# Peterson v. Secretary of Health and Human Services

> United States Court of Federal Claims · November 24, 2025

URL: https://www.frixlaw.com/law-library/cases/11208110

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** November 24, 2025
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Brian H. Corcoran
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/11208110

## How later opinions describe it (automated extraction)

- noting that Moberly “addresses the petitioner’s overall burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 22-322V

*************************
*
HEATHER PETERSON, * Chief Special Master Corcoran
*
Petitioner, * Filed: October 30, 2025
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
*************************

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

4
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

5
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).

6
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.

7
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.

8
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

9
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).

10
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 file

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11208110. Public record. Not legal advice.