# Gardner v. Secretary of Health and Human Services

> United States Court of Federal Claims · January 17, 2024

URL: https://www.frixlaw.com/law-library/cases/10736460

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** January 17, 2024
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Thomas L. Gowen
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10736460

## How later opinions describe it (automated extraction)

- explaining that “to require identification and proof of specific biological mechanisms would be inconsistent with the purpose and nature of the vaccine compensation program”
- holding that Congress created a system in which “close calls regarding causation are resolved in favor of injured claimants”

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: December 21, 2023

* * * * * * * * * * * * *
ROBERT JOSEPH GARDNER, *
*
Petitioner, * No. 17-1851V
*
v. * Special Master Gowen
*
SECRETARY OF HEALTH * Entitlement; Off-Table Injury;
AND HUMAN SERVICES, * Significant Aggravation; Influenza
* (“Flu”) Vaccination; Multiple
Respondent. * Sclerosis (“MS”).
* * * * * * * * * * * * *
David Charles Richards, Christensen & Jensen, P.C., Salt Lake City, UT, for petitioner.
Kimberly Shubert Davey, U.S. Department of Justice, Washington, D.C., for respondent.

RULING ON ENTITLEMENT 1

On November 29, 2017, Robert Joseph Gardner (“petitioner”), filed a petition for
compensation under the National Vaccine Injury Compensation Program. 2 Petitioner alleged
causation-in-fact between an influenza (“flu”) vaccine which he received on December 1, 2014,
which caused him to suffer acute disseminated encephalomyelitis (“ADEM”) and/or that the flu
vaccine caused or significantly aggravated his multiple sclerosis (“MS”). Petition at Preamble
(ECF No. 1). After review of all of the evidence submitted by the parties, 3 for the following
reasons, I find that Petitioner has presented preponderant evidence that the influenza vaccine

1
Pursuant to the E-Government Act of 2002, see 44 U.S.C. § 3501 note (2012), because this decision contains a
reasoned explanation for the action in this case, I am required to post it to a publicly available website. This decision
will appear at https://www.govinfo.gov/app/collection/uscourts/national/cofc or on the Court of Federal Claims
website. This means the decision will be available to anyone with access to the Internet. Before the decision is
posted on the court’s website, each party has 14 days to file a motion requesting redaction “of any information furnished
by that party: (1) that is a trade secret or commercial or financial in substance and is privileged or confidential;
or (2) that includes medical files or similar files, the disclosure of which would constitute a clearly unwarranted
invasion of privacy.” Vaccine Rule 18(b). “An objecting party must provide the court with a proposed redacted
version of the decision.” Id. If neither party files a motion for redaction within 14 days, the decision will be posted
on the court’s website without any changes. Id.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National Childhood Vaccine Injury
Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended, 42 U.S.C. §§ 300aa-10 to 34 (2018) (hereinafter
“Vaccine Act” or “the Act”). Hereinafter, individual section references will be to 42 U.S.C. § 300aa of the Act.

3
Pursuant to Section 300aa-13(a)(1), in order to reach my conclusion, I have considered the entire record including
all of the medical records, statements, expert reports, and medical literature submitted by the parties. This opinion
discusses the elements of the record I found most relevant to the outcome.
aggravated his underlying MS and caused a severe tumefactive MS when a milder, garden
variety MS would more likely have occurred but for the vaccination.

I. Procedural History

Petitioner timely filed his claim on November 29, 2017. See Petition. The case was
assigned to my docket on November 30, 2017. See Notice of Assignment (ECF No. 4). After
petitioner filed medical records, respondent filed a status report on August 16, 2018, indicating
that the medical records were sufficiently complete for an analysis of his claim and requested a
deadline to file a Rule 4(c) report. (ECF No. 14).

Respondent filed a Rule 4(c) report on October 4, 2018, in which respondent noted that
following the DICP review of the case, the case was not appropriate for compensation under the
terms of the Act. Respondent’s Report (“Resp. Rept.”) at 1 (ECF No. 16). An initial status
conference was held on October 24, 2018, in which I ordered petitioner to file additional medical
records and an expert report. See Scheduling Order at 2 (ECF No. 17). Petitioner filed additional
medical records on January 11, 2019. Petitioner’s Exhibit (“Pet. Ex.”) 11-18 (ECF No. 20). On
May 30, 2019, petitioner filed initial expert reports from Marcel Kinsbourne, M.D., a pediatric
neurologist, and Vera Byers, M.D., Ph.D. 4 an immunologist. Pet. Ex. 25 (ECF No. 27); Pet. Ex.
48 (ECF No. 28). Petitioner also filed an expert report and a review letter from petitioner’s
treating neurologist, John Foley, M.D. 5 Pet. Ex. 62; Pet. Ex. 63 (ECF No. 29).

4
The qualifications of Dr. Kinsbourne and Dr. Byers will not be enumerated in this ruling because the Court will not
be considering their expert reports. Tr. 527-28. I held a status conference in October 2019 and explained to
petitioner my concern with the expert reports filed at that time given the complexity of this case. Petitioner elected
to retain new experts.

Dr. Foley, petitioner's treating neurologist, filed two expert reports and testified in the entitlement hearing. Pet. Ex;
5

62; Pet. Ex. 63. He received his medical degree from the Medical College of Wisconsin and did a residency in
neurology at the University of Utah Medical Center. Pet. Ex. 64 at 1. He is an expert in neurology and multiple
sclerosis, and serves as The Director of the Rocky Mountain Multiple Sclerosis Clinic, which services
approximately 4,200 patients a year. Id. at 2; see also Tr. 97. He is also the President of the Rocky Mountain MS
Research Group and is an elected Fellow in the American Academy of Neurology. Pet. Ex. 64; Tr. 97-98. Dr. Foley
himself sees 40-50 patients a week. Tr. 98. Petitioner offered Dr. Foley as an expert in the field of neurology with a
special concentration in multiple sclerosis, and he was admitted as such. Tr. 100.

2
On September 20, 2019, respondent filed responsive expert reports from Thomas
Forsthuber, M.D., 6 and Subramaniam Sriram, M.D. 7 Resp. Ex. A (ECF No. 34); Resp. Ex. B
(ECF No. 35). A Rule 5 status conference was held on October 23, 2019, and I ordered petitioner
to submit supplemental expert reports to better address the nature of multiple sclerosis in the
very rare tumefactive form, 8 the possible immune mechanisms, and the rapid timing of the
aggravation seen in this case. See Scheduling Order (ECF No. 38). On July 30, 2020, petitioner
filed an initial expert report from Lawrence Steinman, M.D. 9 Pet. Ex. 66 (ECF No. 50). On

6
Dr. Forsthuber is a Professor of Immunology at the University of Texas at San Antonio and an Adjunct Professor
of Pathology and Microbiology & Immunology at UT Health Sciences Center in San Antonio. Resp. Ex. C at 1
(ECF No. 37). He is board certified in Anatomical and Clinical Pathology. Tr. 437. He serves as the senior editor for
expert review in Clinical Immunology and is on the editorial board of several medical and scientific journals. Id. Dr.
Forsthuber graduated from medical school in Germany in 1986 and completed an internship in Medicine in 1987.
Resp. Ex. C at 2. In 1993, Dr. Forsthuber passed the United States Medical Licensing Examinations in Basic
Medical Sciences and Clinical Sciences. Id. In 1993, Dr. Forsthuber completed a postdoctoral fellowship in
immunology at the University of California, Los Angeles. Id.; see also Tr. 434-35. He passed his licensing
examination in 1995 and was issued a medical license in Ohio in 1996. Resp. Ex. C at 2. In 1998, he completed a
residency in pathology at the University Hospitals Cleveland. Id. at 3. He testified that his research focuses on
autoimmune diseases, particularly multiple sclerosis. Tr. 434-35. He also testified that he has published numerous
papers related to MS and experimental autoimmune encephalomyelitis (“EAE”). Respondent offered Dr. Forsthuber
as an expert in the field of immunology, and he was admitted as such. Id. at 439.
7
Dr. Sriram is board certified in Internal Medicine and Neurology. Resp. Ex. B at 1. He is Professor of
Experimental Neurology and Pathology, Microbiology, and Immunology at Vanderbilt University Medical Center.
Resp. Ex. D at 2. He also serves as Director of the Multiple Sclerosis Clinic at Vanderbilt, where he takes care of
over 1,200 patients in the outpatient clinic and 900 patients with MS. Id.; Tr. 318. He obtained a Bachelor of
Medicine and a Bachelor of Surgery from the University of Madras in Madras, India. Resp. Ex. D at 1. He
completed a residency in internal medicine at Wayne State University in 1976 and completed a residency in
neurology at Stanford University in 1979, where he also served as chief resident. Resp. Ex. D at 1. He went on to
complete a post-doctoral fellowship in neuroimmunology. Id. Dr. Sriram has published numerous peer-reviewed
medical articles regarding demyelinating diseases of the central nervous system. Id. at 9-19. Dr. Sriram testified that
he is board certified in internal medicine and neurology and continues to practice in the state of Tennessee. Tr. 317.
Respondent offered Dr. Sriram as an expert in the field of neurology and multiple sclerosis, and he was admitted as
such. Tr. 320.
8
The respondent filed a paper by Alghatani et al, entitled Tumefactive Demyelinating Lesions: A comprehensive
review. The article defined a tumefactive lesion as one that is an acute, large (greater than 2 cm), tumor-like
demyelinating lesion in the CNS that may occur with surrounding edema, mass effect and ring enhancement.
Hussein Algahtani et al., Tumefactive demyelinating lesions: A comprehensive review, 14 Multiple Sclerosis and
Related Disorders 72, 72 (2017); Resp. Ex. A-1 at 1 (ECF No. 34). It is a rare variant of MS occurring in an
estimated 1-3 per 100,000 cases of MS. Algahtani et al., supra, at 72; Resp. Ex A-1 at 1.
9
Dr. Lawrence Steinman is a Professor in the Departments of Neurology and Neurological Sciences and Pediatrics
and Genetics at Stanford University Medical Center. Pet. Ex. 67 at 1. Dr. Steinman received his undergraduate
degree from Dartmouth College in 1968 and graduated from Harvard University Medical School in 1973. Id. He
completed a residency in pediatrics in 1974 and a residency in pediatric and adult neurology in 1980, both at
Stanford University Hospital. Id. Dr. Steinman is board certified in Psychiatry and Neurology. Id. at 2. Dr. Steinman
has cared for adult and pediatric patients with various forms of inflammatory neuropathy, including, GBS,
transverse myelitis, acute disseminated encephalomyelitis, neuromyelitis optica and multiple sclerosis. Pet. Ex. 66 at
1. Additionally, Dr. Steinman has served on multiple National Institute of Health's (“NIH”) expert panels pertaining
to vaccination, including the Advisory Committee on Pertussis Immunization and the Immunological Sciences
Study Section. Id. at 2. Dr. Steinman was awarded the Charcot Prize for Lifetime Achievement in 2011 from the
International Federation of MS Societies for his work in multiple sclerosis research, and he was elected to the
National Academy of Sciences in 2015. Pet. Ex. 67 at 2. Dr. Steinman listed nearly 600 publications on his

3
September 21, 2020, respondent filed a supplemental expert report from Dr. Forsthuber. Resp.
Ex. E (ECF No. 51).

I held a status conference on November 23, 2020 and ordered the parties to find a
mutually agreeable time for an entitlement hearing in 2021 and to file supplemental reports from
Dr. Steinman and Dr. Forsthuber. ECF No. 54. I also ordered petitioner to file updated medical
records. Id. An Entitlement Hearing was set for October 27-29, 2021. See Hearing Order (ECF
No. 55).

On February 16, 2021, petitioner filed a supplemental expert report from Dr. Steinman.
Pet. Ex. 85 (ECF No. 60). Respondent filed a supplemental report from Dr. Forsthuber on March
31, 2021. Resp. Ex. F (ECF No. 61). In preparation for the entitlement hearing, petitioner filed
prehearing submissions on September 1, 2021, and October 13, 2021, and respondent filed his
prehearing submissions on September 27, 2021, and October 15. (ECF Nos. 66, 69, 76, 80).

An entitlement hearing was held on October 27-29, 2021 on Zoom with the Court sitting
in Annapolis, Maryland, the petitioner and counsel in the Salt Lake City, Utah area, respondent’s
counsel in Washington, D.C., and experts appearing from Salt Lake City, Utah, Palo Alto,
California, San Antonio, Texas and Nashville, Tennessee. Following the entitlement hearing,
petitioner filed a post hearing brief on February 28, 2022, and respondent filed his post hearing
brief on April 29, 2022. Pet. Post Hearing Brief (ECF No. 94); Resp. Post Hearing Brief (ECF
No. 95). Petitioner filed a post hearing brief reply on June 9, 2022. Pet. Post Hearing Reply (ECF
No. 100). Respondent filed a sur-reply on June 24, 2022. Resp. Sur-Reply (ECF No. 101). In
petitioner’s post hearing brief, a section was included to strike or otherwise discount Dr. Sriram’s
testimony based on his lack of credible testimony on his credentials. 10

The matter is now ripe for adjudication.

II. Legal Standard

curriculum vitae. Id. at 5-48. Additionally, Dr. Steinman has previously testified before the Vaccine Court as an
expert in neurology and neuroimmunology. Tr. 202-03. Petitioner offered Dr. Steinman as an expert in neurology
and neuroimmunology, particularly with regard to MS, and he was admitted as such. Id.at 203-04.
10
Citing to Contreras, petitioner argues that Dr. Sriram misrepresented his membership as a Fellow in the American
Academy of Neurology. See Pet. Post Hearing Brief at 9-12; Contreras v. Sec’y of Health & Hum. Servs., 116 Fed.
Cl. 472, 483 (Fed. Cl. 2014). Petitioner argues that the misrepresentation of his credentials calls into question the
credibility of his entire testimony, as “it is conceivable that Dr. Sriram would do the same on the important matters
regarding Mr. Gardner’s medical records.” Pet. Post Hearing Brief at 11-12. Respondent explained that Dr. Sriram is
in fact “a member of two professional neurological associations, the American Academy of Neurology and the
American Neurological Association.” Resp. Post Hearing Brief at 23. Dr. Sriram is a member of the American
Academy of Neurology and a Fellow of the American Neurological Association, his curriculum vitae contains that
correct information, and Dr. Sriram misspoke at the hearing. Id. at 24. Petitioner’s argument is completely
unpersuasive in the present case, as Dr. Sriram is a qualified expert to opine on the neurological theory in this case.
He is board-certified in Internal Medicine and Neurology. Resp. Ex. B at 1. He is Professor of Neurology and
Microbiology and Immunology and head of the Multiple Sclerosis (“MS”) Clinic at Vanderbilt Medical Center,
where he takes care of over 1,200 patients in the outpatient clinic, and 900 patients with MS. Id. Tr. 313, 318.
Therefore, he is qualified to opine on this case and his opinion will not be discounted based on a mere misstatement
during the entitlement hearing.

4
The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
300aa-10(a). “Congress designed the Vaccine Program to supplement the state law civil tort
system as a simple, fair, and expeditious means for compensating vaccine-related injured
persons. The Program was established to award ‘vaccine-injured persons quickly, easily, and
with certainty and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7
(1996) (quoting H.R. Rep. No. 908, at 3, reprinted in 1986 U.S.C.C.A.N. 6287, 6344).

A petitioner bears the burden of establishing his or her entitlement to compensation from
the Vaccine Program. The burden of proof is by a preponderance of the evidence. § 300aa-
13(a)(1). A petitioner may prevail by proving either that (1) the vaccinee suffered an injury listed
on the Vaccine Injury Table with onset beginning within a corresponding time period following
receipt of a corresponding vaccine (a “Table Injury”), for which causation is presumed or that (2)
the vaccinee suffered an injury that was actually caused by a vaccine. §300aa-11(c)(1)(C)(i-ii).
Under either method, however, the petitioner must also show that the vaccinee “suffered the
residual effects or complications of the illness, disability, injury, or condition for more than six
months after the administration of the vaccine.” § 300aa-11(c)(1)(D)(i).

In the present case, petitioner does not allege a Table injury. Instead, petitioner alleges that
he suffered an off-table significant aggravation of multiple sclerosis as a result of the flu
vaccination on December 1, 2014. Pet. Post-Hearing Brief at 1. Thus, petitioner bears the burden
of establishing actual causation.

The Vaccine Act defines significant aggravation as “any change for the worse in a
preexisting condition which results in markedly greater disability, pain, or illness accompanied
by substantial deterioration of health.” § 300aa-33(4). The United States Court of Federal
Claims established the governing six-part test for off-Table significant aggravations in Loving.
Petitioner must prove by a preponderance of the evidence:

(1) The person’s condition prior to administration of the vaccine, (2) the person’s
current condition (or the condition following the vaccination if that is also
pertinent), (3) whether the person’s current condition constitutes a ‘significant
aggravation’ of the person’s condition prior to vaccination, (4) a medical theory
causally connecting such a significantly worsened condition to the vaccination, (5)
a logical sequence of cause and effect showing that the vaccination was the reason
for the significant aggravation, and (6) a showing of a proximate temporal
relationship between the vaccination and the significant aggravation.

Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (2009); see also W.C. v. Sec’y of
Health & Human Servs., 704 F.3d 1352, 1357 (Fed. Cir. 2013) (adopting this test as the proper
legal standard for significant aggravation claims brought under the Vaccine Act). Loving prongs
four, five, and six are derived from the Federal Circuit’s test for off-Table actual causation cases.
See id. at 143; see also Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir.
2005).

The Federal Circuit clarified Loving prongs 3, 4, and 5 in Sharpe, further defining the
requirements for petitioners to successfully demonstrate a cause-in-fact significant aggravation
claim. Sharpe v. Sec’y of Health & Human Servs., 964 F.3d 1072 (Fed. Cir. 2020). Loving

5
prong three only requires a comparison of a petitioner’s current, post-vaccination condition with
his pre-existing pre-vaccination condition. Id. at 1082. A petitioner is not required to
demonstrate an expected outcome or that his post-vaccination condition was worse than such an
expected outcome. Id. at 1081.

Loving prong four requires petitioner to provide only a “medical theory causally
connecting [petitioner’s] significantly worsened condition to the vaccination.” Id. at 1083
(quoting Loving, 86 Fed. Cl. at 144). In other words, a petitioner is “required to present a
medically plausible theory demonstrating that a vaccine ‘can’ cause a significant worsening” of
the condition. Id. (citing Pafford ex. rel. Pafford v. Sec’y of Health & Human Servs., 451 F.3d
1352, 1356-57 (Fed. Cir. 2006)). A petitioner may be able to establish a prima facie case under
Loving prong four without eliminating a pre-existing condition as the cause of his significantly
aggravated injury. Id. (citing Walther v. Sec’y of Health & Human Servs., 485 F. 3d 1146, 1151
(Fed. Cir. 2007) (noting that “the government bears the burden of establishing alternative
causation . . . once petitioner has established a prima facie case”)).

Loving prong five requires a petitioner to show “a logical sequence of cause and effect
showing that the vaccination was the reason for the significant aggravation.” Id. at 1085 (quoting
Loving, 86 Fed. Cl. at 144). In other words, petitioner must show that the vaccination “did” cause
a worsening of petitioner’s underlying disorder. Id. “The sequence of cause and effect is usually
supported by facts derived from petitioner’s medical records. Althen, 418 F.3d at 1478; Andreu
v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1377 (Fed. Cir. 2009); Capizzano v. Sec’y of
Health & Human Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006). In determining causation, a
special master should consider the causation opinions of the treating providers as “treating
physicians are likely to be in the best position to determine whether ‘a logical sequence of cause
and effect shows that the vaccination was the reason for the injury’” Cappizano, 440 F.3d at
1280.

In determining whether a petitioner is entitled to compensation, a special master must
consider the entire record and is not bound by any particular piece of evidence. § 13(b)(1)
(stating that a special master is not bound by any “diagnosis, conclusion, judgment, test result,
report, or summary” contained in the record). Furthermore, a petitioner is not required to present
medical literature or epidemiological evidence to establish any Althen prong. The special master
essentially must weigh and evaluate opposing evidence in deciding whether a petitioner has met
his or her burden of proof. Andreu, 569 F.3d at 1380; see also Grant v. Sec’y of Health &
Human Servs., 956 F.2d 1144, 1149 (Fed. Cir. 1992).

In Vaccine Act cases, expert testimony may be evaluated according to the factors for
analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579,
594-96 (1993); see also Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339 (Fed.
Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999). In Vaccine Program cases, these factors are used in the weighing of the scientific
evidence actually proffered and heard. Davis v. Sec'y of Health & Human Servs., 94 Fed. Cl. 53,
66–67 (2010) (“uniquely in this Circuit, the Daubert factors have been employed also as an
acceptable evidentiary-gauging tool with respect to persuasiveness of expert testimony already
admitted”), aff'd, 420 F. App'x 973 (Fed. Cir. 2011). The flexible use of the Daubert factors to

6
determine the persuasiveness and/or reliability of expert testimony in Vaccine Program cases has
routinely been upheld. See, e.g., Snyder v. Sec'y of Health & Human Servs., 88 Fed. Cl. 706,
742-45 (2009).

Where both sides offer expert testimony, a special master's decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec'y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe v. Sec’y of Health & Human Servs., 219 F.3d 1357, 1362 (Fed. Cir. 2000)). However,
nothing requires the acceptance of an expert's conclusion “connected to existing data only by the
ipse dixit of the expert,” especially if “there is simply too great an analytical gap between the
data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner,
522 U.S. 146 (1997)). Weighing the relative persuasiveness of competing expert testimony
based on a particular expert's credibility is part of the overall reliability analysis to which special
masters must subject expert testimony in Vaccine Program cases. Moberly v. Sec’y of Health &
Hum. Servs., 592 F.3d 1315, 1325-26 (Fed. Cir. 2010) (“[a]ssessments as to the reliability of
expert testimony often turn on credibility determinations”); see also Porter v. Sec'y of Health &
Human Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court has unambiguously explained
that special masters are expected to consider the credibility of expert witnesses in evaluating
petitions for compensation under the Vaccine Act”).

Close calls regarding causation must be resolved in favor of the petitioner. Althen, 418
F.3d at 1280 (holding that Congress created a system in which “close calls regarding causation
are resolved in favor of injured claimants”); Knudsen v. Sec’y of Health & Human Servs., 35
F.3d 543, 551 (Fed. Cir. 1994) (“If the evidence [on alternative cause] is seen in equipoise, then
the government has failed in its burden of persuasion and compensation must be awarded.”).

III. Summary of Relevant Facts

A. Prior Medical History before the December 1, 2014, Vaccination

On November 16, 2010, petitioner underwent an annual physical examination and
petitioner’s primary care physician (“PCP”), Dr. John Richards, wrote, “1. Last tetanus shot was
more than 10 years ago. Did get a flu shot.” Pet. Ex. 4 at 3. Petitioner testified during the
entitlement hearing that he did not regularly get an annual flu shot, but that he had received one
“four or five years, six years, [before this one] something like that.” Tr. 59. After some
discussion during the hearing, the undersigned stated that “… it’s not completely definitive and,
if that flu shot was the one that was primarily at issue in this case, we might look…for a more
definitive record.” Id. at 432. On further review of the record from the November 2010 physical,
it appears that petitioner’s PCP asked about the tetanus and flu vaccines and administered the
tetanus vaccination. Pet. Ex. 4 at 3-4. As the flu shot is an annual shot, it is most likely that Mr.
Gardner was would have also received the flu vaccine, if he had not yet received it that year.
This would also be consistent with petitioner’s recollection that he had received the flu vaccine
several years before. See Tr. 59. As such, the undersigned has determined that “more likely than
not [petitioner] did receive the flu shot in [2010].” Id. at 433.

7
Petitioner lives in Utah with his wife, Kim Gardner and their three children, and he holds
both a bachelor’s degree and master’s degree in music. Pet. Affidavit (“Aff.”) ¶ 3 (ECF No. 1).
Mr. Gardner was 37 years old at the time of the 2014 vaccination. Pet. Ex. 4 at 7. Petitioner was
working as a store manager for a local restaurant. Pet. Aff. ¶ 4. Other than as described below,
petitioner had no disability prior to the vaccination. He testified that he was able to walk, run,
play with his kids, engage in athletics, coach his children’s sports teams, and lift things at work.
Tr. 92-93.

On June 13, 2014, petitioner sought vision care from an optometrist at Riverton Family
Eye care for changes to his vision, including “cloudy [or] dim” vision in his left eye. Pet. Ex. 2 at
1-6. Petitioner was diagnosed with rhegmatogenous retinal detachment 11 and ser-ous retinal
detachment 12 and was referred to the University of Utah Moran Eye Center. Id. at 3. Dr. Trent
Richards, an ophthalmologist at the Moran Eye Center, noted that petitioner continued to have
blurred vision in his left eye that began on or about June 11, 2014 and progressed with “some
pain when looking all the way to one side or the other.” Pet. Ex. 3 at 1. Dr. Richards noted that
petitioner had “been completely healthy,” other than the blurry vision, and a dilated fundoscopic
examination revealed left eye optic neuritis. Id. at 2.

On June 13, 2014, petitioner underwent an MRI of the brain which was “unremarkable
with no stigmata of MS [but] consistent with left-sided optic neuritis.” Pet. Ex. 3 at 3. On August
5, 2014, petitioner followed up with Dr. Judith Warner, a neuro-ophthalmologist at the Moran
Eye Center. Id. at 8-9. Petitioner noted that there had been “some improvement of the vision”
over the last six weeks. Dr. Warner personally reviewed his MRI and, in an addendum to her
report, she noted that there was no evidence of demyelination but there was enhancement at the
globe of the optic nerve. Id. Dr. Warner added that “his Aquaporin receptor antibody was
negative, arguing against neuromyelitis optica…however, his ANA was positive with the Slc-70
also positive.” Id. Petitioner elected to receive a course of IV steroids and was advised to follow
up with Dr. Warner in one month. Id.

At his December 1, 2014 physical examination, petitioner told Dr. Richards, “in the last
week his left leg, mostly on his foot but up to his lower left abdomen-feels almost like it has pins
and needles. Comes and goes and nothing seems to make it worse. First time he felt it as a heat
sensation on his anterior left thigh.” Pet. Ex. 4 at 6. This is consistent with the history petitioner
provided when he was admitted to Intermountain Medical Center on December 12, 2014, where
he noted that, “around November of [2014], he began having parasthesias and numbness on his
left leg” Pet. Ex. 11 at 8. At a later appointment on January 19, 2015, petitioner reported that he
first noticed tingling in his left leg in August of 2014 and noticed cognitive changes, including
difficulty with word finding, in September 2014. Pet. Ex. 6 at 2. However, there were no
contemporaneous medical appointments between August and December 2014 discussing these

11
Rhegmatogenous retinal detachment is the most common form of retinal detachment. Types and Causes of Retinal
Detachment, National Eye Institute (Dec. 23, 2020), https://www nei.nih.gov/learn-about-eye-health/eye-conditions-
and-diseases/retinal-detachment/types-and-causes-retinal-detachment.
12
I can find no definition for the term “ser-ous retinal detachment,” and, as such, conclude that it may be a typo for
“serious.” However, as mention of retinal detachment is not made again upon subsequent eye examinations by
ophthalmologists at the University of Utah Moran Eye Center, I conclude that the optician’s diagnosis of retinal tear,
which he said was hard to see, was probably in error.

8
issues. During that time, petitioner continued to work a full-time job, was active with musical
groups, and played actively with his children. Tr. 7-8.

B. December 1, 2014 – December 9, 2014

On December 1, 2014, petitioner presented to his PCP, Dr. John Richards, for a physical
examination. Pet. Ex. 4 at 6. He went for a physical because his wife’s company was providing
incentives for employees and their families to have annual physicals. Tr. 40. Petitioner noted
that “in the last week his left leg, mostly in his feet but up to his lower left abdomen – feels
almost like it has pins and needles.” Pet. Ex. 4 at 6. He reported that there was a “heat sensation
on the anterior left thigh” when he first felt it and that the feeling comes and goes. Id. Petitioner
also informed Dr. Richards that his uncle had recently been diagnosed with MS. Id. Petitioner
received the flu vaccine at this appointment., Id. Dr. Richards performed a complete physical
exam and noted full range of motion in ankles, knees, back, shoulders and elbows. Vision was
good and extraocular muscles appeared normal. Id.

Mrs. Gardner testified that “between the December 1, visit and the December 10 visit,
things started to get worse fast…[petitioner] had the weird muscle spasms, seizure thing,
couldn’t get warm, and then his leg started to get a lot worse…it started to go numb. He wasn’t
getting better.” Tr. 15. Petitioner testified that he was in training at work and on his feet and his
right leg stopped working “basically at my ankle. But it didn’t stop me from going to work and
standing on my feet. It didn’t stop me from driving to work.” Tr. 59. He testified that, after a
few days, his right leg stopped responding, and he thought he might have had a pinched nerve.
Id. On December 7, 2014, petitioner called into work and told them he was sick, as he was
“feeling extremely cold and achy and [he] was barely able to use [his] right leg.” Pet. Aff. ¶ 5.
The progress notes from Wednesday, December 10, 2014, stated that “this last Monday he came
in for his blood tests, when the [medical assistant] noticed he was having difficulty walking and
set him up to see me today. His right leg has felt worse since Monday. While standing there he
can hardly lift his right leg up. His memory has not been as good as it has been, and his brain
feels ‘foggy.’ ” Pet. Ex. 4 at 9. While there was some dispute as to whether the notation of “this
last Monday,” referred to the Monday before the December 10 appointment, December 8, or
whether it referred to the original December 1, appointment, the undersigned concluded that the
reference to “this last Monday” refers to December 8, 2014. Tr. 428. While there was no record
of the blood work filed, the fact that Dr. Richards did a full physical exam, as described above,
with no notation of trouble walking or weakness in the right leg on December 1, and that the
December 10, note used the phrase “this last Monday” (emphasis added) when referring to the
blood draw appointment when the medical assistant noticed that he was having trouble walking
and set up the December 10 appointment, the context strongly supports the reference to the date
of the blood draw as being December 8, 2014.

C. December 10, 2014: return to PCP

On December 10, 2014, ten (10) days after the flu vaccination, petitioner returned to Dr.
Richards, reporting “tingling” in his left side and on the left side of his abdomen that “started a
couple weeks ago and is still present.” Pet. Ex. 4 at 9. He stated that his “skin was burning
and…did not have any strength in [his] right leg and…had a sudden limp.” Pet. Aff. ¶ 6.

9
Petitioner also noted “trouble walking” and that 2-3 days following the December 1, 2014 visit,
his right leg “stopped working [and went] intensely numb, including his whole thigh and leg
from the foot to the bottom of his right chest.” Pet. Ex. 4 at 9. Petitioner noted his brain felt
“foggy.” Id. Dr. Richards found that petitioner’s muscles in his right leg were significantly
weaker than the left and he continued to have difficulty walking. Id. Mr. Gardner testified that he
did not have any bowel or bladder problems until the day he went into the hospital. Tr. 61. None
were noted in the medical record before that date.

D. December 12, 2014: Intermountain Medical Center Emergency Room and admission
to the hospital.

On December 12, 2014, petitioner presented to Intermountain Medical Center Emergency
Room when he lost his ability to walk and “completely lost the use of [his] right leg…[and]
could not control [his] bladder or…bowels.” Pet. Ex. 5 at 14; Pet. Aff. ¶ 7. He and his wife
testified that he could not urinate at all on the morning of December 12. Petitioner’s wife
testified that she had to go into work that day, and, when she left, petitioner had crawled into the
bathroom. Tr. 18. However, when she returned about an hour and a half later, petitioner was still
in the floor and was unable to move. Id. Mrs. Gardner testified that, at this point, she became
scared and dragged him down the steps and got him into the car to go to the hospital. Id. She
decided to go straight to Intermountain Medical Center where there would be neurologists, as
they had been having a hard time finding one since he saw Dr. Richards on December 10, 2014.
Id. Petitioner was admitted to Intermountain Medical Center through the emergency room by
neurologist Dr. Huan on December 12, 2014. Dr. Huan noted the past diagnosis of optic neuritis.
She also noted that petitioner had some paresthesias and numbness on his left leg but no
weakness around November. She described the f1u shot that he received 2 weeks prior to his
presentation to the hospital. Pet. Ex. 17 at 1.

The neurologic examination revealed a left afferent pupillary defect. Both pupils were
reactive, and petitioner had decreased visual field on the peripheral of the right eye and the left
lower quadrant of the left eye. Id. at 2. The lower extremity exam showed that petitioner was
“completely plegic with no movement at all in the right leg” and had normal movement in the
left leg. Id. He had a T4-5 sensory level bilaterally, with elevated tone on the right. His strength
in the arms was 5/5 with normal bulk. He had no sensory loss in the arms. Id. The diagnosis was
“new onset myelopathy symptoms with right 1eg plegia and T5 sensory level along with new
symptom of right likely right optic neuritis.” Id. Petitioner also had “mild cognitive complaints”
at that time. Id. Overall, Dr. Huan felt petitioner’s symptoms were “suggestive of a
demyelinating process.” She ordered MRIs and other testing. Id.

After admission, petitioner underwent a brain MRI which revealed a peripherally
enhancing intra-axial lesion centered in the left anterior temporal lobe, which was a “prominently
T1 hypointense, T2 hyperintense, and somewhat heterogeneously FLAIR hyperintense intra-
axial lesion.” Pet. Ex. 17 at 12. The lesion demonstrated “prominent nearly complete peripheral
enhancement, measuring 4.6 x 4.2 x 3.8 cm in AP, craniocaudal and transverse dimensions
respectively.” Id. A “very thin rim of surrounding parenchymal T2 and FLAIR hyperintense
vasogenic edema” was demonstrated. Id. at 13. The radiologist interpreting the study noted that

10
“the appearance was most typical of active tumefactive demyelinating disease involvement.” Id.
There was age-appropriate cerebral volume. Id.

Petitioner also underwent a cervical spine MRI which revealed a prominent abnormal
signal change and C6-T1 cord expansion with prominent enhancement at C7 to T1. Pet. Ex. 5 at
20-21.
The radiologist’s impression was as follows:

Given the prior left optic neuritis, current right optic neuritis, the large peripherally
enhancing left anterior temporal lobe lesion, and the prominent fairly diffusely
enhancing T2 [hyperintense] lesion in the cord at C7 and T1 on accompanying
cervical and thoracic spine MRI exams and given previously negative workup for
neuromyelitis optica and history of recent immunization, differential diagnosis
would first include acute disseminating encephalomyelitis with transverse myelitis.
[Neuromyelitis optica] would still be of consideration, as well as multiple sclerosis
and viral myelitis.

Id. at 16. On December 12, 2014, petitioner was admitted with possible problems including
“probable multiple sclerosis [and] history of optic neuritis.” Pet. Ex. 5 at 113. The assessment
included “nearly definite multiple sclerosis.” Id. at 114. On December 14, 2014, petitioner
underwent a lumbar puncture which showed two white blood cells, an elevated myelin basic
protein, and no oligoclonal bands. Id. at 146, 161. Petitioner was discharged from the hospital to
Intermountain Medical Rehabilitation Center on December 16, 2014, with diagnoses including
multiple sclerosis, optic neuritis, and urinary retention. Id. at 161, 199. The discharge summary
noted that petitioner had received a three-day course of intravenous steroids and had “no
improvement.” Id. at 161.

E. Medical Records from December 2014 through 2016

On December 22, 2014, petitioner underwent a follow-up brain and cervical spine MRI.
Pet. Ex. 5 at 319-22. The brain MRI continued to demonstrate the inferior left temporal lobe T1
hypointense and T2 hyperintense lesions which measured approximately 4.4 x 4.2 x 2.8 cms.
Since the prior exam, there was significantly decreased edema associated with this lesion. The
enhancement had also minimally decreased particularly within the more posterior left temporal
lobe. The radiologist indicated that these findings are consistent with tumefactive multiple
sclerosis with mild treatment response. Id. at 320.

The brain MRI also showed a mild enhancement of the right infraorbital optic nerve, and
a mild asymmetric atrophy of the right infraorbital optic nerve. Id. The cervical MRI showed an
enhancing intramedullary lesion extending from the inferior endplate of C6 now extending
through the mid-T2 vertebrae. Id. at 322. There was now a T2 hyperintense signal in the central
gray matter pattern on the axial view. The lesion was slightly asymmetric to the right, similar to
the prior MRI. Id. The findings were consistent with the progression of disease. Id. In his
affidavit Mr. Gardner recounted that, during his hospitalization, he was seeing physical
therapists, occupational therapists, speech pathologists, psychologists, neurologists and countless
nurses. Aff. ¶ 8-11. While in rehabilitation, his condition worsened with essentially complete

11
paralysis of the right leg and new onset weakness in the left leg. Tr. 120-21. He also developed
additional cognitive deficits and speech problems with continued bowel and bladder
incontinence. See Pet. Ex. 327.

Petitioner was ultimately discharged from the Intermountain Medical Rehabilitation
Center on January 9, 2015 and required stand-by assistance with activities of daily living at home
(“ADLs”). He required assistance with complex tasks. Pet. Ex. 5 at 631-633. His discharge
diagnoses were MS, lower extremity paraplegia, T4 sensory level, optic neuritis, cognitive
deficits, urinary retention, constipation, and urinary tract infection. Id. at 631. Mrs. Gardner
testified that upon discharge from the rehabilitation hospital “he [couldn’t] move his legs…he
[couldn’t] remember anything.” Tr. 22.

On January 19, 2015, petitioner presented to neurologist, Dr. John Foley, the Director of
the Rocky Mountain Multiple Sclerosis Clinic. Pet. Ex. 6 at 1. Dr. Foley recorded an extensive
history and noted the petitioner’s optical symptoms began on June 11, 2014, when he was
diagnosed with left optic neuritis. Id. By August 2014, petitioner noticed tingling in his left leg
that lasted for several months, and by September 2014, petitioner started to notice cognitive
changes such as “difficulty finding words.” Id. at 1-2. Dr. Foley noted that, within a day or two
of petitioner receiving the flu vaccination in question, he “became ill with nausea and flu-like
symptoms requiring him to take a day off from work.” Id. He called in sick on December 7, 2014
seven days after the vaccination. Pet. Aff. ¶ 5. Within 1 or 2 days more, petitioner was
experiencing “increased cognitive difficulties, right blurred vision, persistent left leg numbness
and paresthesia, and new right lower extremity weakness as well as urinary retention.” Pet. Ex. 6
at 2. Dr. Foley conducted a full examination which showed that petitioner had mild weakness in
his upper extremities, with a lower extremity strength of 0/5. Id. at 3. He noted that petitioner
had received three days of IV steroids and a lumbar puncture that revealed no oligoclonal bands.
The only abnormality was elevated myelin basic protein at 423. Id. at 2. While in rehab his
symptoms worsened and in addition to his right lower extremity plegia, he began to note new left
lower extremity weakness. Id. Dr. Foley’s note reported significantly increased edema with
minimally decreased enhancement of the left temporal lobe lesion. The spinal lesion showed
some progression from C6-T1 to C6-T2 on the repeat scan with enhancement. Id. He received
five days of plasmapheresis from December 27 – 31, 2014. and reported no improvement in leg
function two days after completion. Id. He presented to the MS Clinic in a wheelchair, reporting
some improvement in lower extremity movement in his toes and feet. His symptom profile over
the last 30 days included severe bladder dysfunction requiring daily self cathing 4 times daily,
sexual dysfunction, moderate fatigue, muscle weakness, muscle spasm, cognitive dysfunction,
imbalance and bowel dysfunction including constipation and mild blurred vision with slurred
speech occurring with increased fatigue. The hospital records documented a T4 sensory level.
He reported normal visual acuity with persistent blurred left peripheral vision. Id. The receipt of
the flu vaccine on December 1, was reported as part of the complete medical chronology. Id.

Dr. Foley ordered repeat MRIs of the brain, the cervical spine, and the thoracic spine,
along with additional blood tests. Id. at 4. At that time, he concluded that petitioner demonstrated
“subacute disseminated encephalomyelitis secondary to flu vaccine.” Id.

12
Forty-five days after the initial MRIs petitioner underwent another MRI of the cervical
spine and brain on January 26, 2015. Pet. Ex. 6 at 6. The cervical spine MRI revealed “mild
fusiform cord lesion from C6-T2 with mild residual post-contrast enhancement but no cord
expansion,” which was similar to the December 2014 MRI. Id. The brain MRI showed “large left
temporal lobe area of white matter T2 signal hyperintensity, with significant interval decrease in
the degree of postcontrast enhancement, only mild residual, and with complete interval
resolution of the previously demonstrated associated edema and mass effect, in fact, there now
appears to be slight volume loss.” Id. at 11-12. Additionally, “the previously suggested changes
of the optic nerves are again noted but less prominent.” Id. at 12.

Dr. Foley referred petitioner to Mountain Land Physical Therapy and Rehabilitation
where he underwent a physical therapy evaluation for paraplegia due to “subacute disseminated
encephalomyelitis.” Pet. Ex. 7 at 8. Petitioner stated that in “February 2015, [he] was able to
stand for short periods with a walker. For the first time in months, [he] was able to crawl upstairs
to get to [his] bedroom and [he] was able to sleep in [his] own bed.” Pet. Aff. ¶ 12. The
examination “revealed decreased lower extremity strength, functional mobility and stability,
which is consistent with impairments associated with MS.” Pet. Ex. 7 at 9. Petitioner attended a
total of 18 physical therapy sessions, ending on May 14, 2015, when the physical therapist noted
that petitioner was “very functional in all his ADLs.” Id. at 43.

Petitioner returned to Dr. Foley on March 9, 2015, and while he reported some
improvement in his strength, he was only able to take steps with his walker, primarily used his
wheelchair at home, and his gait remained restricted. Pet. Ex. 6 at 24. Dr. Foley noted that
petitioner’s “spinal cord disease clearly was related to his flu shot. This generated massive
inflammation at the level of the lower cervical and upper thoracic spine with grossly enhancing
lesion in the left temporal lobe consistent with ADEM post vac[cination] and recrudescence of
probable multiple sclerosis.” Id. at 24. Petitioner also reviewed all the written materials regarding
Tysabri 13 and wished to proceed with the treatment. Id.

During a May 19, 2015, visit with Dr. Foley, he noted that while petitioner’s “clinical
status since beginning Tysabri [was] markedly improved,” he tested positive for neutralizing
antibodies and suffered from an allergic reaction to the infusion on April 6, 2015, and Dr. Foley
concluded that “he is not a good candidate for retrial with Tysabri” on September 10, 2015. Id. at
28-30. During the physical exam, petitioner had full strength in all extremities and was able to
ambulate 500 feet unassisted. Id. Due to his hospitalization and ongoing weakness petitioner was
unable to “work from December 6, 2014, through May 2015,” and he returned to work on May
27, 2015. Pet. Aff. ¶ 14. Petitioner testified that when he returned to work, he was “sensitive to
heat,” his eyesight felt “as if somebody smears Vaseline on eyeglasses,” and he is “constantly in
pain.” Tr. 47-48. Further, he stated that he had other issues such as “keeping [his] balance,” and
feeling “tired.” Id. at 48.

13
Tysabri is an immunomodulator, which stops certain cells of the immune system from reaching the brain and
spinal cord and causing damage. Tysabri treatment protocol includes a one hour infusion, once a month.
(https://www.tysabri.com/).

13
On August 21, 2015, petitioner returned to Dr. Foley with complaints of “moderate
fatigue…mild muscle spasms…mild memory/thought process deficits, mild imbalance, mild
pain, moderate loss of vision…moderate blurred vision, mild bladder dysfunction, mild bowel
dysfunction, mild sexual dysfunction, mild heat sensitivity.” Pet. Ex. 6 at 33. The impression
included “[relapsing remitting multiple sclerosis] RRMS,” and recommendations to undergo
“neurocognitive testing [and] ophthalmologist visit to delineate vision loss.” Id. at 34.

Petitioner returned to Dr. Foley’s office on August 26, 2015, reporting that two weeks
earlier a relapse began with vision loss, and ongoing complaints of mild memory/thought process
deficits, mild numbness and muscle spasms, mild loss of vision and vision loss, and mild bowel
and bladder dysfunction. Pet. Ex. 6 at 36. Under “impression,” it noted “RRMS with relapse
including bilateral visual field defects,” and the plan included “IVSM [intravenous Solu-Medrol]
x 3 here starting today, [follow-up] with Dr. Warner 14 at Moran.” Id. at 37. Petitioner was
“forced to quit [his] job in August 2015 because of the inability to perform simple tasks, and
because [he] had suddenly lost vision in both eyes.” Pet. Aff. ¶ 16.

On September 9, 2015, petitioner returned to see Dr. Foley and reported that his “vision
is getting worse.” Pet. Ex. 6 at 46. The plan included adding two more days of IVSM via home
health and the infusion clinic, and to follow up with Dr. Foley regarding disease-modifying
therapy (“DMT”) and a follow-up visit with Dr. Warner. Id. at 46-47. The next day petitioner
presented to ophthalmologist, Dr. Jean Tabin, a colleague of Dr. Warner, at the Moran Eye
Center with complaints of “decreased visual acuity.” Pet. Ex. 3 at 15. Petitioner noted that his
vision “has gone dark…and getting worse every day.” Id. Dr. Tabin concluded that petitioner
demonstrated “left homonymous bilateral field defects in visual field, 15 …relapsing remitting
multiple sclerosis [history of] optic neuritis OS (left eye), possible parenchymal MS lesion.” Id.
at 17. Petitioner was also referred to “neuro-ophthalmology for a second opinion [and an] MRI.”
Id. The same day petitioner revisited with Dr. Foley to discuss “therapeutic options,” because
petitioner had “over the month of August [2015]…developed profound optic neuritis [in both
eyes].” Pet. Ex. 6 at 49-50. Dr. Foley recommended against Tysabri based on the previous
allergic reaction, and to try Tecfidera or a “trial of Rituxan off label as well.” Id. at 50. Petitioner
underwent a brain MRI on September 14, 2015, which found,

The large areas of T2 signal hyperintensity and rim-like enhancement most
consistent with new large areas of demyelinating disease involving the right
parieto-occipital periventricular white matter and left frontal lobe with a small area
of paramedian anterior left parietal vertex involvement as well. Findings consistent
with active demyelination. Left temporal lesions has improved and shows no
significant enhancement on today’s study.

Pet. Ex. 8 at 1. Mr. Gardner also had a cervical-thoracic spine MRI performed on the same day.
The radiologist noted that there was “ill-defined abnormal T2 and STIR hyperintensity in the

14
Dr. Warner is a Neuro-opthalmologist with a practice at John A. Moran Eye Center at the University of Utah.
15
Homonymous hemianopsia is defective vision or blindness in half of the visual field affecting the right halves or
the left halves of the visual fields in both eyes. Dorland’s Illustrated Medical Dictionary (33d ed. 2020).

14
lower cervical and upper thoracic cord from C6 to T2.” Id. at 3. There was no abnormal contrast
enhancement. The expansion seen in 2014 was no longer present and there is probably mild
atrophy in the cord at these levels. Id.

On September 29, 2015, about ten months after the beginning of the major event,
petitioner was again seen by Dr. Warner. Pet. Ex. 13 at 38. Dr. Warner noted a history of optic
neuritis in petitioner’s left eye, which began in June 2014, and in late July “sudden vision loss
left eye, no eye pain, then right eye vision loss with no pain, then flare up of memory loss,
speech problems, bowel problems, weakness in his legs but not as severe as in December.” Id. at
39. She added that petitioner’s “vision has not changed, cannot see with his left eye; vision [in]
right eye came back but not to the baseline…overall getting better but very slow.” Id.

Petitioner returned to Dr. Warner on November 10, 2015. She noted, “following
aggressive treatment of his demyelinating disease his vision had improved to 20/20.” Pet. Ex. 3
at 42. Dr. Warner noted that he had received “weekly IV methylprednisolone for 4 weeks.” Id.
Petitioner returned to Dr. Foley the next day, on November 11, 2015, and Dr. Foley’s impression
included “RRMS [Relapsing Remitting Multiple Sclerosis] on Tecfidera full dose 240 mg 1 po
BID x 3 16 months and is feeling better. He received multiple doses of IVSM – 3 in August, 2 in
September and 3 in October…continue Tecfidera and recheck blood tests in 3 months…schedule
follow-up in 3 months.” Pet. Ex. 6 at 52. On January 20, 2016, petitioner returned to Dr. Foley,
who classified his condition as “relatively stable,” and petitioner complained of “difficulty with
visual acuity primarily in the lower half of his left eye visual field…[and] fairly significant
cognitive decline.” Id. at 59.

On March 15, 2016, petitioner returned for a follow-up to neuro-ophthalmologist Dr.
Warner. Pet. Ex. 3 at 61. Dr. Warner noted that his vision had improved “slightly.” He continued
to have a defect on his left eye, but the homonymous hemianopia had nearly resolved. Id.
Petitioner returned to Dr. Foley on July 27, 2016, with concerns about his short-term memory
loss, with a note that the Tecfidera treatment was going well. Pet. Ex. 6 at 62.

F. April 2017 – August 2021: Subsequent Course Including Follow-up imaging.

Petitioner returned to Dr. Foley eight months later, on March 27, 2017, and reported no
major relapses. Pet. Ex. 6 at 69. Further, Dr. Foley’s impression remained “presumed MS,” with
the “possibility of ADEM appear[ing] less likely given the relapse.” Id. at 71. Repeat brain and
cervical spine MRIs were performed on April 3, 2017. Pet. Ex. 8 at 3-8. The brain MRI
demonstrated improvement “since 9/14/2015. Id. A very large, tumefactive area of T2 and
FLAIR signal abnormality in the left frontal lobe seen on 9/14/2015 has decreased significantly
in size, previously measuring over 6 cm in AP diameter, and currently measuring about 4.1 cm.”
Id. at 6. The radiologist concluded, “findings presumably representing tumefactive plaque, with
interval improvement,” with “new increased signal intensity with associated volume loss in the
anterior body of the corpus callosum which is felt to represent Wallerian degeneration related to
the large left frontal lobe lesion.” Id. at 7-8.

16
This abbreviation means one by mouth. two times a day for three months.

15
The cervical spine MRI demonstrated “abnormal T2 and STIR hyperintensity in the
lower cervical and upper thoracic cord [which] is again seen, but is quite ill-defined currently.”
Id. at. 4. Further, there was “no definite new signal abnormality nor abnormal contrast
enhancement in the cervical cord.” Id.

On April 5, 2018, petitioner had follow-up MRIs which were compared to the April 3,
2017 MRIs. See Pet. Ex. 18. The brain MRI demonstrated “mild cerebral atrophy for the age of
40 [and] multiple lesions compatible with multiple sclerosis.” Id. at 2. The MRI of the cervical
spine demonstrated “marked abnormal myelomalacia 17 of the cervical spinal cord beginning at
the mid C6 level [with] thinning of the cervical spinal cord, the size of the lesions has increased
when compared to prior examination of one June 2015.” Id. at 4.

Later that month, on April 17, 2018, petitioner returned to Dr. Foley with complaints of
worsening memory, “word finding difficulty, articulation…difficulty understanding instructions
and recall of information. Learning new things can be difficult…episode of bilateral vision loss
for several weeks, had to quit his job.” Pet. Ex. 14 at 14. Petitioner continued “to have right sided
warm, burning pain, constantly present, worse in evenings…generally weak [and] unable to
build muscle bulk.” Id.

At the time of filing of petitioner’s affidavit, petitioner stated that he “had less endurance,
less coordination…difficulty multitasking, and problems with both [his] short and long-term
memory and [he had] trouble recalling words.” Pet. Aff. ¶ 16.

Petitioner returned to Dr. Foley on July 10, 2018, where he recommended new MS
medications including Ocrevus and Gilenya. Pet. Ex. 14 at 18. Dr. Foley noted that petitioner felt
that “his neurological status is declining over time and recognizes the need for an effective DMT
[disease modifying therapy].” Id. Petitioner returned to Dr. Foley for a follow-up on October 2,
2018 with complaints of “some weakness, cognitive dysfunction and fatigue [and] some bowel
and bladder dysfunction.” Id. at 21. Petitioner also noted that he recently tried weightlifting
which “caused severe weakness and fatigue for several days…he does some light walking for
exercise now.” Id. Petitioner had started on Gilenya and “tolerated first dose well.” Id.

On November 13, 2018, petitioner had a follow-up appointment with Dr. Foley. In the
“History of Present Illness” section of the record, Dr. Foley wrote, “[ petitioner] returned to work
in June 2015 but was unable to complete the job and in August to September 2015 he developed
a large central scotomata bilaterally in his primary field of vision [and] was unable to continue
work. He was on disability until September 2017 when Social Security felt he was able to return
to work…he then attempted to return to work and in September 2017 noted onset of significant
cognitive impairment.” Id. He is now not working and disabled but not recognized by SS [social
security].” Id. at 24. Under “Impression,” Dr. Foley wrote:

multiple sclerosis with significant exacerbation immediately following influenza
vaccine…at the present time he is 100% disabled primarily at this point secondary
to cognitive dysfunction…his symptomatology is directly related to the influenza
vaccine he received. He likely did have a propensity for underlying multiple

17
Myelomalacia is morbid softening of the spinal cord. Dorland’s Illustrated Medical Dictionary (33d ed. 2020).

16
sclerosis which was severely exacerbated by the influenza injection. He likely
would’ve had a significantly more benign course to his MS had he not received the
influenza vaccine.

Id. at 26.

On November 30, 2018, petitioner presented to Becky Bailey, PhD, for a
neuropsychological examination. Pet. Ex. 95. Dr. Bailey noted that his “current MS symptoms
included continued incontinence, chronic right-leg nerve pain, memory loss, speech dysfunction
(e.g., word finding problems), and vision problems.” Id. at 4. The diagnostic impression included
“a number of areas of cognitive weakness (motor, processing speed, verbal fluency, auditory
learning, multitasking), but one of the most disabling areas of concern is his loss of social skills
and ability to read others.” Id. at 8. Additionally, petitioner “demonstrates executive function
difficulties involved in carrying out planned behavior quickly, effectively and efficiently as well
as likely organic apathy.” Id. Dr. Bailey also documented mild to moderate impairment in
memory, significant depression and difficulty learning new things which likely resulted in the
loss of a job at the VA which he had held for just four months. Id.

Petitioner returned to Dr. Foley on January 20, 2020, for “MS follow-up.” Pet. Ex. 96 at
9. Petitioner continues to complain “of the right lower extremity weakness, difficulty with
learning and memory and loss of vision involving the left eye lower half of his visual field…he
remains 100% disabled. He also remains on Gilenya every other day.” Id. Further, Dr. Foley
noted that petitioner has “relatively stable symptomatology post ADEM with the cord
involvement…he does have significant cognitive dysfunction, motor dysfunction, and
hyperesthesia of the right leg together with persistent visual field loss OS [left eye].” Id. at 11.

Follow-up brain and cervical spine MRIs were conducted on August 26, 2020. See Pet.
Ex. 96. The brain MRI demonstrated that the “demyelinating brain lesions have not significantly
changed when compared to prior examination but continued to demonstrate demyelination in the
left anterior frontal lobe, left anterior parietal lobe and right-side white matter.” Id. at 43. The
cervical spine MRI demonstrated “unchanged appearance of the demyelinating cervical spinal
cord lesion without convincing new or enhancing lesions.” Id. at 42. The cervical and thoracic
MRI confirmed an unchanged long segment of chronic demyelination from C6 to T3-4. Id at 44.
On September 22, 2020, petitioner returned to Dr. Foley and was noted to be “relatively
stable…[but] continues to have difficulty with cognitive issues.” Id. at 6. Dr. Foley wrote that
petitioner has a “history of clear-cut optic neuritis followed by an acute disseminated
encephalomyelitis-type event. He did have subsequent bilateral optic neuritis a few months later.
It remains unclear whether this is residual ADEM or continuing MS.” Id. at 8.

In March 2021, petitioner returned to Dr. Foley for a telehealth consultation with
complaints of “right sided abdominal pain that moves down into his leg periodically…blurred
vision and difficulty concentrating…vision loss in the left inferior lateral visual field.” Pet. Ex.
96 at 4. Dr. Foley recommended remaining “off of DMT 18 for now [and] wait[in] to receive
COVID-19 vaccine until more information is available.” Id. at 5. In August 2021, petitioner
returned to Dr. Foley, and he wrote that petitioner has “significant residual neurological

18
DMT is disease modifying therapy.

17
compromise. due to his post axonal ADEM/MS.” Id. at 1. Dr. Foley’s impression was
“significant residual from acute disseminated encephalomyelitis with extensive involvement in
the cervical and thoracic spinal cord.” Id. at 3.

Mrs. Gardner testified that her husband’s “most common relapse symptoms include
fatigue…hard time moving his legs…bowels are a constant issue.” Tr. 32. At the hearing,
petitioner testified that he was still experiencing leg and hip pain “every day,” along with
cognitive problems, memory problems, and brain fog. Tr. 81. He explained that brain fog means
he “start[s] a sentence with the intention of including one particular word, and if I don’t use the
word quickly enough at the beginning of the sentence, by the time I get to where I’m going to
place that word in that sentence, I’ve already forgotten what the word was in my own sentence.”
Tr. 81-82. He explained that his memory problems manifest as having issues “forming new
memories.” Id. at 82-83. While petitioner is engaged in conversations, he “can’t recall the point
of the conversation…[and] might close a conversation without realizing that the person I was
talking to was about to say something.” Id. at 84.

Petitioner explained that while he has not experienced any large-scale flares as he
experienced in 2014-2015 he continues to have “small, short events, but nowhere near as extreme
as the paralysis. The lack of putting words together, the lack of cognizance, all of that – all of those
and the eyesight…you can stack all of those up, that’s one really big event for me.” Tr. 86.

III. Analysis

1. Loving Prong One: Petitioner’s condition before receiving the flu vaccine.

As detailed in the facts section above, petitioner appeared to be somewhat healthy before
receiving the vaccine. He was a 37-year-old husband, and father of three, who was noted to have
a “very healthy exam” during a physical on November 16, 2010. Pet. Ex. 16 at 1-8. At that
appointment petitioner’s PCP wrote, “1. Last tetanus shot was more than 10 years ago. Did get a
flu shot.” Pet. Ex. 4 at 3. He had only a few appointments in the intervening four years for
allergies and sinus infections. Id.

At the December 1, 2014, appointment for a physical, petitioner reported to his PCP, Dr.
Richards, that in the last week he had felt something almost like pins and needles mostly in the
left foot but at times going up to the abdomen and also reported that he had had a recent left eye
problem with optic nerve inflammation that was not helped by steroids. Otherwise, his physical
examination was normal. His range of motion was good in his hips, knees, ankles, back, shoulder
and elbows. His eye movement was good. eyes looked normal. All other systems were normal
leaving the question of the pins and needles in the left leg. Pet. Ex. 16 at 9-10.

Petitioner’s wife testified that, prior to the December events, petitioner was very active,
spontaneous, and fun. He was in good health. He loved music and was in bands and composed
for groups. He would run and chase the kids. He was tall and was into sports. When he started to
have an eye problem in the summer, they had been working in the yard and she thought that he
might have had allergies or something in his eye. Tr. 7-9. Dr. Steinman noted that petitioner was
in relatively good health, he was “working, driving, being a great dad.” Tr. 264.

18
The parties stipulated that “prior to his receipt of the flu vaccination, petitioner had a
history of optic neuritis.” Joint Submissions at 1 (ECF No. 80). The parties also stipulated that
“prior to his receipt of the flu vaccination, petitioner likely had multiple sclerosis.” Id.

In mid-June 2014, approximately 6 months prior to the flu vaccine in question, petitioner
started to get blurry vision in the inferior aspect of his left eye. Pet. Ex. 3 at 1. After a
comprehensive eye exam showed stage 2 nerve edema in his left eye, petitioner underwent a
brain MRI on June 13, 2014, which showed optic nerve enhancement at the globe and “no
stigmata of MS.” Pet. Ex. 3 at 3. Additionally, petitioner had a negative Aquaporin receptor
antibody, and positive ANA and Slc-70. Id. at 8. The experts agree that petitioner was
diagnosed with optic neuritis in June 2014. See Pet. Ex. 25 at 1; Pet. Ex. 66 at 7; Resp. Ex. A at
4; Resp. Ex. B at 6. Dr. Foley testified that the “clinical examination by the neuro-
ophthalmologist in June of 2014 clearly validated the concept that he had a real optic neuritis of
the left eye.” Tr. 119. Dr. Steinman testified “that [petitioner] had an episode of something called
optic neuritis. It wasn’t diagnosed at that time as multiple sclerosis, but with retrospective view,
that may have been the first clinically apparent attack.” Tr. 205-06.

Respondent points to various parts of the medical record that demonstrate “clinical
symptoms of a demyelinating disease in the weeks before his December 1, 2014 vaccination.”
Resp. Post Hearing Brief at 27. These symptoms included pins and needles sensation in his left
leg, and some trouble with word finding. See Pet. Ex. 4 at 1-2, 6; Pet. Ex. 10 at 2; Pet. Ex. 5 at
113. Dr. Foley further testified that, since Dr. Richards did not perform a basic neurological
exam, he “can’t absolutely say that …the pins and needles couldn’t have been a prodrome of
some kind of an MS attack.” Id. at 120. During cross-examination, Dr. Steinman stated that “in
hindsight” the cognitive difficulties and pins and needles sensation were “probably” symptoms
of his yet undiagnosed MS. Tr. 297-98.

Further, Dr. Sriram testified that in his opinion petitioner had lesions in his cervical spine
prior to vaccination, and that petitioner’s “symptoms began a few days before his vaccination
with the development of the sensory abnormalities on his left leg and this would indicate to me
that he already had some inflammation in his spinal cord…[w]hether a vaccine can aggravate
and perpetuate or expand an ongoing developing lesion is not something that is known to occur.”
Tr. 363-64. In response, Dr. Foley testified that it is “speculation” for Dr. Sriram to believe that
petitioner’s lesions in his brain and spine started in September or October in 2014 because “we
don’t have an MRI, and the data of intervening neurological events is at best extremely weak and
driven primarily by the patient’s self-report without examination confirmation.” Tr. 599.

Taking into consideration the diagnosed optic neuritis, pins and needles sensation in
petitioner’s left leg and mild cognitive changes such as difficulty finding words, it is most likely
that petitioner had MS before the vaccine at issue. However, other than the optic neuritis,
petitioner had at most mild symptoms of tingling in the left leg prior to the vaccination. He was
very active with his kids, with musical groups, working a full-time job and generally not
experiencing symptoms of significant illness.

19
2. Loving Prong Two: Petitioner’s condition after receiving the vaccine.

Based on the undersigned’s review of the medical records set forth above, petitioner had
sensory symptoms in the left foot and leg that came and went prior to his physical exam and
vaccination on December 1, 2014. The record establishes that after the vaccination, petitioner’s
condition significantly worsened.

Within a couple of days after the vaccination petitioner developed flu like symptoms but
did not initially have new neurological symptoms. He called in sick to work on December 7,
because he felt achy and cold and was barely able to use his right leg. Up to that point, he was in
training, was working on his feet, and was driving to work. Tr. 59. He testified that it took a few
days and eventually his right leg stopped responding. He thought he might have had a pinched
nerve. Id.

In his first expert report, Dr. Foley wrote, “within 1-2 days [petitioner] became ill with
nausea and flu-like symptoms requiring him to take time off from work. He called in sick on
December 7, [2014]. Within 1 or 2 more days after he experienced flu like symptoms he
experienced increased cognitive difficulties, right blurred vision, persistent left leg numbness and
paresthesia, and new right lower extremity weakness, as well as urinary retention.” Pet. Ex. 62 at
1. He saw a medical assistant for a blood draw on December 8, 2014, and she noticed that he
was having trouble walking. She scheduled him to see Dr. Richards again on December 10,
2014. At this appointment the right leg weakness and dysfunction was documented but he was
still able to walk on his own. By December 12, he could not walk at all, and his wife had to drag
him to the car to go to the hospital. Dr. Foley testified that petitioner’s initial disease course in
December 2014 “would be more typical of a real severe ADEM…sort of an atypical MS,
because…he had a single major event.” Tr. 115.

The parties stipulated that on December 10, 2014, “petitioner saw his primary care
physician and reported that, ‘two or three days’ after his flu vaccination, his right leg ‘stopped
working’ and that it went ‘intensely numb,” including the ‘whole thigh and leg,’ ‘[from] the foot
to the bottom of the right chest.” Joint Submission at 2.

As noted above, on December 1, 2014, the date of the vaccination, petitioner presented to
Dr. Richards and reported that in the last week before his visit, his left leg from his feet to his
abdomen had some “pins and needles” which came and went. Pet. Ex. 16 at 9 (emphasis added).
Dr. Richards noted petitioner’s prior optic neuritis diagnosis and that MS had been ruled out
through the MRI. Id. Dr. Richards recorded the nerve irritation in petitioner’s left leg and ordered
the flu shot. Id. His physical was otherwise normal including full range of motion in all his
joints.

When petitioner returned to Dr. Richards on December 10, 2014, due to “trouble
walking,” and tingling in his left leg that had “started a couple of weeks ago.” Pet. Ex. 16 at 14.
Further, petitioner noted that 2-3 days after the vaccination his right leg “stopped working [and]
went intensely numb” from the bottom of his right chest to his foot. Id. Mrs. Gardner testified
that “between the December 1, [2014] visit and the December 10, [2014] visit, things started to

20
get worse fast…he had weird muscle spasms, seizure thing, couldn’t get warm, and then his leg
started to get a lot worse, really, really fast.” Tr. 15.

Petitioner presented to the emergency room (“ER”) on December 12, 2014, when he lost
his ability to walk because of a paralyzed right leg. Pet. Ex. 5 at 11. The admission note
indicated that he was a good historian and reported the prior NMO diagnosis. It indicated that in
about November he began noticing some paresthesias in his left leg but not weakness. About
five days ago, he started having numbness in the left leg up to about T5 and had hyperesthesia
and neuropathic pain in the left hip and torso. This developed into weakness to the point where
his right leg was completely plegic today. He was unable to urinate, and a Foley catheter was
placed. He also noticed some right eye pain with no loss of acuity. He came into the ER
because of this progression of symptoms. Pet. Ex. 11 at 7. On physical exam, his right pupil was
larger than the left (4 mm to 2.5 mm). He appeared to have a left afferent pupillary defect with
reactivity in both eyes and some decrease in visual fields bilaterally. He did have an occasional
misplaced word but was otherwise cognitively intact. Id. at 9-11.

On physical exam in the emergency room, petitioner was calm and articulate and able to
describe his history in detail. He was able to ambulate with the right knee locked. On sensory
exam, he complained of decreased sensation and hyperesthesia from his feet to the nipple level
bilaterally. He was unable to lift his right leg against gravity at the knee and was unable to lift
the right leg off the bed with hip flexion. There was marked weakness on the right leg with no
dorsiflexion or plantar flexion. The left leg appeared normal. He had normal proprioception
bilaterally and normal response to light touch but was severely hyperesthetic to pinprick on the
right side as compared to the left. Pinprick on the right appeared to cause severe discomfort. He
was oriented to person, place and time and his cognition was baseline. His recall for recent
events appeared to be intact. Pet. Ex. 11 at 11. Based on the above presentation and
examination, Dr. Chloe Huan, a neurologist, admitted him to the hospital for extensive
evaluation, imaging and lab work. Id. at 12.

A brain MRI conducted on the same day revealed a previously unseen, enhancing
tumefactive lesion in the left anterior temporal lobe, “measuring 4.6 x 4.2 x 3.8 cm…suggestive
of acute tumefactive demyelinating disease involvement in this patient with brain MRI a few
months ago reportedly negative for intracranial lesions.” Pet. Ex. 17 at 12-13. The enhancement
indicates that the lesion is new and active, and the location on the left side of the brain would
correlate with right-sided symptoms, such as the new right-sided visual problems and lower
extremity sensory loss experienced by petitioner. Id. at 15-16. Petitioner also underwent a
cervical spine MRI which revealed prominent abnormal signal change and C6-T1 associated
cord expansion with prominent enhancement at C7 to T1. Pet. Ex. 5 at 20-21. The radiologist
noted:

Given the prior left optic neuritis, current right optic neuritis, the large partially
peripherally enhancing left anterior temporal lobe lesion, and the prominently
enhancing T2 hyperintense lesion in the right dominant C6-T1 cord on
accompanying cervical and thoracic spine MRI exams, and given previously
negative workup for neuromyelitis optica (NMO) and history of recent
immunization, differential diagnosis would first include acute disseminating

21
encephalomyelitis (ADEM) with transverse myelitis. NMO would still be
consideration, as well as multiple sclerosis and viral myelitis.

Pet. Ex 5 at 16. As noted by Dr. Foley, compared to the initial MRI performed in June
2014, the second round of MRIs performed on December 12, 2014, showed significant
progression. Dr. Foley testified that the MRI images were,

significantly worse than a standard presentation of multiple sclerosis…we didn’t
have spinal cord imaging, but we had brain imaging as of June of 2014 that revealed
only optic neuritis and no lesion burden in the brain. So, over this time frame, to
develop this kind of picture, I would really say was kind of more acutely reactive.
The prior brain MRI was essentially normal except for the left optic neuritis.

Tr. 111-12. With this dramatic change in the MRIs of the brain and spinal cord, petitioner rapidly
lost his ability to walk, he experienced changes in his cognition, such as difficulty finding words,
and he also experienced blurriness in his right eye. Pet. Ex. 5 at 113. His physical examination
on December 13, 2014, revealed decreased sensation to light touch from his left toe to T5 level,
and his right leg was paralyzed. Id. Petitioner also demonstrated constipation and urinary
retention. Id.

Mr. Gardner underwent a second MRI of the brain and cervical spine on December 22,
which was compared to the first from December 12. The brain MRI showed a slight decrease in
edema and enhancement from the prior scan consistent with tumefactive multiple sclerosis. It
also showed enhancement of the right intra-orbital optic nerve with atrophy although a full optic
scan was not done. Pet. Ex. 5 at 320. In contrast to the brain scan which showed some mild
improvement, the cervical MRI documented an enhancing intramedullary lesion from the inferior
endplate of C6 through the mid T2 vertebral body. This lesion resulted in expansion of the
cervical cord. In addition, on axial view there was T2 hyperintensity in the central grey matter.
The length and width of the cervical lesion increased significantly from the prior scan. Id. at 322.

Mr. Gardner was discharged to the Intermountain Rehab Center on December 16, 2014
where he remained until January 9, 2015. He received a three-day course of intravenous steroids
without improvement. While in rehabilitation, his condition worsened with essentially complete
paralysis of the right leg and new onset weakness in the left leg. He also developed additional
cognitive deficits and speech problems with continued bowel and bladder incontinence. His
diagnosis on discharge was multiple sclerosis, lower extremity paraplegia, T4 sensory level,
optic neuritis, cognitive deficits, urinary retention, constipation, and urinary tract infection. Pet.
Ex. 5 at 631.

Dr. Foley testified that these lesions did improve and the insult was largely monophasic
except for an additional attack of optic neuritis with some mild MS symptoms in August 2015
which they treated at that time. Tr. 156. Dr. Foley put him on disease modifying therapy,
initially Techfidera and then Ocrefus and finally Gilenya but he is now off MS medications.

Today, petitioner is dependent on his wife, and has not been able to be employed. Tr. 81.
He continues to suffer from cognitive impairments, including word finding, brain fog and

22
memory problems. Tr. 81-83. Physically, he still experiences leg and hip pain, gets tired easily,
cannot be intimate with his wife, and continues to suffer a blind spot “on the bottom left corner
of [his] left eye,” that it is “constantly blurry.” Id. at 84. Additionally, he is sensitive to
temperature changes and has experienced “small, short” flare-up events, but “nowhere near as
extreme as the paralysis,” experienced in December 2014. Id. at 86.

There is no question that petitioner’s physical condition, and ability to function became
significantly worse in the 10 to 12 days after the vaccination. His symptoms began with pins and
needles on the left and some visual blurriness on the left at the time of vaccination, progressing
to right leg paralysis, right optic neuritis, urinary retention, and bilateral paresthesias with what
appeared to be increasing levels of cognitive deficits by December 12, 2014. His condition
continued to worsen during his hospitalization and rehabilitation with significant deterioration in
cognition and minimal improvement in physical function. All of the above required an extended
hospitalization and rehabilitation. While he did not have an MRI immediately before his
vaccination, he did have one in June 2014 that showed optic neuritis on the left side only but was
otherwise normal with no evidence of MS. His symptoms at the time of vaccination were quite
mild compared to those that developed by December 12, 2014. The MRIs done in response to his
worsening condition showed dramatic, enhancing changes from the prior scan that appear to
have occurred concurrently with the worsening of symptoms. The December MRIs also
demonstrated a significant enhancing cervical/thoracic lesion as described above. This change in
signs, symptoms and imaging satisfies Loving Prong Two.

3. Loving Prong Three: Petitioner’s change in condition constitutes a significant
aggravation.

As provided above, the Vaccine Act defines a significant aggravation as “any change for
the worse in a preexisting condition which results in markedly greater disability, pain, or illness
accompanied by substantial deterioration of health.” § 300aa-33(4). The Vaccine Act requires
only a comparison of a petitioner’s current or post-vaccination condition with his pre-vaccination
condition. Sharpe v. Sec'y of Health & Hum. Servs., 964 F.3d 1072, 1078 (Fed. Cir. 2020).

When Dr. Foley was asked by the Court about the possibility of an inflammatory process
occurring between the time of the flu vaccine on December 1, 2014, and the MRI on December
12, which showed large lesions and massive enhancement, he responded that “the timing of this
obviously is critical, and absent any MRIs prior to the influenza injection, it is essentially
impossible for us to know.” Tr. 123-24. Dr. Foley testified that if you take from the point of
injection, he nearly immediately notices some sort of reactive symptoms that suggest some
systemic reaction to the flu shot. After a few days he starts to notice more neurological
symptoms. Importantly, Dr. Foley explained that the spinal cord, especially the anterior spinal
cord, where corticospinal tracts are located, is very small, less than a half dollar around, so lesion
formation there is rapidly transmitted into clinical symptoms. Id. at 124. In petitioner’s case, he
only had some pins and needles paresthesias prior to the injection. Then, there are a couple of
days where it seems that he reacted negatively to the flu shot but does not necessarily have
worsened neurological symptoms. Then petitioner really starts to get much worse, to the point
where his wife has to drag him down the stairs, taking an hour to get him into the car. Id. By
December 12, 2014, he has right leg paralysis, severe weakness and bladder dysfunction. Id.

23
This evolution of symptoms correlates with him suffering tumefactive lesion formation with
massive gadolinium enhancement suggestive of an active, open blood-brain barrier and blood
cord barrier. Dr. Foley explained that an acute inflammatory lesion in the spinal cord that is
gadolinium enhancing is going to manifest very, very rapidly as clinical symptoms. So, Dr. Foley
stated that his inclination was that sometime in the first week after having the flu shot, he
developed at least a spinal cord lesion that became nearly immediately symptomatic. Id. at 125.

When asked about the large tumefactive lesion, Dr. Foley testified that it was primarily in
the temporal lobe into the frontal lobe on the left side, and would induce speech dysfunction,
cognitive dysfunction, processing slowing, probably emotional abnormalities. He pointed to Mrs.
Gardner’s testimony that petitioner could hardly talk by the end of his admission and explained
why more of petitioner’s cognitive symptoms manifested during his rehabilitation stay.
Specifically, Dr. Foley explained that cerebral lesions, especially those that originate in the white
matter association area, “can take a little bit longer to manifest with clinical symptoms.” Id. at
125. In addressing the timing, Dr. Foley stated that “in a hypothetical, I think it…it’s possible
that he was going into what would have been a low-grade kind of minimal relapse that really got
exacerbated by the antigenic stimulus.” Id. In agreement with Dr. Foley, Dr. Steinman wrote that
“the [flu] vaccine massively accelerated the severity and extent of [petitioner’s] disease, multiple
sclerosis.” Pet. Ex. 66 at 6.

Dr. Foley testified that in retrospect, the June 2014 optic neuritis diagnosis fulfilled the
first McDonald 19 criteria, and the second, separate in time McDonald criteria was confirmed by
the abnormal MRIs from December 12, 2014. Tr. 118. As a treating physician, Dr. Foley noted
during a visit on January 19, 2015, that petitioner’s “spinal cord disease clearly was related to his
flu shot. This generated massive inflammation at the level of the lower cervical and upper
thoracic spine together with a grossly enhancing lesion on the left temporal lobe consistent with
ADEM post vax and recrudescence of probable multiple sclerosis.” Pet. Ex. 6 at 24. Clinically,
this was demonstrated in petitioner by December 12, 2014, when he lost his ability to walk. Pet.
Ex. 5 at 14. Dr. Foley testified that this was an atypical presentation of MS, and, but for the prior
optic neuritis, he would have called it frank ADEM. However, with the prior optic neuritis and
no other evidence of brain lesions on the MRI from June 2014, Dr. Foley testified that “we have
to describe it as an atypical MS with a single monophasic severe episode that was ADEM-like.
Short of doing a biopsy of the brain that is the best that we can say.” Tr. 117-18.

Referring to his explanation of the narrow spinal cord, Dr. Foley explained that “the tight
binding correlate of expanding inflammation in a very small space, in a very critical space in the
spinal cord will induce inability to walk and complete failure of bowel, bladder and sexual
function very rapidly. There is not a lot of margin there.” Id. at 143. His theory, he explained is
“that the bulk of that lesion burden, gadolinium enhancement, and cord enlargement developed
within the first few days after getting the influenza vaccine.” Tr. 143.

19
The McDonald criteria, last revised in 2017, are the most recent diagnostic criteria for multiple sclerosis
combining clinical, imaging, and laboratory evidence. Alan J. Thompson, et al., Diagnosis of multiple sclerosis:
2017 revisions of the McDonald criteria, 17 Lancet Neurol. 162, 162 (2018). The McDonald criteria for the
diagnosis of MS is often referred to as disseminated in time and disseminated in space and can refer to separate
episodes or radiologic findings. Id. Dr. Foley explained in his testimony, in the present case, the McDonald criteria
for MS “is essentially two episodes, separated in space and time.” Tr. 105.

24
Dr. Foley explained that the blood brain barrier is opened in response to an antigenic
stimulus, and, “then circulating immune cells will rush into certain areas that are usually
perivenular…and those inflammatory cells, if they aggregate in sufficient numbers will start to
do a couple things.” Id. at 121-22. One is that they can swell the spinal cord or the brain giving
them a “swollen look with acute inflammation” as occurred in this case. Id. Dr. Foley testified
that this swelling can put pressure on things like the corticospinal tract, which is the major motor
tract going to the legs and it can compromise bowel and bladder function. Id. At the same time,
the inflammatory aggregates also start exerting a negative effect on the neuronal pools which
ultimately lead to atrophy seen in scans years later. Id. at 122. Dr. Foley noted that this was a
monophasic event and that petitioner’s MRIs have remained stable, but he testified that there is
permanent compromise that is now manifest by myelomalacia or a shrinkage of the spinal cord
related to the initial lesion burden during the monophasic event. Id. at 140-41. Petitioner also has
disproportionate atrophy in the left temporal, frontal-temporal regions of the brain related to the
lesion burden in the monophasic event. Dr. Foley indicated that Mr. Gardner will have
permanent cognitive compromise, bowel, bladder and sexual compromise and when he gets
fatigued, he still uses a cane. Tr. 140-41. Dr. Sriram testified that “these lesions were massively
enhanced on December 12, [2014] and they weaned off by January 22, [2015], these large
lesions…last longer than three to four months, so it’s up a timeline for the beginning of this
sometime in October, November. That’s my best guess because these large lesions don’t
suddenly come up and suddenly disappear.” Tr. 342.

Dr. Steinman, in agreement with Dr. Foley, stated that while it is possible that petitioner
had lesions and MS prior to the vaccination, there is no way to definitively know. After receiving
the vaccine, petitioner progressively developed significant new symptoms over the ensuing days
and weeks. The increase in lesions seen in the December 12, 2014 MRIs correlated with
worsening symptoms in the time period from December 1, 2014 to December 12, 2014. The
increased symptoms and lesions represent a very substantial worsening of his condition,
constituting a “significant aggravation.” Tr. 205-06.

The cause of the worsening will be addressed below, under Loving prong five,
considering whether the vaccine was more likely than not the cause of petitioner’s condition
becoming worse. However, there is no question that Mr. Gardner’s signs and symptoms became
much worse in the days to weeks after the vaccination than they were before. Petitioner therefore
satisfies Loving prong three as having experienced a significant aggravation of his condition.

4. Loving Prong Four (Althen Prong One): Petitioner has established a reliable and
reputable theory of how the flu vaccine can cause the significant aggravation of
multiple sclerosis.

Under Althen prong one, the causation theory must relate to the injury alleged. Thus, a
petitioner must provide a “reputable” medical or scientific explanation, demonstrating that the
vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56. The theory
must be based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y of
Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). However, the theory need only be
“legally probable, not medically or scientifically certain.” Id. at 549. However, the theory still
must be based on a “sound and reliable medical or scientific explanation.” Id. at 548. The

25
Federal Circuit explained in Althen that “while [that petitioner’s claim] involves the possible link
between [tetanus toxoid] vaccination and central nervous system injury, a sequence hitherto
unproven in medicine, the purpose of the Vaccine Act’s preponderance standard is to allow the
finding of causation in a field bereft of complete and direct proof of how vaccines affect the
human body.” Althen, 418 F.3d at 1280 (emphasis added).

A. Petitioners’ Experts’ Opinions Regarding Loving Prong Four (Althen
Prong One): Dr. Foley and Dr. Steinman

Dr. Foley, as the primary multiple sclerosis specialist treating Mr. Gardner, opined early
in the course of treatment that he believed that the flu vaccine triggered this event. He explained
that he is the Director of the Rocky Mountain Multiple Sclerosis Clinic, which takes care of
about 4,200 patients a year from throughout the intermountain west, primarily with multiple
sclerosis but also with other disorders such as ADEM and NMO. Tr. 97. He referred to the
literature regarding vaccination and ADEM and indicated that the correlation with MS in the
literature is less robust but that it is there. He said that he has no doubt on a clinical basis that it
occurs, as he has taken care of multiple patients with MS occurring after vaccination. Tr. 145.
As detailed above he explained his theory of antigenic stimulation that can arise from an
infection or a vaccination. He indicated that onset or relapse happens more frequently from
infection but does also occur after vaccination.

Dr. Steinman agreed with Dr. Foley as to the likelihood of vaccine causation and opined
that there was homology between components of the 2014-2015 flu vaccine (received by
petitioner) and components of myelin, in particular myelin oligodendrocyte glycoprotein or
MOG that could give rise to molecular mimicry. Pet. Ex. 66. Dr. Steinman presented the theory
of molecular mimicry, which explains how the introduction of the flu vaccine can cause an
autoimmune response against myelin, and can cause significant aggravation of MS via an open
blood-brain barrier. See Pet. Ex. 66; Pet. Ex. 85. He defined MOG as a molecule that is “almost
exclusively expressed in the central nervous system…and it’s come to be understood that it’s one
of the myelin antigens that is attacked in multiple sclerosis.” Tr. 219. Dr. Steinman further
testified that “the components of the influenza vaccine sensitized Mr. Gardner to MOG,” because
there exists “a molecular similarity between what’s in the vaccine that he actually received and
MOG itself.” 20 Tr. 222. He opined that because the components of the flu vaccine that Mr.
Gardner received in 2010 and the one that he received in 2014 were identical in relevant parts
that it is likely that he had a rapid recall response to the 2014 vaccine. Tr. 251-53.

Dr. Steinman demonstrated his theory in three steps. Initially he utilized the BLAST
database made available by the National Institute of Health to perform a BLAST search to look
for any similarities between MOG and the components of the flu vaccine. Pet. Ex. 66 at 14 He
chose MOG because it is a protein that is attacked in optic neuritis, MS, and ADEM. Tr. 223.
The BLAST search lines up two proteins and asks where they align, which is step one. His

20
Dean M. Wingerchuk & Brian G. Weinshenker, Neuromyelitis optica spectrum disorder diagnostic criteria:
Sensitivity and specificity are both important, 23 Multiple Sclerosis J. 182, 182–84 (2017) [Pet. Ex. 93]; Maureen A.
Mealy et al., Vaccines and the association with relapses in patient with neuromyelitis optica spectrum disorder, 23
Multiple Sclerosis & Related Disorders 78, 78–82 (2018) [Pet. Ex. 94].

26
BLAST search identified a sequence in which there were six out of eight amino acids in a row
that were identical between MOG and the hemagglutinin in the influenza vaccine. Tr. 224. He
testified that they concluded years ago, as published in Scientific American, that you need five
out of twelve amino acids to be identical in a consecutive stretch, and you could get ADEM. Tr.
224. The BLAST search revealed “the sequence TGMEVGWY [which] has 6 of 8 amino acids
in common between the flu vaccine and MOG which he testified is sufficient to cause clinically
relevant neuroinflammation.” Pet. Ex. 66 at 14. Dr. Steinman testified that this sequence
similarity could be sufficient to cause aggravation of MS by molecular mimicry,” and he opined
that “the components of the influenza vaccine most likely sensitized Mr. Gardner to MOG
[because of] a molecular similarity between what’s inside the vaccine that he actually received
and MOG itself.” Tr. 221-22.

To support his theory, in his second step, Dr. Steinman discussed the Gautam papers,
which were studies done in his lab at Stanford, and which demonstrated in two papers that as few
as four native myelin basic protein amino acids were sufficient to stimulate myelin basic protein
T cells and cause experimental autoimmune encephalitis (“EAE”) in mice. EAE is a murine
model of the human autoimmune disease, multiple sclerosis. Pet. Ex. 78; Pet. Ex. 79. In a
subsequent paper published in 1998, Gautam and colleagues demonstrated that a viral peptide
with limited homology to a self-peptide can induce clinical signs of EAE. They stated that T
helper cells recognize foreign peptides bound to MHC class II molecules on antigen presenting
cells and that their studies suggest that the exposure to pathogens may stimulate the self-reactive
T cell repertoire such that it may trigger or exacerbate autoimmunity and cause paralysis in
mice. 21 Pet. Ex 79 at 7. Gautam observed that Wucherpfennig and colleagues 22 provided strong
evidence that peptides derived from certain viruses and bacteria could stimulate myelin basic
protein specific T cell clones generated from MS patients. In the 1998 Gautam paper they
demonstrated that EAE in mice can be induced by a cross-reactive viral peptide with limited
homology and provided evidence for molecular mimicry triggered by a virus. Id. at 10. Dr.
Steinman also cited to a paper by Root-Bernstein 23 that demonstrates molecular mimicry
between Group A Streptococcus and or coxsackievirus and cardiomyocytes giving rise to
rheumatic heart disease. Root-Bernstein used a similar BLAST search approach and accepted
homology of five identical amino acids in ten to demonstrate molecular mimicry in this context.
Pet. Ex. 88. In this step Dr. Steinman explained that Gautam and other papers showed “an
autoimmune response can begin even if the molecular mimicry is not quite exact.” 24 Pet. Ex. 66

21
Anand 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, 63 (1998).
22
Kai Wucherpfennig, et al., Recognition of the Immunodominant Myelin Basic Protein by Autoantibodies and
HLA-DR2-restricted T Cell Clones from Multiple Sclerosis Patients, 100 J. Clinical Investigation 1114 (1997). [Pet.
Ex. 73].
23
Robert Root-Bernsein, Rethinking molecular mimicry in rheumatic heart disease and autoimmune myocarditis:
laminin, collagen IV, CAR, and B1AR as initial targets of disease, Frontiers in Pediatrics, Aug. 2014, at 1. [Pet. Ex.
88].
24
Anand Gautam, et al., A Polyalanine Peptide with only Five Native Myelin Basic Protein Residues Induces
Autoimmune Encephalomyelitis, 176 J. Exp. Med. 605, 605-09 (1992). [Pet. Ex. 77]; Anand Gautam et al., Minimum
structural requirements for peptide presentation by major histocompatibility complex class II molecules:

27
at 9; Tr. 237. He referred to a paper by Srinivasappa 25 which demonstrated that almost 4% of
antiviral monoclonal antibodies also reacted with self-proteins. Tr. 236. Dr. Steinman testified
that complete identity of amino acids in the relevant peptide could give disease 80 percent of the
time, and if you reduce the number of identities, you still get disease 40 percent of the time. Tr.
239. He emphasized that the experiments that they can do within the scope of the Vaccine
Program are limited so that in proposing a theory based on peer reviewed literature, as he has
here, he is showing that the vaccine with six of eight identities between it and MOG could cause
disease. He acknowledged that the theory cannot be proven to a certainty, emphasizing that it is
not possible to do specific experiments on the petitioners in vaccine cases. Id. at 241. However,
these papers provide preponderant evidence of how cross reactivity between a vaccine and MOG
can cause disease which is what he believes occurred in this case. Id.

In the third step in refining his molecular mimicry theory, Dr. Steinman referenced the
Immune Epitope Database (IEDB) to determine if that sequence had been studied by others. The
database is known as the Immune Epitope Database, which “catalogs experimental data on
antibody and T cell epitopes studied in humans, non-human primates, and other animal species in
the context of infectious diseases, allergy, autoimmunity, and transplantation.” Pet. Ex. 66 at 14.
Dr. Steinman also utilized the Influenza Research Database in the third filtration step. Id. at 14-
15. He testified that “the third step is really illuminating,” by asking if “anyone else report[ed]
that TM sequence of eight amino acids, did anyone else study it, report it, publish it, and they
did, and it’s found in both the hemagglutinin of the influenza, and it’s found in MOG.” Tr. 225.

The assays for the sequences “included a large number of studies from peer reviewed
publications…demonstrating viral neutralization, proliferation, and production of pathogenic
cytokines in human cells.” Pet. Ex. 66 at 18. Referencing the sequence alignments in his first
expert report, Dr. Steinman testified that “the protein is broken up into peptide fragments, and
these size peptide fragments can usually elicit an immune response, and they can actually – even
a fragment as small as eight amino acids can elicit ADEM in an experimental animal.” Tr. 232.

He explained that the TMEGY segment has been shown to be part of what humans
actually respond to in the hemagglutinin of influenza and also that it has been studied in great
detail in dissecting the nature of the immune response to MOG itself. Tr. 244-45. Dr. Steinman
testified that the TGMVDGWY epitope is part of the hemagglutinin portion of the H1N1
component of the vaccine. He indicated that many papers found through the IEDB referenced
the TMGV et cetera peptides we are looking at overlapping peptides of about 20 amino acids in
length. He explained that in an ideal situation, experiments could be conducted where the length
of the peptide was shortened repeatedly to see if it could be determined exactly what part of the
peptide became the landing pad for the immune response in a patient. However, those types of
experiments are not possible in the context of a vaccine case. Nevertheless, he found that the
reference to this peptide in the IEDB supported his theory as it appears to be a region where the
human immune response to influenza is targeted. Id. at 247. He also explained a chart of all of

Implications in induction of autoimmunity, 91 Proceedings of the National Academy of Sciences 767 (1994). [Pet.
Ex. 78]
25
Javaraiah Srinivasappa, et al., Molecular Mimicry: Frequency of Reactivity of Monoclonal Antiviral Antibodies
with Normal Tissues, 57 J. Virology 397 (1986).

28
the types of assays that were done to show that this is a region that is a landing pad in MOG.
They used binding to HLA. They used B cell assays. They used a huge number of T cell assays
to show that this region could elicit cytokines associated with multiple sclerosis, like gamma
interferon and IL-17 and that it could cause experimental disease exacerbation. Tr. 249. As such,
he found that the multiple references to this peptide in the IEDB helped support his theory as to
how the vaccine could cause an aggravation of MS in Mr. Gardner.

On cross examination Dr. Steinman was asked about the e-values, or expect values, in
the BLAST search step. Dr. Steinman explained that the e-values were designed to compare one
entire protein to another, which have much longer stretches of amino acids. However, the
immune system does not respond to entire proteins but rather to short stretches after the antigen
is chopped up and presented to the immune system through the HLA molecule. It is these short
stretches that are relevant to the immune system response to the H1N1 molecules and to MOG.
Tr. at 288. Dr. Steinman testified “that’s why I go through the two other steps of the
filtration…first [to] look for any alignment.” Id. at 287. He explained that “the reason BLAST
started out [was] they wanted to know how similar one protein was to another. I’m not interested
in the whole protein. I’m interested in defined regions because the immune system doesn’t scan
whole proteins. It chops up the protein using enzymes called proteases and chops it up into short
amino acid sequences that then bind to HLA molecules.” Id. at 288. Further, he testified that “I
don’t care about the expect value number, because that’s not what the immune system cares
about.” Id. at 289. While Dr. Steinman testified that he is “completely aware of the expect
values,” he stated that he doesn’t “think they’re relevant to the analysis that I’m doing for what
the immune system might be interested in.” Id. at 288. There is little doubt but that foreign
pathogens such as the flu virus are chopped up inside cells and short segments are presented to
the immune system on MHC molecules on the surface of the cell. Antibodies and T cells
recognize short segments of pathogens called epitopes and mount the immune defense based
upon that recognition. Dr. Steinman’s theory is based upon recognition of short segments or
epitopes that have similarity between the ingredients in the vaccine and components of myelin
such as MOG. He argued that the Gautam and Root Bernstein papers among others demonstrate
that short segments have been shown to cause clinically meaningful disease and that the third
step in his filtration system has demonstrated that others are interested in the segment that he
identified as being likely to be immunologically significant in causing cross reactivity and
aggravation of MS.

Regarding onset, Dr. Steinman agreed that petitioner suffered some symptoms within two
to three days following the flu vaccine at issue. Tr. 250. He testified that the onset is particularly
appropriate “if this were a recall response.” Id. at 251. Dr. Steinman testified that a corollary to
the recall response to petitioner is an injection of tuberculin, and that “if you actually had been
exposed to tuberculin or had tuberculosis, that arm might look red and angry in 24 hours or
less.” 26 Id. at 251. He further testified that “recall immunity is very fast…sometimes the very fast
response is not necessarily in a neutralizing antibody. It’s in a memory killer T cell.” Id. at 252.

26
Tiromourougane Serane, et al., Tuberculin Test Can Be Read After 24 Hours in Adolescent Children, 60 J.
Tropical Pediatrics 157 (2014) [Pet. Ex. 105]; Lin Fan, et al., Variation of Mycobacterium tuberculosis Antigen-
Specific IFN-γ and IL-17 Responses in Tuberculin Skin Test (TST)-Positive Human Subjects, PloS One, Aug. 2012.
[Pet. Ex. 106]; T. Kardjito & J.M. Grange, Immunological and Clinical Features of Smear-Positive Pulmonary
Tuberculosis in East Java, 61 Tuberculosis, 231 (1980. [Pet. Ex. 107].

29
Referring to petitioner’s medical records from November 2010, Dr. Steinman noted that
Mr. Gardner had received the flu vaccine available in that year as I have concluded was most
likely to be the case. He explained that the flu vaccine in 2010 contained the same HIN1 virus as
the 2014 flu vaccine, which is sufficient to mount a rapid recall response. Tr. 253. Thus, Dr.
Steinman concluded that there is sufficient identity between the influenza vaccine administered
to petitioner in 2014 and the one he received in 2010, with structural similarities known to be
targeted in MS to cause a faster recall response. Pet. Ex. 66 at 20. Dr. Foley testified that the
enhancing lesions suggest a very open blood brain barrier at the time of vaccination which
together with the concept of a recall response helps to explain the rapid onset of the aggravation
of Mr. Gardner’s disease. Dr. Foley testified that this type of response is-

usually due to a stimulus of some sort, and what happens then is circulating immune
cells will rush into certain areas that are usually perivenular [around a vein]…those
inflammatory cells, if they aggregate in sufficient numbers…can swell the spinal
cord or the brain…and the swelling can actually put pressure on things like the
corticospinal tract which is your major motor tract going to the legs, and it can
compromise bowel and bladder function.

Tr. 121-22.

B. Respondent’s Experts’ Opinions Regarding Loving Prong Four (Althen
Prong One): Dr. Sriram and Dr. Forsthuber

Dr. Forsthuber argued that the three-step filtration system Dr. Steinman used to
demonstrate a theory that the flu vaccine could aggravate petitioner’s MS is not reliable. Tr. 440.

Regarding the first step, Dr. Forsthuber testified that a BLAST search is a
“bioinformatics approach to enter sequences which are either nucleotide sequences, meaning
DNA or RNA, or amino acid sequences from proteins in a software package that’s available via
the National Institutes of Health.” Tr. 441. He testified that the “BLAST was not designed as an
immunological tool…BLAST only shows you whether there is a certain level of similarity in
nucleotides or amino acids between your protein that you’re interested in versus other proteins.”
Id. at 442.

Dr. Forsthuber argues that even if the BLAST step were an effective tool for identifying
immunological relationships, the comparison between MOG and the flu vaccine is not significant
because of their high e-values. Tr. 447. He explained that e-values are used to determine whether
or not the match is meaningful. Id. at 444-45. A meaningful e-value is lower and a non-
meaningful e-value is higher. Id. Dr. Forsthuber relies on the National Institute of Health criteria
that any e-value is significant if it is less than or equal to 0.00001. Id. at 445. He said that the e-
value for the comparison between the 2009 California influenza strain and MOG was 0.1. Id. at
447. He said he would never consider this as a similarity. Id. at 449.

He pointed to an article by Trost et al. which addressed bacterial sequences, suggesting
that about 50,000 perfect sequences, each 9 amino acids long, are shared between 40 bacterial

30
proteomes and about one third of the human proteome. 27 The Trost article concluded that “our
past and present data tend to exclude a causal mechanistic role for molecular mimicry in the
genesis of autoimmunity.” Resp. Ex. E-11 at 3.

Dr. Forsthuber opined that “the ‘sequence similarity’ for which Dr. Steinman claims
molecular mimicry is only 3 amino acids interspersed by two not matching amino acids and then
another three amino acids and not 8 amino acids which perfectly match.” Tr. 451. (Dr. Steinman
testified that the match he referenced was 6 of 8 amino acids that matched not 8 of 8 and that 6
of 8 can be enough to induce autoimmunity) Referring to the Trost article, Dr. Forsthuber
testified that the “sequence similarity between bacteria and humans is frequent.” Tr. 450. The
authors in Trost, “examined for amino acid sequence similarity” between bacterial proteomes
and the human proteome. Resp. Ex. E-11 at 1. The article found that “the bacteria-versus-human
nonamer (nine amino acids) overlap is numerically defined by 47,610 total perfect matches
disseminated through 10,701 human proteins.” Id. Dr. Forsthuber explained that “these short
amino acid similarities, even up to nine amino acids, are so frequent that it is conceptually very
difficult to say that these short sequences are causing molecular mimicry.” Tr. 450-51. Dr.
Forsthuber concluded that this research undermines any possible role of molecular mimicry and
that if it did have a role due to the extensive overlap, the incidence of autoimmunity should occur
at a rate of 100 percent. Id. at 450-52. The Court asked Dr. Forsthuber to clarify exactly what the
paper said, and Dr. Forsthuber responded that “the paper is more careful…[and] they’re a little
more cautious in their wording,” regarding the possible matches needed to induce autoimmunity
via molecular mimicry. Tr. 451-52. Further, Dr. Forsthuber argued that even if MOG is
significant in multiple sclerosis, the amino acid sequence outlined by Dr. Steinman does not
include matches for the essential positions of the MOG sequence that researchers have identified
as critical for T cell responses and induction of an autoimmune disease. Resp. Post Hearing
Brief; Tr. 455.

Regarding the second step, Dr. Forsthuber distinguished the approach used by Dr.
Steinman and the papers he relied on by Gautam. Tr. 461-62. Dr. Forsthuber argued that, in
order to rely on the Gautam papers, two facts are necessary to induce an immune response. The
first is that the relevant peptide must bind to the MHC molecule, and secondly the T cells need
specific amino acids in defined positions in order to react. Id. at 463-64. He further argued that
Dr. Steinman does not know “definitively” exactly which of the six out of eight amino acids
would be correct to induce a reaction, and, therefore, without that knowledge his theory is pure
speculation. He later testified that the positions of amino acids “are actually not so critical, but
what’s in [the] position is critical…if the wrong amino acid is in the wrong position, you’ll lose
binding.” Id. at 473. Further, “you can’t predict just by looking at the sequence…it’s impossible
to predict what would bind. It’s simply not possible…the chances that you’re getting a wrong
amino acid in the right position are much higher than getting by chance the right amino acid in
the right position.” Id. at 474 (emphasis added).

Regarding the third step, Dr. Forsthuber stated that the influenza research database and
the immune epitope database are not two distinct steps because they are pulling the same data.
Tr. 480. He explained, as did Dr. Steinman, that the IEDB database “provides researchers with

27
Brett Trost, et al., Bacterial peptides are intensively present throughout the human proteome, 1 Self/Nonself 71
(2010). [Resp. Ex. E-11].

31
the tools to search whether epitopes…that they have identified in their research…have been
reported by someone else. It gives you some tools where you can try to identify epitopes on your
own that could potentially induce T cell responses or B cell responses.” Id. Dr. Forsthuber then
explained that the exact eight amino acid sequence identified by Dr. Steinman was not present by
itself in the database, therefore no one “has ever found immune reactivity to those two eight
amino acid sequences.” Id. at 481-82. It is part of a longer sequence between positions 35 and 55
in mice which is often looked at by researchers. Citing to a paper by Mendel, Dr. Forsthuber
testified that “just because a sequence is listed in IEDB does not mean that actually your
sequences that is part of a larger sequence has meaning in inducing immune responses.” 28 Tr.
486; Resp. Ex. E-6. Dr. Forsthuber explained that while the sequences identified by Dr.
Steinman are in mouse models, the Mendel paper indicated that positions 40-48 are the relevant
positions for inducing disease in mice, and this sequence does not match Dr. Steinman’s alleged
mimics. Tr. 486; Resp. Ex. E at 24.

He additionally testified that “the reports on the influenza epitopes are after infection,”
not after vaccination. Tr. 492. He stated that when “we immunize an animal or a human being
with a protein, the immune system only responds to a few regions on this protein…the immune
system doesn’t respond to…every sequence in this protein, just against a few of those regions.
And during infection, typically more epitopes are induced as compared to vaccination.” Id. at
493. Therefore, Dr. Forsthuber argued that the alleged mimic identified by Dr. Steinman is not
capable of inducing inflammation or disease.

Dr. Forsthuber argued that Dr. Steinman’s theory is not supported in the scientific
community and has not been subjected to peer review. Dr. Steinman points to the Root-Bernstein
paper as evidence that scientists have used similar methods. Dr. Forsthuber testified that the
Root-Bernstein paper uses a different approach in which the authors conduct “BLAST searches
and LALIGN searches,” and if the sequences match 60% of the time, it is significant, if it is less
then it is a meaningless comparison. Tr. 497-498. Therefore, Dr. Forsthuber argued that Root-
Bernstein “would have discarded this result and these sequences as being meaningless, based on
simply that they fall below the Blast significance standard.” Tr. 498.

Dr. Sriram argued that the flu vaccine has not been shown to cause or aggravate MS, and
it also doesn’t impact the production of MOG antibodies. He discussed multiple studies that
examined the relationship between vaccination and the clinical or radiological worsening of an
autoimmune condition, and said that they have failed to substantiate these claims. Resp. Ex. B at
7. He cited to a paper by Hapfelmeier et al., which looked to see “whether the onset of MS,
which is often a relapse, is preceded by a vaccination, and they looked at three different
autoimmune diseases, MS, Crohn’s Disease, and psoriasis.” 29 Tr. 380. The study used a cohort of
12,000 patients with MS and found that vaccines were not associated with a higher likelihood of

28
Itzhak Mendel et al., Delineation of the minimal encephalitogenic epitope within the
immunodominant region of myelin oligodendrocyte glycoprotein: diverse V beta gene usage by T cells
recognizing the core epitope encephalitogenic for T cell receptor V beta b and T cell receptor V beta a H-2b mice,
26 Eur. J Immunol. 2470 (1996). [Resp. Ex. E-6].

Alexander Hapfelmeier et al., A large case-control study on vaccination as risk factor for multiple sclerosis, 93
29

Neurology, 908 (2019). [Resp. Ex. B-3].

32
an MS diagnosis.” Id. at 381. Dr. Sriram explained that the study found that vaccines “protected,
to some degree…the risk of MS, to the extent that it was reducing the onset of an MS event.” Id.
He also cited to a study by Confavreux, which studied the relationship between multiple vaccines
and risk of MS relapse. 30 The study concluded that “there was no increase in the specific risk of
relapse associated with tetanus, hepatitis B, or influenza vaccination.” Id. at 1. A review by
Mailand similarly concluded after a systematic literature review that there is “no change in risk
of developing [MS] after vaccination against…seasonal influenza.” 31 Tr. 388; Resp. Ex. B-1.

Dr. Sriram acknowledged that the possible protective effect was likely because the
vaccine reduced the likelihood of the patient developing the wild infection, in this case influenza
which he agreed can trigger an MS attack. Tr. 383-84. He also agreed that these studies did not
rule out rare occurrences of MS after vaccination. He said there is no way to rule out rare events.
Tr. 395-86.

Dr. Forsthuber testified that there has been extensive research on whether the flu vaccine
case cause or aggravate experimental autoimmune encephalomyelitis (“EAE”) in mice and stated
that the research demonstrated that the flu vaccine has no effect on the course of EAE in mice.
Tr. 499; Resp. Ex. F-3. Dr. Forsthuber cited to an article by Stojkovic, which found increased
anti-MOG antibodies detected in all of the mice with EAE, and no difference in anti-MOG
antibodies found between vaccinated and unvaccinated mice with EAE. Id. Dr. Forsthuber
testified that since MOG antibodies are the basis of Dr. Steinman’s theory, this study undermines
his theory. Dr. Forsthuber testified that the mice models in EAE are more like ADEM models,
but we call it MS and the model doesn’t perfectly replicate everything that happens in humans.
So, we know there are limitations. Tr. 498.

C. Discussion and Conclusion Regarding Loving Prong Four (Althen Prong
One):

Under Althen prong one, petitioner must set forth a medical theory explaining how the
vaccine could have caused his significant aggravation. Andreu, 569 F.3d 1367, 1375 (Fed. Cir.
2009); Pafford, 451 F.3d at 1355-56. This prong requires petitioner to make an evidentiary
showing that the vaccine “can” cause the injury alleged. Pafford, 451 F.3d at 1356.

The causation theory must relate to the injury alleged. The petitioner must provide a
sound and reliable medical or scientific explanation that pertains specifically to this case,
although the explanation need only be “legally probable, not medically or scientifically certain.”
Knudsen, 35 F.3d at 548-49. Recently, in Kottenstette, the Federal Circuit reiterated that proof of
causation does not “require identification and proof of specific biological mechanisms[.]”
Kottenstette v. Sec’y of Health & Hum. Servs., 861 F. App’x 433, 440-41(Fed. Cir. 2021) (citing
Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 549 (Fed. Cir. 1994)). Causation “can
be found in vaccine cases…without detailed medical and scientific exposition of the biological

30
Christian Confavreux et al., Vaccinations and the risk of relapse in multiple sclerosis, 344 The New England
Journal of Medicine 319 (2001). [Resp. Ex. B-2].
31
Mia Mailand & Jette Fredriksen, Vaccines and Multiple Sclerosis: A Systematic Review, 264 J. Neurol. 1035
(2016). [Resp. Ex. B-1].

33
mechanisms.” Knudsen, 35 F.3d 543, 548-49 (Fed. Cir. 1994). I

[Text truncated at 120,000 characters. The full text is on the page linked above.]

---

Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10736460. Public record. Not legal advice.