VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_22-vv-01408
Package ID: USCOURTS-cofc-1_22-vv-01408
Petitioner: ANNAMMA VARUGHESE
Filed: 2022-09-30
Decided: 2026-07-23
Vaccine: influenza
Vaccination date: 2021-09-21
Condition: transverse myelitis
Outcome: denied
Award amount USD: 

AI-assisted case summary:
Annamna Varughese, a 66-year-old woman, received an influenza vaccination on September 21, 2021. Three days later, she presented with chest pain, back pain, leg weakness, numbness, and nausea, reporting a gradual onset of symptoms over two days, placing onset the day after vaccination. She was initially evaluated for Guillain Barré Syndrome (GBS) or a spinal cord lesion. Later, her primary care provider suspected transverse myelitis (TM), and a repeat MRI suggested a "progression of demyelinating or inflammatory process." She was treated with IV Solu-Medrol. A VAERS report submitted by the pharmacy indicated symptom onset on September 22, 2021. Her neurologist, Dr. Sengul, noted an impression of "idiopathic transverse myelitis, likely provoked by vaccine." The petitioner's expert, Dr. Steinman, proposed a theory of molecular mimicry, suggesting the flu vaccine's hemagglutinin shared amino acid sequences with neurofascin, a molecule implicated in TM. Respondent's experts, Dr. Merkler and Dr. He, disagreed, citing a lack of epidemiological evidence linking the flu vaccine to TM and challenging the molecular mimicry theory and the rapid onset timeframe. The Special Master found that the petitioner failed to establish a sound and reliable medical theory under Althen prong one, as the literature did not support neurofascin as a cause of acute TM and the molecular mimicry theory was not sufficiently demonstrated. Furthermore, the Special Master found that the onset of TM within 24 hours was too short to be causally related, even assuming a recall response, thus failing Althen prong three. Although Dr. Sengul's opinion suggested a vaccine provocation, it was not sufficiently supported by reasoning regarding the timing or mechanism. Consequently, the Special Master denied the petition for compensation, finding insufficient proof of causation.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_22-vv-01408-0
Date issued/filed: 2026-09-01
Pages: 26
Docket text: PUBLIC DECISION (Originally filed: 07/23/2026) regarding 56 DECISION of Special Master. Signed by Special Master Daniel T. Horner. (cd) Service on parties made.
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 1 of 26
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 22-1408V
Filed: July 23, 2026
Special Master Horner
ANNAMMA VARUGHESE,
Petitioner,
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Kirk Tripp Otto, Siri & Glimstad, LLP, Richmond, VA, for petitioner.
Mallori Browne Openchowski, U.S. Department of Justice, Washington, DC, for
respondent.
DECISION1
On September 30, 2022, petitioner filed a petition under the National Childhood
Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging that she suffered
transverse myelitis (“TM”) caused by the influenza (“flu”) vaccination that she received
on September 21, 2021. (ECF No. 1.) For the reasons set forth below, I conclude that
petitioner is not entitled to an award of compensation.
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
1 Because this document contains a reasoned explanation for the action taken in this case, it must be
made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or
at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government
Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic
Government Services). This means the document will be available to anyone with access to the
internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact
medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy.
If, upon review, I agree that the identified material fits within this definition, I will redact such material from
public access.
2 All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-
10-34.
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 2 of 26
received it in the United States; suffered a serious or long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination, and the petitioner is
automatically entitled to compensation, unless it is affirmatively shown that the injury
was caused by some factor other than the vaccination. § 300aa-13(a)(1); § 300aa-
11(c)(1)(C)(i); § 300aa-14(a).
In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines ex rel. Sevier v. Sec’y of Health & Human Servs.,
940 F.2d 1518, 1525 (Fed. Cir. 1991). In this case, petitioner has not alleged an injury
that appears on the Vaccine Injury Table. 42 C.F.R. § 100.3(a). Therefore, petitioner
must demonstrate causation-in-fact.
The showing of causation-in-fact must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1278-79; Hines, 940 F.2d at 1525. Under that
standard, petitioner must show that it is “more probable than not” that the vaccination
was the cause of the injury. Althen, 418 F.3d at 1279. She need not show that the
vaccination was the sole cause but must demonstrate that the vaccination was at least
a “substantial factor” in causing the condition at issue and was a “but for” cause.
Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).
Thus, petitioner must supply “proof of a logical sequence of cause and effect showing
that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278 (quoting
Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992)).
Ultimately, petitioner must satisfy what has come to be known as the Althen test, which
requires: (1) a medical theory causally connecting the vaccination and the injury; (2) a
logical sequence of cause and effect showing that the vaccination was the reason for
the injury; and (3) a showing of proximate temporal relationship between vaccination
and injury. Id.
A petitioner may not receive a Vaccine Program award based solely on his or her
assertions; rather, the petition must be supported by either medical records or by the
opinion of a competent physician. § 300aa-13(a)(1). Medical records are generally
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 3 of 26
viewed as particularly trustworthy evidence because they are created
contemporaneously with the treatment of the patient. Cucuras v. Sec’y of Health &
Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, medical records and/or
statements of a treating physician’s views do not per se bind the special master to adopt
the conclusions of such an individual, even if they must be considered and carefully
evaluated. § 300aa-13(b)(1). A petitioner may rely upon circumstantial evidence. See
Althen, 418 F.3d at 1280. Moreover, the Althen court noted that a petitioner need not
necessarily supply evidence from medical literature supporting petitioner’s causation
contention, so long as the petitioner supplies the medical opinion of an expert. Id. at
1279-80. While scientific certainty is not required, that expert’s opinion must be based
on “sound and reliable” medical or scientific explanation. Boatmon v. Sec’y of Health &
Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).
Cases in the Vaccine Program are assigned to special masters who are
responsible for “conducting all proceedings, including taking such evidence as may be
appropriate, making the requisite findings of fact and conclusions of law, preparing a
decision, and determining the amount of compensation, if any, to be awarded.” Vaccine
Rule 3(b)(1). Special masters must ensure each party has had a “full and fair
opportunity” to develop the record but are empowered to determine the format for taking
evidence based on the circumstances of each case, including having the discretion to
decide cases without an evidentiary hearing. Vaccine Rule 3(b)(2); Vaccine Rule 8(a);
Vaccine Rule 8(d). Special masters are not bound by common law or statutory rules of
evidence but must consider all relevant and reliable evidence in keeping with
fundamental fairness to both parties. Vaccine Rule 8(b)(1).
II. Procedural History
Petitioner filed medical records, a Vaccine Adverse Event Reporting System
(“VAERS”) report, declarations by petitioner and her spouse, and a Statement of
Completion in October of 2022. (ECF Nos. 7-8; Exs. 1-6.) The case was initially
assigned to another special master. (ECF Nos. 10-11.) Petitioner filed additional
medical records in August of 2023 (ECF No. 18; Ex. 7), and respondent then filed his
Rule 4(c) Report in September of 2023 (ECF No. 21). Respondent recommended
against compensation, arguing that petitioner’s medical records were inadequate to
meet the Althen test and stressing that symptom onset occurred within 24 hours of
vaccination. (Id. at 8-9.)
The parties then exchanged multiple rounds of expert reports, with
neuroimmunologist Lawrence Steinman, M.D., opining on petitioner’s behalf (Exs. 8,
51,3 52), and neurologist Alexander Merkler, M.D., and immunologist You-Wen He,
M.D., Ph.D., opining on respondent’s behalf (Exs. A, C, E-F). Thereafter, the previously
presiding special master directed respondent to file a motion for a ruling on the written
3 Petitioner filed Dr. Steinman’s first supplemental report at ECF No. 29-1 without proper bates stamping.
However, for the purposes of this decision, Dr. Steinman’s first supplemental report will be referred to as
Exhibit 51, the exhibit designation reflected on the notice of filing (ECF No. 29).
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 4 of 26
record after the parties confirmed they would not file further expert reports. (ECF No.
37; Non-PDF Scheduling Order, filed Feb. 10, 2025.)
The case was subsequently reassigned to the undersigned in February of 2025
(ECF No. 38), and respondent filed his motion for a ruling on the written record on May
1, 2025 (ECF No. 45). That motion is fully briefed as of August 6, 2025. (ECF No. 47
(petitioner’s response); ECF No. 50 (respondent’s reply).) Based on my review of the
docket, the record, and the parties’ briefs, I agree that the parties have had a full and
fair opportunity to develop the record and that it is appropriate to resolve this case on
the existing record.4 See Vaccine Rule 8(d); Vaccine Rule 3(b)(2); Kreizenbeck v. Sec’y
of Health & Human Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020).
III. Factual Summary
The facts of this case are largely not disputed and need not be discussed at
length. Petitioner received the flu vaccination at issue on September 21, 2021, at 66
years of age. (Ex. 3, p. 7.) Although she was not in perfect health, her prior medical
history is not at issue. Three days after her vaccination, on September 24, 2021,
petitioner presented to the emergency department with complaints of chest pain
radiating to her back with bilateral leg weakness and numbness as well as nausea. (Ex.
4, p. 683.) At that time, she reported a gradual onset of symptoms over the course of
two days, placing onset the day after vaccination. (Id.) Petitioner’s initial neurological
exam was unremarkable; however, she was admitted to the hospital for observation and
a workup for possible Guillain Barré Syndrome (“GBS”). (Id. at 686-87.) On September
26, 2021, petitioner was discharged with a differential diagnosis of GBS versus a spinal
cord lesion versus polyradiculopathy. (Id. at 679-80.) However, when petitioner later
followed up with her primary care provider for ongoing symptoms (Id. at 632-41), the
primary care provider felt that transverse myelitis (“TM”) was likely, and petitioner was
advised to return to the emergency department after a repeat MRI suggested
“progression of demyelinating or inflammatory process” (Id. at 381-85, 620, 624-45,
641). Petitioner was admitted to neurology and completed a five-day course of IV Solu-
Medrol. (Id. at 320, 376-85).
On October 10, 2021, the pharmacy where petitioner received her vaccination
submitted a VAERS report indicating that petitioner experienced symptoms, which were
later diagnosed as transverse myelitis, beginning on September 22, 2021, the day after
vaccination. (Ex. 5, pp. 1-2.) Petitioner continued to treat and evaluate for possible
transverse myelitis. (See generally Ex. 4.) Ultimately, she sought a second opinion
from neurologist Buse Sengul, M.D., on February 28, 2022. (Id. at 184-89.) Dr.
Sengul’s impression was, “66-year-old woman with longitudinally expansile transverse
myelitis, negative AQ P4 and MOG antibodies, paraneoplastic panel negative as well as
cancer screening. This is truly an idiopathic transverse myelitis, likely provoked by
4 In connection with her motion response, petitioner filed additional medical literature. (ECF No. 48; Exs.
54-59.) In reply, respondent argued the additional literature is inapposite but did not object to its filing.
(ECF No. 50, pp. 2-3.)
4

Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 5 of 26
vaccine, which can be seen with MOGAD although she remains to be seronegative.”
(Id. at 188.) Notably, however, the history recorded by Dr. Sengul does not document
the preceding vaccination. (Id. at 184.) Accordingly, it is unclear what Dr. Sengul’s
understanding was with regard to the latency between petitioner’s flu vaccination and
the onset of her TM, though petitioner did consistently report a 24-hour onset both
before and after this evaluation. (Id. at 159, 356, 683; Ex. 5, pp. 1-2.)
Declarations by petitioner and her spouse are consistent with the above. (See
Exs. 1-2.) Neither petitioner nor respondent has identified any treating physician
opinion as informative of the cause of petitioner’s condition apart from the above-
referenced notation by Dr. Sengul. (See ECF Nos. 1, 21, 45, 47.)
IV. Expert Summary
a. Petitioner’s initial report by Dr. Steinman5
Dr. Steinman opined that the condition at issue is TM. (Ex. 8, p. 8.) However,
although petitioner suffered TM, she tested negative for the two known antigens
associated with TM, MOG and AQP-4, suggesting she did not mount an immune
response to either antigen. (Id. at 8-9.) Instead, Dr. Steinman suggested that
petitioner’s TM is explained by molecular mimicry resulting from cross-reaction between
components of the flu vaccine and neurofascin, a molecule found at the Node of
Ranvier in the central and peripheral nervous systems that has been implicated in TM
as well as neuromyelitis optica spectrum disorder (“NMOSD”). (Id. at 9, 12 (citing
Matthew N. Rasband & Elior Peles, The Nodes of Ranvier: Molecular Assembly and
Maintenance, 8 COLD SPRING HARBOR PERSPECTIVES BIOLOGY, 2016, at 1 (Ex. 17); Fang
Guo & Yong-Bo Zhang, Clinical Features and Prognosis of Patients with Guillain-Barré
and Acute Transverse Myelitis Overlap Syndrome, 181 CLINICAL NEUROLOGY &
NEUROSURGERY 127 (2019) (Ex. 18); Jun-ichi Kira et al., Anti-Neurofascin Autoantibody
and Demyelination, 130 NEUROCHEMISTRY INT’L, 2018, at 1 (Ex. 19); Kun Jia et al., Anti-
Neurofascin-155 Antibody-Positive Neuromyelitis Optica Spectrum Disorders, 398 J.
NEUROLOGICAL SCIS. 16 (2019) (Ex. 20)).) Specifically, Dr. Steinman indicated that a
BLAST6 search confirmed that influenza hemagglutinin contained in the Fluad vaccine
5 Dr. Steinman received his medical degree from Harvard University in 1973. (Ex. 9, p. 1.) He completed
a surgical internship and two residencies, one in neurology and one in pediatrics, at Stanford University
Hospital. (Id.) Thereafter, Dr. Steinman completed a fellowship in chemical immunology at Weizmann
Institute of Science and also served as a visiting fellow at the National Institutes of Health. (Id.) He
maintains his license to practice medicine in California and is board-certified in neurology. (Id. at 2; Ex. 8,
p. 1.) Currently, Dr. Steinman serves as a Professor at Stanford University, Departments of Neurology
and Neurological Sciences, Pediatrics, and Genetics. (Ex. 9, p. 1.) In his clinical practice, he cares for
patients with neuroinflammatory disorders, including transverse myelitis. (Ex. 8, p. 1.) Dr. Steinman has
co-authored over 600 peer-reviewed publications, with a focus on neuroinflammation in the nervous
system. (Id.; Ex. 9, pp. 5-51.)
6 Basic Local Alignment Search Tool (“BLAST”) “finds regions of similarity between biological sequences.
The program compares nucleotide or protein sequences to sequence databases and calculates the
statistical significance of the matches. BLAST can be used to infer functional and evolutionary
relationships between sequences as well as help identify members of gene families.” Blast Local
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 6 of 26
shares a six of ten amino acid sequence with neuorfascin, AGSGIIISDT (hemagglutinin)
versus AGDTIIFRDT (neurofascin). (Id. at 23-24.)
Dr. Steinman opined that this degree of homology is relevant based on his
citation to a number of papers, which he described as demonstrating that sequences of
five out of 12 identical amino acids have been shown to be sufficient to trigger
neuroinflammation. (Ex. 8, pp. 15, 24 (citing Anand M. Gautam et al., A Polyalanine
Peptide with Only Five Native Myelin Basic Protein Residues Induces Autoimmune
Encephalomyelitis, 176 J. EXPERIMENTAL MED. 605 (1992) (Ex. 27); Anand M. Gautam et
al., Minimum Structural Requirements for Peptide Presentation by Major
Histocompatibility Complex Class II Molecules: Implications in Induction of
Autoimmunity, 91 PNAS 767 (1994) (Ex. 28); Anand M. Gautam et al., A Viral Peptide
with Limited Homology to a Self Peptide Can Induce Clinical Signs of Experimental
Autoimmune Encephalomyelitis, 161 J. IMMUNOLOGY 60 (1998) (Ex. 29)).) He also
asserted that the significance of this finding is further supported by the Immune Epitope
Database (“IEDB”),7 which shows that “APAAGDTIISL” has been studied in humans.
(Id. at 25.) However, although Dr. Steinman included a screenshot documenting the
IEDB search results, the screenshot does not indicate what has been observed about
this antigen. (See id.)
Additionally, Dr. Steinman indicated that “AGDTIFRDT,” the sequence identified
in neurofascin, is in a region of the immunoglobulin domain between Ig4 and Ig5, which
means it is “capable of interactions with the extracellular milieu where antibody and T
cell receptor might interact.” (Ex. 8, p. 26 (citing Lucas M. Chataigner et al., Structural
Insights into the Contactin-1 Neurofascin 155 Adhesion Complex, 13 NATURE
COMMC’NS, 2022, at 1 (Ex. 39)).) He opined that “[a]n antibody targeting this region
would more likely than not disrupt paranodal architecture.” (Id.) Dr. Steinman indicated
that neurofascin also has “remarkable homology” with GlialCAM, which is also highly
related to Contactin-1. (Id. at 22, 26 (citing Tobias V. Lanz et al., Roadmap for
Understanding Mechanisms on How Epstein-Barr Virus Triggers Multiple Sclerosis and
for Translating These Discoveries in Clinical Trials, 12 CLINICAL & TRANSLATIONAL
IMMUNOLOGY, 2023, at 1 (Ex. 35)).) The above referenced sequence “AGDTIIFRDT” is
adjacent to the homology between GlialCAM and neurofascin, which occurs at
“TIIFRDT.” (Id. at 27.) Dr. Steinman did not explicitly indicate why the similarity
between neurofascin and GlialCAM is relevant; however, in substantiating that a five of
12 amino acid sequence can support molecular mimicry, he cited a paper by his own
research group demonstrating that the Epstein-Barr virus can cause multiple sclerosis,
another central nervous system demyelinating condition, via molecular mimicry
involving GlialCAM. (Id. at 18-19 (citing Tobias V. Lanz et al., Clonally Expanded B
Alignment Search Tool, NAT’L LIBR. MED., https://blast.ncbi.nlm.nih.gov/Blast.cgi (last visited July 15,
2026).
7 The Immune Epitope Database (“IEDB”) “catalogs experimental data on antibody and T cell epitopes
studied in humans and other animal species in the context of infectious diseases, allergy, autoimmunity
and transplantation. The IEDB also hosts epitope prediction and analysis tools.” IMMUNE EPITOPE
DATABASE & TOOLS, https://www.iedb.org/ (last visited July 15, 2026).
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 7 of 26
Cells in Multiple Sclerosis Bind EBV EBNA1 and GlialCAM, 603 NATURE 321 (2022) (Ex.
30)).)
Because onset of petitioner’s TM occurred about 24 hours post-vaccination, Dr.
Steinman indicated that “there MUST be a recall response” to explain the timing in this
case. (Ex. 8, p. 27.) Thus, he confirmed that petitioner received flu vaccinations in
2019-2021. (Id. at 27-28 (citing Ex. 3, pp. 5-7).) He opined that all three vaccines “had
enormous degrees of homology.” (Id. at 28.) That is, “[a]ll three vaccines including the
2021-2022 vaccine had at least 5 identical amino acids in the stretch of hemagglutinin
with the sequence in the 2022 vaccine – AGSGIIISDTP – shared with the neurofascin
mimic.” (Id. at 30.) Thus, he opined there is “a high likelihood” that there would be a
recall response from the two prior vaccines. (Id.) Dr. Steinman indicated that a recall
response can result in neurologic symptoms within a day or two based on two
epidemiologic papers by Schonberger et al. and Park et al. respectively, and an
experimental study by Lai et al. (Id. at 31-33 (citing Lawrence B. Schonberger et al.,
Guillain-Barre Syndrome Following Vaccination in the National Influenza Immunization
Program, United States, 1976-1977, 110 AM. J. EPIDEMIOLOGY 105 (1979) (Ex. 40);
Yong-Shik Park et al., Clinical Features of Post-Vaccination Guillain-Barré Syndrome
(GBS) in Korea, 32 J. KOREAN MED. SCI. 1154 (2017) (Ex. 41); Wendy Lai et al.,
Transcriptional Control of Rapid Recall by Memory CD4 T Cells, 187 J. IMMUNOLOGY
133 (2011) (Ex. 47)).) Dr. Steinman asserted that the Lai et al. study shows that a recall
response can occur as early as 6 hours after antigenic exposure and the Schonberger
et al. study described an increased risk of GBS 0-1 days after vaccination. (Id. at 32-33
(citing Lai et al., supra, at Ex. 47; Schonberger et al., supra, at Ex. 40, p. 8 fig. 5).)8 He
also indicated that tuberculin tests, which can be read as positive within 24 hours,
further demonstrate that antigen-specific recall responses can occur within that
timeframe. (Id. at 32 (citing Tiroumourougane V. Serane & Bhuvaneswari
Kothendaraman, Brief Report: Tuberculin Test Can Be Read After 24 Hours in Children,
60 J. TROPICAL PEDIATRICS 157 (2014) (Ex. 43); Lin Fan et al., Variation of
Mycobacterium tuberculosis Antigen-Specific IFN-γ and IL-17 Responses in Healthy
Tuberculin Skin Test (TST)-Positive Human Subjects, 7 PLOS ONE, 2012, at 1 (Ex. 44);
T. Kardjito & J.M. Grange, Immunological and Clinical Features of Smear-Positive
Pulmonary Tuberculosis in East Java, 61 TUBERCLE 231 (1980) (Ex. 45)).)
Given that Dr. Steinman has opined that a medical theory exists to explain how
petitioner’s vaccine can cause TM, and given that he opined that a recall response can
explain how that can occur within one day of vaccination, Dr. Steinman further opined
that there is a logical sequence of cause and effect that demonstrates that petitioner’s
vaccination did cause her injury. (Ex. 8, pp. 38-39.) In addition to the sequence of
events he proposed, he noted that petitioner had no infectious illness at the time of her
8 Dr. Steinman further highlighted that the bar graph in figure 5 shows that there were more cases of GBS
observed on days 0-1 than on days 35 and 41. (Ex. 8, p. 33 (discussing Schonberger et al., supra, at Ex.
40, p. 8 fig. 5).) Based on my review of his report and my experience in prior cases, Dr. Steinman is
presumably asserting that this finding is significant because, while it remains controverted that the day 0-
1 cases reflect a causal relationship, it is generally not disputed that days 35 and 41 fall within the period
of elevated risk. (Id.)
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vaccination and that none of her preexisting conditions are known to provoke TM. (Id.
at 39.)
b. Respondent’s initial report by Dr. Merkler9
Dr. Merkler agreed that petitioner suffered TM and that the onset of her condition
occurred about 24 hours following her flu vaccination. (Ex. A, pp. 5-6.) He also agreed
that petitioner’s TM was not found to be related to any other condition, meaning that it
was idiopathic. (Id. at 6.) However, citing the lack of any clear epidemiologic signal, Dr.
Merkler did not agree that the flu vaccine can cause TM. (Id. at 6-7 (citing ADVERSE
EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY (Kathleen Stratton et al. eds., 2012)
[hereinafter 2012 IOM Report] (Ex. 50, pp. 338-39); AGENCY FOR HEALTHCARE RSCH. &
QUALITY, NO. 14-E002-EF, SAFETY OF VACCINES USED FOR ROUTINE IMMUNIZATION IN THE
UNITED STATES (2014) (Ex. A, Tab 5);10 Roger Baxter et al., Acute Demyelinating Events
Following Vaccines: A Case-Centered Analysis, 63 CLINICAL INFECTIOUS DISEASES 1456
(2016) (Ex. A, Tab 2) (see also Ex. C, Tab 3)).) Regarding Dr. Steinman’s molecular
mimicry theory, Dr. Merkler acknowledged that neurofascin autoimmunity has been
suggested vis-à-vis GBS but disagreed that neurofascin has been implicated in the
pathology of TM. (Id. at 7 (citing Harald Prüss et al., Neurofascin as Target of
Autoantibodies in Guillain-Barré Syndrome, 124 BRAIN, 2011, at 1 (Ex. A, Tab 8); Emily
K. Mathey et al., Neurofascin as a Novel Target for Autoantibody-Mediated Axonal
Injury, 204 J. EXPERIMENTAL MED. 2363 (2007) (Ex. A, Tab 7); O. Stich et al., Prevalence
of Neurofascin-155 Antibodies in Patients with Multiple Sclerosis, 364 J. NEUROLOGICAL
SCIS. 29 (2016) (Ex. A, Tab 10)).) He also disagreed that Dr. Steinman’s findings
supporting molecular mimicry between the Epstein-Barr virus and GlialCAM can be
generalized to other molecular exposures. (Id.) And, in any event, even if crediting Dr.
Steinman’s theory, Dr. Merkler did not agree that exposure to vaccination can result in
neuroimmunological complication within 24 hours, opining instead that such an injury
would take anywhere from five days to weeks to develop. (Id. at 6-8 (citing
9 Dr. Merkler received his medical degree from New York University School of Medicine in 2010. (Ex. B,
p. 1.) He completed an internship in internal medicine and a residency in neurology at New York
Presbyterian Hospital -Weill Cornell Medical College in 2011 and 2014 respectively, serving as chief
resident in his final year. (Id.) Thereafter, Dr. Merkler completed a fellowship in neurocritical care at
Cornell/Columbia University and earned a Master’s Degree in Clinical and Translational Investigation from
Cornell University. (Id. at 2; Ex. A, p. 1.) He maintains his medical license in New York and is board-
certified in neurology with subspeciality certification in neurocritical care. (Ex. B, p. 2; Ex. A, p. 1.)
Currently, Dr. Merkler serves as an Assistant Professor of Neurology and Neuroscience at Weill Cornell
Medical College and the Brain and Mind Research Institute. (Ex. A, p. 1; Ex. B, p. 2.) Additionally, he
serves as an attending neurologist at New York Presbyterian Hospital, where he routinely cares for
patients with neurological disorders, including transverse myelitis. (Ex. B, p. 2; Ex. A, p. 1.) Dr. Merkler
has co-authored over 100 peer-reviewed publications on neurological disorders. (Ex. B, pp. 14-22; Ex. A,
p. 1.)
10 Some of the articles of medical literature referenced in Dr. Merkler’s initial report at Exhibit A were filed
by respondent with erroneous bates stamping. For example, the notice of filing designates the report
authored by the Agency of Healthcare Research and Quality as Exhibit A, Tab 5 (see ECF No. 44-1);
however, the bates stamping marks the report as Exhibit C, Tab 5. For the purposes of clarity, this
decision refers to the medical literature filed at ECF No. 44 by the exhibit designations reflected on the
notice of filing.
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Schonberger et al., supra, at Ex. 40; Divya Mamootil & Anmol Grewal, Viral Versus
Vaccine-Associated Acute Transverse Myelitis with Neuromyelitis Optica
Immunoglobulin G Antibody and Myelin Basic Protein: A Case Report, 14 CUREUS,
2022, at 1 (Ex. A, Tab 6); Chumpol Anamnart et al., Newly Diagnosed Neuromyelitis
Optica Spectrum Disorders Following Vaccination: Case Report and Systematic
Review, 58 MULTIPLE SCLEROSIS & RELATED DISORDERS, 2022, at 1 (Ex. A, Tab 1); Chris
Wu et al., Case Report: Hemorrhagic Longitudinally Extensive Transverse Myelitis,
CASE REPS. NEUROLOGICAL MED., 2016, at 1 (Ex. A, Tab 12); Marcelo Adriano da Cunha
e Silva Vieira et al., Transverse Myelitis with Brown-Sèquard Syndrome After H1N1
Immunization, 70 ARQUIVOS DE NEURO-PSIQUIATRIA 555 (2012) (Ex. A, Tab 11); Isabelle
Korn-Lubetzki et al., H1N1 Vaccine-Related Acute Transverse Myelitis, 13 ISRAEL MED.
ASS’N J. 249 (2011) (Ex. A, Tab 4); Li Gui et al., Acute Transverse Myelitis Following
Vaccination Against H1N1 Influenza: A Case Report, 4 INT’L J. CLINICAL & EXPERIMENTAL
PATHOLOGY 312 (2011) (Ex. A, Tab 3)).) Accordingly, he opined that it is more likely
than not that petitioner’s vaccination was not a causal factor in her development of TM.
(Id. at 8.)
c. Respondent’s initial report by Dr. He11
Like Dr. Merkler, Dr. He opined that, although TM can be parainfectious and
post-vaccinal TM has been reported, epidemiologic evidence has not indicated that
vaccines cause TM. (Ex. C, pp. 5-6 (citing INST. OF MED., Influenza Vaccine: Transverse
Myelitis, in ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY 309-10 (Kathleen
Stratton eds., 2012) (Ex. C, Tab 2)12; Baxter et al., supra, at Ex. C, Tab 3; Matthew Z.
Dudley et al., The State of Vaccine Safety Science: Systematic Reviews of the
Evidence, 20 LANCET INFECTIOUS DISEASES e80 (2020) (Ex. C, Tab 4); Agency for
Healthcare Rsch. & Quality, Safety of Vaccines Used for Routine Immunization in the
United States, at 1 (unpublished manuscript) (Ex. C, Tab 5)).)13 He additionally
stressed that between 15-30% of cases of TM remain classified as idiopathic after
thorough evaluation. (Id. at 5 (citing Benjamin Greenberg, Transverse Myelitis:
11 Dr. He received his medical degree in 1986 from The Fourth Military Medical University in Xian, China.
(Ex. D, p. 1.) In 1996, he earned his Ph.D. in immunology from the University of Miami School of
Medicine. (Id.) Thereafter, he served as a senior fellow at the Howard Hughes Medical Institute and the
University of Washington, Department of Immunology. (Id.) Since completing his fellowship training, Dr.
He has held various academic appointments at Duke University School of Medicine. (Id.) Currently, he
serves as a Professor Integrative Immunobiology in the Department of Integrative Immunobiology and as
Director for an advanced immunology course. (Id.; Ex. C, p. 1.) Dr. He has been conducting research in
immunology since 1986 with a focus on innate and adaptive immunity against viral infections, as well as
tumors. (Ex. C, p. 1.) He has co-authored over 100 peer-reviewed publications on immunology. (Id. at 2;
Ex. D, pp. 7-18.)
12 Both Dr. Steinman and Dr. He provided as a reference the 2012 IOM report entitled: ADVERSE EFFECTS
OF VACCINES: EVIDENCE AND CAUSALITY. (Ex. 50; Ex. C, Tab 2.) Dr. Steinman filed a copy of the entire
report whereas Dr. He only filed a section of the report that explicitly focuses on TM and the flu vaccine.
(Compare Ex. 50, with Ex. C, Tab 2.) Therefore, both of these exhibits refer to the same 2012 report.
13 Some of the docket text accompanying respondent’s filing incorrectly identifies Dr. He’s initial report as
Exhibit A, duplicative of the designation for Dr. Merkler’s initial report. However, the exhibit itself is
correctly bates stamped as Exhibit C.
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Case 1:22-vv-01408-UNJ Document 60 Filed 09/01/26 Page 10 of 26
Etiology, Clinical Features, and Diagnosis, UPTODATE (last updated Jan. 23, 2024) (Ex.
C, Tab 1)).)
Regarding Dr. Steinman’s molecular mimicry theory, Dr. He opined that three
scientific findings have “strongly challenged” the theory of molecular mimicry: (1)
massive sequence sharing between microbial pathogens and human proteome; (2)
frequent detection of cross-reactive antibodies and T lymphocytes in humans; and (3)
advances in the understanding of host tolerance mechanisms. (Ex. C, p. 7.) Thus, he
opined:
Given these many layers of immune regulatory/tolerant mechanisms, the
critical determinant of autoimmune disease development upon antigen
stimulation is the strength/ extent of the immune activation induced by the
overall immunological encounters (either infections or immunizations), not
the molecular mimicry (aka linear sequence or structural homologies)
between foreign antigens and self-proteins. On rare occasions, strong
immune activation conditions such as certain types of infections and potent
immune stimulations can break the many layers of immune regulatory
mechanisms to cause autoimmune diseases. However, there is no
evidence to support that seasonal influenza vaccine can induce strong
immune activation to break immune tolerance to cause TM.
(Id. at 11.) Moreover, Dr. He opined that the specific sequence homologies discussed
by Dr. Steinman “are entirely expected.” (Id. at 16.) For example, Kanduc et al.
showed that a stretch of six consecutive amino acids in H5N1 influenza virus shares
sequence similarity with 2,332 different human proteins. (Id. (citing Darja Kanduc et al.,
Massive Peptide Sharing Between Viral and Human Proteomes, 29 PEPTIDES 1755
(2008) (Ex. C, Tab 7, tbl. 6)14).) Dr. He criticized the studies by Gautam et al. because
they used complete Freund’s adjuvant, “a powerful immune adjuvant,” which means the
molecular mimics “are not working by themselves.” (Id. at 13 (discussing Gautam et al.,
supra, at Ex. 27; Gautam et al., supra, at Ex. 28; Gautam et al., supra, at Ex. 29.)
When juxtaposed with other studies, such as Lanz et al., Dr. He opined that the
evidence shows that “the critical determinant of autoimmune disease development upon
antigen stimulation is the strength/extent of the immune activation induced by the
overall immunological encounters (either infections or immunizations), not the molecular
mimicry (aka linear sequence or structural homologies) between foreign antigens and
self-proteins.” (Id.)
Dr. He also disagreed that 24-hours would be enough time for the
immunopathogenesis at issue. (Ex. C, pp. 16-17.) Instead, he opined that it takes at
least three days for the innate immune response to develop and seven to ten days for
activation of the adaptive immune response following antigen exposure. (Id. at 16
14 Respondent filed the Kanduc et al. article referenced by Dr. He in his report as Exhibit C, Tab 7.
However, the filing appears to be incomplete. While the filing suggests that the article includes twelve
pages total, only the first four pages of the article are viewable. Pages five through twelve are blank with
the exception of the bates stamping.
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(citing Matthew A. Williams & Michael J. Bevan, Effector and Memory CTL
Differentiation, 25 ANN. REV. IMMUNOLOGY 171 (2007) (Ex. C, Tab 29, p. 2 fig. 1); Lina
Sun et al., T Cells in Health and Disease, 8 SIGNAL TRANSDUCTION & TARGETED THERAPY,
2023, at 1 (Ex. C, Tab 30, p. 5 fig. 3)).) He opined that the Lai et al. study is not
informative because it did not examine an in vivo immune response, explaining that
[t]he fast response to antigen-stimulation by memory T cells is well-
established in the immunology field. However, the CD4+ T cell activation
in vitro was not subjected to the multiple layers of host regulatory
mechanisms as in vivo, therefore, using the in vitro kinetics of memory
CD4+ T cell response to make conclusion that memory CD4+ T cells will
rapidly attack self-tissue in vivo is scientifically unreliable.
(Id. at 17 (discussing Lai et al., supra, at Ex. 47).) Dr. He also disagreed with Dr.
Steinman’s interpretation of the data within the Schonberger et al. study. (Id. at 17-18
(discussing Schonberger et al., supra, at Ex. 40).)
d. Dr. Steinman’s first supplemental report
In response to respondent’s experts, Dr. Steinman questioned the value of the
Baxter et al. study relative to this case given that the seasonal flu vaccine changes each
year. (Ex. 51, pp. 1-2, 4 (discussing Baxter et al., supra, at Ex. A, Tab 2).) Although
respondent’s experts cite Baxter et al. as an example of a study that found no
association between the flu vaccine and TM, Dr. Steinman pointed out that the study
was published in 2016 and examined the season flu vaccines for 2007 through 2012.
(Id. at 1-2 (citing Baxter et al., supra, at Ex. A, Tab 2, p. 2 tbl. 1).) By contrast, Dr.
Steinman noted that his theory is specific to components of the 2019 through 2021
vaccines, which were not contained in the prior years examined by Baxter et al. (Id. at
2.) Dr. Steinman suggested the 2012 IOM report likewise could not have addressed a
vaccine formulation that did not yet exist at that time. (Id. at 2-3 (discussing 2012 IOM
Report, supra, at Ex. 50).) Dr. Steinman also further defended his interpretation of the
Schonberger et al. study as supporting a one-day post-vaccination onset. (Id. at 7-9
(discussing Schonberger et al., supra, at Ex. 40).) Furthermore, he seemed to
characterize the treating physicians’ diagnosis of idiopathic transverse myelitis as a
failure to consider the vaccine as a potential cause. (Id. at 1.)
Noting in particular the positive reception for the 2022 study by Lanz et al., Dr.
Steinman does not accept Dr. He’s opinion that molecular mimicry is an outdated
theory. (Ex. 51, pp. 4-5 (discussing Lanz et al., supra, at Ex. 30).) And, whereas Dr.
Merkler opined that the findings from Lanz et al. cannot be generalized to other
molecular mimics, Dr. Steinman reiterated the view that the Lanz et al. study’s findings,
especially when coupled with the prior Gautam et al. studies, does support the
proposition that five identical amino acids out of a sequence of 12 can trigger clinically
relevant neuroinflammation. (Id. at 3 (discussing Lanz et al., supra, at Ex. 30; Gautam
et al., supra, at Ex. 27; Gautam et al., supra, at Ex. 28; Gautam et al., supra, at Ex. 29).)
Moreover, Dr. Steinman disagreed with Dr. He’s criticism of the Gautam et al. studies’
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use of complete Freund’s adjuvant, explaining that within the studies some peptides,
such as Ac3.5.6 did not induce paralysis despite the use of the adjuvant. (Id. at 5-7
(citing Gautam et al., supra, at Ex. 27).) Therefore, the use of the adjuvant did not
invalidate the findings. (Id. at 6-7.)
e. Dr. Merkler’s supplemental report
In his second report, Dr. Merkler stressed the validity of a diagnosis of idiopathic
TM as “well-established in medical practice and is applied when a thorough
investigation fails to identify a known cause.” (Ex. E, p. 1 (citing Transverse Myelitis
Consortium Working Group, Proposed Diagnostic Criteria and Nosology of Acute
Transverse Myelitis, 59 NEUROLOGY 499 (2002) [hereinafter TM Consortium] (Ex. E, Tab
3)).) Idiopathic TM accounts for as many as 19% of patients diagnosed with TM. (Id.
(citing Olwen C. Murphy et al., Identification of Specific Causes of Myelopathy in a
Large Cohort of Patients Initially Diagnosed with Transverse Myelitis, 442 J.
NEUROLOGICAL SCIS., 2022, at 1 (Ex. E, Tab 1)).) The diagnosis of idiopathic TM is
correct in this case because “all other possible etiologies for which there are diagnostic
tests approved for human use by the FDA, including infections, and autoimmune
diseases were ruled out based on [the] available clinical data.” (Id.) Although Dr.
Merkler does not dispute Dr. Steinman’s observation that the Baxter et al. study and
2012 IOM report pre-dated the vaccination at issue in this case, he opined that these
publications remain informative of the broader understanding of the potential
relationship between vaccines and TM. (Id. (discussing Baxter et al., supra, at Ex. A,
Tab 2; 2012 IOM Report, supra, at Ex. 50).) Dr. Merkler stressed that he does not
disparage the molecular mimicry hypothesis, but he maintained that it “is an interesting
hypothetical mechanism and does not establish causality in this case without robust
supporting epidemiological evidence to confirm it.” (Id. at 2.) And, while Dr. Merkler
acknowledged that some autoimmune phenomena can develop rapidly in rare cases,
“the latency period for the onset of transverse myelitis after an immunological trigger is
longer than 24 hours.” (Id.) He opined that isolated case reports of TM occurring in
such a timeframe do not imply causation. (Id.)
f. Dr. He’s supplemental report
In response to Dr. Steinman’s assertion that the Baxter et al. study and 2012
IOM report are not informative of the specific molecular mimics he identified, Dr. He
responded that “no matter how many homologies (aka, molecular mimics) can be found
between the 2021 influenza vaccine and host proteins, mere sequence homologies will
not cause autoimmune diseases as the IOM clearly stated.”15 (Ex. F, p. 2.) Dr. He
indicated that
[T]he IOM committee has unequivocally stated that “Both naturally
occurring and postinfectious cross-reactive antibodies and T cells are
15 Dr. He also noted that the Dudley et al. study cited in his initial report was from 2020. (Ex. F, p. 2
(citing Dudley et al., supra, at Ex. C, Tab 4).)
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relatively common and most frequently not pathogenic. Cross-reacting
antibodies can also be secondary to nonspecific tissue injury rather than
involved in primary injury to the tissue. Moreover, in some circumstances,
infection with viruses that express antigens having immunologic cross-
reactivity with self-proteins can actually protect against autoimmune
disease in certain animal models.”
(Id. at 2-3 (quoting 2012 IOM Report, supra, at Ex. 50, pp. 99-100).)
Thus, Dr. He reiterated his view that autoimmune disease development is
explained by the strength and extent of the immune response at issue rather than the
presence of molecular mimicry. (Ex. F, p. 3.) He opined that Dr. Steinman’s opinion
lacks “a balanced view on the ying and yang force of the host immune system.” (Id.)
Dr. He clarified that there is no argument as to the validity of the Gautam et al. studies,
but reiterated that these studies underscore the need for a strong immune activation to
break immune tolerance. (Id. at 4 (discussing Gautam et al., supra, at Ex. 27; Gautam
et al., supra, at Ex. 28; Gautam et al., supra, at Ex. 29).) Moreover, these studies are
mostly focused on the innate immune system. (Id.)
Dr. He also maintained that, even accounting for the presence of a recall
response, the timeframe between petitioner’s vaccination and onset of her TM is too
short for a vaccine-induced activation of innate and adaptive immune responses leading
to attack of neural tissue. (Ex. F, p. 5.) While the innate immune response is fully
functional within three days, it takes the adaptive immune response at least seven days
to be fully activated. (Id. (citing Richard Warrington et al., An Introduction to
Immunology and Immunopathology, 7 ALLERGY ASTHMA & CLINICAL IMMUNOLOGY, 2011,
at 1 (Ex. F, Tab 1);16 Williams & Bevan, supra, at Ex. C, Tab 29; Bali Pulendran & Rafi
Ahmed, Immunological Mechanisms of Vaccination, 12 NATURE IMMUNOLOGY 509 (2011)
(Ex. C, Tab 24); Michael J. Carter et al., The Antibody-Secreting Cell Response to
Infection: Kinetics and Clinical Applications, 8 FRONTIERS IMMUNOLOGY, 2017, at 1 (Ex.
F, Tab 2)).) Moreover, antigen-specific B cells do not become antibody secreting cells
until at least 8 days after a primary vaccination and at least five days after a secondary
vaccination. (Id. at 5-6 (citing Carter et al., supra, at Ex. F, Tab 2, p. 9 fig. 2).)17 A recall
response does not develop until day four post-vaccination and both B cells and antigen-
specific T cells take at least five days to activate and expand. (Id. at 5 (citing Carter et
al., supra, at Ex. F, Tab 2; Williams & Bevan, supra, at Ex. C, Tab 29).) Thus,
according to Dr. He, it is “impossible” for T and B cells to be activated within two days of
a flu vaccination even in the context of a recall response. (Id.) Dr. He disagreed again
16 In his report, Dr. He’s bibliography indicates that reference 4 refers to: J.S. Marshall et al., An
Introduction to Immunology and Immunopathology, 14 ALLERGY ASTHMA & CLINICAL IMMUNOLOGY 49
(2018). (See Ex. F, p. 8.) However, this decision cites the article respondent actually filed. (See Ex. F,
Tab 1.)
17 Figure two is a line graph comparing the relative frequency of antigen-specific antibody secreting cells
by day as among bacterial and viral infections, primary vaccination, and secondary vaccination. (Carter
et al., supra, at Ex. F, Tab 2, p. 9 fig. 2.) The figure reflects that only the line for bacterial and viral
infection rises above the x-axis before day four. (See id.)
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with Dr. Steinman’s interpretation of the Schonberger et al. data and stressed that
Schonberger et al. examined GBS rather than TM. (Id. (discussing Schonberger et al.,
supra, at Ex. 40).)
g. Dr. Steinman’s second supplemental report
In his final report, Dr. Steinman stressed that respondent’s suggestion that
petitioner’s TM is idiopathic – which he characterized as a euphemism for “I don’t know”
– must be balanced against his presentation of a causal explanation that should be
considered sound and reliable. (Ex. 52, p. 1.) And, regarding Dr. Merkler’s emphasis
on epidemiology, he indicated that it would not be realistic to expect any epidemiology
to be available given the recency of the specific flu vaccine formulations at issue. (Id.)
He charged that Dr. Merkler seeks scientific certainty. (Id. at 1-2.) In that regard, he
cited an additional study as validation of the findings of Lanz et al. (Id. at 2 (citing Neda
Sattarnezhad et al., Antibody Reactivity Against EBNA1 and GlialCAM Differentiates
Multiple Sclerosis Patients from Healthy Controls (Jan. 5, 2025) (unpublished
manuscript) (Ex. 53))18.)
Dr. Steinman agreed with Dr. He’s statement that the immune system involves
“ying and yang” forces. (Ex. 52, p. 4.) However, in response to Dr. He’s statement that
“mere sequence homologies will not cause autoimmune disease,” Dr. Steinman
indicated
Petitioner’s theory goes far beyond showing “mere sequence homologies”.
The hierarchical search describes regions in the vaccine that have met the
criteria of four peer reviewed papers, the three Gautam papers and the Lanz
paper, and now a fifth paper cited here as Supplementary Reference 1. In
addition, the region in the vaccine has been studied by others and is
described extensively in Petitioner’s reports.
(Id. at 3.)
Dr. Steinman also disagreed with Dr. He’s citation to Carter et al. (Ex. 52, p. 4.)
According to Dr. Steinman, the chart depicted in Dr. He’s report, though it comes from
the Carter et al. paper, does not actually reflect the data generated by the study. (Id.
(discussing Carter et al., supra, at Ex. F, Tab 2, p. 9 fig. 2).) In fact, citing Table 1 within
the study, he observed that in most instances measurements were not even taken until
day 7. (Id. at 4-5 (citing Carter et al., supra, at Ex. F, Tab 2, pp. 4-7 tbl. 1).) Dr.
Steinman reiterated his reliance on the Schonberger et al. and Park et al. papers. (Id.
at 5 (citing Schonberger et al., supra, at Ex. 40; Park et al., supra, at Ex. 41).)
18 The manuscript was subsequently published in March of 2025. See Neda Sattarnezhad et al.,
Antibody Reactivity Against EBNA1 and GlialCAM Differentiates Multiple Sclerosis Patients from Healthy
Controls, 10 PNAS, 2025, at 1. However, petitioner did not file the publication as an exhibit in this case.
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V. Analysis
a. Althen prong one
Under Althen prong one, petitioner must provide a “reputable medical theory,”
showing that the subject vaccine can cause the type of injury alleged. Pafford v. Sec’y
of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (quoting Pafford v.
Sec’y of Health & Human Servs., No. 01-0165V, 2004 WL 1717359, at *4 (Fed. Cl.
Spec. Mstr. July 16, 2004), mot. for rev. denied, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d
1352 (Fed. Cir. 2006)). Such a theory need only be “legally probable, not medically or
scientifically certain.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49
(Fed. Cir. 1994). Petitioner may satisfy the first Althen prong without resort to medical
literature, epidemiological studies, demonstration of a specific mechanism, or a
generally accepted medical theory. See Andreu v. Sec’y of Health & Human Servs.,
569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of Health & Human
Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). However, “[a] petitioner must provide
a ‘reputable medical or scientific explanation’ for [the proposed causal] theory. While it
does not require medical or scientific certainty, it must still be ‘sound and reliable.’”
Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019)
(citation omitted) (first quoting Moberly v. Sec’y of Health & Human Servs., 592 F.3d
1315, 1322 (Fed. Cir. 2010); then quoting Knudsen, 35 F.3d at 548-49). That is,
although petitioners are not required to prove their theories in any one way, they must in
all events support their proffered theory with sound and reliable scientific explanation,
Boatmon, 941 F.3d at 1359, and provide evidence that establishes on balance that the
vaccine at issue can more likely than not cause the injury at issue, Cerrone v. Sec’y of
Health & Human Servs., 146 F.4th 1113, 1120-23 (Fed. Cir. 2025).19
In his motion, respondent argues that relying on the concept of molecular
mimicry broadly would be too generic to support a theory of causation.20 (ECF No. 45,
19 In the motion papers, the parties debated whether a plausible theory of causation is sufficient to meet
petitioner’s burden of proof under Althen prong one (ECF No. 45, p. 11; ECF No. 47, pp. 7-11), with
respondent ultimately arguing in his reply brief that the Federal Circuit resolved the question in Cerrone,
which was issued subsequent to the filing of petitioner’s brief (ECF No. 50, pp. 1-2 (citing Cerrone, 146
F.4th at 1121 n.3)). I agree with respondent, but I also stress that Cerrone did not announce a new
standard. As respondent indicated in his initial brief (ECF No. 45, p. 11), the Federal Circuit has long held
that a plausible theory of causation is insufficient in this program. Cerrone, 146 F.4th at 1121
(emphasizing that “we have repeatedly stated that ‘simply identifying a ‘plausible’ theory of causation is
insufficient for a petitioner to meet her burden of proof.’” (quoting LaLonde v. Sec’y of Health & Human
Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014))).
20 Consistent with what respondent argues here, prior cases have explained that molecular mimicry is “a
generally accepted scientific principle,” but “mere invocation of the scientific term does not carry a
petitioner’s burden in a Program case.” Deshler v. Sec’y of Health & Human Servs., No. 16-1070V, 2020
WL 4593162, at *20 (Fed. Cl. Spec. Mstr. July 1, 2020) (citing Forrest v. Sec’y of Health & Human Servs.,
No. 14-1046V, 2019 WL 925495, at *3 (Fed. Cl. Spec. Mstr. Jan. 28, 2019)). In particular, identifying
sequence homology is not enough standing alone because, as Dr. He stressed, being able to identify a
homology “does not necessarily mean the similarity has significance to the immune system.” Tullio v.
Sec’y of Health & Human Servs., No. 15-51V, 2019 WL 7580149, at *15 (Fed. Cl. Spec. Mstr. Dec. 19,
2019), aff’d, 149 Fed. Cl. 448 (2020); see also Caredio ex rel. D.C. v. Sec’y of Health & Human Servs.,
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pp. 12-13.) Instead, petitioner must show that it applies to the specific vaccination and
condition at issue. (Id. (citing W.C. v. Sec’ of Health & Human Servs., 704 F.3d 1352,
1360 (Fed. Cir. 2013)).) In this case, however, no scientific studies are available that
associate the flu vaccine with TM. (Id. at 13-15.) Moreover, respondent argues that Dr.
Steinman’s theory is speculative. (Id. at 15-17.) In light of Dr. He’s opinion, respondent
argues that an immune response to vaccination cannot be equated to an infection-
induced immune response and, therefore, Dr. Steinman’s reliance on papers such as
Lanz et al. and Bjornevik et al. that study EBV infection as a cause of MS is misplaced.
(Id. at 15-16 (discussing Lanz et al., supra, at Ex. 30; Kjetil Bjornevik et al., Longitudinal
Analysis Reveals High Prevalence of Epstein-Barr Virus Associated with Multiple
Sclerosis, 375 SCIENCE 296 (2022) (Ex. 31)).) Dr. Steinman’s use of BLAST to compare
neurofascin and influenza hemagglutinin is otherwise insufficient without more. (Id. at
16-17.)
In response, petitioner stresses that, though medical literature is valuable,
petitioner is permitted to rely on circumstantial evidence and is not obligated to
demonstrate scientific certainty, especially given the rarity of the condition at issue.
(ECF No. 47, pp. 11-12.) Petitioner contends that in the search for medical proof,
respondent’s experts impermissibly “downplay” Dr. Steinman’s opinion. (Id. at 11.)
Petitioner notes that prior petitioners have been found entitled to compensation for TM
resulting from various vaccinations.21 (Id. at 12.) TM is known to be an autoimmune
inflammatory condition affecting the spinal cord that can be post-infectious and,
moreover, the National Institute of Neurological Disorders and Stroke (“NINDS”)
recognizes that TM may also present as a post-vaccination phenomenon. (Id. at 13
(citing Transverse Myelitis, NAT’L INST. NEUROLOGICAL DISORDERS & STROKE,
https://www.ninds.nih.gov/health-information/disorders/transverse-myelitis (last
reviewed Nov. 28, 2023) (Ex. 14)).) Petitioner challenges the notion that the available
epidemiology is informative. (Id. at 13-17.) Describing the steps included in Dr.
Steinman’s reports, petitioner endorses Dr. Steinman’s reliance on molecular mimicry to
explain how the flu vaccine can cause TM (Id. at 17-23), and she cites prior cases in
No. 17-0079V, 2021 WL 4100294, at *31 (Fed. Cl. Spec. Mstr. July 30, 2021) (“[D]emonstration of
homology alone is not enough to establish a preponderant causation theory.” (emphasis omitted) (citing
Schultz v. Sec’y of Health & Human Servs., No. 16-539V, 2020 WL 1039161, at *22 n.24 (Fed. Cl. Spec.
Mstr. Jan. 24, 2020))), mot. for rev. denied, No. 17-79V, 2021 WL 6058835 (Fed. Cl. Dec. 3, 2021).
Thus, for example, in Brayboy, an omnibus proceeding addressing autoimmune premature ovarian
insufficiency, the special master found it sufficient that the petitioners had, more robustly, “identified
cross-reaction between components of the vaccine and proteins in the body that are directly responsible
for the health and productivity of the organ at issue,” while also noting that further requiring additional
steps, or insisting on direct, testable evidence would impermissibly heighten petitioner’s burden of proof.
Brayboy v. Sec’y of Health & Human Servs., No. 15-183V, 2021 WL 4453146, at *19 (Fed. Cl. Spec.
Mstr. Aug. 30, 2021). Ultimately, when assessing theories based on molecular mimicry in light of
petitioner’s preponderant burden of proof, “[t]he line must be drawn somewhere between speculation and
certainty.” Id.
21 Specifically, petitioner cites White v. Secretary of Health & Human Services, No. 15-1521V, 2019 WL
7563239 (Fed. Cl. Spec. Mstr. Dec. 19, 2019) (finding the HPV vaccine caused TM) and Le v. Secretary
of Health & Human Services, No. 16-1078V, 2023 WL 3049203 (Fed. Cl. Spec. Mstr. Mar. 30, 2023)
(finding the Tdap vaccine caused TM). (ECF No. 47, p. 12.)
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which Dr. Steinman’s use of BLAST and citation to the Gautam et al. papers have been
accepted (Id. at 23).22 She is critical of respondent’s experts’ competing opinions. (Id.
at 24-33.)
It is not necessary to resolve the parties’ competing positions on molecular
mimicry more broadly. Even crediting the applicability of molecular mimicry to TM and
accepting arguendo Dr. Steinman’s use of BLAST and his reliance on the Gautam et al.,
Lanz et al., and Bjornevik et al. papers, I am not persuaded as a threshold matter that
petitioner has preponderantly demonstrated that TM can be explained by an
autoimmune attack on neurofascin, as Dr. Steinman’s proffered theory requires.23
Absent Dr. Steinman’s specific molecular mimicry theory, the evidence on this record,
including the additional literature petitioner filed in connection with her motion response,
is not otherwise sufficient to meet petitioner’s preponderant burden of proof under
Althen prong one. Ultimately, Dr. Steinman cited four publications to support
neurofascin as found in the Node of Ranvier as having been implicated in TM. (Ex. 8,
pp. 8-9, 22 (citing Rasband & Peles, supra, at Ex. 17; Guo & Zhang, supra, at Ex. 18;
Kira et al., supra, at Ex. 19; Jia et al., supra, at Ex. 20).) However, although these
papers do support the general idea that neurofascin may be affected by demyelination
in the central nervous system, there are several reasons why they do not readily
support Dr. Steinman’s theory in this case.
First, contrary to what Dr. Steinman suggests, none of these papers invoke an
attack against neurofascin as an explanation specifically for the pathogenesis of acute
monophasic TM as is at issue in this case. One case series does discuss an
autoimmune attack against the Nodes of Ranvier as a potential explanation for
“GBS/ATM overlap syndrome;” however, that case report does not seek to implicate
neurofascin antibodies. (Guo & Zhang, supra, at Ex. 18, pp. 4-5.) Instead, they note
only that three of the subjects tested positive for anti-ganglioside antibodies. (Id. at 2.)
Rather, the literature cited by Dr. Steinman as a whole generally discusses neursofasin
antibodies in the context of chronic conditions including MS, NMOSD, and CIDP.
22 Specifically, petitioner cites Pasco v. Secretary of Health & Human Services, No. 16-500V, 2022 WL
6616736 (Fed. Cl. Spec. Mstr. Sept. 23, 2022); Mullins v. Secretary of Health & Human Services, No. 19-
320V, 2024 WL 4045424 (Fed. Cl. Spec. Mstr. Aug. 8, 2024); Gardner v. Secretary of Health & Human
Services, No. 17-1851V, 2023 WL 9288070 (Fed. Cl. Spec. Mstr. Dec. 21, 2023); White, 2019 WL
7563239. (ECF No. 47, p. 23.)
23 Of course, petitioner is not obligated to come forward with a specific biologic mechanism to meet her
burden of proof. Kottenstette v. Sec’y of Health & Human Servs., 861 F. App’x 433, 440-41 (Fed. Cir.
June 15, 2021) (citing Knudsen, 35 F.3d at 549 and Simanski v. Sec’y of Health & Human Servs., 671
F.3d 1368, 1384 (Fed. Cir. 2012)). However, because she does seek to meet her burden of proof under
Althen prong one at least in part via presentation of such a mechanism – in this case, molecular mimicry
– the soundness of that assertion must be assessed. E.g., Howard v. Sec’y of Health & Human Servs.,
No. 16-1592V, 2022 WL 4869354, at *24 (Fed Cl. Spec. Mstr. Aug. 31, 2022) (“[P]etitioners are never
required to establish [a] mechanism—but they often attempt to do so, and therefore it is reasonable to
evaluate their success in the effort.”), mot. for rev. denied sub nom., Howard v. United States, No. 16-
1592V, 2023 WL 4117370 (Fed. Cl. May 18, 2023), aff’d per curiam sub nom., Howard v. Sec’y of Health
& Human Servs., No. 2023-1816, 2024 WL 2873301 (Fed. Cir. June 7, 2024).
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Second, even for those conditions that are more explicitly discussed, this
literature characterizes a role for neurofascin antibodies as merely an “emerging” area
of research (Kira et al., supra, at Ex. 19, p. 6; see also Jia et al., supra, at Ex. 20, p. 3
(noting that “further studies are needed to elucidate the pathogenesis of NMOSD in
relation to the presence of antibodies against . . . [neurofascin]155”)), undercutting the
suggestion that an autoimmune attack against neurofascin is an accepted cause of any
condition, let alone TM by extension. For example, Dr. Merkler noted on respondent’s
behalf that a later study by Stich et al. was unable to find a difference in the prevalence
of neurofascin 155 antibodies as between MS patients and controls. (Ex. A, p. 7
(discussing Stich et al., supra, at Ex. A, Tab 10, p. 3).) Indeed, Dr. Steinman initially
raised an attack against neurofascin because he had noted that petitioner tested
negative for antibodies against two targets more commonly associated with TM, MOG
and AQP-4. (Ex. 8, pp. 8-9.)
Third, the literature suggests that anti-neurofascin antibodies, as antibodies
against paranodal proteins, “are associated with unique features and these conditions
are collectively termed nodopathy or paranodopathy.” (Kira et al., supra, at Ex. 19, p.
1.) Indeed, these papers note that injury to neurofascin is viewed as a potential
explanation for conditions that combine both peripheral and central nervous system
damage. (Jia et al., supra, at Ex. 20, p. 1; Kira et al., supra, at Ex. 19, pp. 3, 6.) Thus,
for example, Dr. Merkler opined that neurofascin is more likely to be important to GBS
or CIDP than to TM. (Ex. A, p. 7.) Even Dr. Steinman’s own report suggests that
neurofascin is more readily implicated in the pathogenesis of GBS. (Ex. 8, p. 22 (stating
that “[i]mmunity to neurofascin is critical to the triggering of inflammatory neuropathy
(GBS), and in some cases transverse myelitis . . .”).)
Prior petitioners have been compensated for post-flu vaccine TM. E.g., Jane
Doe 93 v. Sec’y of Health & Human Servs., No. [redacted], 2011 WL 2326966 (Fed. Cl.
Spec. Mstr. May 9, 2011); J.S. v. Sec’y of Health & Human Servs., No. 14-851V, 2018
WL 11731139 (Fed. Cl. Spec. Mstr. Apr. 9, 2018); Songero v. Sec’y of Health & Human
Servs., No. 18-300V, 2025 WL 3013090 (Fed. Cl. Spec. Mstr. Oct. 3, 2025). However,
given the cause-in-fact context, petitioners do not always succeed in demonstrating that
the flu vaccine can cause TM. E.g., Caves v. Sec’y of Health & Human Servs., No. 07-
443V, 2010 WL 5557542 (Fed. Cl. Spec. Mstr. Nov. 29, 2010), mot. for rev. denied, 100
Fed. Cl. 119 (2011), aff’d per curiam, 463 F. App’x 932 (Fed. Cir. 2012); Bowling v.
Sec’y of Health & Human Servs., No, 18-109V, 2023 WL 6846491 (Fed. Cl. Spec. Mstr.
Sept. 20, 2023); Johnson v. Sec’y of Health & Human Servs., No. 18-410V, 2025 WL
1942989 (Fed. Cl. Spec. Mstr. June 17, 2025). Moreover, the undersigned is not aware
of any prior TM case in which a petitioner has presented the specific neurofascin-based
molecular mimicry theory advanced in this case.
A limited number of prior cases discuss neurofascin, but they all involved
conditions other than TM and, moreover, often rejected or did not reach the question of
whether molecular mimicry against neuorfascin was preponderantly supported. In fact,
consistent with the above, these cases mostly involved peripheral nerve disorders.
Davis v. Sec’y of Health & Human Servs., No. 14-978V, 2022 WL 1654743, at *33 (Fed.
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Cl. Spec. Mstr. Apr. 27, 2022) (alleging the flu vaccine caused CIDP in which one of the
theories presented by Dr. Steinman involved molecular mimicry between a component
of the flu vaccine and contactin-1 and neurofascin; however, the special master did not
reach any conclusions about this theory as there was no record evidence of the
presence of either contactin-1 or neurofascin in petitioner); H.C. v. Sec’y of Health &
Human Servs., No. 16-4V, 2022 WL 2825395, at *28 (Fed. Cl. Spec. Mstr. May 9, 2022)
(alleging the flu vaccine caused Ramsay Hunt syndrome in which Dr. Zamvil proposed
homology between flu A hemagglutinin and contactin-associated protein and/or
neurofascin, which was ultimately rejected); Gatto v. Sec’y of Health & Human Servs.,
No. 21-924V, 2025 WL 972817, at *6-7, 20-21 (Fed. Cl. Spec. Mstr. Feb. 28, 2025)
(alleging that the meningococcal vaccine caused GBS in which Dr. Steinman identified
homology between the diphtheria toxin and contactin and neurofascin; however, the
Chief Special Master rejected Dr. Steinman’s theory); Borgelt v. Sec’y of Health &
Human Servs., No. 23-1051V, 2026 WL 267899, at *20-21 (Fed. Cl. Spec. Mstr. Jan. 5,
2026) (finding that the record did not preponderantly support petitioner’s theory that the
flu vaccine can worsen anti-neurofascin CIDP). In one prior case, Dr. Steinman
presented multiple proposed homologies, including against neurofascin, to explain how
a vaccine can cause ADEM, a central nervous system demyelinating disorder. Mullins
v. Sec’y of Health & Human Servs., No. 19-320V, 2024 WL 4045424 (Fed. Cl. Spec.
Mstr. Aug. 8, 2024). However, although the petitioner in that case was found entitled to
compensation, molecular mimicry against neurofascin was not isolated as being
dispositive of the special master’s Althen prong one analysis and, in fact, the special
master explicitly remarked that she would have reached the conclusion that vaccines
can cause ADEM even if petitioner has not presented any of the multiple examples of
potential homology. Id. at *45; see also Byrd v. Sec’y of Health & Human Servs., No.
20-1476V, 2024 WL 4003061 (Fed. Cl. Spec. Mstr. July 8, 2024) (similarly finding
petitioner entitled to compensation for GBS caused by the pneumococcal vaccine where
multiple molecular mimics were proposed, including one against neurofascin).
In light of all of the above, petitioner has not presented preponderant evidence on
this record of a sound and reliable medical theory that demonstrates that the flu vaccine
can cause TM.
a. Althen prong three
The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. That term
has been equated to the phrase “medically-acceptable temporal relationship.” Id. at
1281. A petitioner must offer “preponderant proof that the onset of symptoms occurred
within a timeframe for which, given the medical understanding of the disorder’s etiology,
it is medically acceptable to infer causation-in-fact.” de Bazan v. Sec’y of Health &
Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a
medically acceptable timeframe must coincide with the theory of how the relevant
vaccine can cause an injury (Althen prong one's requirement). Id.; Shapiro v. Sec’y of
Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), mot. for recons. denied after
remand, 105 Fed. Cl. 353 (2012), aff’d per curiam, 503 F. App’x 952 (Fed. Cir. 2013);
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Koehn v. Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl.
Spec. Mstr. May 30, 2013), mot. for rev. denied sub nom., C.K. v. Sec’y of Health &
Human Servs., 113 Fed. Cl. 757 (2013), aff’d sub nom., Koehn v. Sec’y of Health &
Human Servs., 773 F.3d 1239 (Fed. Cir. 2014).
Here, there is no dispute that petitioner’s TM developed as little as 24 hours after
the vaccination at issue.24 (ECF No. 45, p. 20; ECF No. 47, p. 38.) Moreover, based on
the medical history discussed above, I conclude that the evidence preponderates in
favor of a finding that onset of petitioner’s TM occurred approximately 24-hours post-
vaccination. (Ex. 4, pp. 159, 683; Ex. 5, pp. 1-2.) What remains controversial is
whether molecular mimicry can manifest a neurologic injury such as TM within 24 hours.
Respondent argues the timing is too short. (ECF No. 45, pp. 20-21.) He
contends that Dr. He persuasively explained that a 24-hour latency is inconsistent with
the multi-step innate and adaptive immune responses necessary to explain how
molecular mimicry would result in TM. (Id. at 20.) He additionally argues that Dr.
Steinman’s reliance on the Schonberger et al. study is unpersuasive. (Id.) Petitioner
argues that the short latency can be explained by a recall response. (ECF No. 47, pp.
37-40.) In particular, petitioner notes Dr. Steinman’s reliance on the Lai et al. study to
demonstrate that CD4 T cells respond to antigen within 6 hours. (Id. at 39.)
Additionally, petitioner observes that Dr. Steinman cited the Schonberger et al. study to
demonstrate that a one-day onset has been seen in humans and not merely in animal
model studies. (Id. at 39-40.)
For purposes of this discussion under Althen prong three, despite having
concluded that petitioner has not met her burden under Althen prong one, I assume
arguendo that a recall response to vaccination could result in the relevant molecular
mimicry.25 Granting petitioner that premise, petitioner has not preponderantly
24 In their briefs, the parties discuss the onset as being “within 24 to 48 hours.” (ECF No. 45, p. 20; ECF
No. 47, p. 38.) This characterization is based on Dr. Steinman’s couching of the timing issue. However,
based on the positions staked out by the experts, the distinction between a 24-hour onset and a 48-hour
onset is immaterial. Dr. Steinman has opined that a 24-hour onset is biologically plausible without
distinguishing a 48-hour onset as being any more plausible and respondent’s experts have, conversely,
opined that anything less than three or four days is implausible.
25 In his motion, respondent also raises within his Althen prong three argument a comment by Dr. He that,
if Dr. Steinman’s hypothesis were correct, then the Baxter et al. study would have detected many more
cases of post-vaccination TM due to immune recall response. (ECF No. 45, p. 20 (discussing Ex. C, p.
19).) Petitioner then devoted significant attention to this issue, arguing that the Baxter et al. data can be
viewed in such a way as to buttress Dr. Steinman’s view. (ECF No. 47, pp. 41-43 (discussing Baxter et
al., supra, at Ex. C, Tab 3; Baxter et al., Supplemental Tables 1 & 2: Relative Risk of Transverse Myelitis
in the 2-42 Day Risk Interval Following Vaccines, Compared to Remainder of the 9 Months Post
Vaccination (Ex. 58) [supplement to Ex. C, Tab 3]).) However, Dr. He’s assertion speaks to his overall
view that an immune response to vaccination would not result in autoimmunity. (Ex. C, pp. 17-18.)
Although Dr. He’s comment was included under the heading “Timing,” I take Dr. He to be stating that the
Baxter et al. study provides evidence that a recall response is no more likely than a primary immune
response to result in autoimmunity, which is not a question that bears directly on whether a recall
response would accelerate the timing of onset relative to a primary response. I do not find it necessary to
resolve this question. Nor do I find petitioner’s reinterpretation of the Baxter et al. data to be persuasive.
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demonstrated that molecular mimicry can cause a neurologic injury within 24-hours,
even in the context of a recall response. Thus, petitioner cannot meet her burden of
proof under Althen prong three for reasons entirely independent of her failure to meet
her burden of proof under Althen prong one. Indeed, the timing of onset is the biggest
issue in this case and would be fatal to petitioner’s case even if she met her burden of
proof under Althen prong one.
Dr. He is persuasive in explaining that even in the context of a recall response,
the overall time needed for the complete immune response to develop is days, not
hours. (Ex. F, pp. 5-6.) Although Dr. Steinman questioned whether a particular graph
cited by Dr. He was supported by underlying study data (Ex. 52, pp. 4-5 (discussing
Carter et al., supra, at Ex. F, Tab 2, p. 9 fig. 2)), he did not actually refute Dr. He’s
assertion as a matter of basic immunologic understanding. In fact, Dr. Steinman
described the graph at issue as “idealized,” not incorrect. (Id. at 5.) But in any event,
Dr. He cited several other publications for the proposition that even a recall response
takes several days to fully develop. (E.g., Warrington et al., supra, at Ex. F, Tab 1;
Williams & Bevan, supra, at Ex. C, Tab 29; Pulendran & Ahmed, supra, at Ex. C, Tab
24.) Moreover, Dr. Steinman himself presented the complete 2012 IOM report on
adverse effects of vaccines, which indicates that a recall response reduces the time for
the initial lag phase of an immune response from 4-7 days for a primary response down
to 1-3 days, meaning that the recall response does not begin to build until after that
initial period of at least 24 hours. (2012 IOM Report, supra, at Ex. 50, p. 87.) Dr.
Steinman’s counter presentation seeking to show that a recall response can
nonetheless result in disease more rapidly is based primarily on three sources of
evidence, none of which is persuasively presented.26
First, Dr. Steinman relies on papers by Lai et al. and Bartholomäus et al. to
demonstrate that CD4 T cells can respond to antigen within six hours and enter the
central nervous system within one to two days. (Ex. 8, pp. 32, 34-35 (citing Lai et al.,
supra, at Ex. 47; Ingo Bartholomäus et al., Effector T Cell Interactions with Meningeal
Vascular Structures in Nascent Autoimmune CNS Lesions, 46 NATURE 94 (2009) (Ex.
49)).) The fact that the Lai et al. study shows an initial T cell response occurring within
six hours is not disputed; however, Dr. He persuasively notes that this finding alone is
not informative. (Ex. C, pp. 16-17.) The fact that T cells respond at six hours within an
in vitro experiment does not necessarily speak to how long it would take these cells to
respond and meaningfully develop in vivo, given the overall interplay of forces that
make up the human immune system. (Id. at 17 (discussing Lai et al., supra, at Ex. 47).)
Moreover, even taking the Lai et al. finding at face value, the time it takes T cells to
initially respond to an antigen is only the first step in what Dr. He explains to be a multi-
26 In reaching this conclusion, I have also considered the fact that petitioner’s treating neurologist, Dr.
Sengul, opined that petitioner’s TM was provoked by her vaccination. (Ex. 4, p. 188.) Although Dr.
Sengul’s opinion is primarily discussed under Althen prong two, the same reasoning applies with respect
to Althen prong three. Even assuming arguendo that Dr. Sengul was opining with specific respect to a
24-hour onset, the available evidence is limited to the mere fact that Dr. Sengul was willing to attribute
petitioner’s TM to vaccination. (See id. at 184-89.) Without more, it cannot be said that Dr. Sengul’s
opinion on this question would be any more reliable than Dr. Steinman’s.
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step process. (Id.) An initial T cell response occurring in as little as six hours does not
imply that the full immune response develops within that timeframe, let alone that it
would result in the manifestation of neurologic injury within that timeframe. Dr.
Steinman cited a prior case in which another special master credited his reliance on the
Lai et al. study. (Ex. 8, p. 35 (discussing E.M. v. Sec’y of Health & Human Servs., No.
14-753V, 2021 WL 3477837 (Fed. Cl. Spec. Mstr. July 9, 2021).) However, in a prior
case I rejected a petitioner’s reliance on the Lai et al. study as support for a rapid onset
of small fiber neuropathy because it showed only that T cells can respond to antigen
challenge within a matter of hours, which is not equivalent to showing that the immune
response can cause neurologic injury in that timeframe. McGill v. Sec’y of Health &
Human Servs., No. 15-1485V, 2023 WL 3813524, at *35-36 (Fed. Cl. Spec. Mstr. May
11, 2023).)
Dr. Steinman also discussed a study by Bartholomäus et al. as further
demonstrating that experimental autoimmune encephalomyelitis studies have shown
that the first T cells sensitized to myelin enter the central nervous system between one
to two-and-a-half days after transfer. (Ex. 8, p. 35 (citing Bartholomäus et al., supra, at
Ex. 49).) However, it is explicitly noted that this occurred “before onset” of the EAE.
(Bartholomäus et al., supra, at Ex. 49, p. 1.) Dr. Steinman stressed that “an
experimental animal would not be able to share with an investigator subtle neurologic
symptoms in a manner that petitioner did.” (Ex. 8, p. 35.) However, I rejected this
reasoning in a prior decision, explaining that: “While Dr. Steinman's point may be
logical, it is inherently speculative. The study's finding was that clinical symptoms
manifested at 3 days. The fact that mice cannot report subjective complaints is a
limitation of the study, not evidence that onset was earlier than actually observed.”
Greenslade v. Sec’y of Health & Human Servs., No. 14-1140V, 2024 WL 3527665, at
*39 (Fed. Cl. Spec. Mstr. June 28, 2024).
Second, Dr. Steinman has also put forward the idea that tuberculin tests, which
can be read as positive within 24 hours, further demonstrate that antigen-specific recall
responses can occur within that timeframe. (Ex. 8, p. 32 (citing Serane &
Kothendaraman, supra, at Ex. 43; Fan et al., supra, at Ex. 44; Kardjito & Grange, supra,
at Ex. 45).) However, tuberculin tests detect a hypersensitivity response, which is not
informative of the type of immune reaction Dr. Steinman otherwise places at issue.
(Williams & Bevan, supra, at Ex. C, Tab 29; Warrington et al., supra, at Ex. F, Tab 1.) I
have explained in prior cases that these tests are not informative of the type of immune
response involved in a recall response resulting in molecular mimicry and autoimmunity.
Defenza v. Sec’y of Health & Human Servs., No. 18-1601V, 2026 WL 473297, at *8
(Fed. Cl. Spec. Mstr. Jan. 7, 2026), mot. for rev. denied, 2026 WL 1742021 (Fed. Cl.
May 29, 2026), appeal docketed, No. 2026-2053 (Fed. Cir. July 20, 2026); see also
Greenslade, 2024 WL 3527665, at *39 (similarly noting that respondent’s expert had
refuted that tuberculin tests are informative of the timing of a recall response and that
Dr. Steinman had not adequately explained the relevance of the cited papers).
Third, Dr. Steinman relies on two epidemiologic studies – Schonberger et al. and
Park et al. – for the proposition that vaccinations have led to neurologic injury in humans
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within one day. As a threshold matter, respondent’s experts reasonably question Dr.
Steinman’s reliance on these papers because they pertain to GBS rather than TM.
(E.g., Ex. A, pp. 7-8; Ex. F, p. 5.) Although both conditions can be demyelinating and
epidemiologic evidence pertaining to GBS has been considered in prior cases in
assessing the time needed for autoimmunity to develop more broadly, TM is a central
nervous system condition whereas GBS is a peripheral nerve disorder. This distinction
should be more carefully considered when assessing edge cases with respect to the
minimum time needed for disease to develop. Indeed, though not dispositive, it is
notable that there is no direct evidence on this record that TM can develop in as little as
24 hours.
But in any event, even accepting these studies as some evidence pertaining to
TM, Dr. Steinman is not persuasive in suggesting that these two studies meaningfully
support a causal relationship between the flu vaccine and GBS occurring just a single
day post-vaccination. As with the Lai et al. study, Dr. Steinman cited a prior case in
which another special master credited his reliance on the Schonberger et al. paper with
respect to a one-day post-vaccination onset. (Ex. 8, pp. 35-36 (discussing
Quackenbush-Baker v. Sec’y of Health & Human Servs., 14-1000V, 2018 WL 1704523
(Fed. Cl. Spec. Mstr. Mar. 14, 2018).) However, in a prior case I addressed Dr.
Steinman’s reliance on both the Schonberger et al. and Park et al. papers in greater
detail, finding that neither provided strong evidence that vaccinations can cause GBS
within 24 hours. Defenza, 2026 WL 473297, at *14-15, *17. There is no doubt that the
Schonberger et al. study is often credited with regard to its overall epidemiologic signal.
However, although Dr. Steinman cites a specific bar graph that shows a number of
cases of GBS occurring on day “0-1” (Ex. 8, p. 33 (discussing Schonberger et al., supra,
at Ex. 40, p. 8 fig. 5)), nothing in the paper calculates that these cases represent an
increased risk. At best, the study observes that there is an increased risk of GBS for
the first full week post-vaccination. (Schonberger et al., supra, at Ex. 40, pp. 7-9.) The
Park et al. study, by contrast, has significant shortcomings. It observes a highly
selective group of people seeking compensation for perceived vaccine injury and,
moreover, does not indicate what criteria the compensating authority uses to adjudge
eligibility. (Park et al., supra, at Ex. 41.) In that regard, it is also suspicious that the
distribution curve among the observed cases is very different from the type of
distribution seen in other studies such as Schonberger et al. (Compare id. at 3 fig. 1,
with Schonberger et al., supra, at Ex. 40, p. 8 fig. 5.) And, finally, because
epidemiology speaks to correlation, epidemiologic findings do not necessarily override
contrary scientific understanding just because epidemiology is also a valuable scientific
tool. Accord Defenza, 2026 WL 1742021, at *10 (explaining that the fact that petitioner
is not obligated to present epidemiologic evidence “does not mean [] that special
masters must overlook the nature and limitations of such evidence”).
Accordingly, petitioner has not presented preponderant evidence on this record
that the timing of the onset of her TM occurred during a period that would support a
causal inference based on the theory of causation she has presented.
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b. Althen prong two
The second Althen prong requires proof of a logical sequence of cause and
effect, usually supported by facts derived from a petitioner’s medical records. Althen,
418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326-27;
Grant, 956 F.2d at 1147-48. Medical records are generally viewed as particularly
trustworthy evidence. Cucuras, 993 F.2d at 1528. However, medical records and/or
statements of a treating physician's views do not per se bind the special master. See
§ 300aa-13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment, test result,
report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y
of Health & Human Servs., 88 Fed. Cl. 706, 745 n.67 (2009) (“[T]here is nothing ... that
mandates that the testimony of a treating physician is sacrosanct—that it must be
accepted in its entirety and cannot be rebutted.”) A petitioner may support a cause-in-
fact claim through either medical records or expert medical opinion. § 300aa-13(a).
The special master is required to consider all the relevant evidence of record, draw
plausible inferences, and articulate a rational basis for the decision. Winkler v. Sec’y of
Health & Human Servs., 88 F.4th 958, 963 (Fed. Cir. 2023) (citing Hines, 940 F.2d at
1528).
Here, respondent argues that the medical records at best include “cursory
statements” that are limited to explaining that petitioner’s TM followed her vaccination.
(ECF No. 45, p. 19 (citing Ex. 4, pp. 159, 188).) However, respondent stresses that
such statements do not constitute causal opinions. (Id. (citing Moberly, 592 F.3d at
1323).) Otherwise, respondent argues that petitioner has not presented any evidence
that would distinguish her own TM from the typical manifestations of idiopathic TM. (Id.
at 18.) Moreover, respondent suggests that petitioner’s success in meeting Althen
prong two is predicated on her satisfaction of Althen prongs one and three, yet he
contends that Dr. Steinman’s theory and reliance on a recall response to explain the
timing of onset are speculative. (Id. at 17-18.)
Petitioner disagrees with respondent’s assessment of the treating physician’s
statements. (ECF No. 47, pp. 35-36.) She quotes her neurologist, Dr. Sengul, as
documenting the opinion that “this is truly an idiopathic transverse myelitis, likely
provoked by vaccine, which can be seen with MOGAD although she remains to be
seronegative.” (Id. at 35 (quoting Ex. 4, p. 188).) She also argues that Dr. Steinman’s
opinion further supports a logical sequence of cause and effect implicating petitioner’s
vaccination as a cause of her TM and stresses that respondent’s experts have not
identified any alternative cause. (Id. at 35-37.)
I cannot agree with respondent’s interpretation of Dr. Sengul’s record. The
statement that petitioner’s TM was “likely provoked by vaccine” cannot reasonably be
reduced to mere acknowledgement of the temporal proximity of the vaccination. Dr.
Sengul’s opinion, as the treating neurologist, is clearly some evidence supporting
petitioner’s case. However, there are three significant reasons why Dr. Sengul’s opinion
does not meaningfully assist petitioner in reaching a preponderance of the evidence
under Althen prong two.
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First, as respondent suggests, Dr. Sengul’s impression arose from a later
neurology evaluation of February 28, 2022. (Ex. 4, pp. 184-89.) The history taken at
that encounter does not confirm that Dr. Sengul was aware of the specific 24-hour post-
vaccination latency at issue. (Id. at 184.) However, as discussed above under Althen
prong three, that latency is not only controverted, but persuasively so. Given that
respondent is persuasive in demonstrating that a 24-hour latency does not support a
causal inference, and given that Dr. Sengul’s record is silent as to the timing of
petitioner’s prior vaccination relative to the onset of her TM, it cannot merely be
assumed that Dr. Sengul’s opinion embraces what the record evidence otherwise
demonstrates would be an implausible causal connection. Instead, considering Dr.
Sengul’s February 28, 2022 record holistically, the more reasonable inference is that Dr.
Sengul was aware only of the fact of the prior vaccination and not the specific timing.
Second, and relatedly, although respondent is not persuasive in arguing that Dr.
Sengul’s notation included no causal opinion at all, that opinion does seem to be based
in significant part on the presence of an assumed temporal relationship between
vaccination and injury. After all, but for noting the vaccine likely “provoked” the TM, Dr.
Sengul otherwise documented that petitioner’s TM was “truly idiopathic.” (Ex. 4, p.
188.) When a treating physician relies in part on temporality to conclude a condition is
vaccine-caused, this is not disqualifying and, in fact, can be “quite probative,” when the
evidence under Althen prongs one and three also supports a causal relationship.
Capizzano, 440 F.3d at 1326. Here, however, petitioner has not met her burden of
proof under either Althen prongs one or three. Even if Dr. Sengul was aware of the 24-
hour latency, a treating physician’s opinion must still be assessed for its reliability.27
Without more, Dr. Sengul’s opinion cannot be said to be any more reliable or any better
supported than Dr. Steinman’s. That is, Dr. Sengul’s opinion as documented does not
present any reasoning or explanation that could account for the issues discussed under
Althen prong three.
And, third, it is difficult to separate Dr. Sengul’s causal opinion from her
explanation that vaccine-provoked TM “can be seen with MOGAD although she remains
to be seronegative.” (Ex. 4, p. 188.) As discussed above relative to Althen prong one,
Dr. Steinman specifically devised a theory of causation based on neurofascin rather
than either MOG or AQP-4 because petitioner was seronegative for either MOG or
AQP4. (Ex. 8, pp. 8-9.) Consistent with Dr. Steinman’s implicit acknowledgement that
a causal relationship based on MOG cannot be demonstrated, Dr. Sengul’s notation on
its face expresses that the lack of a positive MOG finding is a reason to at least doubt
that petitioner’s TM was vaccine-caused. Nonetheless, Dr. Sengul still couches the
27 E.g., Veryzer v. Sec’y of Health & Human Servs., 100 Fed. Cl. 344, 355 (2011) (explaining that “[t]he
special master properly assessed the probative value of the statements provided by petitioner’s
physicians . . .”), aff’d per curiam sub nom., Veryzer v. United States, 475 F. App’x 765 (Fed. Cir. 2012);
Hughes v. Sec’y of Health & Human Servs., No. 16-930V, 2021 WL 839092, at *20 (Fed. Cl. Spec. Mstr.
Jan. 4, 2021) (noting that “[t]he views of treating physicians should be weighed against other, contrary
evidence also present in the record . . .”), mot. for rev. denied, 154 Fed. Cl. 640 (2021); see also Caves v.
Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 136-37 (2011) (noting special masters must consider,
but are not bound by, treating physician opinions), aff’d per curiam, 463 F. App’x 932 (Fed. Cir. 2012).
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possibility of vaccine-causation on the fact that it has been shown that vaccination can
result in MOG antibody-mediated disease. Thus, Dr. Sengul’s opinion does not readily
support the application of Dr. Steinman’s theory of causation because Dr. Sengul
entertained vaccine-causation based on the premise that, despite negative testing,
petitioner might have undergone an immune response to MOG, which is different than
the immune response Dr. Steinman theorized.
Petitioner otherwise argues that a logical sequence of cause and effect is
supported by Dr. Steinman’s opinion. (ECF No. 47, pp. 35-37.) However, this
argument fails in light of the fact that Dr. Steinman’s opinion has not been credited
under either Althen prong one or prong three. Petitioner also argues that it is significant
that no other cause of her TM is in evidence. (Id. at 36.) However, although petitioners
can rely on the absence of other causes to help carry their burden of proof, Walther v.
Sec’y of Health & Human Servs., 485 F.3d 1146, 1151 (Fed. Cir. 2007), “neither a mere
showing of a proximate temporal relationship between vaccination and injury, nor a
simplistic elimination of other potential causes of the injury suffices, without more, to
meet the burden of showing actual causation.” Althen, 418 F.3d at 1278 (citing Grant,
956 F.2d at 1149). Respondent is persuasive in suggesting that there is nothing
available on this record that distinguishes petitioner’s own TM from idiopathic TM. (ECF
No. 45, p. 18.) Moreover, as respondent’s experts noted, idiopathic TM is well-accepted
as a diagnosis. (E.g., Ex. C, p. 5; Ex. E, p. 1.) Indeed, that was Dr. Sengul’s actual
diagnosis. (Ex. 4, p. 189.)
Accordingly, petitioner has not presented preponderant evidence on this record
of a logical sequence of cause and effect that demonstrates that the flu vaccine did
cause her own TM.
VI. Conclusion
Regardless of the cause of petitioner’s condition, I am mindful of the pain and
suffering she has endured. Moreover, I appreciate that, at first blush, the onset of TM
occurring the day after a flu vaccine offers a striking coincidence. However, for all the
reasons discussed above, the onset of petitioner’s TM occurred too soon after
vaccination to be causally related and petitioner has not met her preponderant burden
of proof under any of the three parts of the applicable Althen test for demonstrating
causation-in-fact. Therefore, pursuant to § 300aa-12(d)(3)(A) and Vaccine Rule 10, this
decision concludes that petitioner is not entitled to an award of compensation. Absent a
timely motion for review, the Clerk is directed to enter judgment dismissing this case for
insufficient proof in accordance with Vaccine Rule 11(a).
IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
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