Peterson v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 22-322V

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HEATHER PETERSON, * Chief Special Master Corcoran

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Petitioner, * Filed: October 30, 2025

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v. *

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SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

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Respondent. *

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Edward Kraus, Kraus Law Group, Chicago, IL, for Petitioner.

Alexa Roggenkamp, U.S. Dep’t of Justice, Washington, DC, for Respondent.

ENTITLEMENT DECISION 1

On March 24, 2022, Heather Peterson filed a petition for compensation under the National

Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petitioner alleges that an

influenza “(flu”) vaccine she received on March 26, 2019, caused her to develop transverse

myelitis “(TM”), and then multiple sclerosis (“MS”). Petition (ECF No. 1) (“Pet.”) at 3. She has

since acknowledged that her TM was the presenting symptom of what was later properly diagnosed

as MS. See Petitioner’s Motion for Ruling on the Record and Memorandum in Support, dated Dec.

27, 2024 (ECF No. 36) (“Mot.”) at 9–11.

Both parties have filed expert reports and have also briefed their positions for resolution of

this matter on the basis of the written record. See Mot.; Respondent’s Brief, dated Mar. 27, 2025

1

Under Vaccine Rule 18(b), each party has fourteen 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). Otherwise, the whole Decision will be available to the public

in its present form. Id.

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) (“Vaccine Act” or “the Act”).

Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

(ECF No. 38) (“Opp.”); Petitioner’s Reply, dated Apr. 28, 2025 (ECF No. 39) (“Reply”). For the

reasons set forth below, I hereby deny entitlement. Petitioner has not established preponderantly

that the flu vaccine can cause MS, or did so to her—and no new medical or scientific thinking

exists on the topic that would better support this causal theory, which I have on many prior

occasions found wanting.

I. Factual Background

Petitioner was born on November 25, 1986 (and was therefore 32 years old when she

received the vaccine at issue). See Pet. at 1. She had a medical history significant for

hypothyroidism, Hashimoto’s Thyroiditis, and Vitamin D deficiency. Ex. 5 at 110; Ex. 1 at 9.

Vaccination and Initial Neurologic Symptoms

On March 26, 2019, Ms. Peterson went to her primary care physician (“PCP”), complaining

of fatigue and flu symptoms. Ex. 7 at 64–66. She had a generally normal examination but was

diagnosed with the flu. Id. Her PCP prescribed Tamiflu, and also administered a flu vaccine. Id.;

Ex. 5 at 1. There is no evidence of any immediate temporal reaction to this vaccination.

Petitioner’s affidavit states that three days later (March 29, 2019), she noted the

development of numbness and tingling of fingertips after holding her infant son during a movie,

but assumed it was transient. Affidavit, dated Mar. 25, 2022, filed as Ex. 14 (ECF No. 10-5)

(“Peterson Aff.”), at 2; Ex. 21 at 77. On the morning of the 30th, however, she awoke with

progressive numbness and tingling from her left upper extremity. Peterson Aff. at 2.

Petitioner maintains (although it does not appear the records relevant to these visits were

filed) that she subsequently sought chiropractic assistance three times in the days thereafter for her

paresthesia concerns. Peterson Aff. at 2. Eventually, however, she felt the numbness spreading to

the left side of her body, then to her right side, and went to the emergency department (“ED”) at

Northwest Community Healthcare on April 2, 2019, for treatment. Id; Ex. 8. at 7. But she was

discharged after no explanation could be provided for her symptoms from the testing she received.

Peterson Aff. at 2.

The next day (April 3, 2019—now a bit more than a week after vaccination), however, Ms.

Peterson awoke with worsened symptoms, and she went back to the ED complaining of left arm

numbness for the prior four days. Ex. 8 at 3–6. She reported that the numbness first ran from her

fingers to her elbow, and the next day, the numbness progressed to her entire left arm and left side.

Id. On exam, she had decreased sensation in her left arm, side, and leg. Id. Her lab results and head

CT were normal, however. Id. The differential diagnosis included MS, and Petitioner was

discharged home and advised to follow-up with neurology. Id.

2

Later that same day, Petitioner visited a different hospital’s ED, again reporting left arm

weakness and paresthesias beginning five days prior while attending a movie (as well as the fact

that she had experienced an upper respiratory infection with rhinorrhea and congestion for a week

around that same timeframe). Ex. 21 at 65–66. She denied other symptoms, some of which are

often viewed as neurologic (such as bladder control or dizziness). Id. at 65. The differential

diagnosis proposed the possibility of a lesion “likely at level of [cervical spine],” although no

imaging had yet been performed, and also deemed MS to be a “significant consideration.” Id. at

66. Ms. Peterson was subsequently admitted to the hospital. Id.

Hospitalization and Evaluation of Condition

While hospitalized, Petitioner was evaluated by neurologist Smriti Wagle, M.D. Ex. 21 at

100–02. On exam, her muscle strength was 4/5, and her deep tendon reflexes were 2/4. Id. An MRI

of the cervical spine (with and without contrast) performed on April 3, 2019, revealed “slightly

expansile oval T2 hyperintense lesion within the spinal cord posteriorly to the left of midline at L3

level there is slight enhancement. It measures about 13 x 7 x 5 mm in the craniocaudal, AP and

transverse dimensions.” Id. at 102, 105.

Lab results included elevated ANA and IgG antibody readings, among other things. Ex. 21

at 105, 131; Ex. 2 at 33, 59. However, eight oligoclonal bands (a well-accepted biomarker of MS)

were seen in her cerebrospinal fluid (“CSF”) testing performed on April 5th (although other signs

of infection were not). Ex. 21 at 125–26 (deeming the oligoclonal bands “supportive of a diagnosis

of multiple sclerosis in the appropriate clinical setting”). Petitioner received IV steroids and was

discharged home on April 5, 2019. Id. at 105.

A few days later (April 8, 2019), Petitioner visited her PCP for follow-up of her left-sided

numbness that she reported began on “3/29/19.” Ex. 7 at 67–68. Her left-hand strength was 4/5,

and she had decreased sensation and impaired coordination. Id. at 69. Her PCP diagnosed myelitis

“possible [secondary to] flu vaccine, but cannot confirm. Could be autoimmune such as MS or

TM.” Id. Petitioner was advised to continue steroids and follow-up with neurology, occupational

therapy (“OT”), and physical therapy (“PT”). Id.

On April 10, 2019, Ms. Peterson had her first PT/OT appointment. Ex. 4 at 111. At this

evaluation, she displayed poor sensory motor control and weakness in her left upper extremity,

and interference with her activities of daily living (“ADLs”). Id. Later that month, she saw again

Dr. Wagle for follow-up. Ex. 6 at 77–80. She had now finished her course of steroids and reported

improved feeling in her leg and better strength in her left arm. Id. On exam, she did not have tremor

or dysmetria, had a normal gait, and could walk unassisted. Id. Dr. Wagle diagnosed acute TM,

and referred Petitioner to an MS specialist. Id. at 79, 80.

3

On May 10, 2019, Petitioner was evaluated by MS specialist Wayne Rubinstein, M.D. Ex.

6 at 81–82. Dr. Rubenstein diagnosed petitioner with non-longitudinally extensive and non-

necrotizing upper cervical TM, temporally related to the March receipt of a flu vaccine. Id. at 84.

Dr. Rubinstein also noted, that “[t]he interval [between vaccination and onset] is short, however,

at 4–7 days.,” and that her CSF findings were “not specific” either for MS or “postvaccinal TM.”

Id.

Approximately two months later (July 9, 2019), Petitioner went back to Dr. Wagle and

reported ongoing left palm numbness (although she had felt baseline strength since engaging in

PT). Ex. 6 at 85–86. By early October, she had been discharged from PT/OT. Ex. 4 at 17–19. And

when she saw Dr. Wagle again that October, she reported only some residual left-hand tingling

and numbness in her left two fingers. Ex. 6 at 90–92. Repeat MRI imaging performed in November

2019 revealed normal results for her brain, but “pathologic intramedullary T2 signal abnormality

within the cervical spinal cord, extending from C2-C3” for her cervical spine. Ex. 5 at 95–98.

Symptoms Relapse in 2020

For nearly a year, Ms. Peterson’s condition was largely quiescent. But in October 2020, a

repeat brain MRI showed “few small foci of demyelination as described above likely reflecting

multiple sclerosis.” Ex. 23 at 58. Around the same time, neurologist Elena Grebenciucova, M.D.,

opined Petitioner likely had some kind of central nervous system demyelinating disease—possibly

MS depending on comparison of earlier MRI imaging. Ex. 9 at 17–19.

On October 16, 2020, Petitioner saw neurologist Thomas Shoemaker, M.D., for an initial

consultation regarding suspected relapsing-remitting MS. Ex. 26 at 20–29. Her history was noted,

as well as the fact that the October 2020 MRIs showed that the lesion in her cervical cord was

stable, but that there was a new small foci in the brain. Id. Dr. Shoemaker diagnosed Petitioner

with MS, opining that “[w]hile it is possible that her partial myelitis may have been provoked by

the influenza vaccination, given the time course as well as the CSF findings[,] this is unlikely.” Id.

at 28 (emphasis added).

Toward the end of October 2020, Petitioner had a telehealth visit with Dr. Grebenciucova

to discuss medications. Ex. 9 at 12–14. A year later, repeat brain and cervical spine MRIs were

performed, and the cervical MRI revealed “[s]table high T2 signal abnormality within the upper

posterior spinal cord suggesting multiple sclerosis” (Ex. 23 at 30), while the brain MRI showed

“[s]ubtle focus of focal high T2 signal adjacent to the left lateral ventricular body posterior aspect

is smaller/less conspicuous than previously” but “[n]o new abnormalities.” Id. at 32. And in early

November 2021, Petitioner had a follow-up visit with Dr. Rubinstein. Ex. 25 at 65–67. Her exam

was essentially normal, and he assessed her with MS, “4/2019 cervical myelitis, temporally post

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vaccinial [sic], with subsequent evolution of cerebral MRI abnormalities.” Id. at 69. No additional

relevant records have been filed.

II. Expert Opinions

A. Petitioner’s Expert – Dr. Carlo Tornatore

Dr. Tornatore is a neurologist, and he prepared two written reports for Petitioner. Report,

dated Nov. 29, 2023, filed as Ex. 29 (ECF No. 27-1) (“First Tornatore Rep.”); Report, dated May

31, 2024, filed as Ex. 54 (ECF No. 33-1) (“Second Tornatore Rep.”).

Dr. Tornatore graduated from Cornell University with a Bachelor of Arts and Sciences in

Neurobiology, and attended Georgetown University Medical Center, where he received a Master

of Science in Physiology. Curriculum Vitae, filed as Ex. 30 (ECF No. 27-2) (“Tornatore CV”) at

2. He subsequently graduated from medical school at Georgetown University School of Medicine,

completing a residency in the Department of Neurology at Georgetown University Hospital. Id.

Dr. Tornatore also completed a fellowship in Molecular Virology at the National Institute of Health

in Bethesda, Maryland. Id. He has published multiple articles addressing demyelinating disorders

and their pathology. Id. at 8–13. Currently, Dr. Tornatore serves as a Professor and Chairman of

the Department of Neurology at Georgetown University Medical Center, Chairman and

Neurologist-in-Chief of the Department of Neurology at Medstar Georgetown University Hospital

in Washington, D.C., and Medstar Health’s Regional Director Neurology. Id. at 3.

First Report

Dr. Tornatore’s first report began with an overview of Petitioner’s medical history. First

Tornatore Rep. at 2–9. But he highlighted a few aspects of that history that he considered

particularly significant to his opinion. He noted, for example, that Ms. Peterson had a prior history

of an autoimmune condition, suggesting “a propensity for immune over-reactivity.” Id. at 9. She

had received the flu vaccine at issue on the same day she sought treatment for a possible wild viral

infection, and Dr. Tornatore deemed this “unusual” and “not the standard of care for treatment of

an acute influenza infection.” Id. at 3. He otherwise noted that within a week of vaccination,

Petitioner’s differential diagnosis already included MS as a possibility, although TM was also

proposed. Id. at 4. While by the summer of 2019 some treaters were opining that her presentation

was not likely MS (and that it could be instead attributed to a post-vaccination reaction), as of the

fall of 2020 her diagnosis was ultimately best characterized as MS, given subsequent imaging and

corroborative CSF findings. Id. at 9.

Petitioner’s treatment records clearly embrace MS as the ultimately proper diagnosis, and

Dr. Tornatore agreed it was a proper diagnosis as well, based on the totality of the record (and in

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particular the conclusions of her treaters). First Tornatore Rep. at 9. He even noted that Petitioner

had tested positive for one known MS biomarker, oligoclonal bands, after CSF testing performed

on April 5, 2019, and he deemed it likely they arose in the context of the initially-observed lesion,

since they “are not found in asymptomatic individuals without MRI findings.” Id. at 14.

Dr. Tornatore’s report nevertheless characterized Petitioner’s condition as vaccine-caused

“TM/CIS,” and he labored hard to isolate his causation analysis to that early aspect of Petitioner’s

medical history. First Tornatore Rep. at 9, 29. He defined TM to be a rare syndrome featuring

spinal cord inflammation, usually occurring “across the width of the spinal cord,” that clinically

manifests with “varying degrees of weakness, sensory alterations and autonomic dysfunction.” Id.

at 10. TM also involves destruction of the nerve myelin sheath, resulting in nerve signal

communication disruption. It is known to be caused by “post-infectious or post-vaccine

autoimmune phenomenon,” although Dr. Tornatore also allowed that TM is associated with MS

itself. Id. at 11, 15; “Transverse Myelitis” – National Institute of Neurologic Disorders and Stroke

(https://www.ninds.nih.gov/health-information/disorders/transverse-myelitis), filed as Ex. 31

(ECF No. 28-1) at 2 (including MS as a condition that “appear[s] to cause transverse myelitis”).

He even stated that some authority now supported the view that this kind of condition might be

more generally referred to as “myelitis,” without regard to the positional location of the

inflammation.” K. Blackburn & B. Greenberg, Revisiting Transverse Myelitis: Moving Toward a

New Nomenclature, 11 Frontiers. Neurol. 1 (2020), filed as Ex. 32 (ECF No. 28-2) at 2 (observing

that not all myelopathies are attributable to inflammation, but can have other mechanisms or

etiologies). TM has, he emphasized, been credibly associated with vaccinations, even if the link

lacks firm epidemiologic proof. First Tornatore Rep. at 15.

Another diagnostic classification that Dr. Tornatore felt was applicable to Petitioner was

“CIS,” or “clinically isolated syndrome.” First Tornatore Rep. at 11–12. He characterized CIS as

featuring a single, monophasic occurrence of a CNS demyelinating event comparable to an MS

flare, but occurring “in a patient not known to have [MS].” Id. at 12 (quoting A. Thompson et al.,

Diagnosis of Multiple Sclerosis: 2017 Revisions of the McDonald Criteria, 17 Lancet Neurol. 162-

73 (2018), filed as Ex. 33 (ECF No. 28-3) (“Thompson”) at 2 Panel 1). But “if a patient is

subsequently diagnosed with [MS], the clinically isolated syndrome was the patient’s first attack.”

Thompson at 2 Panel 1. Ms. Peterson, Dr. Tornatore noted, in fact could not yet have been

diagnosed with MS (even if it could be suspected, as treaters seem to have surmised) because she

could not demonstrate her satisfaction of the “dissemination in time or space” MS criterion—that

she developed CNS lesions in different locations and at different times. First Tornatore Rep. at 12,

13. (As discussed in greater detail below, Dr. Tornatore’s characterization of CIS as a component

of an MS diagnosis (when the facts prove to support the latter) rather than as a free-standing

separate occurrence, is an important concession in evaluating causation in this matter).

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Ms. Peterson, Dr. Tornatore opined, demonstrated a single lesion on her cervical spine that

was enhancing 3 when viewed by MRI in early April 2019, and which Dr. Tornatore deemed likely

to have been no less than two to three weeks old (meaning it could have predated vaccination).

First Tornatore Rep. at 13–14. However (and based on the contention that Petitioner’s symptoms

started on “5/8/2019”—something wholly unsupported by the medical record), 4 he deemed it

reasonable to “surmise that the inflammatory process in the spinal cord started on or around

3/31/2019, which would correlate nicely with the 4/4/2019 MRI.” Id. at 14. Of course—given Dr.

Tornatore’s assertion that the lesion could have been at least two weeks old, it would still predate

vaccination (and hence could not be assumed to have caused its development).

From the foregoing, Dr. Tornatore attempted to construct a causation theory that would

connect Petitioner’s receipt of the flu vaccine to what transpired not long after. The immune

system’s built-in capacity to avoid autoimmune attack, he noted, could break down (and hence

promote such cross-reactive damage). First Tornatore Rep. at 16. Vaccines provoke an immune

response comparable to an infection. Id. Thus, vaccines (he reasoned transitively) are as capable

of provoking autoimmune disease as wild infections, and he outlined any number of mechanisms

by which this was possible. Id. at 16, (listing antigenic mimicry between foreign and self-antigens

and “epitope spreading” (in which a response to foreign antigen causes nonspecific reactions by

other immune cells), among other things), 18–22.

The wild flu virus could specifically, Dr. Tornatore contended, provoke just such a

response, and he cited an item of literature in support. First Tornatore Rep. at 17–18; S. Markovic-

Plese et al., High Level of Cross-Reactivity in Influenza Virus Hemagluttinin-Specific CD4+ T-

Cell Response: Implications for the Initiation of Autoimmune Response in Multiple Sclerosis, 169

J. Neuroimm. 31 (2005), filed as Ex. 43 (ECF No. 29-4) (“Markovic-Plese”). Thus, “T cells that

recognized influenza antigens found in the influenza vaccine can likewise recognize CNS

antigens,” making a “downstream autoimmune response” possible. First Tornatore Rep. at 18.

Markovic-Plese, however, does not support causation as firmly as Dr. Tornatore suggests.

In it, researchers derived a clone of a “T helper” cell (a kind of T cell that aids B cells in their

production of antibodies in the adaptive immune response to foreign pathogens) from the serum

of an existing MS patient who was then also experiencing an influenza A infection, using it in vitro

3

See Robinson v. Sec’y of Health & Hum. Servs., No. 14-952V, 2021 WL 2371721, at *16 (Fed. Cl. Spec. Mstr. Apr.

12, 2021) (“[b]efore a patient has an MRI with contrast, they are injected intravenously with a contrast dye called

gadolinium. In a healthy person, or in an MS patient not having a flare, that dye should remain in the bloodstream.

However, if an MS patient is symptomatic, the gadolinium will leak into the brain through an opening in the blood-

brain barrier and will show as an enhancing image on MRI”). Thus, imaging that reveals an “enhancing” lesion

evidences active disease process.

4

It is possible that the reference to a May 2019 onset is a typographical error. Regardless, it lacks any record support.

Why did Petitioner even seek medical intervention in April 2019, if not for treatment the symptoms later deemed to

be an initial presentation of MS? Dr. Tornatore also does not later attempt to distinguish these initial symptoms from

Petitioner’s MS diagnosis.

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to compare cross-reactive potential with different peptides relating to myelin basic protein—a

“putative autoantigen in MS.” Markovic-Plese at 32. And Markovic-Plese’s authors did in fact

identify mimicking peptide sequences that were also cross-reactive. Id. at 37. Of course, the

authors aimed not to identify possible causes of MS, but instead to learn about ways to improve

vaccine function in order to “provide a longer-lasting protection against viral infections and

possibly decrease their effect on initiation of relapses in MS.” Id. Moreover, the article says

nothing about the capacity of a nonadjuvanted and inactivated flu vaccine to cause disease in this

manner—and did not even test what the actual target antigen in MS would be.

Another item of literature referenced by Dr. Tornatore as evidence of a direct association

between vaccination and MS is also far less supportive of his theory than he allows. See First

Tornatore Rep. at 16–17; A. Langer-Gould et al., Vaccines and the Risk of Multiple Sclerosis and

Other Central Nervous System Demyelinating Diseases, 71 JAMA Neurol. 12:1506-13 (Oct.

2014), filed as Ex. 42 (ECF No. 29-3) (“Langer-Gould”). Langer-Gould was an epidemiologic,

case-controlled study of 780 vaccinated individuals diagnosed with MS or a different CNS-

oriented demyelinating disease, comparing them to 3,885 control subjects, with a primary focus

on the risk from the Hepatitis B or HPV vaccines (although its subjects had also received the flu

vaccine). Langer-Gould at 1508, 1509. Dr. Tornatore emphasized Langer-Gould’s finding that in

fact there was a statistically-significant increased risk of CNS onset within 30 days of receipt of

any vaccine for the studied group—consistent with the idea that in individuals with “subclinical

autoimmunity,” a vaccine might act as a “pro-inflammatory cofactor”—in much the same way an

intercurrent infection might prompt an MS relapse/flare. First Tornatore Rep. at 16–17; Langer-

Gould at 1512.

Langer-Gould, however, not only reached a different ultimate determination, but is not

even all that supportive of the secondary conclusion that has in other cases 5 resulted in its embrace

as supportive of MS causation. Its authors’ primary conclusion was that there was “no long-term

association of vaccines with an increased risk of MS”—contrary to Dr. Tornatore’s theory writ

large. Langer-Gould at 1512. At the same time (and more consistent with the causation theory

embraced in this case), however, Langer-Gould did observe “a short-term increase in risk after

vaccination of any type” in a younger population, seemingly supportive of what is alleged herein.

Id.

But Langer-Gould’s authors actually qualified significantly this aspect of their study’s

findings. They noted that because overall there was no greater exposure risk to MS from

vaccination over time, “[t]his argues against causality because the risk in the vaccinated group

5

See, e.g., Doles v. Sec’y of Health & Hum. Servs., 2025 WL 1177875, at *8 (Fed. Cir. Apr. 23, 2025). In Doles, the

Federal Circuit found that Langer-Gould’s determination of a heightened risk of MS symptoms in a specific sample

of patients and a narrow timeframe could reasonably be given evidentiary weight by a special master in finding a

vaccine had significantly aggravated a claimant’s MS, even if the study did not reach statistically significant

conclusions as to the association.

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should remain elevated regardless of whether the time window between exposure and clinical

disease expression is defined as 15 days or 3 years.” Langer-Gould at 1512 (emphasis added). So

what, then, did their findings about risk in a shorter timeframe post-vaccination actually suggest?

Langer-Gould deemed those results to be consistent with the fact that proinflammatory immune

stimulation was as much of a risk for existing MS patients (who often experience flares due to a

variety of environmental factors) as those who may be experiencing “subclinical autoimmunity,”

causing a hastening of “symptom onset.” Id. In other words, the findings showed that individuals

who were already experiencing MS in some form might see their disease manifest sooner in the

wake of vaccination, or experience a flare—but the vaccine had not caused the underlying

subclinical condition (and more than the cause of a flare would provide an etiologic explanation

for a person’s MS in the first place). Id. (“vaccines (like infections) may accelerate the transition

from subclinical to overt autoimmunity in patients with existing disease”) (emphasis added)). 6

The occurrence of just one vaccination event, moreover, could in turn stimulate a

“progressive inflammatory disorder,” in Dr. Tornatore’s opinion. First Tornatore Rep. at 22–25.

For support, Dr. Tornatore referenced an article involving “the marmoset model of MS.” Id. at 22;

B. t’Hart, Experimental Autoimmune Encephalomyelitis in the Common Marmoset: A

Translationally Relevant Model for the Cause and Course of Multiple Sclerosis, 6 Primate Biol.

17 (2019), filed as Ex. 50 (ECF No. 30-2) (the “Marmoset Paper”). Dr. Tornatore maintained that

this article highlighted (via animal model experiments involving “experimental autoimmune

encephalomyelitis,” or “EAE”—a known scientific animal model for MS) one particular

experiment, in which animals immunized with mimics for a particular nerve myelin component

(myelin oligodendrocyte glycoprotein, or “MOG”) go on to develop MS-like CNS lesions, and in

turn a progressive disease course comparable to human MS. First Tornatore Rep. at 22–25.

Dr. Tornatore found significant that this kind of experiment discussed in the Marmoset

Paper revealed that “one need not have a humoral response against MOG to have an immune

response (cellular in nature).” First Tornatore Rep. at 25. 7 And he noted that, in fact, molecular

amino acid sequence homology can be shown between hemagglutinin in the flu vaccine and MOG

peptides (based on Dr. Tornatore’s own “BLAST” search). 8 Thus, it was scientifically conceivable

6

Langer-Gould actually noted (in an earlier section of the article discussing existing literature on the topic of vaccine

causation) that studies involving the HPV vaccine that seemed to support an association with CNS demyelination had

observed in many of their studied subjects that they “had symptoms at the time of vaccination”—and thus the vaccines

had only hastened “the transition from subclinical to clinical disease”—not caused it. Langer-Gould at 1507.

7

Humoral means “pertaining to elements dissolved in the blood or body fluids, e.g., humoral immunity from

antibodies in the blood as opposed to cellular immunity.” Humoral, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=23202&searchterm=humoral (last visited Oct. 30, 2025).

8

Basic Local Alignment Search Tool (“BLAST”) is a medical/scientific internet resource that assists researchers in

finding regions of similarity between biological sequences of amino acids. The program compares nucleotide or

protein sequences to sequence databases and calculates the statistical significance. BLAST, U.S. National Library of

Medicine, https://blast.ncbi.nlm.nih.gov/Blast.cgi (last visited Oct. 30, 2025). A BLAST search involves review of an

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not only that the flu vaccine could result in this specific kind of MS-associated damage, but also

that it might do so independent of the creation of antibodies against this specific CNS-associated

nerve tissue component.

A careful reading of the Marmoset Paper, however, reveals that it stands for far less (and

even contradicts the concept of vaccine causation of MS). For starters, the main thrust of the article

was its author’s defense of this particular form of animal EAE study as scientifically worthwhile,

despite objections to the ethics of such animal model research. Marmoset Paper at 19. With that

goal, the article reviews numerous published marmoset-model studies involving MS, emphasizing

the benefits of their findings in increasing medical science’s comprehension of MS from many

angles. The Marmoset Paper acknowledged, however, that questions have been raised about how

relevant its findings actually are to human MS (although the paper’s author is clearly in the camp

of favoring animal model EAE experiments for the study of MS). Id. at 22–23.

Yet the Marmoset Paper also makes numerous statements regarding MS’s likely

pathogenesis that run counter to a causal foundation in Petitioner’s case: that administration of a

single dose of flu vaccine could begin a disease process culminating in MS. For example, it notes

that some marmoset-specific experiments shed light on the possibility that “MS might not be

elicited by infection . . ., but by primary injury inside the central nervous system.” Marmoset Paper

at 18 (emphasis added). It later notes that this possibility could be characterized as the “inside-out

paradigm,” in which lesions within the CNS drive disease processes due to a “physiological

response to sustained excess antigen turnover in diseased tissues (the primary lesion).” Id. at 22;

see also id. at 21 (“[t]he pathological hallmark of MS and the most likely cause of the accumulating

neurologic deficits is the lesion”).

The Marmoset Paper acknowledges uncertainty as to whether this paradigm has been

proved over an “outside-in” scheme (where “MS is triggered by an external factor”—here, a

vaccine), but its author clearly seems to disfavor the latter. Marmoset Paper at 31. In fact, its author

writes that “data obtained in the marmoset EAE model are strongly supportive for the inside-out

paradigm.” Id. at 22 (emphasis added). Thus, although the Marmoset Paper does reference a

number of MS-relevant studies, and some could be reasonably invoked to show how a foreign

antigen like a vaccine component might have sufficient homologic similarity with nerve-related

tissues for an autoimmune cross-reaction to occur, they are referenced to bulwark the model’s

value—not because the author believes this is how MS likely occurs. This calls into question the

fundamental assumption of Dr. Tornatore’s theory—that a single vaccination could cause a

resulting pathogenic cascade that fundamentally occurs in the CNS. And the Marmoset Paper even

expressly states that vaccination does not cause MS. Id. at 29 (“[t]he consideration that MS is

online database to “compare[ ] nucleotide and protein sequences, to search for a homology between the … vaccine

and [the body’s myelin basic protein].” Montgomery v. Sec’y of Health & Hum. Servs., No. 15-1037V, 2019 WL

2511352, at *5 (Fed. Cl. Spec. Mstr. May 21, 2019).

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obviously not elicited by injection of an antigen/adjuvant formulation but develops spontaneously”

points toward the need for research about how a CNS lesion might result in myelin damage that is

reflected by clinical symptoms) (emphasis added). 9

Dr. Tornatore further sought to establish how evidence of the existence of oligoclonal

bands (a known biomarker for MS, and here seen in Petitioner’s CSF testing in April 2019—at the

time she was hospitalized) was supportive of a vaccine-encouraged disease process. First

Tornatore Rep. at 14. He deemed it likely that their emergence coincided with the lesions then

observed on MRI, but identified the bands as potential evidence for peripherally-introduced

immune activity. C. Beseler et al., The Complex Relationship Between Oligoclonal Bands,

Lymphocytes in the Cerebrospinal Fluid, and Immunoglobulin G Antibodies in Multiple Sclerosis:

Indication of Serum Contribution, 12 PLOS ONE 10:1 (Oct. 2017)

(https://doi.org/10.1371/journal.pone.0186842), filed as Ex. 36 (ECF No. 28-6) (“Beseler”).

Beseler (drawing upon other studies supporting a “strong connection between IgG

[antibodies] in the peripheral blood and that in the CNS of MS patients”) sought to evaluate the

serum and CSF findings in a sample of 115 subjects, 91 of which had been diagnosed with MS.

Beseler at 2. The authors concluded, among other things, that there were nonlinear but “complex”

associations between the number of oligoclonal bands and CSF IgG, on the one hand, and serum

IgG. Id. at 4. But they also proposed that their data raised a question as to how “intrathecal IgG”

(meaning in the CSF) could possibly be produced given the amounts they saw, and they tentatively

proposed that this was due to blood serum-derived IgG. Id. at 9.

Beseler’s authors only advanced this concept as a hypothesis, and they referenced a fairly-

old article (published in 1971—but not apparently filed in this case) as “compelling” support for

evidence of “antibody-mediated demyelination in MS.” Beseler at 11. Beseler certainly does not

stand for the conclusion that oligoclonal bands come from outside the CNS. But Dr. Tornatore

deemed it further proof that “an inflammatory event in the periphery could trigger an immune

response that ultimately will result in a CNS inflammatory event”—and here, that peripheral event

could be vaccine-mediated. First Tornatore Rep. at 14. (This contention did not, however, explain

(a) why it should be assumed one event—peripheral inflammation—would have temporal priority

over a CNS event, as opposed to something beginning in the CNS that later shows up in the

9

In addition, Dr. Tornatore’s first report referenced unfiled experiments or studies discussed in the Marmoset Paper,

as well as their data. See, e.g., First Tornatore Rep. at 23 (reproducing a portion of “Figure 2” of Marmoset Paper (p.

19)). This Figure seems itself to have been derived from a different item of literature referenced in the Marmoset Paper

but published in 1998. Marmoset Paper at 18 (referencing ’t Hart et al., Histopathological Characterization of

Magnetic Resonance Imaging- Detectable Brain White Matter Lesions in a Primate Model of Multiple Sclerosis: A

Correlative Study in the Experimental Autoimmune Encephalomyelitis Model in Common Marmosets (Callithrix

jacchus), 153 Am. J. Pathol. 649–63 (1998) (see Marmoset Paper at 57 (bibliography)). But the underlying article

itself does not appear to have been filed in this case.

11

periphery, or (b) how the oligoclonal bands—which are understood to be evidence of CNS harm,

get into the CNS in the first place. 10

The remainder of Dr. Tornatore’s report involved his review of the other causation prongs.

See generally First Tornatore Rep. at 25–29. With respect to the “did cause” prong, Dr. Tornatore

maintained that the record established a “logical sequence of cause and effect” from vaccination

to onset. Id. at 25. Thus, Petitioner received the vaccine while (likely) ill with a wild flu infection;

those two factors worked synergistically together; this causes an autoimmune response; and the

autoimmune reaction led to sensory symptoms several days later. Id. at 25–26. But other than the

circumstances of Petitioner’s vaccination and the post-vaccination onset of her first neurologic-

like symptoms, Dr. Tornatore pointed to no other record proof supporting the conclusion that the

flu vaccine she received was likely causal of her MS. And he also did not explain how he

differentiated vaccine-caused TM from the circumstances in which initially-diagnosed TM

actually reflected a first instance of MS (as is clearly so in this case).

Dr. Tornatore devoted a bit more effort to delineating the basis for his opinion that the

timeframe from vaccination to onset was medically acceptable. First Tornatore Rep. at 26–29. He

noted that it was difficult to identify “risk intervals,” given the rarity of “vaccine-precipitated TM.”

Id. at 26. But (citing a publication by the Institutes of Medicine (“IOM”)), he observed that the

known timeframes for the adaptive immune response to a foreign antigenic stimulus provided a

reasonable framework that could be relied upon in this context. Id; Adverse Effects of Vaccines:

Evidence and Causality, Institute of Medicine (K. Stratton et al., eds. 2012), filed as Ex. 51 (ECF

No. 30-3) (“2012 IOM Rep.”), at 58. Here, an immune response could be evident within up to

three days of vaccination—and an article specific to a different CNS-impacting demyelinating

disease (acute disseminated encephalomyelitis, or “ADEM”) established that a two-to-28-day

timeframe was a likely risk interval post-vaccination. A. Rowhani-Rahbar et al., Biologically

Plausible and Evidence-Based Risk Intervals in Immunization Safety Research, 31 Vaccine 271–

77 (2012), filed as Ex. 52 (ECF No. 30-4) (“Rowhani-Rahbar”). And articles involving flu vaccine-

associated peripheral neuropathies reached a comparable conclusion. L. Schonberger et al.,

Guillain-Barre Syndrome Following Vaccination in the National Influenza Immunization

Program, United States, 1976-1977, 110 Am. J. Epid. 2:105-23 (1979), filed as Ex. 53 (ECF No.

30-5) (“Schonberger”). As a result, Petitioner’s onset (which he proposed occurred four to nine

days post-vaccination) fit well within these intervals. First Tornatore Rep. at 28.

10

Beseler also acknowledged the significance of oligoclonal bands in MS—among other things, they may be

explanatory of how a patient’s MS progresses from an initial CIS. Beseler at 2 (“OCBs are associated with increased

levels of disease activity and disability, a greater risk of second attack, the conversion from a clinically isolated

syndrome (CIS) to early [relapsing-remitting MS], and greater brain atrophy”).

12

Second Report

Dr. Tornatore’s supplemental report grouped by topic his reactions to aspects of the report

from Respondent’s expert, Dr. Subramaniam Sriram. First, he questioned Dr. Sriram’s opinion

that Petitioner could not credibly have yielded CSF testing results suggestive of an immune

reaction due to a peripherally-administered vaccine the week prior. Second Tornatore Rep. at 1–

2. He reemphasized the fact that Ms. Peterson was vaccinated while likely ill with a respiratory

infection (perhaps influenza), increasing the likelihood of an overactive immune reaction. Id. at 1.

This was, he maintained, evidenced by both her slightly-elevated IgG and ANA levels, tested ten

days post-vaccination, and was otherwise consistent with the timeframe for a vaccine-caused

immune response. Id. at 1, 2. He also again argued (citing Beseler) that contrasting CSF evidence

of normal-range IgG levels “strongly suggested that the [oligoclonal bands] seen in the CSF were

de novo” (Id. at 2), and thus could have appeared after other instigating factors (here, vaccine-

induced cross-reactive autoantibodies) responsible for the pathogenesis of MS. (This argument, it

should be noted, is somewhat inconsistent with the idea that very-recent peripheral inflammation

was seeping into the CSF (since it did not even show up in this testing), and does not otherwise

negate the conclusion that tests demonstrating the presence of oligoclonal bands are evidence of a

source inside the CNS as the reason for initial MS symptoms—a concept that articles like the

Marmoset Paper readily concede have significant scientific support).

In challenging Dr. Sriram’s contentions about the sequence of events leading to the

appearance of the oligoclonal bands (a recognized biomarker for MS), Dr. Tornatore deemed Dr.

Sriram “absolutely incorrect” in arguing that they can be present before radiologic evidence of

CNS lesions is apparent. Second Tornatore Rep. at 2, 3. The article offered for this contention by

Dr. Sriram revealed evidence of lesions on MRI in all four case subjects discussed, but without a

history of neurologic symptoms. B. Hakiki et al, “Subclinical MS”: Follow-Up of Four Cases, 15

Eur. J. Neurol. 858–61 (2008), filed as Ex. A Tab 4 (ECF No. 31-5) (“Hakiki”). In two of the

cases, however, CSF testing revealed the presence of oligoclonal bands (and thus it cannot be said

for those instances when the bands appeared in relationship to the radiologic evidence of lesions),

while testing was not performed in a third—and hence only one case subject revealed no evidence

of oligoclonal bands after imaging. Hakiki at 2–3. Hakiki’s authors otherwise say nothing about

when the bands likely appear in conjunction with lesion development.

Dr. Tornatore also endeavored to show, with ample citations to a number of scientific

studies, that EAE model experiments had confirmed different aspects of his causation theory. See

generally Second Tornatore Rep. at 7–10. Many of the studies he invoked were, however, more

than 20 to 30 years old—raising the reasonable question why, if these articles so implicated a role

for vaccination in sparking MS (or TM), there were not more recent studies confirming their

purported findings. See, e.g., D. Ziegler et al., Experimental Allergic Neuritis-Like Disease in

Rabbits After Injection with Influenza Vaccines Mixed with Gangliosides and Adjuvants, 42 Infec.

13

& Immun. 2:824–30 (1983), filed as Ex. 63 (ECF No. 34-1) (research published 42 years ago); U.

Jahnke, Sequence Homology Between Certain Viral Proteins and Proteins Related to

Encephalomyelitis and Neuritis, 229 Science 282–84 (1985), filed as Ex. 64 (ECF No. 34-2)

(research conducted more than 40 years ago).

One article that was more recently published, however, was offered by Dr. Tornatore to

explain how the EAE model can be used “to induce oscillatory symptoms typical of the relapsing-

remitting disease . . . , similar to that found in MS patients.” C. Procaccini et al., Animal Models

of Multiple Sclerosis, 759 Eur. J. Pharmac. 182–91 (2015), filed as Ex. 72 (ECF No. 33-9)

(“Procaccini”). Like the Marmoset Paper, Procaccini is a review article mostly aiming at

bulwarking the utility of different research models for the study of MS. Procaccini at 188. And it

also notes the extent to which these models do not fully replicate MS—including the fact that one

model discussed mimics MS through a “virus-induced pathology” (congruent with the contention

here that vaccination could induce disease), even though in MS in humans, “persistent viral

infection of the CNS has not been demonstrated.” Id. at 187. But Procaccini does mention some

animal models that have observed how MS-like disease could be induced by direct immunization

with MBP-derived peptides or reactive T cell clones. Id. at 183–84. From this, Dr. Tornatore

opined those studies about “longitudinally extensive TM” (“LETM”) 11—a form of TM he

acknowledges was not descriptive of Petitioner’s first MS incidence—provided evidence for how

a flu vaccine might prompt disease. Second Tornatore Rep. at 8.

Research regarding TM, Dr. Tornatore maintained, provided helpful evidence even though

MS is the injury in question. Again, referencing the Marmoset Paper, he opined that “a single

antigen” that sparks one disease process (here, manifesting initially as what could be—but was

not—a self-limiting case of TM) could, via other autoimmune mechanisms result in greater harm.

Second Tornatore Rep. at 17. He specifically identified “epitope spreading”—a mechanism in

which an initial immune response against a specific antigen expands over time to include responses

against new epitopes on the same or entirely different ones, causing expansion of an autoimmune

disease 12—as a way that “multiple additional autoantigens can become targeted and persistent,

leading to progressive disease.” Id. But Dr. Tornatore offered no additional independent research

or literature standing for the proposition that MS is thought to be propagated in this manner, and/or

has the potential to become a secondary injury after the “first hit” of TM due to an initial cross-

reaction followed by more widespread epitope spreading.

11

Dr. Tornatore in fact included a chart setting forth the findings of several articles specifically looking at LETM.

Second Tornatore Rep. at 4–5. I discuss some of these herein (although since MS is facially a distinguishable disease,

I do not in detail review each article).

12

See Guzman v. Sec’y of Health & Hum. Servs., No. 15-736V, 2019 WL 2723392, at *26 (Fed. Cl. Spec. Mstr. May

14, 2019) (explaining that epitope spreading is “a process in which invading agents accelerate an ongoing autoimmune

process by local activation of antigens presenting as a result of the existence of immune complexes.”)

14

In so contending, Dr. Tornatore relied upon the notion that mimicry between flu vaccine

antigens and peptide sequences in MBP was a likely mechanism for how injury occurred. Second

Tornatore Rep. at 9–10. Indeed, he contended MBP was the target of attack in these cross-reactive

instances, contrary to Dr. Sriram’s arguments. Id. at 12–15. To support his argument, he cited yet

another study more than 20 years old. B. Bielekova et al., Encephalitogenic Potential of the Myelin

Basic Protein Peptide (Amino Acids 83-99) in Multiple Sclerosis: Results of a Phase II Clinical

Trial with an Altered Peptide Ligand, 6 Nat. Med. 10: 1167–75 (Oct. 2000), filed as Ex. 67 (ECF

No. 34-5) (“Bielekova”). Bielekova’s authors sought to alter a specific peptide T-cell receptor in

the MBP (for a group of eight patients already suffering from relapsing-remitting MS—and hence

a distinguishable group from Petitioner), in order to suppress disease activity. Bielekova at 1167.

They found instead, however, that three of the patients experienced exacerbations, and were able

to identify two where the alterations were deemed to highlight the “encephalitogenic potential” of

the peptide at issue. Id. at 1168, 1170, 1172

Dr. Tornatore opined that Bielekova’s findings (notably, with respect to less than half of

an eight-person sample) were highly significant, and he devoted two pages of his second report to

reproducing charts, figures, and block quotes from the article. Second Tornatore Rep. at 13–16.

He deemed it to constitute “strong evidence that immunization with peptides that bear resemblance

to MBP can result in acute inflammatory events in the CNS.” Id. at 16. But this contention greatly

exaggerates Bielekova’s findings. For one thing, Bielekova’s authors were mainly focused on

attempting to identify helpful immune therapies for treatment of MS, and hence did not aim to

ascertain MS causes, making its overall focus distinguishable from what is at issue in this case.

Bielekova at 1173. In addition, it involved a very small sample of patients who had MS—with no

evidence provided by Dr. Tornatore of follow-up research confirming its findings, or more

obviously extending them to other contexts. And Bielekova does not measure the impact of receipt

of a flu vaccine on existing MS patients.

An even more compelling reason to give Bielekova less weight than Dr. Tornatore

proposed lies in the fact that a core premise it embraces has not since been corroborated.

Bielekova’s authors (writing in 2000—thus 25 years ago), stated that the “current pathogenic

concept of MS . . . assumes that autoreactive T cells are activated in susceptible individuals most

likely by cross-reactive foreign agents.” Bielekova at 1173. 13 This foundational premise is

congruent with Dr. Tornatore’s theory in this case, in which the “foreign agent” of vaccination is

the instigating factor. And yet that premise has not been since confirmed by medical science—and

indeed, articles like the Marmoset Paper undermine its reliability. Moreover, the experiment in

13

Notably, Bielekova offers as a reference for this contention a foundational work (not filed in this case) about

molecular mimicry and its capacity to cause production of cross-reacting antibodies capable of instigating an

autoimmune disease. Bielekova at 1173 n.49 (referencing R. Fujinami & M. Oldstone, Amino Acid Homology Between

the Encephalitogenic Site of Myelin Basic Protein and Virus: Mechanism for Autoimmunity, 230 Science 1043–45

(1985)). This evidence speaks more to the general reliability of molecular mimicry as a mechanistic concept than it

supports the contention in this case that this is the relevant mechanism by which MS likely occurs.

15

Bielekova involved direct transmission of peptides, not induction of cross-reactive antibodies. It

is thus a category error to treat as interchangeable “immunization” with direct injection of peptides

for a specific purpose and receipt of inactivated flu antigens contained in a vaccine. At bottom,

Bielekova may suggest that MBP is the situs for further nerve damage in existing MS patients, but

it does not establish that damage begins here—let alone due to cross-reactivity from antibodies

generated by a vaccine.

Dr. Tornatore also endeavored to supplement his arguments about a vaccine-induced cross-

reactive process in other ways. For example, he contended that a number of articles establish that

flu vaccine antigens have been associated with antibodies discovered in the serum of patients with

LETM. Second Tornatore Rep. at 6; N. Nakamura et al., Neurologic Complications Associated

with Influenza Vaccination: Two Adult Cases, 42 Intern. Med. 2:191–94 (Feb. 2003), filed as Ex.

59 (ECF No. 33-6) (“Nakamura”). Nakamura, however, is only a case study report, and identified

two instances in which distinguishable CNS-impacting neurologic conditions (TM and acute

disseminated encephalomyelitis) were observed after receipt of a flu vaccine—and to the extent

the article discusses MS, it notes that the greater risk of the impact of a flu infection warrants

vaccination. Id. at 194. Another article (specifically considering the distinguishable peripheral

neuropathy of Guillain-Barré syndrome) also showed how flu vaccine-derived antibodies likely

relevant to the disease process in question could arise. I. Nachamkin et al., Anti-Ganglioside

Antibody Induction by Swine (A/NJ/1976/H1N1) and Other Influenza Vaccines: Insights into

Vaccine-Associated Guillain-Barré Syndrome, 198 J. Infec. Dis. 15:226–33 (July 2008), filed as

Ex. 61 (ECF No. 33-8). Of course, proof that the flu vaccine can lead to a different disease is not

particularly robust evidence that it will do so for other, different diseases—and this is true even if

the diseases both involve nerve demyelination.

The post-vaccination timeframe in which Petitioner’s neurologic symptoms manifested

was, Dr. Tornatore reiterated, consistent with reliable science on the subject, despite Dr. Sriram’s

arguments to the contrary. In so arguing, Dr. Tornatore contended that Dr. Sriram had

misinterpreted a chart from Rowhani-Rahbar. Second Tornatore Rep. at 16–17; Rowhani-Rahbar

at 273 Fig. 2. Dr. Sriram had contended that the chart demonstrated that an autoimmune process

driven by vaccination was most likely to occur no sooner than one week post-vaccination (and

hence faster than what Petitioner experienced). But Dr. Tornatore noted that the dates where mean

values, allowing for the possibility of a shorter onset. Second Tornatore Rep. at 17. This argument

may be correct, but it does not rebut the likelihood that “more often than not” onset would occur

in a longer timeframe than the one at issue in this case.

Dr. Tornatore otherwise repeated arguments comparable to those he advances in other

cases where he serves as an expert (arguments that I have repeatedly deemed wanting in

persuasiveness and reliability in many prior decisions). He contended that the rarity of vaccine

injuries rendered epidemiologic evidence a probative nullity in Program cases (Second Tornatore

16

Rep. at 3)—an argument that essentially advances a legal opinion about what evidence bears on a

vaccine injury claim that not only exceeds his competence as a medical expert, but is wrong (from

the standpoint of the Program’s consistent treatment of such evidence as relevant). 14 He then went

on to argue that due to injury rarity, case reports of TM post-vaccination warrant special emphasis,

citing a number as highly relevant and persuasive. Id. at 4–6.

Dr. Tornatore also performed his own “in silica” peptide homology sequence review,

comparing an amino acid peptide string in MBP with influenza A, and observing a homologic

sequence that he noted “has been found to be encephalitogenic” in an animal study performed

nearly 40 years ago. Second Tornatore Rep. at 11, 12; N. Potter et al., Immunochemical Specificity

of Antisera Raised Against the Encephalitogenic Peptide SH624, Residues 59-74 of the Myelin

Basic Protein, 12 Neurochem. Rs. 1:9–14 (1987), filed as Ex 66 (ECF No. 34-4) (“Potter”). I have,

however, noted repeatedly in prior decision that showings of “naked” homology do not appreciably

advance the contention that mimicry between vaccine antigenic components and a self-tissue

establishes a likely mechanism for an autoimmune disease. 15 And Potter (like other experiments

discussed in other articles filed in this case) involves direct “immunization” with MBP peptides,

distinguishable from the effect of a vaccine (where the possibility of a comparable cross-reaction

is lower—and impact more likely muted).

B. Respondent’s Expert – Dr. Subramaniam Sriram

Dr. Sriram is also a neurologist, and he prepared a single written report. Report, dated Mar.

15, 2024, filed as Ex. A (ECF No. 31-1) (“Sriram Rep.”).

Dr. Sriram received a Bachelor of Medicine and a Bachelor of Surgery from the University

of Madras in Madras, India. Curriculum Vitae, filed as Ex. B (ECF No. 32-1) (“Sriram CV”) at 1.

He then served as an intern and resident at Wayne State University and completed a residency in

neurology at Stanford University, where he also served as chief resident and eventually completed

a post-doctoral fellowship in neuroimmunology. Id. He is board-certified in both neurology and

internal medicine. Id. He also holds academic positions as a professor of experimental neurology

and therapeutics as well as an associate professor in molecular biology and immunology. Id. 2. Dr.

Sriram is heavily involved in clinical work as he directs the Multiple Sclerosis Clinic at Vanderbilt

University Medical Center where he sees roughly 1450 patients a year. Sriram Rep at 1. In

addition, he runs a basic science laboratory looking at pathways that promote neurologic repair.

14

See Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009) (“[a]lthough . . . a claimant

need not produce medical literature or epidemiological evidence to establish causation under the Vaccine Act, where

such evidence is submitted, the special master can consider it in reaching an informed judgment as to whether a

particular vaccination likely caused a particular injury”).

15

See Schultz v. Sec’y of Health & Hum. Servs., No. 16-539V, 2020 WL 1039161 (Fed. Cl. Spec. Mstr. Jan. 24, 2020)

(“[m]ere demonstration of theoretical homology alone, based on computer-driven searches involving databases of

amino acid sequences, does not carry the day.”).

17

https://www.vumc.org/neurology/person/subramaniam-sriram-mbbs (last visited Oct. 30, 2025).

In addition, Dr. Sriram has published numerous articles on various aspects of clinical and immune

mediated diseases of the nervous system. Sriram CV at 9–21; Sriram Rep. at 1.

Like Dr. Tornatore, Dr. Sriram’s expert report began with a review of Petitioner’s relevant

medical history. Sriram Rep. at 2–4. He also commented on MS, defining it as a chronic CNS

inflammatory disease involving demyelination. Id. at 4. MS usually presents clinically with

symptoms of “dysfunction of either optic nerves, brainstem, or spinal cord,” followed by relapse

symptoms which can vary in their severity. Id. Its diagnosis requires evidence of lesions in the

brain or spinal cord “disseminated in space and time” (meaning appearing in different places and

at different times). Id. at 4, 5. Although MS is understood to likely be autoimmune in its

mechanism, no specific antigenic autoantibody responsible for it has been identified, and it has no

known cause. Id. at 5.

Acute TM, by contrast, is restricted to the spinal cord, and involves evidence of different

kinds and levels of neurologic dysfunction, typically below the level of the lesion. Sriram Rep. at

6. “Incomplete” forms of TM usually involve asymmetrical deficits “with variable degree of

paralysis of arms and legs” plus autonomic dysfunction. Id. at 7. And this form of TM is very often

seen as an MS relapse. Id.

Dr. Sriram deemed Petitioner’s MS diagnosis (which he clarified to properly be relapsing-

remitting MS) 16 to have full record support. Sriram Rep. at 5. He agreed that as of Petitioner’s

initial early-April presentation, her exam work-up was enough to establish CIS, and there was

proof of one lesion. Id. But as her symptoms evolved, “it is clear that her initial presentation of

myelitis was in fact the first episode of MS.” Id. He felt that her initial symptoms (predominantly

left-sided tingling and numbness that later spread on that side, coupled with a cervical (meaning

close to the neck) lesion) reflected the kind of incomplete myelitis that would characterize an MS

initial flare. Id. at 2–3, 7.

Unlike Dr. Tornatore, however, Dr. Sriram did not consider Petitioner’s initial CIS

presentation (which hinted at MS, even if that diagnosis could not then have been formally applied)

to have any analytic importance with respect to the causation issues raised by this case. As he

observed, “TM is the most common initial presentation of MS,” but “it does not follow that since

Ms. Peterson did not meet the criteria of MS at onset of her symptoms,” the initial TM-like

symptoms could be evaluated in isolation as a separate injury (even if in theory it prompted what

followed). Id. at 9. Rather, “she had MS from the start”—not TM that “then developed into MS.”

16

Relapsing-remitting Multiple Sclerosis (“RRMS”) is the most common course of MS. It “can be characterized as

either active (with relapses and/or evidence of new MRI activity over a specified period of time) or not active, as well

as worsening (a confirmed increase in disability following a relapse) or not worsening.” Relapsing-Remitting Multiple

Sclerosis (RRMS), National Multiple Sclerosis Society, https://www.nationalmssociety.org/understanding-ms/what-

is-ms/types-of-ms/relapse-remitting-ms (last visited Oct. 30, 2025).

18

Id. Accordingly, “[t]he question here is not the relationship between Flu vaccine and TM/CIS but

its relationship to MS,” and literature specific to TM was irrelevant for that purpose. Id. at 10.

The flu vaccine was not likely capable of causing MS, Dr. Sriram contended. Sriram Rep.

at 8–9. He noted that MS patients are “highly studied,” and the causes for flares/exacerbations

have been looked at extensively—yet vaccines have not been deemed associated. Id. at 8; F.

DeStefano et al., Vaccinations and Risk of Central Nervous System Demyelinating Disease in

Adults, 60 Arch. Neurol. 504–09 (Apr. 2003), filed as Ex. A-2 (ECF No. 31-3) (“DeStefano”)

(case-control study comparing instances of MS or optic neuritis in 450 subjects (compared to 950

healthy controls) found no increased risk of onset or recurrence/flares after receipt of a number of

vaccines, including flu vaccine).

More recent studies arrived at similar conclusions. A. Hapfelmeier et al., A Large Case-

Control Study on Vaccination as Risk Factor for Multiple Sclerosis, 93 Am. Ac. Neurol. 9:e908–

16 (2019), filed as Ex. A-5 (ECF No. 31-6) (“Hapfelmeier”), at e909, 914–15 (case control study

of German population of more than 12,000 MS patients compared to over 200,000 controls; over

a five-year period, incidence of new-onset MS not greater for recipients of large number of

vaccines, including flu, than control group). Indeed, Hapfelmeier tentatively proposed, given its

findings, that vaccination might be protective against MS. Hapfelmeier at e915–16. And Dr.

Sriram deemed these studies to confirm what neurology specialists already understood to be the

case. If, he reasoned, medical science even suspected that an “aberrant immune response” due to

vaccination could spark MS, it would be testing blood serum as well as CSF for proof when MS

was suspected, but it does not. Sriram Rep. at 11–12 (“[w]e don’t test patients for an immune

response to MBP in either their blood or CSF”).

Other aspects of Dr. Tornatore’s causation reasoning were called into question by Dr.

Sriram. He noted that proposing a mimicry-driven autoantibody cross-reaction as the mechanistic

driver of MS relied on the idea that “the autoantigen driving MS is a myelin antigen and very likely

Myelin basic protein and the [flu vaccine] hemagglutinin is the antigenic culprit.” Sriram Rep. at

11. But “there is very little evidence that MBP is the antigen in MS,” adding that his own research

into the topic had not identified an autoantibody to MBP as causal—let alone one produced in

response to vaccination. Id. And he disputed that evidence from the Marmoset Paper about

mimicry or cross-reactivity involving MOG proteins was relevant, noting that “MOG associated

disease (MOGAD) 17 is not MS,” and is instead treated as a distinguishable neurologic condition.

Id.

17

“Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD)” is defined as “an autoimmune

condition where your immune system (antibodies) mistakenly attacks parts of you center nervous system. MOG is

part of the protective cover that surrounds nerves (myelin) in your brain, spinal cord and eyes (optic nerves).” Myelin

Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD), Cleveland Clinic,

https://my.clevelandclinic.org/health/diseases/myelin-oligodendrocyte-glycoprotein-antibody-disease-mogad (last

visited Oct. 30, 2025).

19

Dr. Sriram also discussed what was the likely onset of Ms. Peterson’s MS. Petitioner had

tested positive for oligoclonal bands at her early April 2019 hospitalization. Sriram Rep. at 3, 5–

6; Ex. 2 at 53. These bands reflect the existence of “antibodies present in the CSF but not in [blood]

serum, indicating that they are made within the CFS.” Sriram Rep. at 6. The fact that these bands

were observed when MRI findings established the existence of a lesion, Dr. Sriram reasoned, was

proof of “an ongoing immune process which predates receipt of the vaccine,” since they were

observed within approximately one week of vaccination—but would have likely taken a longer

period of time to be produced. Id. at 7, 8. He deemed it “highly unlikely that the antibodies present

in the CNS . . . developed in the periphery and moved to the CNS within seven days” of

vaccination—and hence the flu vaccine could not have caused them to appear. Id. at 8.

In so arguing, Dr. Sriram disputed Dr. Tornatore’s contention that because oligoclonal

bands would generally not be found in asymptomatic individuals, “the MS had to begin at the onset

of the initial symptoms.” Sriram Rep. at 9. Treaters would not think to perform CSF testing unless

a person’s clinical presentation suggested the presence of a neurologic condition that could reflect

MS. Id. Thus, the oligoclonal bands could certainly exist before onset of clinical symptoms. Dr.

Sriram referenced Hakiki to show case report instances of what could be called “subclinical” MS,

where (he contended) it was shown that “patients who had normal MRIs of their brains but spinal

fluid studies showing positive oligoclonal bands and who on follow up went on to develop MS.”

Id.

In fact, the Hakiki case reports involved individuals whose imaging revealed unanticipated

CNS lesions consistent with MS, but before clinical manifestations had occurred (although the

imaging was performed because of nonspecific neurologic concerns (cervical trauma, headaches,

tiredness, etc.). Hakiki at 859–60. And not all the case report subjects revealed the presence of

oligoclonal bands. Thus, Dr. Sriram has misstated Hakiki’s findings, as Dr. Tornatore alleges—

although the article otherwise does not shed light on the question of what evidence of oligoclonal

bands says about when a person’s MS likely began. It also underscores the general notion that MS

onset certainly can predate clinical symptoms—consistent with Dr. Sriram’s more general

argument.

Dr. Sriram also distinguished evidence, like Beseler, that Dr. Tornatore had relied upon to

contend that different categories of immunoglobulins found in the CSF likely came from the

serum—noting that in fact the issue really was where the oligoclonal bands came from. Sriram

Rep. at 10. They were “present only in the CSF and not in serum,” and hence they could reflect

only “intrathecal synthesis” of immune cells reflecting inflammation in the CNS. Thus, their

existence could not be assumed to be due to peripheral immune activity that had migrated to the

CNS and instigated the disease process, as would be required under Dr. Tornatore’s theory.

20

Dr. Sriram did not accept Dr. Tornatore’s more general contentions of what a reasonable

post-vaccination timeframe would be for vaccine-induced MS. Sriram Rep. at 12–14. To

substantiate this argument, Dr. Tornatore had referenced Rowhani-Rahbar, which involved a risk

interval for ADEM after infection, and hence was not precisely relevant to the context of purported

MS due to vaccination. Rowhani-Rahbar at 273; Sriram Rep. at 12 (“we are not dealing with an

infection but rather a vaccine, which unlike an active infection is not [a] proliferating and dividing

organism”), 14. In addition, a closer reading of Rowhani-Rahbar suggested the true, greatest risk

interval was no less than approximately six days—longer than Petitioner’s post-vaccination onset.

Id. at 13; Rowhani-Rahbar at Fig 2 at 273. And even the studies discussed in Rowhani-Rahbar

involved longer risk intervals than the three to four days at issue in this matter. Sriram Rep. at 13–

14; Rowhani-Rahbar at 275.

Thus, the kind of immune response that would need to occur before manifestation of

clinical symptoms suggestive of a neurologic issue (consistent with Petitioner’s presentation)

would not occur in the short, post-vaccination timeframe at issue. Sriram Rep. at 14. Even the

Marmoset Paper studies, which discussed various EAE studies, did not observe disease

development (and only after immunizing the animal subjects with both a highly-powered

adjuvant 18 designed to elicit observable changes, plus direct myelin antigens–not just vaccines that

might indirectly elicit antibodies to those antigens) sooner than seven days later. Marmoset Paper

at 23. And this was consistent with studies Dr. Sriram had conducted and published upon. C. Du

et al., Administration of Dehydroepiandrosterone Suppresses Experimental Allergic

Encephalomyelitis in SJL/J Mice, 167 J. Immunol. 12:7094–101 (2001), filed as Ex. A-3 (ECF

No. 31-4), at 7098 Fig. 6 (animal study involving MS model; five days elapsed before subjects

receiving MBP-primed immune cells manifested clinical symptoms). And none of this explained

how oligoclonal bands would appear in CSF testing as early as they did in this case. Sriram Rep.

at 14.

III. Procedural History

The Petition was filed in March 2022, and assigned to another special master in August of

that same year, before being transferred to me in February 2023. After Respondent’s Rule 4(c)

Report contesting entitlement was filed in June 2023 (ECF No. 24), Petitioner filed Dr. Tornatore’s

first expert report that fall. The process of filing expert reports and other supportive items of

medical literature was completed in July 2024, and I thereafter set a schedule for resolving the case

18

“Freund Adjuvant” is defined as “a water-in-oil emulsion incorporating antigen, in the aqueous phase, into

lightweight paraffin oil with the aid of an emulsifying agent. On injection, this mixture [] induces strong persistent

antibody formation. The addition of killed, dried mycobacteria, e.g., Mycobacterium butryicum, to the oil phase

(Freund complete a.) elicits cell-mediated immunity (delayed hypersensitivity), as well as humoral antibody

formation.” Freund Adjuvant, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=55029 (last visited Oct. 30, 2025).

21

via ruling on the record. The parties have since filed briefs in support of their respective positions,

and the matter is fully ripe for resolution.

IV. Parties’ Arguments

Petitioner

Petitioner maintains all three prongs of the test for causation established by the Federal

Circuit in Althen v. Sec’y of Health & Hum. Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). Br. at

9. But she frames her overall argument with a specific understanding of her diagnosis and medical

history. Id. at 9–11. She emphasizes the fact that as of April 2019, she had been “diagnosed by two

different neurologists” with TM or CIS, and that this was a proper understanding of the medical

facts at that initial period of her treatment. Id. at 9, 10. TM, she emphasizes, is “understood” to be

both a post-infectious or post-vaccine phenomenon, and that it is also on a “continuum” of

demyelinating conditions. Id. at 10. Later on, and as her condition progressed, she was properly

diagnosed with MS—but “her flu vaccination was not just the trigger of an acute demyelinating

event, but also responsible for initiating what was subsequently understood/identified as a chronic

demyelinating condition.” Id. at 11.

Regarding the first, “can cause” Althen prong, Petitioner deems Dr. Tornatore’s opinion to

be sufficiently reputable to meet the preponderant evidentiary test. Br. at 11–12. He offered a

mechanism of molecular mimicry between the flu vaccine antigens and nerve myelin, and even

showed that the flu vaccine did possess sufficient amino acid sequential homology to MOG

peptides for a cross reaction to be possible. Id. at 21. She also noted that many prior decisions in

the Program have found “that it is medically plausible for MS to be caused by vaccinations in

certain circumstances” (Id. at 24) and cited a number of such decisions. Id. at 22–23. (As noted

below, however, it is legally erroneous to characterize a claimant’s Althen prong one burden as

requiring only a showing of plausibility).

Petitioner emphasized the recognized scientific validity of that theory—both generally and

specifically as an explanation for some comparable demyelinating diseases. Br. at 12–15. Dr.

Tornatore further provided specific evidence that this mechanism could explain how the flu

vaccine can cause CNS demyelination akin to what is experienced in MS. Id. at 17–18 (referencing

Markovic-Plese and Langer-Gould). An initial cross-reactive autoantibody attack triggered by

vaccination could lead to a “progressive inflammatory disorder such as MS,” as the different

studies referenced in the Marmoset Paper (in particular involving MOG peptides) revealed. Id. at

19-20). And Bielekova revealed MS exacerbation could occur in patients exposed to an MBP

peptide—suggesting that a chronic response was possible if antigens with homology to myelin, of

the sort contained in the flu vaccine, were introduced to the immune system. Id. at 20–21.

22

With respect to the second, “did cause” prong, Petitioner emphasized that she both had a

demonstrated autoimmune propensity pre-vaccination, and was also likely experiencing an

infectious process at the time of vaccination, making it likely her immune system was “activated

in a manner that would likely cause unbalanced synergistic local inflammation.” Br. at 26. Her

subsequent development of TM close-in-time to vaccination was evidence that this had occurred.

Id. And her initial treaters in April 2019 allowed for the possibility that the vaccine explained her

injury (although Petitioner cannot point to doctors who later made the MS diagnosis also

expressing that tentative view). Id. at 27–28.

Finally, Petitioner contends that she can meet the third Althen prong governing timing. Her

TM manifested within four days of vaccination, and eight days after vaccination enhancing lesions

were revealed on MRI. In Dr. Tornatore’s view, such a lesion would be no more than two to three

weeks old—and therefore could have been generated at the time of vaccination or not long after.

Br. at 29. Overall, a timeframe of CNS demyelination occurring within four to nine days post-

vaccination was consistent with Dr. Tornatore’s theory, and supported by independent items of

literature like Rowhani-Rahbar. Id. at 29–30.

In Petitioner’s Reply, she maintains that Respondent mischaracterizes her legal burden

under Althen—arguing that Prong One only requires her to “provide a sound and reliable, plausible

medical theory showing how the vaccine can cause the injury in question,” not that she must

“provide a theory that establishes, by preponderance, a true or correct explanation of how the

vaccine does cause the injury.” Reply at 2 (emphasis in original). Such a mischaracterization,

explains Petition, is “clearly an elevation of [her] burden,” and that where “some medically

plausible theories may fall short in terms of how sound and reliable the Special Master deems them

to be does not mean a petitioner must show by preponderant evidence that a theory is “true” or

“correct” to prevail in an off-table claim. Id. at 4. Petitioner, however, emphasizes her

understanding that her burden of proof is clearly one of preponderance of the evidence, and that

she is in no way suggesting it is less than that. Id. at 6.

She also argues that she has provided more than a “bare assertion of molecular mimicry,”

and that proving that specific epitopes in the vaccine and the nervous system cross-react with one

another” similarly elevates her burden of proof. Id. Instead, Petitioner contends that special masters

are to consider the totality of the evidence when assessing a petitioner’s theory—not whether a

specific mechanism, including molecular mimicry, has been proven. Id. at 7. Despite Respondent’s

contention that the pathogenesis of MS is not clear or fully known, Petitioner nevertheless,

maintains that the uncertainty regarding the pathogenesis of MS does not defeat her claim. Id. at

13. Rather, what is already known about the nature and pathogenesis of CNS demyelinating

conditions and the immunological impact of the flu vaccine, is sufficient, according to Petitioner,

to conclude that she has met her preponderant burden. Reply at 13.

23

Finally, Petitioner contends that her concurrent influenza infection at the time of her

vaccination only strengthens her support needed to prove a logical sequence of cause and effect.

Id. at 17. Specifically, Petitioner argues that her concurrent influenza infection “significantly

augment[ed] the immune response to not only influenza antigens but also resulting in aberrant

autoimmune response against CNS antigens.” Id. Moreover, Respondent has not provided any

evidence to the contrary, according to Petitioner. Id. She concludes her reply disagreeing with

Respondent regarding a medically acceptable timeframe—noting that her initial TM/CIS

symptoms and subsequent development of MS is consistent with her overall medical theory. Id. at

18.

Respondent

Respondent denies that Petitioner has preponderantly established any of the Althen

causation test prongs. With respect to the first prong, Petitioner relies on a lesser “biologically

plausible” standard of proof, when in fact this prong is subject to the same preponderance

requirement that applies to the other two. Opp. at 10–11. And Petitioner did not otherwise meet

the “can cause” prong with sufficient reliable evidence. As Dr. Sriram established, many large-

scale epidemiologic studies have found no association between the flu vaccine and MS. Id. at 11

(citing Hapfelmeier, DeStefano). Articles like Langer-Gould were actually consistent in their

conclusions. Id. at 11–12. And existing medical guidelines cited by Dr. Sriram supported the

conclusion that the scientific community did not deem the flu vaccine to pose a risk to MS patients.

Id. at 12.

Respondent deemed the components of Dr. Tornatore’s opinion to be inadequately

supported. His reference to molecular mimicry, for example, was too general (a criticism often

directed against its invocation in other cases). Opp. at 12–13 (citations omitted). And where Dr.

Tornatore tried to be more specific to the issues at hand when asserting molecular mimicry, he

faltered. For example, much of his theory relied on attempting to show mimics between flu vaccine

antigenic components and MBP—even though “there is very little evidence that MS is mediated

by MBP.” Id. at 13. Indeed, MS’s pathogenesis remains “unclear,” and therefore it could not be

assumed to be driven by a vaccine as an environmental trigger and in the manner proposed by Dr.

Tornatore. Id. at 13, 14. And the various items of literature offered to bulwark Dr. Tornatore’s

theory either over-relied on MBP associations (Markovic-Plese, Bielekova), did not actually show

a pathogenic response to demonstrated mimicry (Markovic-Plese), or involved individuals who

already had MS (Bielekova). Id. at 14–15. Thus, the showing of homology between putative flu

vaccine antigenic components and MOG was not enough of a basis for the conclusion that a cross-

reactive process driven by autoantibodies produced in response to vaccination could cause MS. Id.

at 16.

24

The Marmoset Paper stood as no better evidence of a vaccine-MS association, Respondent

contended. Opp. at 15–16. Dr. Tornatore identified within this paper the discussion of a different

study, in which it was demonstrated that direct immunization of animal subjects with MOG-

homologous peptides could result in EAE characterized by chronic demyelination. But not only

was EAE not a particularly good match for MS (as Dr. Sriram established), but its focus on MOG

made it even less applicable in this context, since autoimmune demyelinating diseases associated

with MOG are distinguishable. Id. at 15–16.

The remaining two Althen prongs, Respondent argued, were also unmet. Although treaters

had observed a temporal association in April 2019 between receipt of the flu vaccine and

Petitioner’s onset, the treater who later diagnosed her with MS in the fall of 2020 (Dr. Shoemaker)

deemed her initial myelitis not to have been vaccine-associated, given the overall medical record

course and evidence. Opp. at 16–17. And her onset was actually no more than three days post-

vaccination—far too fast for an antibody-driven process due to vaccination to have occurred. Id.

at 18. Evidence relied upon for the timeframe Petitioner favored, like Rowhani-Rahbar, involved

different vaccines or CNS conditions. Id. at 18–19.

V. Applicable Law

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that

he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—

corresponding to one of the vaccinations in question within a statutorily prescribed period of time

or, in the alternative, (2) that her illnesses were actually caused by a vaccine (a “Non-Table

Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §

11(c)(1)(C)(ii)(I); see also Moberly, 592 F.3d at 1321; Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). 19 There is no Table claim for MS as an injury after

the receipt of any covered vaccine—so such a claim can only sound in causation-in-fact.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance

of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that

leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence

before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s

existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. V. United States, 6 Cl. Ct.

476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).

19

Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding

authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings

concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,

124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,

2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

25

Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d

867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not

only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”

Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344,

1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.

Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

rather, the petition must be supported by either medical records or by the opinion of a competent

physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a

Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal

Circuit in Althen, 418 F.3d at 1278: (1) a medical theory causally connecting the vaccination and

the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason

for the injury; and (3) a showing of proximate temporal relationship between vaccination and

injury.”

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners

must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the

type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a

petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”

Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must

only be “legally probable, not medically or scientifically certain.” Id. at 549.

Petitioners may satisfy the first Althen prong without resort to medical literature,

epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical

theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing

Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not empowered by

statute to conclusively resolve what are essentially thorny scientific and medical questions, and

thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of

the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence

standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden

placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v. Sec'y of

Health & Hum. Servs., 121 Fed. Cl. 230, 245 (2015), vacated, 844 F.3d 1363 (Fed. Cir. 2017).

In discussing the evidentiary standard applicable to the first Althen prong, the Federal

Circuit has consistently rejected the contention that it can be satisfied merely by establishing the

proposed causal theory’s scientific or medical plausibility. See Cerrone v. Sec'y of Health & Hum.

Servs., 146 F.4th 1113, 1122 (Fed. Cir. 2025); Kalajdzic v. Sec’y of Health & Hum. Servs., No.

2023-1321, 2024 WL 3064398, at *2 (Fed. Cir. June 20, 2024) (arguments “for a less than

preponderance standard” deemed “plainly inconsistent with our precedent” (citing Moberly, 592

26

F.3d at 1322)); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019);

see also Howard v. Sec'y of Health & Hum. Servs., 2023 WL 4117370, at *4 (Fed. Cl. May 18,

2023) (“[t]he standard has been preponderance for nearly four decades”), aff’d, 2024 WL 2873301

(Fed. Cir. June 7, 2024) (unpublished). And petitioners always have the ultimate burden of

establishing their overall Vaccine Act claim with preponderant evidence. W.C., 704 F.3d at 1356

(citations omitted); Tarsell v. United States, 133 Fed. Cl. 782, 793 (2017) (noting that Moberly

“addresses the petitioner’s overall burden of proving causation-in-fact under the Vaccine Act” by

a preponderance standard).

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

supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,

569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956

F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions

and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d

at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored

in vaccine cases, as treating physicians are likely to be in the best position to determine whether a

‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)

(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly

trustworthy evidence, since they are created contemporaneously with the treatment of the patient.

Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

Medical records and statements of a treating physician, however, do not per se bind the

special master to adopt the conclusions of such an individual, even if they must be considered and

carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment,

test result, report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y

of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing . . . that mandates

that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and

cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the

opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their

suppositions or bases. The views of treating physicians should be weighed against other, contrary

evidence also present in the record—including conflicting opinions among such individuals.

Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious

for special master to weigh competing treating physicians’ conclusions against each other), aff’d,

698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,

2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.

Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between

the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the

phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant

27

proof that the onset of symptoms occurred within a timeframe which, given the medical

understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan

v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what

is a medically acceptable timeframe must align with the theory of how the relevant vaccine can

cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.

Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d

mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,

2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. denied (Fed. Cl. Dec. 3,

2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Legal Standards Governing Factual Determinations

The process for making determinations in Vaccine Program cases regarding factual issues

begins with consideration of the medical records. Section 11(c)(2). The special master is required

to consider “all [] relevant medical and scientific evidence contained in the record,” including “any

diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the

record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,

condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained

in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then

required to weigh the evidence presented, including contemporaneous medical records and

testimony. See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is

within the special master’s discretion to determine whether to afford greater weight to

contemporaneous medical records than to other evidence, such as oral testimony surrounding the

events in question that was given at a later date, provided that such determination is evidenced by

a rational determination).

Medical records that are created contemporaneously with the events they describe are

presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s

health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed.

Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his

contemporaneous medical records, the special master’s decision to rely on petitioner’s medical

records was rational and consistent with applicable law”), aff’d sub nom. Rickett v. Sec’y of Health

& Hum. Servs., 468 F. Appx. 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption

is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people

honestly report their health problems to those professionals; and (iii) medical professionals record

what they are told or observe when examining their patients in as accurate a manner as possible,

so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez

v. Sec’y of Health & Hum. Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.

Apr. 10, 2013); Cucuras v. Sec’y of Health & Hum. Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993

28

F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to

accurately report the onset of their daughter’s symptoms”).

Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03-1585V, 2005 WL

6117475, at *20 (Fed. Cl. Dec. 12, 2005). Indeed, contemporaneous medical records are generally

found to be deserving of greater evidentiary weight than oral testimony—especially where such

testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also Murphy v. Sec’y

of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd, 968 F.2d 1226 (Fed. Cir.), cert. denied,

506 U.S. 974, 113 S. Ct. 463, 121 L.Ed.2d 371 (1992) (citing United States v. United States

Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral testimony which is

in conflict with contemporaneous documents is entitled to little evidentiary weight.”)).

There are, however, situations in which compelling oral testimony may be more persuasive

than written records, such as where records are deemed to be incomplete or inaccurate. Campbell

v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the factual

predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19 (“’[w]ritten

records which are, themselves, inconsistent, should be accorded less deference than those which

are internally consistent’”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination

regarding a witness’s credibility is needed when determining the weight that such testimony should

be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,

1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to

contemporaneous medical records, such testimony must be “consistent, clear, cogent, and

compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Hum. Servs.,

No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In determining the

accuracy and completeness of medical records, the Court of Federal Claims has listed four possible

explanations for inconsistencies between contemporaneously created medical records and later

testimony: (1) a person’s failure to recount to the medical professional everything that happened

during the relevant time period; (2) the medical professional’s failure to document everything

reported to her or him; (3) a person’s faulty recollection of the events when presenting testimony;

or (4) a person’s purposeful recounting of symptoms that did not exist. Lalonde v. Sec’y of Health

& Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In making

a determination regarding whether to afford greater weight to contemporaneous medical records

or other evidence, such as testimony at hearing, there must be evidence that this decision was the

result of a rational determination. Burns, 3 F.3d at 417.

29

C. Determining Matter on Record Rather Than at Hearing

I have determined to resolve this case based on written submissions and evidentiary filings.

My determination is consistent with the Vaccine Act and Rules, which not only contemplate but

encourage special masters to decide petitions (or components of a claim) on the papers where (in

the exercise of their discretion) they conclude that such a means of adjudication will properly and

fairly resolve the case. Section 12(d)(2)(D); Vaccine Rule 8(d). The Federal Circuit has affirmed

this practice. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1365–66 (Fed. Cir.

2020). It simply is not the case that every Vaccine Act claim need be resolved by hearing—even

where the petitioner explicitly so requests.

D. Review of Medical Literature

Both parties filed numerous items of medical and scientific literature in this case, but not

every filed item factors into the outcome of this Decision. While I have reviewed all the medical

literature submitted in this case, I discuss only those articles that are most relevant to my

determination and/or are central to Petitioner’s case—just as I have not exhaustively discussed

every individual medical record filed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322,

1328 (Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record

evidence even though he does not explicitly reference such evidence in his decision”) (citation

omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. Appx. 875, 884 (Fed. Cir.

2013) (“[f]inding certain information not relevant does not lead to—and likely undermines—the

conclusion that it was not considered”).

ANALYSIS

I. MS and its Treatment in the Vaccine Program as a Putative Vaccine Injury

A. Medical Characteristics of MS

The parties agree that Petitioner was accurately diagnosed with relapsing-remitting MS,

despite how treaters characterized her initial presentation. As noted in P.M. v. Sec'y of Health &

Hum. Servs., No. 16-949V, 2019 WL 5608859, at *21 (Fed. Cl. Spec. Mstr. Oct. 31, 2019):

MS is a demyelinating CNS disease. See Taylor v. Sec’y of Health & Human

Servs., No. 13-700V, 2018 WL 2050857, at *21 (Fed. Cl. Spec. Mstr. Mar.

9, 2018). It likely has an autoimmune pathogenesis. W.C. v. Sec’y of Health

& Human Servs., No. 07-456V, 2011 WL 4537877, at *3 (Fed. Cl. Spec.

Mstr. Feb. 22, 2011), mot. for review den’d, 100 Fed. Cl. 440 (2011), aff’d,

704 F.3d 1352 (Fed. Cir. 2013). Patients diagnosed with MS typically

experience multiple episodes of CNS demyelination separated in time and

30

space (meaning throughout the CNS), concurrent with a progressive, if

remitting and relapsing, decline in their overall health course. Taylor, 2018

WL 2050857, at *21. An MRI can be used to corroborate the dissemination

in space and time requirement, and often reveals old lesions as well as

enhancing/new lesions. Id. Symptoms can include numbness or weakness

in the body, loss of vision, tremors, unsteady gait, slurred speech, and

dizziness. Id.

Significantly, medical science still does not understand why MS begins, or why its

symptoms later recur—and no study has been generated supporting the proposition that a one-time

neurologic “hit” can thereafter initiate what becomes a chronic injury (although the research into

the MS-Epstein Barr virus (“EBV”) connection is promising). 20 There are thus no widely-accepted

known specific causes of MS—and no particular antibodies associated with it either. Yet many

other demyelinating diseases—MOGAD, for example—do have associated antibodies, which at a

minimum constitute biomarkers of the relevant disease even if medical science is not precisely

confident that the antibodies in question drive it.

B. Program Decisions Involving MS as Vaccine Injury

Special masters have sometimes been persuaded by causation theories that certain vaccines

could cause, or worsen, MS. See, e.g., Jane Doe v. Sec'y of Health & Hum. Servs., No. 13-471V,

2023 WL 4741993, at *29 (Fed. Cl. Spec. Mstr. July 25, 2023) (hepatitis B vaccine significantly

aggravated subclinical MS), mot. for review den’d on other grounds, 2023 WL 6474093 (Fed. Cl.

Oct. 5, 2023); Robinson v. Sec'y of Health & Hum. Servs., No. 14-952V, 2021 WL 2371721, at

*25 (Fed. Cl. Spec. Mstr. Apr. 12, 2021) (flu vaccine caused MS); Hitt v. Sec’y of Health & Human

Servs., No. 15-1283V, 2020 WL 831822, at *9–10 (Fed. Cl. Spec. Mstr. Jan. 24, 2020) (entitlement

for petitioner based in part on finding that Respondent’s expert had conceded the flu vaccine can

cause MS); Br. at 22–23 (citations omitted I have not joined in this view, however—and the case

against such a theory is far more scientifically reliable and persuasive (as discussed below).

In addition, certain CNS demyelinating diseases that manifest in an acute and monophasic

manner, like TM or ADEM, have been reasonably associated with vaccines in many prior Program

matters, based on sound medical science. MS is not the same, however. Compare Raymo v. Sec’y

of Health & Human Servs., No. 11-654V, 2014 WL 1092274, at *23 (Fed. Cl. Spec. Mstr. Feb.

24, 2014) (finding causal relationship between flu vaccine and TM), with Wei-Ti Chen v. Sec’y of

Health & Human Servs., No. 16-634V, 2019 WL 2121208, at *22 (Fed. Cl. Spec. Mstr. Apr. 19,

20

Recent studies have posited an association between MS and an EBV infection. See, e.g., Jaye v. Sec’y of Health &

Hum. Servs., No. 20-672V, 2024 WL 3691413, at *3–5, (Fed. Cl. Spec. Mstr. July 18, 2024). But claimants cannot

persuasively invoke these studies in the context of other vaccines—especially since there is no EBV vaccine to begin

with that could be analogized to any covered vaccine.

31

2019) (determining there was insufficient evidence provided to support a causal connection

between the flu vaccine and petitioner’s subsequent development of neuromyelitis optica spectrum

disorder, which is chronic and relapsing/remitting, like MS).

There are several compelling reasons for treating MS differently from ADEM or TM,

despite their overlapping features. MS is chronic and persistent, and often can be subclinical for

lengthy periods of time. And its symptomatic flares (common to relapsing/remitting MS) can be

triggered by a wide array of external environmental factors. L.Z. v. Sec'y of Health & Hum. Servs.,

No. 14-920V, 2018 WL 5784525, at *6 (Fed. Cl. Spec. Mstr. Aug. 24, 2018). But the trigger for

such a flare, whatever its nature, cannot be said to have “started” the underlying disease process

ab initio.

By contrast, more self-limiting and monophasic neurologic injuries are understood to

occasionally be triggered by the single impact of an external stimulus, such as a wild infection—

and hence reasoning that the same kind of monophasic illness could also begin with the single

instance of vaccine exposure has far greater power. But no infectious cause for MS has yet been

identified (except for the nascent EBV research). In addition (and as noted in my discussion of the

Marmoset Paper), it is not at all clear whether MS is a disease that occurs from the “outside-in”—

driven by external stimuli to the immune system that works its way inward, to the spine and brain.

Marmoset Paper at 22. It may well be the case that lesions within the CNS are responsible for the

subsequent symptoms—and that their generation does not occur due to an external/environmental

trigger.

Because of this distinction, it is scientifically unreliable to apply the analytic framework

relevant to how some vaccines may cause acute, self-limiting demyelinating nerve injuries to a

chronic, often-insidiously-developing disease like MS. Samuels v. Sec'y of Health & Hum. Servs.,

No. 17-071V, 2020 WL 2954953, at *18–19 (Fed. Cl. Spec. Mstr. May 1, 2020) (finding

petitioner’s actual injury was MS, an illness far less associated with vaccination than one-time

acute CNS demyelinating events like ADEM); Pek v. Sec'y of Health & Hum. Servs., No. 16-

0736V, 2020 WL 1062959, at *17 (Fed. Cl. Spec. Mstr. Jan. 31, 2020) (determining that evidence

and expert reports did not provide sufficient proof that a progressive, chronic demyelinating

condition like MS could be initiated by the flu and Tdap vaccines); Wei-Ti Chen, 2019 WL

2121208, at *22; Hunt v. Sec’y of Health & Human Servs., No. 12-232V, 2015 WL 1263356, *15

(Fed. Cl. Spec. Mstr. Feb. 23, 2015) (denying entitlement where MS was the alleged injury, but

the literature offered only discussed a causal relationship between vaccines and ADEM).

Relying upon such reasoning, I have repeatedly rejected causation theories that many

different covered vaccines are capable of causing (or worsening) MS. See, e.g., Garris v. Sec'y of

Health & Hum. Servs., No. 22-1354V, 2025 WL 2401999 (Fed. Cl. Spec. Mstr. June 20, 2025)

(hepatitis B vaccine not shown to be causal of MS); Porch v. Sec'y of Health & Hum. Servs., No.

32

17-802V, 2023 WL 21875 (Fed. Cl. Spec. Mstr. Jan. 3, 2023) (MMR vaccine did not cause MS);

P.M., 2019 WL 5608859 (flu vaccine not shown to be capable of worsening MS); Samuels, 2020

WL 2954953, at *19–21 (Tdap vaccine not established to be causal of MS); Pek, 2020 WL

1062959, at *16–17 (flu and Tdap vaccines not causal of MS); P.M., 2019 WL 5608859, at *22–

27 (flu vaccine not shown to be able to worsen MS or to have done so to specific claimant); L.Z.,

2018 WL 5784525 (flu vaccine and MS). Although other special masters may have been more

solicitous of this causation theory, I am not required to endorse their determinations (any more

than they were obligated to accept my reasoning). And while the existence of contrary decisions

seem to suggest that the relevant science is equivocal on the issue, I have found (based upon my

own carefully-considered reasoned decisions) that it unquestionably is not.

II. Petitioner’s Initial Presentation of TM/CIS Does not Define her Proper Diagnosis

Petitioner’s causation theory is based in part on an inconvenient fact, and one she endeavors

through her expert to evade. As evidenced by the totality of the record, she was properly diagnosed

with MS—and it is just as clear that her MS first manifested with symptoms that could have been

a single and monophasic instance of TM—but unfortunately proved not to be. In addition, there is

far better medical and scientific support for a single instance of TM to be caused by an

environmental trigger akin to vaccination (since infections are known to lead to CNS

demyelination), than with respect to MS.

What to do? Dr. Tornatore’s solution was to focus upon Petitioner’s medical history in the

fairly immediate post-vaccination timeframe (March-April 2019), rather than place those

presenting neurologic symptoms in the context of her ultimate (and evidentiarily-supported) MS

diagnosis. He thus emphasizes the fact that Petitioner’s admittedly close-to-vaccination

presentation would be consistent with TM and CIS—had Petitioner not also gone on to meet the

other MS criteria. Of course, that is in fact what happened—and literature filed by Petitioner in

this case clearly establishes that TM can be an initial presenting clinical manifestation of MS.

It is not difficult to discern why Petitioner would want to frame her claim around the initial

diagnosis of TM—an oft-compensated injury that is far better known to be post-infectious (and

even post-vaccinal) than MS. But the evidence does not allow the conclusion that Petitioner’s TM

was unrelated to her later MS diagnosis. Rather, applicable independent evidence strongly

supports the conclusion that a person who first experiences a myelitis-like presentation, coupled

with proof of a lesion characteristic of TM, but who later meets the diagnostic criteria for MS,

suffered from MS—not two separate diseases. And this record establishes that as time progressed,

Petitioner’s treaters (taking into account the entirety of her medical history) noted that she had not

experienced a single isolated event of TM. Indeed—there were signs early on, recognized by

treaters, that Ms. Peterson might actually have MS. Ex. 26 at 21.

33

It cannot be assumed that simply because a vaccine might be shown capable of triggering

a single, acute instance of a CNS-impacting demyelinating disease, like TM, that this in turn means

that MS presenting with TM is also necessarily vaccine-caused. When MS is later diagnosed, an

initial flare that is TM-like is almost always understood to be part of the MS disease process. The

MS diagnosis is not deemed incidental or secondary to the initial TM diagnosis, or something that

could be avoided with proper treatment—it subsumes it. Thus, Petitioner’s initial TM-like

symptoms cannot credibly be viewed in isolation in this case. And it does not matter if treaters

initially viewed a first presenting neuropathic symptom as TM alone—since they usually do so

without knowing enough of a patient’s total presentation to understand the true picture.

Relying on such logic, I have dismissed several cases where MS proves to be the

evidentiarily-supported diagnosis, even though the petitioner’s initial symptoms seemed to first-

responding treaters to reflect TM, ADEM, or a comparable acute demyelinating neuropathy. See,

e.g., Morgan v. Sec’y of Health & Human Servs., No. 15-1137V, 2019 WL 7498665, at *16 (Fed.

Cl. Spec. Mstr. Dec. 4, 2019), mot. for review den’d, 148 Fed. Cl. 454 (2020), aff'd, 850 F. App'x

775 (Fed. Cir. 2021); Caruso v. Sec'y of Health & Human Servs., No. 15-200V, 2017 WL 5381154,

at *12–13 (Fed. Cl. Spec. Mstr. Oct. 18, 2017), mot. for review den'd, 137 Fed. Cl. 386 (2018).

Other special masters have also so concluded. See, e.g., Juranek v. Sec'y of Health & Hum. Servs.,

No. 19-226V, 2025 WL 399501, at *33–34 (Fed. Cl. Spec. Mstr. Jan. 8, 2025) (flu vaccine not

shown to be capable of aggravating MS). It was not established in such cases that reasoning

specific to how a vaccine might cause a monophasic, one-time CNS injury applied to a larger-

scale, chronic injury.

Taking all of the foregoing into account, I do not find on the basis of this record that

Petitioner’s initial, TM-like presentation can be cabined off, for causation purposes, from her later

MS diagnosis. MS is the injury at issue, despite the nature of Petitioner’s initial symptoms—and

therefore the claim must be analyzed as one seeking to prove that the flu vaccine could cause MS,

and did so here. That is the evidence-based, medically-appropriate way to evaluate the claim, as

persuasively recognized by Dr. Sriram. See Sriram Rep. at 9.

III. Petitioner Has Not Carried Her Althen Burden of Proof

I find none of the Althen prongs satisfied in this case. I address them in the order consistent

with how they are presented in the Althen decision.

34

A. Prong One

1. The Evidence Does not Support the Conclusion that

MS Is Understood to Evolve From TM

At its core, Petitioner’s causation theory operates in part according to this syllogism: (a)

the flu vaccine can cause TM; (b) TM is often a presenting symptom of MS; (c) therefore, the flu

vaccine can cause MS. See, e.g., Br. at 25 (“if the evidence supports a finding that TM can be

triggered by a vaccine, the same evidence can support a finding that MS can be triggered by a

vaccine—the pathogenesis and features of the initial injury is the same—whether it ultimately

results in an acute or chronic condition depends on host factors”). But this reasoning is ultimately

fallacious. Indeed, the fact that Petitioner was accurately diagnosed with MS weighs heavily

against the conclusion that her receipt of a flu vaccine could explain everything that came after.

As discussed above, MS (which has no known trigger—unlike TM in some cases) is a

different entity from TM, even if the two overlap. MS is not understood to be post-infectious in

the way TM is. And as evidence Petitioner offered shows, it may actually begin entirely within the

CNS, with outward clinical manifestations downstream from the appearance of lesions (rather than

something impacting the periphery and subsequently invading the CNS, as is true of many viral or

bacterial infectious processes). See, e.g., Marmoset Study at 22. It is reasonable to conclude that

when an individual presents with myelitis-like symptoms that could constitute TM or something

comparable, but then goes on to meet the other clinical and testing criteria for MS, the MS is the

cause of the TM.

It is certainly plausible (although that is not the standard of proof applicable to this claim—

as noted above and below) that a petitioner might be able to show (via reliable independent medical

or scientific evidence) that vaccine-caused instances of TM “set up” a person to later experience

MS—comparable to what Vaccine Act claimants accomplish in other kinds of cases. 21 If vaccines

can trigger CNS demyelination of one sort, they could theoretically be responsible for causing

21

There are, in fact, other kinds of Program claims where petitioners can preponderantly show that an initial vaccine

injury has a greater, secondary/collateral health impact. Thus, in many seizure disorder cases, petitioners have

succeeded in demonstrating that a first seizure provoked by a vaccine-induced fever could later lower a child’s

threshold for seizures, causing a snowball effect and leading to a greater seizure condition with attendant brain damage.

See, e.g., Weaver v. Sec’y of Health & Hum. Servs., No. 16-1494V, 2022 WL 12542485 (Fed. Cl. Spec. Mstr. Sept.

23, 2022), reversed in part, vacated in part, 164 Fed. Cl. 608 (2023), remanded, 2023 WL 3836239, at *2 (Fed. Cl.

May 8, 2023 (determining on remand that vaccines induced a febrile seizure that caused and significantly aggravated

the child’s seizure disorder; no evidence of an underlying genetic cause for the disorder had been supplied); Ginn v.

Sec’y of Health & Hum. Servs., No. 16-1466, 2021 WL 1558342, at *6 (Fed. Cl. Spec. Mstr. Mar. 26, 2021) (finding

that “a brief febrile seizure triggered by vaccinations can be the starting point for the development of epilepsy.”). More

prosaically, syncope after vaccination is a recognized Table injury—and in such instances, damages are almost always

dependent on proof that a person’s initial fainting from receipt of a vaccine caused them to experience some form of

serious consequential harm (such as injury to the cranium or face).

35

progressive or relapsing forms of comparable illnesses. But nothing has been offered in this case,

direct or indirect, to suggest that MS is understood by medical science to proceed in this manner—

that its occurrence is likely dependent on some initial autoimmune event triggered by an

environmental factor. 22 None of the articles in this case specific to MS propose that individuals

who experience TM are subsequently more likely to develop MS due to the first illness. (At most,

articles like Langer-Gould support the conclusion that individuals already suffering from MS sub-

clinically could have their symptoms manifestations hastened due to vaccination—but that is not

consistent with a causation determination).

At bottom, it has not at all been preponderantly shown that TM likely “causes” MS. It is

accordingly erroneous to view in isolation the first clinical manifestation of MS as a separate

instance of vaccine-caused TM, when in fact that first symptom was (in retrospect) the precursor

of something worse (and that likely was already underway). TM itself does not unerringly lead to

MS in any event. And the kinds of environmental factors that can cause limited forms of CNS

demyelination or nerve injury are not equally causative of MS.

2. Petitioner Mistakenly Relies on a Plausibility Standard

An overarching legal mistake evident in Petitioner’s briefing is the extent to which she

appears to rely on a standard of plausibility, rather than preponderance, in proving her causation

theory. See, e.g., Br. at 14, 24. In Cerrone, however, the Federal Circuit made clear that the lesser

standard of scientific/medical plausibility does not govern the first Althen prong. Cerrone, 146

F.4th at 1122. Rather, a claimant must demonstrate it is “more likely than not” that the vaccine in

question can cause the relevant injury. This is the standard I am applying in my analysis—and

overall, I have not found it met.

3. Dr. Tornatore Has Not Established that MS Likely Begins

Due to Cross-Reactivity with Nerve Myelin Components

Petitioner correctly notes that she is not required by Program case law to offer a mechanism

for how the flu vaccine could cause MS (Br. at 11)—but then Dr. Tornatore goes ahead and

attempts to do so in any event. Obviously, when an expert offers a mechanistic explanation in the

context of their causation opinion, a special master may reasonably evaluate the probative strength

of that showing. Bender v. Sec’y of Health & Hum. Servs., No. 11-693V, 2018 WL 3679637, at

*28 (Fed. Cl. Spec. Mstr. July 2, 2018) (explaining that petitioner had not offered any direct

22

One can envision many forms of evidence that might help prove this point. For example, studies that showed how

effective treatment of TM could prevent the subsequent onset of MS could credibly aid the theory that what causes

TM can secondarily cause MS. But I am not aware of any such studies—whether filed in this case or even in

existence—suggesting that a dysregulated immune response thought associated with TM could, if not arrested, result

in a chronic disease.

36

scientific or medical evidence associating the relevant vaccines and TM, but instead attempted to

bulwark her case via a discussion of mechanisms by which any vaccine might cause the alleged

injury at hearing, and thus, it was therefore reasonable to evaluate her success on that front).

Dr. Tornatore’s opinion reflects what many experts attempt to do when similarly faced with

proving how a vaccine could initiate an autoimmune process. He endeavors to identify an amino

acid sequence from a component of the flu vaccine, and a mimicking sequence from a target

antigen from nerve tissues (here, MBP); he offers some evidence that the target has been shown to

be cross-reactive from reputable studies involving neuropathic harms; and he seeks to root all of

the above in the context of MS.

But this showing fails, for the reasons I have often stated in prior cases. McKown v. Sec'y

of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr. July 15,

2019) (explaining that “merely chanting the magic words ‘molecular mimicry’ in a Vaccine Act

case does not render a causation theory scientifically reliable, absent additional evidence

specifically tying the mechanism to the injury and/or vaccine in question” (emphasis omitted)). In

isolation, molecular mimicry is a reliable scientific concept that can explain how autoimmune

diseases occur—but it is not a blanket explanation for every single possible autoimmune disease,

and it has not in this case been shown to be a likely explanation for MS’s pathogenesis, despite its

relevance to other demyelinating disease processes. Thus,

(a) homology demonstrations alone, based on amino acid sequence

similarity, do not establish vaccination is likely to cause an antibody-driven

cross-reaction,

(b) MS has not been shown to be mediated at the outset (as opposed to

during disease course, in the midst of damaging processes already

underway) by an autoimmune attack on MBP, or MOG for that matter, and

(c) many of the studies offered to suggest that MS could be so driven

involve either direct transfer of peptide sequences based on the goal of a

cross-reaction, occur in the context of an animal study intended to provoke

an experimentally-observable response (like EAE), or involve existing MS

patients (rather than disease initiation)—and hence are not comparable to

the immune stimulation provided by vaccination.

In the end, this was yet another case in which a Petitioner attempts to offer the otherwise-

reliable medical theory of molecular mimicry—which “works” in conjunction with some kinds of

demyelinating autoimmune diseases—as an explanation for how a vaccine could spark an entirely

37

different autoimmune disease, but without linking up all elements of the theory with sufficient

reliable scientific or medical evidence.

4. The “Marmoset Paper” Does not Constitute Novel

Scientific Thinking Supportive of Petitioner’s Causation Theory

Despite Petitioner’s embrace of the Marmoset Paper as reflecting critical and recent

thinking about MS’s pathogenesis bearing on this case, a careful reading of the article reveals less

support for causation than Petitioner supposes. The main thrust of this article is a defense of a

particular form of animal EAE study, and while it reviews various other published marmoset-

subject studies that bear on the case, Marmoset Paper was not directly intended to comment on the

kinds of issues at stake in this matter. Moreover, its author not only outlines an “inside out”

pathogenic theory for MS inconsistent with a peripherally-administered vaccine causing systemic

inflammation that subsequently goes to the CNS, but seems to favor that explanation (while

admitting that medical science still knows too little about MS’s pathogenesis to fully rule out any

explanation for it). Marmoset Paper at 22.

In addition, even if the Marmoset Paper’s primary focus is ignored and weight is given to

the results of the studies it references, the article does not appreciably advance the concept that a

peripherally-administered flu vaccine could spark an aberrant immune process leading to MS. Its

discussion of MOG, for example, did not involve the generation of anti-MOG antibodies against

this myelin-found protein due to vaccination, but instead direct transfer of peptides already known

to be homologous. In addition, the discussed study was not itself ever filed in this case—and MOG

is not likely particularly relevant to MS in any event. 23

Given the foregoing, how does the Marmoset Paper actually assist Petitioner’s case? It is

facially equivocal in concluding whether any environmental factor like vaccination could even

trigger the disease process (although it clearly does not rule this possibility out). It offers a reasoned

defense of EAE marmoset models in investigating MS, but the merits of different experimental

methodologies or approaches are not all that relevant to whether the flu vaccine can cause MS.

And the specific studies it mentions that do go to the questions of causation disputed in this case

only offer limited support for an external trigger as initiating MS, while supporting alternative

23

Current medical science favors MOG-associated demyelinating diseases (MOGAD) as distinguishable from MS—

not that it is believed that MOG antibodies likely drive MS in any manner. See, e.g., Garris, 2025 WL 2401999, at

*10 (“MS patients are not commonly found to possess anti-MOG antibodies in the first place”). In addition, the

Marmoset Paper was published six years ago, and relied on studies from prior to that time. See generally Marmoset

Paper at 49-58 (bibliography). Thus, while it is hardly outdated, it does not reflect the most up-to-date thinking on the

relevance of MOG antibodies to MS. And again, the goal of the Marmoset Paper (to defend this kind of model for MS

research) should be kept in mind as well, since its author is unapologetically seeking to demonstrate the importance

of the model—a different aim from defending the accuracy of MOG-oriented studies when applied to MS.

38

etiologies that would rule out vaccine causation if found to be scientifically correct. I thus do not

find the Marmoset Paper warrants the significance Petitioner or her expert has proposed it merits.

5. Other Literature Filed in this Case is Inapposite or

Fails to Preponderantly Support Flu Vaccine-MS Causation

Many items of literature offered by Dr. Tornatore involve distinguishable injuries (see, e.g.,

Schonberger (Guillain-Barré syndrome), Rowhani-Rahbar (ADEM), and Nakamura (TM and

ADEM)), or vaccines (Langer-Gould (focus on Hepatitis B and HPV)). I reasonably give such

literature a bit less weight in comparison to articles more specific to MS.

Even those more MS-oriented items of literature were less helpful to the Petitioner’s case

than billed. Markovic-Plese, for example, demonstrated cross-reactivity in the context of an

existing MS patient, and thus does not stand as robust proof that the flu vaccine’s antigens can

prompt MS ab initio, via autoantibody cross-reactivity. Bielekova relies on uncorroborated

assumptions about MS’s potential propagation from an external/environmental insult, involved a

very small sample of subjects, and (in a study that actually aimed to seek ways to better treat MS)

reached inadvertent conclusions about cross-reactivity with MBP that does not suggest MS likely

initiates in this manner.

Langer-Gould (which has in other cases been relied upon as evidence that vaccines might

hasten MS’s clinical manifestations) actually stands for the greater conclusion that commonly

administered vaccines (like the flu vaccine) are not reliably associated with MS. To the extent it

suggests otherwise, its findings are simply consistent with the understanding that an immune

stimulus can produce MS clinical symptoms (flares in existing patients; first manifestations in

individuals with sub-clinical courses)—not that the vaccine’s immune stimulation causes MS. And

there are at the same time—and in addition to Langer-Gould—other epidemiologic studies

standing for the conclusion that the flu vaccine does not likely cause MS. See, e.g., Hapfelmeier.

6. Not Enough is Yet Known About MS’s Etiology

To Credibly Implicate Vaccines in its Pathogenesis

In many vaccine injury cases, a claimant can point to the fact that a vaccine’s wild viral or

bacterial analog is itself associated with the alleged injury. Here, by contrast, there is no

comparable known infectious basis for MS relevant to the vaccines covered in the Program. A.

Hernandez et al., Multiple Sclerosis, in THE AUTOIMMUNE DISEASES 735, at 745 (N. Rose and I.

Mackay, eds., 2014 (Fifth Ed.)). Dr. Sriram endorsed this view as a neurologist conversant with

the study and treatment of MS—along with the concurrent fact that MS’s cause remains unknown,

and even that the theory that it proceeds via an autoimmune process has many holes left to be

filled. Sriram Rep. at 4–5.

39

Dr. Tornatore of course attempted to maintain the opposite. But although he clearly

possesses the expertise needed to opine on the subject, he did not link his theories (in a case in

which he was acting as an advocate, well-aware of the legal requirements for a successful Vaccine

Act claim) to evidence that would establish that his opinion possesses wide-spread support in the

medical community. Ultimately, it was not shown in this case that enough is known about MS to

conclude that a foreign/environmental agent could likely instigate it (and in fact, items of literature

like the Marmoset Paper seem to deem this unlikely). While at some later point a study might

better elucidate how some environmental factor analogous to vaccination could spark MS, that

kind of reliable research remains to be performed. The studies and articles filed in this case may

establish that within MS’s ongoing processes cross-reactivity leading to demyelination occurs—

but this is not the same as evidence suggesting vaccination instigates it.

7. Dr. Tornatore’s Personal Expertise Was Not Enough

to Render his Overall Opinion Sufficient to Establish

His Proposed Theory by a Preponderance

Petitioner undoubtedly found in Dr. Tornatore an expert with significant personal expertise

in the study and treatment of MS, and he was well-qualified to offer an expert opinion in this case

(even if his knowledge of immunology as a separate discipline is somewhat comparatively less

than his grasp of neurology). But as I recently observed in a different matter also involving Dr.

Tornatore’s work as an expert, “I discount the opinion offered on Petitioner's behalf more than I

find fault in the personal qualifications of the expert espousing it.” Kazcerowski v. Sec’y of Health

& Hum. Servs., No. 21-758V, 2025 WL 2798865, at *38 (Fed. Cl. Spec. Mstr. Aug. 28, 2025).

I have the same reaction here to Dr. Tornatore’s opinion. While logically presented, it over-

relied on the assumption that what can cause TM can also cause MS, put too much emphasis on a

showing of homology of the sort repeatedly rejected as evidentiarily sufficient, and assumed things

about MS’s course or etiology that are not fully accepted in the medical community (even if the

articles selected to prove these contentions contained reliable conclusions about the studies they

considered).

I was not required to accept Dr. Tornatore’s ipse dixit. Rather, I am ultimately to base my

decision on the evidence offered in this case. And I do not find that the balance of proof favors

causation, even applying the Program’s preponderant standard of “fifty percent and a feather”—

for that standard is not easy to meet even if it does not require certainty. Hodges v. Sec'y of Health

& Hum. Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (in causation-in-fact cases, “the heavy lifting

must be done by the petitioner, and it is heavy indeed”). Dr. Tornatore’s opinion was based on

partial evidence that did not effectively link up into a persuasive causation theory. He relied too

much on somewhat-stale studies, blanket applications of molecular mimicry to a context in which

40

it may not work, and assumptions about MS’s etiology—including in particular that it likely begins

due to an external/environmental trigger.

B. Prong Two

Petitioner has also not preponderantly established that the flu vaccine she received “did

cause” her MS. Treaters certainly did not link the two. And to the extent they discussed both, it

was only to acknowledge the fact that Petitioner’s MS onset literally post-dated vaccination (hence

a mere temporal relationship). Ex. 6 at 48. At most, at the time it was possible that Petitioner had

only experienced a one-time, monophasic injury, TM, treaters allowed for an association. But later

treaters who diagnosed Petitioner’s MS, like Dr. Shoemaker, expressly discounted the flu vaccine

as a causal factor. Ex. 6 at 84. Thus, the actual injury Petitioner experienced was not deemed likely

associated with the flu vaccine.

Admittedly, the record does establish Petitioner received the flu vaccine while apparently

suffering from the flu—an occurrence Dr. Tornatore deemed significant. First Tornatore Rep. at

3. But there is no evidence Petitioner experienced any kind of unusual, post-vaccination reaction

that would suggest an aberrant immune response (perhaps characterized by excessive

inflammation). Rather, within three days of vaccination, she began to experience neurologic-like

symptoms that later reflected her MS onset. Petitioner has not otherwise established that receipt of

a flu vaccine while experiencing an intercurrent infection is contraindicated or suggests a risk.

C. Prong Three

The timeframe in which Petitioner’s neurologic symptoms presented was too short,

measured from the date of vaccination, to be deemed medically acceptable (even if I were to

assume the flu vaccine “can cause” MS).

First, the record best supports the conclusion that Petitioner’s early, MS-associated

symptoms—numbness and tingling—manifested March 29, 2019, no later than three days post-

vaccination, when she (by her own admission) began experiencing numbness and tingling that lead

her to seek chiropractic help, followed by ED visits on April 2 and 3, 2019, and then to her

hospitalization, when TM was first proposed as explanatory. Peterson Aff. at 2; Ex. 7 at 67.

This timeframe is far too short for a disease involving not only actual clinical

manifestations, but manifestations attributable to or associated with lesions identified on MRI only

a few days after clinical symptoms occurred. Dr. Sriram persuasively established that an antibody-

mediated disease process (which is how Petitioner’s injury would unfold if her theory were

accepted) would not likely occur in so short a timeframe—and Dr. Tornatore did not convincingly

rebut these contentions, over-relying on literature specific to other kinds of diseases like Guillain-

41

Barré syndrome or ADEM. (The experts’ disagreement about the relationship between the

oligoclonal bands and lesion imaging findings was ultimately without moment, for there is no

dispute that by the time they were observed, Petitioner’s MS had begun—three days post-

vaccination. And the oligoclonal bands only corroborate that Petitioner’s initial symptoms did not

constitute simply a one-time occurrence of a form of myelitis).

Second, the evidence of enhancing lesions (meaning more recent) as revealed by

Petitioner’s MRIs (first performed April 3, 2019) raises the strong possibility that Petitioner’s MS

already existed at the time of vaccination a week before. I have noted in other cases that lesions

often predate symptoms in MS. Porch, 2023 WL 21875, at *21 (noting that MS is a chronic disease

process impacting the CNS and that it “can be subclinical and symptomatically silent for a longer

period of time, with MS-characteristic brain lesions often discovered in the absence of symptoms,

or non-recent lesions discovered only after clinical manifestations”). Even Dr. Tornatore allowed

that the lesions could be as “old” as two to three weeks by the time they were observed—a

timeframe which could support the determination that the lesions began developing up to two

weeks prior to vaccination. It cannot be concluded on this record that it is likely the lesions sprung

into existence within a week of vaccination and also concurrent with appearance of actual

symptoms.

Indeed, if Petitioner’s lesions existed for more than seven days from when they were

discovered, it is likely her MS preceded vaccination—meaning the vaccine could not have caused

it. McDaniel v. Sec'y of Health & Hum. Servs., No. 17-1322V, 2023 WL 4678688, at *33 (Fed.

Cl. Spec. Mstr. June 26, 2023) (finding that Petitioner could not satisfy Althen prong two where

onset of immune-mediated myopathy occurred before vaccination). The fact that Petitioner was

only diagnosed with MS later, after treaters were able to factor in a combination of clinical

evidence with test results, does not mean it likely began post-vaccination as well. Flowers v. Sec'y

of Health & Hum. Servs., No. 20-285V, 2024 WL 2828211, at *12 (Fed. Cl. Spec. Mstr. May 8,

2024) (“[i]t is a foundational matter of Vaccine Program law that onset occurs at first manifestation

of a symptom, regardless of whether the disease it foretells could be diagnosed at that time—and

thus whether the onset symptoms would be clearly understood to reflect the start of the illness”),

mot. for review den’d, 173 Fed. Cl. 613 (2024).

Of course, articles like Langer-Gould support the conclusion that the flu vaccine could (in

a younger population) hasten the clinical “arrival” of MS—seeming to open the door to the

possibility that Petitioner’s vaccination still played some role in “unmasking” her MS. But this is

not the same as a finding that the flu vaccine directly caused or triggered it (nor could it have been

responsible for a process that was already underway at the time of vaccination). And as Langer-

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Gould determined, the ultimate risk from vaccination was low no matter when the MS symptoms

appeared. 24

IV. This Matter was Appropriately Dismissed Without Trial

I am opting to dismiss this case on the existing record, and without holding a hearing.

Determining how best to resolve a case is a matter that lies generally within my discretion, but I

shall explain my reasoning.

Prior decisions have recognized that a special master’s discretion in deciding whether to

conduct an evidentiary hearing “is tempered by Vaccine Rule 3(b),” or the duty to “afford[] each

party a full and fair opportunity to present its case.” Hovey, 38 Fed. Cl. at 400–01 (citing Rule

3(b)). But that rule also includes the obligation of creation of a record “sufficient to allow review

of the special master’s decision.” Id. Thus, the fact that a claim is legitimately disputed, such that

the special master must exercise his intellectual faculties in order to decide a matter, is not itself

grounds for a trial (for if it were, trials would be required in every disputed case). Special masters

are expressly empowered to resolve fact disputes without a hearing—although they should only

so act if a party has been given the proper “full and fair” chance to prove their claim.

In addition, there is another overarching consideration at play. Special masters are

intended to develop “on the job” expertise from deciding entitlement in the numerous Vaccine

Act claims that exist at the Court of Federal Claims. Hodges, 9 F.3d at 961 (“Congress assigned

to a group of specialists, the Special Masters within the Court of Federal Claims, the unenviable

job of sorting through these painful cases and, based upon their accumulated expertise in the

field, judging the merits of the individual claims”) (emphasis added). Over time, the special

masters become conversant in the kinds of theories presented in certain cases, and whether those

theories have sufficient scientific and/or factual validity. And those theories often overlap from

one case to the next. So where a theory of causation is reasonably doubted—and that doubt stems

from the special master’s prior exposure to the theory in many prior cases—that theory should

not be entertained anew (except where the claimant can point to novel scientific or medical

understanding sufficient to breathe life into a theory previously deemed wanting). Only by doing

so can special masters ensure that the Program focuses on fairly compensable claims, and

husband their judicial resources in an efficient manner.

My review of the record here plus Petitioner’s arguments have convinced me that she did

not preponderantly establish that the flu vaccine can cause MS. I reach that determination on the

basis of Dr. Tornatore’s reports, which were clear in their arguments. I did not need to litigate the

24

Notably, Petitioner has not alleged a claim of significant aggravation in this case—and I do not find it has been

shown the flu vaccine can worsen an existing case of MS. In fact, I have found precisely the opposite in several prior

matters. See, e.g., L.Z., 2018 WL 5784525, at *22 (rejecting petitioner’s claim that the flu vaccine significantly

aggravated his pre-vaccination MS).

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matter via a live proceeding to reach the determination I have. The inquisitorial function of special

masters in the Vaccine Program compels them to steer cases in the most sensible direction, based

on the facts presented as well as the special master’s experience with comparable claims.

Because my preliminary review of the filings did not suggest (based on my experience with

comparable cases) that this matter was likely to succeed, I asked Petitioner to establish whether,

and how, I might be wrong. Despite due opportunity, Petitioner has not succeeded in doing so.

CONCLUSION

A Program entitlement award is only appropriate for claims supported by preponderant

evidence. Petitioner cannot make such as showing. She therefore is not entitled to compensation.

In the absence of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the

Court SHALL ENTER JUDGMENT in accordance with the terms of this Decision. 25

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

25

Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices

renouncing their right to seek review.

44