to 

produce the risk for SIDS. Id. at 31, 240. In other words, infection operates as a “neurochemical” 

risk factor. He explained that infection stimulates the production of peripheral cytokines, which can 

have central nervous system effects, such as fever. Id. at 33. He stated that some of these 

cytokines—the predominant ones produced in response to an infection, such as IL1β, TNF-α, and 

IL-6—are active in the medulla in modulating synaptic activity of the serotonin and GABAergic 

networks, and can interact to suppress or reduce the firing of serotonin neurons and increase the 

firing of inhibitory GABA neurons, thereby reducing the medulla’s response to apnea or rising 

carbon dioxide levels or hypoxia (low levels of oxygen) in the short term.14 Id. at 33-34, 37-39. In 

an infant with a defective brainstem, who has reduced levels of 5-HT activity to begin with, the 

cytokine-caused inhibition can reduce response to the point that the infant does not recover from 

apnea, hypoxia, or excessive carbon dioxide levels. Id. at 39. In support of the proposition that 

mild infections can act as an external stressor via cytokine interaction with the CNS, Dr. Miller 

cited articles by Rognum, Kadhim, and Vege.15

Other than upper respiratory and gastrointestinal infections, Dr. Miller could not identify

any other infections that have been identified as a risk factor for SIDS. Tr. at 89. Fever, he noted, 

can be caused by other types of infection, and he believed fever was in and of itself an independent 

risk factor for SIDS.16 Id. at 87-89. 

 

14 Dr. Miller acknowledged that the Chen and Miller article, submitted by Dr. McCusker, indicates that 

immune stimulation can result in increases in 5-HT, and therefore augmentation of the arousal mechanism. 

Tr. at 40 (referencing Resp. Ex. C-15, Guo-Lin Chen & Gregory M. Miller, Advances in Tryptophan 

Hydroxylase-2 Gene Expression Regulation: New Insights into Serotonin—Stress Interaction and Clinical 

Implications, 159B AM.J. OF MEDICAL GENETICS 152 (2012)). However, he stated that this increase takes 

time to occur, and would occur hours after a stimulus, whereas in the context of an immediate hypoxic event 

resulting in death within minutes to an hour, there would not be enough time for the feedback loop to effect 

this result. Tr. at 41, 135 (citing Pet. Ex. 61, Jianping Wang & Adrian J. Dunn, Mouse Interleukin-6 

Stimulates the HPA Axis and Increases Brain Trytophan and Serotonin Metabolism, 33 NEUROCHEM. INT.

143 (1998)). 

15 Pet. Ex. 36, Ingvar Rognum et al., Interleukin-6 and the Serotonergic System of the Medulla Oblongata in 

the Sudden Infant Death Syndrome, 118 ACTA. NEUROPATHOL. 519 (2009); Pet. Ex. 34, Hazim Kadhim et 

al., Distinct Cytokine Profile in SIDS Brain: A Common Denominator in a Multifactorial Syndrome?, 61 

NEUROLOGY 1256 (2003); Pet. Ex. 39, Ashild Vege & Torleiv Ole Rognum, Sudden Infant Death Syndrome, 

Infection and Inflammatory Responses, 42 FEMS IMMUN. & MED. MICROBIOL. 3 (2004).

16 In support of this, Dr. Miller cited the following: Pet. Ex. 27, Hannah C. Kinney, Brainstem Mechanisms 

Underlying the Sudden Infant Death Syndrome: Evidence from Human Pathologic Studies, 51 DEV.

PSYCHOBIOL. 223, 223 (2009) (In this article, hyperthermia is listed as an extrinsic stressor, which Dr. Miller 

said is the same thing as fever. Tr. at 139. Dr. McCusker testified that hyperthermia could be caused by 

factors such as overbundling. Id. at 193); Pet. Ex. 39, Ashild Vege & Torliev Ole Rognum, Sudden Infant 

Death Syndrome, Infection and Inflammatory Responses, 42 FEMS IMMUN. & MED. MICROBIOL. 3, 4 (2004) 

(Discusses the Triple Risk Model and hyperthermia as a component of the vicious cycle of SIDS); Pet. Ex. 
12

In support of his position that the 5-HT system is critical for recovery from apnea and that 

certain cytokines play a role in reducing recovery from apnea, Dr. Miller cited studies by 

Stoltenberg, Froen, and Brambilla.17 Tr. at 70. As for the mechanism of interaction between the 

peripheral cytokines and the central nervous system, he stated that the peripheral cytokines 

“probably cross the blood-brain barrier, although there are proposals whereby [they] might signal 

across it without actually getting to it, but have an interaction with the central nervous system that is 

a physiological synaptic interaction rather than an inflammatory interaction.” Id. at 35. Dr. Miller

stated that this process would not produce inflammation in the brain, as the cytokine action is one of 

physiological neurotransmitter modulation, not inflammatory activity. Id. at 35, 81. 

Reaching outside of the traditional extrinsic risk factors listed in the Triple Risk Model of 

SIDS, Dr. Miller testified that vaccines could be an extrinsic risk factor contributing to SIDS. Tr. at

41. He acknowledged, however, that Dr. Kinney has not studied vaccinations in relation to SIDS. 

Id. When asked whether he was the first medical professional, outside of the Vaccine Program, to 

assert that vaccination is an external risk factor in Dr. Kinney’s triple risk model, Dr. Miller said 

that it had not been done “in the specific terms of Dr. Kinney’s research,” but that there is 

“abundant literature associating vaccinations with SIDS.” Id. at 92. He asserted that he had cited 

literature from multiple people that associated vaccines as a possible mechanism leading to SIDS. 

Id. at 92-93. When asked to cite a particular paper where someone has postulated that an external 

risk factor for SIDS is vaccination, he cited a case report by Balci,18 in which he thought the authors 

suggested vaccines were an external risk factor under the Triple Risk Model in the sudden 

unexpected death of twin infants shortly post-vaccination, based on the proximity in time of death 

to vaccination. Id. at 91-95. Dr. Miller also noted that a case report by Ottaviani19 mentions that 

one of the triggers of SIDS in that case could have been vaccination. Id. at 141-42. In his written

report, he cited several additional papers reporting cases of SIDS following infant vaccinations. See

Pet. Ex. 22 at 7. When pressed, however, Dr. Miller admitted that he was not sure anyone has 

“connected all those dots” between cytokines, cytokine production by vaccines, and vaccines 

specifically being a risk factor for SIDS in vulnerable infants. Tr. at 96. And, in fact, the Balci 

authors themselves specifically note that “studies have shown that vaccinations are not associated 

with an increased risk of SIDS.” Pet. Ex. 58 at 5. 

 

37, Kadhim et al. Interleukin-2 as a Neuromodulator Possibly Implicated in the Physiopathoogy of Sudden 

Infant Death Syndrome, 480 NEUROSCIENCE LETTERS 122, 122 (2010) (Says SIDS victims often have 

preceding mild infections inflammatory conditions, like post-vaccinal fever). 

17 Pet. Ex. 32, Lauritz Stoltenberg et al., Changes in Apnea and Autoresuscitation in Piglets After 

Intravenous and Intrathecal Interleukin-1β Injection, 22 J. PERINAT. MED. 421 (1994); Pet. Ex. 33, J. 

Frederik Froen et al., Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in 

Piglets: Implications for Sudden Infant Death Syndrome, 105 PEDIATRICS (2000); Pet. Ex. 35, D. Brambilla 

et al., Interleukin-1 Inhibits Firing of Serotonergic Neurons in the Dorsal Raphe Nucleus and Enhances 

GABAergic Inhibitory Post-Synaptic Potentials, 26 EUR. J. NEUROSCIENCE 1862 (2007).

18 Pet. Ex. 58, Yasemin Balci et al., Simultaneous Sudden Infant Death Syndrome, 14 J. OF FORENSIC AND 

LEGAL MED. 87 (2007).

19 Pet. Ex. 42, Giulia Ottaviani et al., Sudden Infant Death Syndrome (SIDS) Shortly After Hexavalent 

Vaccination: Another Pathology in Suspected SIDS?, 448 VIRCHOWS ARCH 100 (2006). 
13

Dr. Miller opined that vaccinations are analogous to mild infection as an extrinsic risk 

factor. Tr. at 42-43. A vaccination, he said, activates the immune system to produce peripheral 

cytokines in the same way as a mild infection—the same cytokines reach the same peaks in the 

same time interval in children who have been vaccinated as in children who have influenza 

infections—and these cytokines have the same effect on the nervous system as those produced by 

infection. Id. at 42-43, 80. In support of the contention that the cytokine levels and effects 

provoked by vaccination are not significantly different than those provoked by infection, Dr. Miller 

cited an article by Kashiwagi et al.

20 The Kashiwagi article discusses an association between the 

DTaP and Hib vaccinations, which C.L. received, to the production of cytokines IL-1β, IL-6 and 

TNF-α—the same cytokines that are produced by infection and those that petitioners theorize are 

implicated in their interpretation of the Triple Risk Model. The study compared levels of 

cytokines21 in the blood serum of vaccine recipients with and without febrile reactions within 24 

hours of vaccination. There was no significant difference between the two groups except that the 

cytokine G-CSF was elevated in individuals with a febrile illness. The significance of this finding 

was not determined. In fact, the authors stated that cytokine production due to vaccines has “not 

been sufficiently investigated.” Pet. Ex. 52 at 3. 

During the hearing, Dr. Miller discussed and criticized a number of the epidemiological 

studies cited by respondent’s experts.22 Dr. Miller stated that in principle, it ought to be possible for 

epidemiological studies to detect vaccination as a risk factor for SIDS, but that with the notable 

exception of the Traversa23 study, “the [epidemiological] studies done to date have not had the sort 

of rigorous definition of populations that are necessary to draw appropriate conclusions [regarding 

vaccination as a risk factor for SIDS].” Tr. at 48, 54-55. Dr. Miller said that the Traversa authors 

emphasized that a complete neuropathological evaluation, including a detailed examination of 

brainstem structure on autopsy, was necessary in order to identify those infants who were at risk 

because of a developmental abnormality of the brainstem. Id. at 54-55. 

 

20 Pet. Ex. 52, Yasuyo Kashiwagi et al., Production of Inflammatory Cytokines in Response to DiphtheriaPertussis-Tetanus (DPT), Haemophilus Influenza Type B (Hib), and 7-Valent Pneumococcal (PCV7) 

Vaccines, 10 HUM VACCINE IMMUNOTHER. 677 (2014).

21 These cytokines include IL-1β, IL-4, IL-6, IL-10, IL-12, IFN-y, MIP-1, TNF-α, PGE2, and G-CSF.

22 For Dr. Miller’s full critique of respondent’s literature, see Tr. at 47-69.

23 Pet. Ex. 43/Resp. Ex. A-13, Giuseppe Traversa et al., Sudden Unexpected Deaths and Vaccinations During 

the First Two Years of Life in Italy: A Case Series Study, PLOS ONE 2011; 6E 16363 (2011). The Traversa 

study was a response to an anecdotal report from Germany of an association between vaccination with a 

hexavalent vaccine in the second year of life and sudden unexpected death in the two days following 

vaccination. Traversa, Pet. Ex. 43 at 1 (referencing Pet. Ex. 40/Resp. Ex. A-14, Rudiger von Kries et al., 

Sudden and Unexpected Deaths After the Administration of Hexavalent Vaccines (Diphtheria, Tetanus, 

Pertussis, Poliomyelitis, Hepatitis B, Haemophilius Influenzae Type B): Is There a Signal?). In the Traversa 

study, the statistically significant increased relative risk was one tenth the size of the effect observed in 

Germany, was confined to the first dose, and “may be partly explained by a residual uncontrolled 

confounding effect of age.” Id.
14

b. Petitioners’ Expert Dr. James Oleske

Dr. James Oleske received his medical degree from the College of Medicine and Dentistry 

of New Jersey in 1971. Curriculum Vitae of Dr. James Oleske, Pet. Ex. 51 at 1. From 1971 to 

1974, he served as a pediatric resident and then a pediatric ambulatory care fellow with the College 

of Medicine and Dentistry of New Jersey. Id. He then completed a pediatric infectious disease and 

immunology fellowship at Emory University Medical School. Id. at 2. Dr. Oleske received a 

master’s degree in Public Health from Columbia University in 1974. Id. at 1. He is licensed to 

practice medicine in New Jersey, with specialties in pediatrics and diagnostic laboratory 

immunology. Id. at 2. Dr. Oleske is certified by the American Board of Pediatrics and the 

American Board of Allergy and Immunology. Id. at 2. He worked with the Brighton Group, which 

is a group led by the centers for Disease Control and Prevention (“CDC”) that focuses on issues of 

vaccine safety. Id. at 9. Currently, Dr. Oleske serves as the director of the division of allergy, 

immunology, and infectious diseases at Rutgers University - New Jersey Medical School. Expert 

Report of Dr. James Oleske, Pet. Ex. 50 at 7. 

Dr. Oleske was not called as a witness at the hearing but submitted an expert report in this 

case. See Pet. Ex. 50. Like Dr. Miller, his proposed medical theory to explain how the vaccines at 

issue can cause death was premised on the Triple Risk Model. Id. at 3-4. In this model, “extrinsic 

and intrinsic risk factors converge in a young infant during a vulnerable window of time” when “the 

still immature, developing brain lacks the adaptive responses to adequately control postnatal 

homeostasis.” Id. at 3. Dr. Oleske stated that studies by the Kinney group have demonstrated that 

infants with SIDS have a latent defect(s) in the medullary serotonergic system, the part of the brain 

that controls autonomic functions, including respiration. Id. at 4. “The normal developmental 

immaturity in homeostasis prevents the ‘at risk’ infant from successfully responding to a number of 

exogenous and endogenous stressors, which ultimately affects critical respiratory and arousal 

functions.” Id. at 4. The infant then stops breathing, and “a disturbance in the usual balance of 

cytokine activity in the arcuate nucleus blocks rather than stimulates a normal arousal signal,” so 

that the infant suffocates. Id. 

Dr. Oleske opined that in the Triple Risk Model, “there is support for the role of cytokines 

as mediators for such failures of respiratory/arousal functions in a susceptible infant during this 

window of vulnerability after immunization.” Pet. Ex. 50 at 4. He stated that “[i]t is now accepted 

that pathological conditions, such as cancers, viral infections, and autoimmune diseases, are 

associated with abnormal cytokine production.” Id. at 5. He said that even if “brain cytokines are 

neuroprotective when they are functioning under normal circumstances . . . . in the vulnerable 

infant, experiencing one or more extrinsic factors, the antigen load of vaccines and adjuvants, can 

become neurodamaging and provide the ‘perfect storm’ for SIDS.” Id. He said that because of the 

absence of negative feedback control occurring in the developing brain of a vulnerable infant at risk 

for SIDS, a given cytokine “may flood and accumulate in the extracellular compartment of tissues 

thereby impairing the cytokine network homeostasis and contributing to local pathogenesis.” Id. at 

5-6.
15

In support of his position that cytokines play a causative role in SIDS, Dr. Oleske cited two 

studies which were also cited by Dr. Miller. First, he cited a study by Kadhim,24 which showed an 

increased level of the cytokine IL-1β in brains of children who died of SIDS. Pet. Ex. 50 at 5. Dr. 

Oleske said that in that 2003 study, the authors postulated that brain injury, such as occurs with 

infection and inflammation,25 could lead to alterations in the cytokine-neurotransmitter interactions, 

leading to changes in the center controlling oxygen/carbon dioxide balance, in turn leading to SIDS. 

Id. Dr. Oleske also cited a 2004 study by Vege,

26 in which the authors suggested that a slight 

infection could increase the risk of SIDS by inducing cytokine IL-6, which in turn increases 

temperature, which then affects respiration. Id. 

Like Dr. Miller, Dr. Oleske expanded on the Triple Risk Model in a novel way, arguing that 

vaccinations act as extrinsic risk factors analogous to the way the infections act as extrinsic risk 

factors—by interfering with the complex cytokine signaling in the brain. Pet. Ex. 50 at 5. 

c. Respondent’s Expert Dr. Christine McCusker

Dr. Christine McCusker earned a Master of Science in 1988, followed by an M.D in 1993, at 

McMaster University, in Hamilton, Ontario. Curriculum Vitae of Dr. Christine McCusker, Resp. 

Ex. D at 2. Her residency training was in pediatrics, at Montreal Children’s Hospital, McGill 

University, from 1993-1996. Id. at 3. She was then a clinical fellow in allergy and immunology at 

McGill University from 1996-1999. Id. Dr. McCusker is board certified in pediatrics. Id. She is 

now a pediatric allergist/immunologist, and sees patients at an allergy and immunology clinic. Tr. 

at 152. She also does clinical and fundamental research in immunology, runs the clinical 

immunology laboratory at McGill, and is division head of the Pediatric Department of Allergy, 

Immunology, and Dermatology. Id. at 151-52. In addition, she teaches medical students in the 

areas of immunology, dermatology, and malignant hematology. Id. at 153. 

Dr. McCusker did not agree with petitioners’ experts that vaccines act as an extrinsic risk 

factor under the Triple Risk Model of SIDS. She noted that vaccines have not been identified by 

Kinney as an external stressor. Tr. at 200. Dr. McCusker stated that recognized extrinsic factors—

“prone and side-sleeping, bed sharing, over-bundling, soft bedding, face covered and recent history 

of upper respiratory tract infection” contribute to the risk for SIDS by effecting a mechanical 

change in an infant’s ability to respire, as opposed to a neurochemical change. Expert Report of 

Christine McCusker, Resp. Ex. C at 5. These are factors that have “the potential to shift the oxygen 

 

24 Dr. Oleske did not include a citation to this source, but it appears to be Pet. Ex. 34, Hazim Kadhim et al., 

Distinct Cytokine Profile in SIDS Brain: A Common Denominator in a Multifactorial Syndrome?, 61 

NEUROLOGY 1256 (2003).

25 Dr. Olekse thus seems to suggest that inflammation may play a causal role, whereas Dr. Miller disagrees. 

Dr. Miller testified that the cytokine action at issue is not inflammatory. See Tr. at 35, 81.

26 Again, Dr. Oleske did not include a citation to this source, but it appears to be Pet. Ex. 39, Ashild Vege & 

Torleiv Ole Rognum, Sudden Infant Death Syndrome, Infection and Inflammatory Responses, 42 FEMS 

IMMUN. & MED. MICROBIOL. 3, 4 (2004).
16

and carbon dioxide balance.” Id. at 4 (citing Kinney27). She testified that URIs in infants 

mechanically impede an infant’s ability to breathe. Tr. at 185. Infants breathe through their noses, 

and congestion caused by a URI obstructs their nose and—because the reflex to breathe through 

their mouth instead does not happen easily for them—nasal congestion contributes to a mechanical 

impediment to breathing. Id. at 184-85. Dr. McCusker stated that there is no literature to support 

the position that URIs are known to affect SIDS through the mediation of cytokines. Id. at 202. Dr. 

McCusker testified that there is literature that addresses the issue of whether infection could be a 

neurochemical risk factor—in particular, she noted a study by Ferrante,28 which researched whether 

there are variations in cytokine or immune-related genes in SIDS that would explain the 

vulnerability of SIDS infants to infection. Tr. at 273. However, the Ferrante study concluded that 

more studies were needed to understand the interplay between different genetic variations and how 

they may contribute to an unfavorable immunologic response. Pet. Ex. 53 at 7. Thus, Dr. 

McCusker disagreed with petitioners’ experts’ comparison of vaccination to a URI.

Dr. McCusker agreed that the Kashiwagi29 study, cited by petitioners for the contention that 

cytokine levels and effects provoked by vaccination are not significantly different than those 

provoked by infection, demonstrates that cytokines are released in response to vaccination. See Tr.

at 231. However, because the study showed that in general, cytokine levels were the same in 

children with and without fever, Dr. McCusker opined that the interaction of those cytokines in both 

the periphery and the CNS must somehow qualitatively differ, leading to differing responses. Tr. at

326. In other words, the study demonstrates that it is not just the presence of a certain level of 

cytokines alone that determines how the CNS responds. Rather, other regulatory factors must come 

into play, and the interaction (of cytokines on the CNS) could be very much dependent on the event

leading to the cyoktine production (i.e. vaccination versus infection). Id. Moreover, the study was 

not designed to examine the effects of cytokines in the brain following vaccination. 

Dr. McCusker agreed with petitioners’ experts that the literature suggests that the 5-HT 

system is implicated in SIDS. Tr. at 190. In infants not intrinsically at risk for SIDS (infants with 

normal homeostatic networks), the mechanical extrinsic stressors would activate the protective 

mechanisms in the brain through the 5-HT system, and correct the respiratory problem. Resp. Ex. C 

at 6. Dr. McCusker explained that Kinney has set forth the hypothesis that in an infant with a 

defective 5-HT system, however, the neurons may require excessive cytokine stimulation to

respond to hypercapnia. Tr. at 201; Resp. Ex. C at 4, 5 (discussing Kinney30). The increased levels 

of cytokines in the SIDS brain are a response to having too much carbon dioxide in the body. Tr. at

201. Dr. McCusker noted, however, that vaccination does not affect carbon dioxide levels. Id. at 

202. 

 

27 Pet. Ex. 28, Hannah C. Kinney et al., The Serotonergic Anatomy of the Developing Human Medulla 

Oblongata: Implications for Pediatric Disorders of Homeostasis, 41 J. OF CHEMICAL NEUROANATOMY 182 

(2011).

28 Pet. Ex. 53, Linda Ferrante & Siri Hauge Opdal, Sudden Infant Death Syndrome and the Genetics of 

Inflammation, 6 FRONTIERS IN IMMUNOLOGY 1 (2015). 

29 Pet. Ex. 52, Kashiwagi, supra note 19.

30 Pet. Ex. 28, Kinney, supra note 26. 
17

However, Dr. McCusker did not agree with petitioners’ experts’ theory that the expression 

of cytokines in the brain contributes to a failure to arouse, thus causing SIDS. Tr. at 179. First, 

there is no evidence that the levels of cytokines detected in the brains of SIDS infants are 

pathologically elevated, as opposed to elevation found in normal brain homeostasis. Id. She 

explained that the view that cytokines found in the brain are pro-inflammatory has changed, and it is 

now understood that they operate as signals of stress in normal brain function, rather than cause 

inflammation. See id. at 172-77. Dr. McCusker discussed an article by Ron-Harel,31 which sets 

forth the current thinking. She explained that early research focused on looking at cytokines in 

pathological states, such as brain infection or autoimmune diseases, and found that they were 

elevated in such states. Id. at 172. More recently, however, research has focused on the role of 

cytokines in normal brain function, and it has become clear that the brain uses cytokines as a 

homeostatic mechanism and normal communication molecules to indicate stress. Id. at 172-73; 

Resp. Ex. C at 3. In the brain, cytokines such as IL-1β and IL-6, which can have a proinflammatory effect in the periphery, are associated with normal brain function. Tr. at 173-75. 

Exogenous stimuli or stressors result in upregulation of cytokines in the central nervous system. Id.

at 172. Thus, Dr. McCusker stated that the literature suggests that the expression of cytokines in the 

SIDS brain is a response to stress. Id. at 179, 182, 200 (citing Kinney32). The presence of an 

increased level of cytokines in the arcuate nucleus of SIDS infants “occur[s] as a response to the 

inciting event rather than an element etiologically linked to the respiratory failure in the vulnerable 

child.” Resp. Ex. C at 5 (referencing Pet. Ex. 3633). 

 

Second, Dr. McCusker testified that what is known about cytokines does not suggest that 

they prevent arousal. Tr. at 179-80. Rather, in the context of sleep, IL-1β and TNF-α have been 

implicated as arousal molecules, with regard to increasing arousal from REM sleep. Id. at 177-78; 

204-08 (discussing Resp. Ex. C-7, C-8, C-9, C-1534). Evidence suggests that “the central functions 

of the cytokines IL1β, IL6 and TNFα at times of infection are to promote fever and to affect the 

sleep architecture by increasing NREM versus REM sleep resulting in more disturbed sleep with 

more frequent arousal while permitting the maintenance of increased body temperature.” Resp. Ex. 

C at 4. This means that cytokines improve, rather than impair, autoresuscitation. Tr. at 208. 

Third, Dr. McCusker testified that cytokine production in response to a vaccination is 

localized and “does not generate significant systemic signaling.” Tr. at 157-70. Dr. McCusker 

testified that cytokine expression is tightly regulated—cytokine responses occur locally, and 

 

31 Resp. Ex. C-3, Noga Ron-Harel et al., Brain Homeostasis is Maintained by “Danger” Signals Stimulating 

a Supportive Immune Response Within the Brain’s Borders, 25(5) BRAIN, BEHAV. IMMUN. 1036 (2011). 

32 Pet. Ex. 28, Kinney, supra note 26.

33 Pet. Ex. 36, Ingvar J. Rognum et al., Interleukin-6 and the Serotonergic System of the Medulla Oblongata 

in the Sudden Infant Death Syndrome, 118 ACTA. NEUROPATHOL. 519 (2009). 

34 Resp. Ex. C-7, Luca Imeri & Mark R. Opp, How (and Why) the Immune System Makes Us Sleep, 10 

REVIEWS NEUROSCIENCE 199 (2009); Resp. Ex. C-8, James M. Clinton et al., Biochemical Regulation of 

Sleep and Sleep Biomarkers, 7 J. OF CLINICAL SLEEP MED. S38 (2005); Resp. Ex. C-9, Charlene E. Gamaldo 

et al., The Sleep-Immunity Relationship, 30 NEUROL. CLIN. 1313 (2012); Guo-Lin Chen & Gregory M. 

Miller, Advances in Tryptophan Hydroxylase-2 Gene Expression Regulation: New Insights into Serotonin—

Stress Interaction and Clinical Implications, 159B AM.J. OF MEDICAL GENETICS 152 (2012). 
18

generally do not generate significant systemic signaling. Id. at 157, 179-81. However, they can 

have systemic effects if the stimulus is sufficient, which can be evidenced by sickness behaviors 

such as fever, fatigue, and irritability. Id. at 159. Dr. McCusker stated that fever comes up as a cofactor in many studies but has not been individually identified as an extrinsic risk factor itself. Id. at

192. Fever is mediated by IL-1, IL-6, and TNF-α. Id. at 263. In cases where systemic effects do 

occur, they happen when cytokine signaling reaches the blood brain barrier and signals through it to 

upregulate cytokines produced in the brain. Id. at 160. She stated that most cytokines probably do 

not actually cross the blood brain barrier, and therefore the peripheral cytokines do not flood into 

the brain. Id. at 161. Again, the presence of increased cytokines in the brain signifies the response 

to stress rather than a cause of respiratory failure. Resp. Ex. C at 5. 

With regard to the epidemiology literature assessing a potential causal connection between 

vaccination and SIDS, Dr. McCusker testified that there have been several studies that have looked 

at whether or not there is an increased frequency of SIDS associated with vaccination in a way other 

than temporal, but she does not find any of the large studies (as opposed to case series and case 

reports) supportive of the hypothesis that vaccines are implicated. Tr. at 212-13. She opined that 

the epidemiological studies performed to date have been sufficient to pick up risk factors such as 

position, URI, and reflux. Id. at 213. Given that vaccinations are likely to occur more frequently 

than URIs in children under the age of six months, she would expect these studies to pick up

vaccines as a risk factor. Id. at 213-14. However, the studies have not done so. 

d. Respondent’s Expert Dr. Hart Lidov

Dr. Hart Lidov received a Ph.D. from Johns Hopkins University in 1980, followed by a 

medical degree in 1982. Curriculum Vitae of Dr. Hart G.W. Lidov, Resp. Ex. B at 1. From 1983 to 

1991, Dr. Lidov was a resident in pediatrics and neurology at Massachusetts General Hospital, and 

a neuropathology and anatomic pathology resident at Brigham and Women’s Hospital. Id. He has 

a special qualification in child neurology from the American Board of Psychiatry and Neurology. 

Id. at 2. Dr. Lidov presently serves as a staff neurologist at Children’s Hospital in Boston, and an 

associate neuropathologist at Brigham and Women’s Hospital. Id. at 3.

Dr. Lidov testified that C.L. fits the Triple Risk Model well—he was the right age, and had 

“some brainstem abnormalities and [] several of the recognized risk factors,” and Dr. Lidov did not 

“see any particular reason to be searching for additional . . . new and novel risk factors.” Tr. at 351-

52. Dr. Lidov does not believe that the things that are accepted as risk factors exert their effect on 

SIDS through cytokines, and he is not aware that cytokines causally contribute to SIDS deaths. Id.

at 339-40, 350. Dr. Lidov did not agree that vaccines, through a mechanism related to cytokines, 

should be accepted as a risk factor for SIDS. Id. at 337-38. He stated that doing so would be new 

and novel, and that he was “not aware of any review in papers or any of the relevant text of risk 

factors for SIDS which mention vaccines whatsoever.” Id. at 337. According to Dr. Lidov, there is 

little or no epidemiological support for vaccines as a risk factor, and the things that are accepted as 

risk factors are accepted because they do have epidemiological support—not just because there is

perhaps a plausible mechanistic reason. Id. at 338. 
19

In his expert report, Dr. Lidov analyzed many of the articles cited by Dr. Miller and 

explained in detail the problems with Dr. Miller’s conclusions.35 He disagreed that the medical 

literature submitted by Dr. Miller supports the theory that cytokines associated with vaccination can 

play a causal role in SIDS. Resp. Ex. A at 6-8; Tr. at 351. Rather, he opined that “the role for 

inflammatory cytokines . . . does not bring a novel factor to light; it simply inserts a mechanistic 

step into the proposition that vaccines increase the risk of SIDS.” Resp. Ex. A at 12. He agreed 

with Dr. McCusker that cytokines could be a response to a stressor, as opposed to a cause of the 

stressor. Tr. at 351. 

Regarding the use of epidemiological studies in general, Dr. Lidov testified that “one gets as 

close a definitive answer from an epidemiologic study as one can get in medicine.” Tr. at 349-50. 

He opined that if petitioners’ theory were true, and vaccines were a sufficient exogenous stressor to 

cause SIDS in intrinsically vulnerable infants of the correct age, epidemiology studies should be 

able to pick it up. Id. at 348; Resp. Ex. A at 11.

e. Evaluation of the Evidence

Althen Prong One requires petitioners to set forth a reliable medical theory explaining how 

the received vaccines could have caused the alleged injury. Althen, 418 F.3d at 1278. While 

scientific certainty is not required to establish causation under the Vaccine Act (Id. at 1279), the 

theory must be supported by a “sound and reliable” medical or scientific explanation. Knudsen, 35 

F.3d at 548. 

i. Petitioners have failed to show that vaccines have been identified as an 

extrinsic risk factor under the Triple Risk Model

Petitioners have failed to show that their interpretation of the Triple Risk Model, as it relates 

to vaccines, is a sound and reliable medical theory. While petitioners’ testimony and medical 

literature showed that the Triple Risk Model may be an accepted mechanism to explain some SIDS 

cases, they failed to show preponderant evidence that vaccines have been identified as an exogenous 

stressor implicated in the Triple Risk Model. Neither Dr. Miller nor Dr. Oleske produced evidence 

that others in the medical community support their opinion that vaccinations operate like infections 

as exogenous stressors for purposes of the Triple Risk Model of SIDS. Dr. Miller claimed that there 

is “abundant literature associating vaccinations with SIDS,” but admitted that he was not sure 

anyone has “connected all those dots” between cytokines, cytokine production by vaccines, and 

vaccines specifically being a risk factor for SIDS in vulnerable infants. Tr. at 92, 96. The literature 

he cited reports cases of SIDS following vaccination, however, these studies and epidemiological 

studies do not identify vaccination as an exogenous risk factor. Upon review, there is little or no 

evidence presented to support petitioners’ position, other than the testimony of Drs. Oleske and 

Miller. A special master does not need to credit “expert opinion testimony that is connected to the 

existing data or methodology ‘only by the ipse dixit of the expert.’” Jarvis v. Sec’y of Health & 

Human Servs., 99 Fed. Cl. 47, 61 (2011) (quoting Cedillo ex rel. Cedillo v. Sec’y of Health & 

Human Servs., 617 F.3d 1328, 1339 (Fed. Cir. 2010). 

 

35 To review Dr. Lidov’s complete analysis of the medical literature cited by Dr. Miller, see Dr. Lidov’s 

expert report, Resp. Ex. A at 7-12.
20

ii. Petitioners have failed to show that URIs act as neurochemical risk 

factors, and that vaccines are comparable to infections as risk factors

Petitioners also failed to show by preponderant evidence that recognized extrinsic risk 

factors, and URIs in particular, act as neurochemical rather than mechanical risk factors. The 

evidence identifies URIs and gastrointestinal infections as risk factors for SIDS. Tr. at 184, 300-01. 

Dr. McCusker testified that the literature discussing “mild infection” as a risk factor generally refers

to URI and GI infections—while a few point to something else, as other infections in infants are 

generally not considered “minor.” Id. at 270. URIs and GI infections cause congestion or reflux, 

both of which affect an infant’s breathing mechanics. Id. at 184. Dr. Miller opined that almost 

none of the extrinsic risk factors are “mechanical” risk factors, and that he was “not aware of any 

literature at all that supports the idea that there’s a mechanical respiratory obstruction . . . in the 

sense of chest wall motion [being] restricted or anything like that, as a cause of SIDS in relation to . 

. . infections.” Id. at 35-36, 99. Dr. Miller agreed, however, that prone sleeping was “an external 

reason that not enough oxygen is getting to the system.” Id. at 99. Dr. McCusker testified that socalled “mechanical” risk factors are those that affect respiration by not only physically impeding the 

infant’s ability to respire, but also by otherwise reducing oxygen intake. Id. at 184-85. For 

example, re-breathing exhaled air occurs when an infant is in the prone position. Id. at 183-84.

Dr. McCusker testified that there is no literature that supports the proposition that infections 

like mild upper respiratory infections are known to affect SIDS through the mediation of cytokines. 

Tr. at 202. Petitioners, on the other hand, cite the Rognum36 and Kadhim37 articles. Rognum found 

elevated levels of IL-6 in the brains of infants who died of CNS infection and SIDS compared to 

those who died of noninfectious sudden deaths. Tr. at 189; Pet. Ex. 36. Likewise, Kadhim found a 

difference in cytokine levels in the arcuate nucleus of SIDS victims versus non-SIDS victims. Pet. 

Ex. 34. However, as Dr. McCusker testified, these are “descriptive” studies demonstrating the 

presence of cytokines in the SIDS brain, and do not establish causation. Tr. at 189. Petitioners rely

on these studies, and Dr. Miller agreed that the Rognum and Kadhim studies “only address the 

expression of cytokines, not the effect of cytokines.” Id. at 100 (referencing Pet. Ex. 34, 36). 

Dr. Miller also cited a review article of studies by Vege and Rognum38 about the 

relationship between URIs and SIDS. The article noted “[s]everal observations of immune 

stimulation in the periphery and of Interleukin-6 elevation in the cerebrospinal fluid of SIDS 

victims explain how infections can play a role in precipitating these deaths.” Tr. at 98 (citing Pet. 

Ex. 39 at 2). Dr. McCusker testified that this article was published in 2004, when the presence of 

IL-6 and IL-1β in the CNS was thought to be pro-inflammatory. Tr. at 183. At that time, it was 

known that increased IL-1 and IL-6 were found in the brains of SIDS infants, and the hypothesis 

was that an external trigger, such as slight infection, could lead to changes in cytokines that could 

lead to sudden death. Id. at 183-86. Now, however, the thinking is that the infections discussed as 

 

36 Pet. Ex. 36, Rognum, supra note 32. 

37 Pet. Ex. 34, Hazim Kadhim et al., Distinct Cytokine Profile in SIDS Brain: A Common Denominator in a 

Multifactorial Syndrome?, 61 NEUROLOGY 1256 (2003).

38 Pet. Ex. 39, Ashild Vege & Torleiv Ole Rognum, Sudden Infant Death Syndrome, Infection and 

Inflammatory Responses, 42 FEMS IMMUN. & MED. MICROBIOL. 3 (2004).
21

risk factors for SIDS (URIs and GI infections), can both lead to mechanical obstruction, as 

discussed above. Id. at 184. 

Petitioners argue that URIs are not the only infections that create a risk factor for SIDS, but 

rather that “mild infection and/or mild inflammatory process[es]” can also be external risk factors. 

Pet. Post-Hearing Brief at 26 (citing Pet. Ex. 3739). Petitioners’ argument appears to hinge on the 

premise that vaccinations promote the production of pro-inflammatory cytokines in the same 

manner as a mild infection. The evidence does not support this premise. As Dr. McCusker 

testified, there are important similarities and differences between an immune response to an 

infection and an immune response to a vaccination. Importantly, cytokine production in response to 

a vaccination is localized and “do[es] not generate significant systemic signaling.” Tr. at 157. The 

inflammatory response stays focused at the site of injection while the adjuvant exerts a depot effect, 

and it takes about 24 to 48 hours for the response to go from the thigh to the local lymph nodes, 

where it remains for about four days. Id. at 164-65. An infection, on the other hand, is a live

organism that infects a cell directly and has the ability to replicate in the body and cause a 

significant immune reaction. Id. at 161-64. The vaccines C.L. received are composed of particulate 

killed organisms, i.e., pieces of organisms. Id. at 164. Administered alone, these particles do not 

elicit much of an immune response beyond a local reaction. Id. at 313. Adjuvants are added to 

vaccines to elicit a greater immune response to protect an individual who may later be exposed to 

the live virus. Id. at 164-65, 313.

iii. Petitioners have failed to show that vaccines cause a cytokine response 

that causes or contributes to SIDS in the manner their experts propose

The undersigned does not take issue with petitioners’ argument that vaccinations result in a 

cytokine release and that some of these cytokines are the same ones released in response to 

infection. Petitioners have failed, however, to show that vaccines cause cytokines to produce an 

abnormal brainstem serotonin response or otherwise act in a manner that causes or contributes to 

SIDS, as their experts postulated. According to petitioners’ theory, premised on the Triple Risk 

Model, a vulnerable infant encounters external stressor(s) during a critical time, resulting in death. 

Tr. at 17-20. In this model, an infant is vulnerable due to a defective serotonergic 5-HT system. 

See id. at 18-19. After reviewing slides of C.L.’s brain, the experts agree that C.L. had 

abnormalities in cells migrating from the rhombic lip, which is evidence that C.L. was a vulnerable 

infant within the Triple Risk Model. Id. at 24, 354. If an infant has a defective 5-HT system, the 

ability to arouse in hypoxic conditions will be compromised. Pet. Post-Hearing Brief at 21. 

Petitioners further theorize: 

If the increased cytokine production secondary to a mild infection or 

inflammatory process (such as vaccination) is superimposed on this 

vulnerable infant, her ability to respond or arouse is further 

compromised. In this regard, the evidence is clear that cytokines such 

as IL-1β have an inhibitory effect on 5-HT neurons, meaning that 

cytokine interaction with 5-HT neurons will decrease their firing and 

thereby dampen the arousal response. 

 

39 Pet. Ex. 37, Hazim Kadhim, et al., Interleukin-2 as a Neuromodulator Possibly Implicated in the 

Physiopathoogy of Sudden Infant Death Syndrome, 480 NEUROSCIENCE LETTERS 122 (2010). 
22

Id. at 21-22 (citing Tr. at 33-34, 37-39; Pet. Ex. 3540; Resp. Ex. C-7

41). The current understanding 

of the role of cytokines, however, as expressed by Dr. McCusker, is that cytokines act to signal the 

occurrence of a pathological process and do not themselves cause a pathologic event. Dr. 

McCusker explained how the understanding of the role of cytokine expression in the brain has 

changed over time. Petitioners’ theory is premised on the idea that the cytokine expression in the 

SIDS brain causes inflammation and SIDS death in a vulnerable infant. While early studies showed 

that the pro-inflammatory cytokine, IL-1β, was present in the brains of SIDS infants, current 

research demonstrates that the brain regularly produces pro-inflammatory cytokines as part of a 

normal, regulatory process. 

Petitioners have also failed to show that cytokine interaction with the 5-HT system 

necessarily operates to suppress arousal in a manner that would lead to a SIDS death. Dr. Miller 

asserted that while cytokines may be arousal molecules in general with regard to the sleep-wake 

cycle, not all arousal is the same. Tr. at 233-35. He said that the papers he presented show a 

suppression of 5-HT activity in the medullary 5-HT network, which is involved in stimulation, 

respiration and arousal from sleep during apnea or hypoxia. Id. Dr. McCusker, however, cited 

medical literature that indicates that cytokines improve, rather than impair, autoresuscitation in the 

context of sleep. Id. at 204-08. In particular, there is evidence in the papers regarding sleep that 

cytokines are involved in arousal. Id. at 298. 

In support of the proposition that the 5-HT system is critical for recovery from apnea and 

that certain cytokines play a role in reducing recovery from apnea, Dr. Miller cited studies by 

Stoltenberg, Froen, and Brambilla.42 Tr. at 70. In the Stoltenberg study, the CNS of newborn 

piglets was infused with IL-1β, and their environment was pumped full of ammonia, causing them 

to become hypoxic. Id. at 70, 209. When the environment was cleared, there was a delay in 

autoresuscitation in animals who had been filled with IL-1β. Id. In the Froen study, one-week old 

piglets were infused with IL-1β and nicotine, and it was found that the combination worsened 

apnea. Id. at 210. Brambilla looked at the effect of exposure to IL-1β of the firing on serotonin 

neurons and GABAergic neurons in the dorsal raphe nucleus of rats in the medulla, and found that it 

suppressed the firing of the serotonin neurons and increased the firing of the GABA neurons. Id. at 

72. 

Dr. McCusker critiqued these studies. First, Dr. McCusker testified that the effect seen by

Stoltenberg is only observed in newborn piglets—possibly equivalent to a three week old human. 

Tr. at 210, 297. There is no evidence that IL-1β does harm after the neonatal period. Id. at 298. In 

 

40 D. Brambilla et al., Interleukin-1 Inhibits Firing of Serotonergic Neurons in the Dorsal Raphe Nucleus and 

Enhances GABAergic Inhibitory Post-Synaptic Potentials, 26 EUR. J. OF NEUROSCIENCE 1862 (2007). 

41 Luca Imeri & Mark R. Opp, How (and Why) the Immune System Makes Us Sleep, 10 REVIEWS 

NEUROSCIENCE 199 (2009).

42 Pet. Ex. 32, Lauritz Stoltenberg et al., Changes in Apnea and Autoresuscitation in Piglets After 

Intravenous and Intrathecal Interleukin-1β Injection, 22 J. PERINAT. MED. 421 (1994); Pet. Ex. 33, J. 

Frederik Froen et al., Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in 

Piglets: Implications for Sudden Infant Death Syndrome, 105 PEDIATRICS (2000); Pet. Ex. 35, D. Brambilla 

et al., Interleukin-1 Inhibits Firing of Serotonergic Neurons in the Dorsal Raphe Nucleus and Enhances 

GABAergic Inhibitory Post-Synaptic Potentials, 26 EUR. J. NEUROSCIENCE 1862 (2007).
23

addition, the quantity and location of cytokines administered to the piglets in the study is not akin to 

cytokines triggered by vaccination. Id. Second, in Brambilla, the researchers took the brains out of 

the rats, bathed them with IL-1β, and then stimulated them and observed changes in the firing. Id. 

One cannot necessarily infer that a decrease in firing means there will be a difference in function.

The finding in animal studies has been that there is not a change in respiration post neonatal period. 

Id. at 298-99. Thus, Dr. McCusker did not agree that the studies showed that cytokines interface 

with the 5-HT neurons in the medulla and affect neurotransmission. Id. at 266. Dr. Lidov agreed, 

finding that the studies collectively have “limited applicability” to Dr. Miller’s conclusions. See

Resp. Ex. A at 7-9. 

In discussing the articles cited by petitioners’ experts regarding the role of cytokines, Dr. 

McCusker demonstrated that the information upon which petitioners’ theory is based is outdated. 

Respondent’s experts provided a detailed discussion on the current understanding of the role of 

cytokines. Petitioners’ experts did little to dispute this current information. Until the role of 

cytokines is better understood through research, the question of whether cytokines act to cause 

pathology, as Drs. Oleske and Miller testified, or act to signal the occurrence of a pathological 

process, as Dr. McCusker testified, remains unanswered. 

Petitioners have failed to demonstrate, by a preponderance of the evidence, that vaccinations 

are exogenous stressors under the Triple Risk Model of SIDS, or act similarly to other exogenous 

stressors that have been identified. Furthermore, even if petitioners were successful in providing

evidence that vaccinations produce cytokine effects in the brain similar to infections, petitioners’ 

theory still fails because they have not shown that the cytokines have a negative impact on the brain 

that would lead to SIDS death. 

(2) Althen Prong Two: Logical Sequence of Cause and Effect

Under Althen Prong Two, petitioners must prove by a preponderance of the evidence that 

there is a “logical sequence of cause and effect showing that the vaccination was the reason for the 

injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner[s] must show 

that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine was the 

‘reason for the injury.’” Pafford, 451 F.3d at 1356 (citations omitted). 

a. Petitioners’ Expert, Dr. Miller

Dr. Miller testified that C.L. died of SIDS and that the vaccines were a substantial 

contributing factor to his death. Tr. at 10-11, 75. Dr. Miller testified that the peak incidence for 

SIDS is between two and three months of age, and that 90% of SIDS cases occur within the first six 

months of life. Id. at 29. Dr. Miller considered C.L. to have been five months old at the time of 

death, as he was born prematurely. Id. at 126. Thus, C.L.’s death occurred within the critical 

developmental period within the Triple Risk Model. 

C.L. was a vulnerable infant, based on several facts. Tr. at 23. First, C.L. was premature, 

and therefore had “even less ability to respond . . . on top of whatever intrinsic vulnerability [he had 

due to his] developmental problem.” Id. at 23, 27. Second, C.L. initially had hypothermia and 

desaturations when feeding, which were clinical signs of brainstem dysfunction. Id. at 23. In 

addition, C.L. was noted to have a dysconjugate gaze and failure to fixate at his two-month wellbaby visit. Finally, based on his review of slides of C.L.’s brain, Dr. Miller agreed with Dr. Lidov 
24

that the slides showed a group of cells that appeared to belong to the inferior olivary nucleus (part 

of the medulla) located out of place, more dorsally in the brainstem. See id. at 11-12, 344-46. Dr. 

Miller stated that the ectopic cells that should have been in the inferior olivary nucleus are “a 

fundamental indication of brainstem and specifically medullary development abnormality.” Id. at 

24.

Dr. Miller stated that “abnormality of the brainstem serotonin or the medullary serotonin 

network” and the brainstem abnormalities seen in C.L., in cells migrating from the rhombic lip to 

the medulla, have been described in SIDS cases as making an infant vulnerable. Tr. at 13-14, 22-

23, 146. Dr. Miller testified that the abnormality points to an underlying developmental 

abnormality in C.L.’s brainstem. Id. at 145. 

Recognized extrinsic risk factors, Dr. Miller testified, include things such as prone sleeping 

position, upper respiratory infection, or smoking in the house. Tr. at 30, 85. He opined that 

extrinsic risk factors act “synergistically” or at least in an additive fashion. Id. at 21, 138. As for 

sleeping position at the time of death, Dr. Miller believed that C.L. died supine, on his back. Id. at 

84. C.L.’s grandmother found C.L. prone, face down. The medical examiner and the staff at the 

hospital observed posterior lividity. Id. at 83-84. Dr. Miller stated that he “tend[s] to trust lividity 

patterns more than [he] trust[s] eyewitnesses.” Id. at 83. Dr. Miller conceded, however, that the 

medical examiner opined that the lividity pattern was “not inconsistent” with C.L. having died 

prone and then moved to his back after death. Id. at 84-85. Even if C.L. was in a prone position, 

Dr. Miller’s opinion that vaccination played a causative role would not change. Id. at 138.

Dr. Miller agreed that gastroesophageal reflux is a risk factor for SIDS. Tr. at 85. However, 

he opined that the fluid found in C.L.’s mouth after death was more likely a response to death and 

resuscitation, rather than a cause of death. Id. at 75.

Dr. Miller opined that the evidence in this case indicated that peripherally produced 

cytokines communicated with C.L.’s central nervous system. Tr. at 36. C.L. exhibited sleepiness, 

tiredness, crankiness, fussiness, irritability, and decreased appetite following his vaccination, 

symptoms which Dr. Miller testified are consistent with cytokine effect on central nervous activity. 

Id. at 36-37, 79. The most classic evidence of peripherally produced cytokines communicating with 

the central nervous system is fever, which C.L. did not exhibit. 

b. Petitioners’ Expert, Dr. Oleske

Dr. Oleske opined that C.L. died of SIDS, and that the immunizations he received were the 

plausible cause of his SIDS death. Pet. Ex. 50 at 2. Dr. Oleske stated that infants with SIDS have 

latent defect(s) in the medullary serotonergic system, and that the “anatomical and epidemiological 

link to SIDS, when viewed in the temporal relationship of multiple vaccine administrations, 

supports a finding of a vulnerable subset of infants.” Id. at 4-5. He opined that vaccines—like 

infections—should be considered an extrinsic risk factor in SIDS cases. Id. at 5. He stated that in 

the vulnerable infant, like C.L., experiencing extrinsic risk factors, cytokines may flood and 

accumulate in the extracellular compartment of tissues, impairing the cytokine network 

homeostasis, and contribute to local pathogenesis. Id. at 5-6. In the brain, the complex cytokine 

signaling “can occasionally be disrupted by an extrinsic factor such as a mild infection or, as in the 

case of [C.L.], the multiple vaccine antigens that he was immunized against...” Id. at 6. However, 

Dr. Oleske did not identify any specific factual support in the record for his theory that the vaccines 
25

C.L. received triggered the release of cytokines. Rather, as support for his opinion that C.L.’s death 

was more likely than not related to his vaccinations, Dr. Oleske cited (1) the proximal temporal 

relationship of the multiple immunizations C.L. received and his SIDS death 48 hours later; (2) the 

“lack of any other plausible cause of death”; and (3) “significant evidence from investigations and 

understanding of the pathophysiologic interactions in the developing infant’s brain suffering from 

SIDS.” Id. at 6. 

c. Respondent’s Expert, Dr. McCusker

Dr. McCusker disagreed with petitioners’ experts’ conclusion that C.L.’s vaccinations 

played a contributing role in his death from SIDS. Supp. Expert Report of Dr. McCusker, Resp. Ex. 

E at 4. First, there was no evidence of cytokine activity in C.L.’s brain. Resp. Ex. C at 4. If C.L.’s 

vaccines had caused an increase of cytokines in his brain, “the resulting effect would most likely 

have been increased arousal and/or fever.” Id. at 5. “The key cytokines activated in the first hours 

of an immune response, IL1B, IL6 and TNF-a, are implicated in the development of systemic 

symptoms such as fever and malaise. In the sleep/arousal centers of the brain these cytokines have 

distinct activities that, in part, increase rather than decrease arousal.” Resp. Ex. E. at 3. C.L. had 

“no reported fever, the usual first clinical sign of systemic cytokine activity.” Id. Further, although 

Dr. McCusker agreed that cytokines are associated with sickness behaviors, she testified that 

cytokines are not the only thing that can cause such behaviors. Tr. at 308. 

Dr. McCusker opined that C.L. had several extrinsic risk factors that put him at risk for 

sudden infant death, and “there’s no evidence that the vaccines were a component here.” Tr. at 232. 

She testified that 99% of SIDS deaths have at least one risk factor for SIDS identified at the time of 

death, and 57% have two. Id. at 284 (citing Resp. Ex. C-1143). It “has been hypothesized that there 

may be synergy, but a single risk factor is sufficient.” Id. at 284. Known extrinsic risk factors for 

SIDS include “prone or side sleeping, bed sharing, over-bundling, soft bedding” as well as smoking

exposure and gastro-esophageal reflux. Pet. Ex. E at 2; Pet. Ex. C at 8. 

Dr. McCusker believed that C.L. was found prone, based on his grandmother’s statement. 

Tr. at 195. Dr. McCusker testified that prone sleeping position may affect breathing in two ways: 

first, by creating a pocket of rebreathable air (higher in carbon dioxide), and second, by 

mechanically preventing abdominal breathing. Id. at 194-95. Also, in C.L’s case, there was 

evidence of milk in C.L.’s mouth and upper airway, and liquid in the crib consistent with reflux, as 

well as a history that he would spit up while he was on his tummy. Id. at 198. Gastro-esophageal 

reflux operates as a mechanical risk factor because it can induce the laryngeal chemoreflex—a 

reflex that induces transient apnea when there is food in the mouth (where the pharynx and 

esophagus meet). Id. at 196-97. Thus, Dr. McCusker concluded that the risk factors for SIDS 

present here included prone sleeping position, and the episodes of regurgitation. Resp. Ex. E at 3.

d. Respondent’s Expert, Dr. Lidov

Dr. Lidov did not believe the vaccines were a substantial contributing factor to C.L.’s death. 

Tr. at 334. He believed that C.L. fit in the Triple Risk Model for SIDS without the need to 

 

43 Resp. Ex. C-11, Trachtenberg, supra note 8 at 630. 
26

implicate vaccinations—C.L. was the right age, had brainstem abnormalities, and several 

recognized risk factors. Id. 351-52.

Dr. Lidov testified that “[m]aleness, prematurity, [and] being prone” are all risk factors for 

SIDS, as is gastro-esophageal reflux. Tr. at 344. Regarding the question of whether C.L. died in a 

prone position, Dr. Lidov testified that the most likely scenario was that C.L.’s grandmother found 

him in a prone position. The posterior lividity was caused by the child being turned over onto his 

back after death. Id. at 343-44, 355.

44

 Dr. Lidov also opined that there was evidence that C.L. had 

refluxed, as the EMT report indicated there was “froth in the mouth and wetness on the sheets.” Id.

at 344. 

Dr. Lidov testified that the abnormalities he observed in C.L.’s medulla indicated that there 

was a malformation in his brainstem, but do not necessarily indicate that there was specifically a 

defect in the neuronal circuits using serotonin as a neurotransmitter. Tr. at 346, 353. Nevertheless, 

Dr. Lidov opined that C.L.’s abnormality was an intrinsic brainstem abnormality contemplated in 

the Triple Risk Model. Id. at 346-47, 354. 

e. Evaluation of the Evidence

Althen Prong Two requires preponderant evidence of a “logical sequence of cause and effect 

showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. This prong 

is sometimes referred to as the “did it cause” test; i.e., in petitioners’ case, the question is whether 

the vaccine (or vaccines) caused the alleged injury. Broekelschen, 618 F.3d at 1345 (“Because 

causation is relative to the injury, a petitioner must provide a reputable medical or scientific 

explanation that pertains specifically to the petitioner’s case . . . .”); Pafford, 451 F.3d at 3. 

Temporal association alone is not evidence of causation. See Grant v. Sec’y of Health & Human 

Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). 

There is not preponderant evidence to support petitioners’ theory that peripheral cytokines 

communicated with C.L.’s central nervous system in the pathological manner described by Dr. 

Miller and Dr. Oleske. Although Dr. McCusker agreed that there is communication between 

peripheral cytokines and the central nervous system, she did not agree that cytokines play a 

pathological role, but rather stated that cytokine expression in the brain is normal. In turn, 

petitioners’ evidence described cytokine expression in the SIDS brain, but did not describe the 

effect of cytokines on the brain. Dr. Miller opined that crankiness, fussiness, irritability, and 

decreased appetite following his vaccination were indications that peripherally produced cytokines 

communicated with C.L.’s central nervous system. Tr. at 37, 79. However, the classic evidence of 

peripherally produced cytokines communicating with the central nervous system is fever, which 

C.L. did not exhibit. See Resp. Ex. E at 3. Even if the evidence were sufficient to support a finding 

that peripheral cytokines communicated with C.L.’s nervous, system, there is no evidence to 

suggest that the communication was causally connected to C.L.’s death. 

 

44 In his written expert report, Dr. Lidov stated that he believed the pattern of lividity indicated C.L. died 

supine, contrary to the grandmother’s account. Resp. Ex. A at 3. However, at the hearing, he testified that 

his opinion changed once he understood the short time interval between C.L.’s death and when he was turned 

over to the prone position. See Tr. at 343. 
27

In addition, as Dr. Lidov explained, C.L. met the criteria for the Triple Risk Model of SIDS 

without the need to consider a speculative risk factor. Tr. at 351-52. C.L. died during the first six 

months of life and had brainstem abnormalities of the type described in the Triple Risk Model. He

had several known intrinsic risk factors for SIDS, including the fact that he was premature and 

male. Id. at 288, 323-24. In addition, there is evidence C.L. experienced gastro-esophageal reflux, 

an extrinsic risk factor for SIDS. Id. at 344. Finally, there is preponderant evidence that C.L. was

found in the prone position—C.L.’s grandmother reported finding C.L. prone, and Dr. Lidov agreed 

that this was the most likely scenario. Id. at 342-43. All experts agree that being prone is a 

significant risk factor for SIDS. 

For these reasons, the undersigned finds that petitioners failed to provide preponderant 

evidence of a logical sequence of cause and effect showing that C.L.’s vaccinations caused his 

death. 

(3) Althen Prong Three: Proximate Temporal Relationship

Under Althen Prong Three, petitioners must provide “preponderant proof that the onset of 

symptoms occurred within a timeframe for which, given the understanding of the disorder’s 

etiology, it is medically acceptable to infer causation-in-fact.” De Bazan, 539 F.3d at 1352. The 

acceptable temporal association will vary according to the particular medical theory advanced in the 

case. See Pafford, 451 F.3d at 1358. A temporal relationship between a vaccine and an injury, 

standing alone, does not constitute preponderant evidence of vaccine causation. See, e.g., Veryzer 

v. Sec’y of Health & Human Servs., 100 Fed. Cl. 344, 356 (2011) (explaining that “a temporal 

relationship alone will not demonstrate the requisite causal link and that petitioner must posit a 

medical theory causally connecting the vaccine and injury”). 

a. Petitioners’ Expert, Dr. Miller

Dr. Miller testified that C.L. received his vaccinations, exhibited abnormal behavior over the 

following day and a half to two days, and then died within 48 hours of immunization. Tr. at 8-9, 28. 

He testified that in the literature that describes a temporal association between vaccination and 

SIDS, the majority of cases have occurred in a window of out to four days post-vaccination, with 

the peak being about 48 hours after vaccination. Id. at 28-29; see also, Pet. Ex. 22 at 7 (citing Pet. 

Exs. 41, 43, 4545). 

b. Petitioners’ Expert, Dr. Oleske

Dr. Oleske noted that C.L. died about 48 hours after receiving his vaccinations. Pet. Ex. 50 

at 2. Dr. Oleske concluded that the proximal temporal relationship of the multiple immunizations 

and C.L.’s SIDS death, along with the lack of other plausible causes of death and evidence from the 

understanding of the pathophysiological interactions in the SIDS brain make C.L.’s death more 

likely than not related to the vaccines he received. Id. at 6. 

 

45 Pet. Ex. 41, B. Zinka et al., Unexplained Cases of Sudden Infant Death Shortly After Hexavalent 

Vaccination, 24 VACCINE 5779 (2005); Pet. Ex. 43, Giuseppe Traversa et al., Sudden Unexpected Deaths 

and Vaccinations During the First Two Years of Life in Italy: A Case Series Study, PLOS ONE 2011; 6E 

16363 (2011). As Dr. Lidov notes in his report, the citation to exhibit 45 appears to be a typographical error, 

as it is a study of H. pylori in mice. 
28

c. Respondent’s Expert, Dr. McCusker

Dr. McCusker explained the sequence of events that occurs after vaccination. When a 

vaccine is administered, the inflammatory response stays focused at the site of injection while the 

adjuvant exerts a depot effect. Tr. at 164-65. It takes about 24 to 48 hours for the response to go 

from the thigh to the local lymph nodes, where it remains for about four days. Id. at 165. 

The “key cytokines active during the first hours of an immune response, IL1B, IL6 and 

TNF-a, are implicated in the development of systemic symptoms such as fever and malaise.” Resp. 

Ex. E at 3. Thus, “[f]ever as a sign of systemic cytokine activity may [] occur after several hours,”

and would generally develop within the first day after receiving a vaccination—from six to twelve

hours after—and is usually gone by 24 to 48 hours. Id.; Tr. at 265-66. Dr. McCusker noted that 

C.L. “had no reported fever, the usual first clinical sign of systemic cytokine activity.” Resp. Ex. E 

at 3.

d. Respondent’s Expert, Dr. Lidov

Dr. Lidov stated that the references cited by Dr. Miller in support of the statement that there 

is an elevated risk for SIDS within the first 48 hours following immunization do not represent a 

statistically significant number of cases. See Resp. Ex. A at 10. 

e. Evaluation of the Evidence 

In the present case, there is a temporal relationship between C.L.’s vaccination and his 

death. However, a temporal relationship alone cannot establish causation, nor is it sufficient on its 

own to meet Althen Prong Three. Veryzer, 100 Fed. Cl. at 356. Rather, there must be 

“preponderant proof that the onset of symptoms occurred within a timeframe for which, given the 

understanding of the disorder’s etiology, it is medically acceptable to infer causation-in-fact.” De 

Bazan, 539 F.3d at 1352 (emphasis added). Under Althen Prong Three, petitioners must establish 

the timeframe for which it is medically acceptable to infer causation, assuming C.L.’s death was 

caused by the vaccination, and they must show that C.L.’s death occurred in that timeframe. See

Shapiro v. Sec’y of Health & Human Servs., 105 Fed. Cl. 353 (Fed. Cl. 2012). Petitioners’ experts 

offered evidence that death 48 hours after vaccination is consistent with the timing of death in 

studies reporting an association between death and vaccination. Thus, petitioners have met their 

burden under Althen Prong Three. 

A temporal relationship between C.L.’s vaccination and his death alone, however, is 

insufficient to establish causation. Petitioners failed to provide preponderant evidence of a reliable 

medical theory and a logical sequence of cause and effect under Althen Prongs One and Two, 

respectively. A temporal relationship alone is not sufficient to establish causation in fact without 

preponderant evidence of the two remaining factors. See Veryzer, 98 Fed. Cl. at 227 (citing Grant, 

956 F.2d at 1148). Thus, petitioners’ failure to meet Althen Prongs One and Two means that they 

cannot be compensated. See, e.g. Koehn v. Sec’y of Health & Human Servs., 2013 WL 3214877 

(Fed. Cl. Spec. MsTr. at May 30, 2013) (citing Hibbard v. Sec’y of Health & Human Servs., 698 

F.3d 1355, 1364-65 (Fed. Cir. 2012) (holding the special master did not err in resolving the case 

pursuant to Prong Two when respondent conceded that petitioner met Prong Three). 
29

V. CONCLUSION

For all of the reasons discussed above, the undersigned finds that petitioners have not 

established entitlement to compensation and their petition must be dismissed. In the absence of a 

timely filed motion for review filed pursuant to Vaccine Rule 23, the clerk is directed to enter 

judgment consistent with this decision.

IT IS SO ORDERED. 

 

s/Nora Beth Dorsey

 Nora Beth Dorsey

Chief Special Master