Gardner v. Secretary of Health and Human Services

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). It is not necessary for a petitioner

to point to conclusive evidence in the medical literature linking a vaccine to the petitioner’s

injury, as long as the petitioner can show by a preponderance of evidence that there is a causal

relationship between the vaccine and the injury, whatever the details of the mechanism may be.

Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1325 (Fed. Cir. 2010).

Petitioner’s expert, Dr. Steinman, opined that there is homology between components of

the flu vaccine and components of myelin in the human body. Pet. Ex. 66. As required by Althen

and other cases in the program, he presented a theory of molecular mimicry and recall response,

which explains how the introduction of the flu vaccine can cause an autoimmune response

against myelin, which can cause significant aggravation of MS beginning within 2-3 days. Pet.

Ex. 66. He concluded that there is sufficient structural similarity between the influenza vaccine,

particularly the H1N1 component administered to petitioner, with components of myelin in the

central nervous system, known to be targeted in optic neuritis, MS, transverse myelitis, and

ADEM.” Pet. Ex. 66 at 20. Further, Dr. Foley opined that the vaccine worked as an antigenic

stimulus which can open the blood brain barrier or, in this case, stimulated immune cells to rush

into the central nervous system via an open blood-brain barrier. He testified that these cells are

usually perivenular and if they aggregate in sufficient numbers, they can cause swelling in the

brain or the spinal cord with acute inflammation as occurred in this case. The swelling can put

pressure on things like the cortico-spinal tract which is the major motor tract going to the legs

and can affect bowel and bladder function as well. Tr. 121-22. Dr. Steinman 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.” Tr. 252.

Dr. Steinman researched his theory by running BLAST searches to look for homologies

between the components of the Flu vaccine and MOG, “a nervous system protein in the myelin

sheath known to be targeted in ADEM…optic neuritis, transverse myelitis and MS.” Pet. Ex. 66

at 12. He found that the sequence TGMEVGYW [which] has 6 of 8 amino acids in a consecutive

peptide in both MOG and the vaccine is sufficient to cause clinically relevant

neuroinflammation. Id. at 14. Based on the three Gautam articles, Dr. Steinman opined that the

stretch of those sequence homologies was sufficient to trigger clinically relevant inflammation.

The first Gautam paper from 1992 demonstrated that the injection of five of twelve, sometimes

nonconsecutive amino acids of myelin basic protein (MBP), are sufficient to trigger EAE in

mice. Pet. Ex. 77. A second article by Gautam demonstrated that a peptide with 4 of 11 MBP

amino acids was able to stimulate CD4 T cells and induce neuroinflammation in mice. Pet. Ex.

78. Dr. Steinman then referenced a third study by Gautam et al, published six years later, that

showed that 5 of 11 amino acids were identical between a herpes virus and MBP, with only 3

consecutive proteins and were capable of inducing EAE in some of the mice. Pet. Ex. 79. The

authors of this paper noted that Wucherpfennig and Strominger have provided strong evidence

that peptides derived from certain viruses and bacteria could stimulate MBP-specific T cell

clones generated from MS patients. Gautam used a similar database search based on MHC and

TCR contact residues and identified a herpesvirus (Saimiri-HVS) peptide with homology to the

disease causing MBP 1-11 peptide. The Gautam group demonstrated for the first time that the

HVS peptide stimulates the MBP 1-11 T cell hybridomas and induces clear clinical signs of EAE

in some mice. Id. The paper recognized that the viral peptide did not stimulate EAE as strongly

as the wild type MBP 1-11 but that it did stimulate all four T cell hybridomas in their

34

experiment. Id. at 8. The authors concluded, “these results indicate that a cross-reactive viral

peptide can stimulate self-reactive T cells.” Id.

Initially, Dr. Forsthuber argued that the Gautam studies required that specific amino acids

needed to be in positions 3 and 6 in order to cause cross reactivity. Subsequently, he clarified

that the positions are not so critical, but it is what is in the positions that is. Tr. 473. He then

testified that different T cells have different preferences for binding and that you cannot predict

what peptides will bind with the MHC molecule and which will stimulate an autoimmune

response. Id. at 475, 479. He cast doubt on the likelihood of molecular mimicry because of the

array of overlapping nine peptide sequences in the human body and in bacteria or viruses. Dr.

Forsthuber contended, that the “activation of T cells by specific peptides is highly complex and

exquisitely sensitive to a delicate balancing act of binding of a peptide to and properly aligning

its sequence within the peptide-binding register of an MHC molecule.” Resp. Ex. E at 6. He

emphasized that typically autoimmune T cells are eliminated making it more complicated than

randomly matching peptides. Tr. 475. However, it would appear that, in the case of the

petitioner, his autoimmune T cells were not eliminated by thymic selection as they appear to be

implicated in a rapidly developing, severe case of tumefactive MS that looked quite similar to the

presentation of ADEM at the outset.

Dr. Forsthuber testified that Dr. Steinman does not know “definitively” exactly which of

the six of eight amino acids would be needed to be in epitopes which would be needed to induce

a reaction. He testified that “you can’t predict just by looking at the sequence…it’s impossible to

predict what would bind…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.” Tr.

474. All in all he testified that because of the multiple factors involved, it was not possible to

definitively predict what peptides would give rise to molecular mimicry and cause disease

because of the complexity of factors he described.

During the course of Dr. Forsthuber’s testimony, I indicated that I understood that it was

very difficult to do the experiments that would lead scientists to be able to understand and predict

the causes of human autoimmune disease such as MS, and that I understood the need to

definitively control the number and placement of the amino acids in laboratory experiments in

order to get reliable results in mice and that the odds of getting the wrong amino acids in the

right place may be high. But I asked Dr. Forsthuber whether, in the real world, part of the

explanation for rare events stimulated by the immune system is because sometimes these things

(the proper alignments) do occur? Most of the time they don’t but sometimes they do? He

answered that that was a good question and that the answer is nobody knows. He felt that the

concept of molecular mimicry based on sequence similarities is too simplistic and that it is more

complicated than that. Tr. 476.

Regarding Dr. Steinman’s testimony about sequences of similar amino acids, I find that

he was providing an example of homology between amino acid sequences in the vaccine and

MOG to illustrate homology as a way to explain the science using readily available resources.

Dr. Steinman explained that he could not perform research on the petitioner, and most likely will

never be able to do research on human subjects in cases in this court. He explained that such

testing would be expensive, would require institutional review board consent, and would involve

35

obtaining of blood or CSF samples from before and shortly after onset which is generally

impossible in the context of a vaccine case. Pet. Ex. 85 at 3. Dr. Forsthuber agreed that this was

a very valid point that Dr. Steinman made. While it would be ideal to look at each molecular

response to a vaccine in an individual petitioner, it is just not possible to test everybody and what

their response against vaccine antigens would be. He agreed that ideally, we could test it, but it

is a very involved process. Tr. 494. To be sure the critical time period for testing both before and

after the onset of symptoms would have long passed by the time a case would be filed in the

program.

Molecular mimicry has been an accepted theory in this Court and Dr. Steinman’s BLAST

search process has been accepted in a variety of cases involving demyelinating diseases, such as

GBS, MS, TM, and ADEM. While prior decisions of special masters are not binding on my

analysis, it is persuasive that molecular mimicry has been accepted in the program as a biological

mechanism involving demyelinating conditions in multiple cases. See, e.g., See Davis v. Sec’y of

Health & Human Servs., No. 14-978V, 2022 WL 1654743 (Fed. Cl. Apr. 27, 2022); Maloney v.

Sec’y of Health & Human Servs., No. 19-1713V, 2022 WL 1074087 (Fed. Cl. Mar. 17, 2022);

Pierson v. Maloney v. Sec’y of Health & Human Servs., No. 17-1136V, 2022 WL 322836 (Fed.

Cl. Jan. 19, 2022); Koller v. Sec’y of Health & Human Servs., No. 16-439V, 2021 WL 5027947

(Fed. Cl. Oct. 8, 2021); E.M. v. Sec’y of Health & Human Servs., No. 14-753V, 2021 WL

3477837 (Fed. Cl. July 9, 2021); White v. Sec’y of Health & Human Servs., No. 15-1521V, 2019

WL 7563239 (Fed. Cl. Dec. 19, 2019); Pasco v. Sec'y of Health & Human Servs., No. 16-500V,

2022 WL 6616736, at *27 (Fed. Cl. Sept. 23, 2022).

Dr. Steinman served as an expert in the Quackenbush-Baker case, in which I found the

theory of molecular mimicry sufficient to explain how the vaccine could cause an aggravation of

an asymptomatic or radiologically isolated MS. Quackenbush-Baker v. Sec'y of Health & Human

Servs., No. 14-1000V, 2018 WL 1704523, at *16 (Fed. Cl. Mar. 14, 2018). I found that

petitioner’s receipt of the flu vaccines in 2009 and 2011 made it more likely than not that she had

a recall response when she received the 2013 flu vaccine, which contained several of the same

components. Id. In that case there was also a rapid onset of MS symptoms. While my prior

decisions or those of other special masters are not binding on my analysis, it is persuasive that

Dr. Steinman’s theories have been accepted as reputable, medical, or scientific mechanisms in

other cases in this court and, in particular, in a case with similar facts to the present one.

The medical literature filed by petitioner establishes that molecular mimicry is a well-

known theory in immunology that has been postulated numerous times in medical literature as a

likely mechanistic theory to explain how infectious agents and vaccines can cause autoimmune

disorders like ADEM, TM, MS, and GBS. Pet. Ex. 66. Fujinami and Whitton described

molecular mimicry as one of three mechanisms that can initiate immunoreactivity leading to

autoimmune disease. Pet. Ex. 75. To be sure, there are skeptics about the theory as evidenced by

the Trost article among others. The quest for definitive proof has been successful only in a

limited number of infections and autoimmune diseases. Nevertheless, molecular mimicry

remains a primary theory of autoimmunity and Dr. Steinman has presented evidence as to how

molecular mimicry triggered by the flu vaccine could have accelerated and aggravated the

petitioner’s MS condition. While I respect the detailed testimony presented by Dr. Forsthuber, I

think the standard for proof that he proposes for analysis of a vaccine case is far higher than the

36

law requires. Congress created the Vaccine Program to recognize that adverse events do occur

as a result of vaccinations. As stated in Althen, The Vaccine Injury Program is designed “to

allow the finding of causation in a field bereft of complete and direct proof of how vaccines

affect the human body.” 418 F.3d at 1280. Both Dr. Steinman and Dr. Forsthuber concede that

the science around molecular mimicry is growing, and definitive conclusions have not yet been

reached in the scientific community. The case law in this program has held that, given the state

of current scientific knowledge, petitioner need not make a specific type of evidentiary showing

or require identification of a specific homology to prove that molecular mimicry is a sound and

reliable theory by a preponderance of the evidence. Requiring proof of specific homology or

proof of identical protein sequences giving rise to disease between the flu vaccine and the central

nervous system in order to prove causation would require scientific certainty, which is a bar too

high. See Knudsen, 35 F.3d at 549 (explaining that “to require identification and proof of specific

biological mechanisms would be inconsistent with the purpose and nature of the vaccine

compensation program”).

The task of this court is not to predict what peptides may give rise to disease through

molecular mimicry in a consistent and foreseeable manner, but rather to analyze whether there is

sufficient evidence to indicate that it could have in this case. I find that Dr. Steinman’s

presentation was sufficient to demonstrate by a preponderance of the evidence that the flu

vaccine received by Mr. Gardner on December 1, 2014 could have and was likely to have been

the cause of the significant aggravation and acceleration of his MS condition. While I recognize

that the theory has not been definitively proven, the testimony supports the concept that rare

events, such as the one that occurred in this case, can be caused by molecular mimicry. This

conclusion was well supported by the testimony of his treating MS specialist, Dr. Foley, who

provided a detailed explanation of the correlation between the progressive onset of symptoms

between December 3, 2014 and December 12, 2014, with the rapid development of a

longitudinally extensive lesion in the cervical and thoracic spine in conjunction with the

tumefactive lesion in the brain. Dr. Foley, early in the course of treatment, felt that the vaccine

was causal in the progression of this disease and indicated that in the course of his extensive

clinical experience treating MS patients that he has come to recognize that onset or aggravation

of the disease is at times caused by vaccines.

For the reasons above, I find that petitioner has demonstrated a sound and reliable

medical theory by preponderant evidence of how the flu vaccine he received on December 1,

2014 could have caused the significant aggravation of pre-existing MS. All of the doctors

advocate vaccination for their MS patients and advocate for vaccination in general, but Dr.

Steinman has demonstrated a theory that is sufficient to explain how the flu vaccine can cause an

aggravation of a mild case of MS, and I have concluded that his theory has satisfied Althen Prong

One.

5. Loving Prong Five (Althen Prong Two): Petitioner has established a logical sequence

of cause and effect between the flu vaccine and the significant aggravation of MS in

his case.

Above, under Loving Prong Three, I concluded that petitioner suffered a significant

aggravation of his prior condition. Under Loving Prong Four (Althen Prong One), I concluded

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that the influenza vaccine could cause an aggravation of a previously mild MS through the

mechanisms of molecular mimicry and recall response. 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.” Loving, 86 Fed. Cl. at 144; see also Althen, 418 F.3d at 1278. This

prong is sometimes referred to as the “did it cause” test; i.e., in this particular case, did the

vaccine logically but not definitely cause the alleged injury. Loving 86 Fed. Cl. at 144.;

Broekelschen, 618 F.3d at 1345 (“Because causation is relative to the injury, a petitioner must

provide a reputable medical or scientific explanation that pertains specifically to the petitioner’s

case”). Temporal association alone is not evidence of causation. See Grant v. Sec’y of Health &

Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992).

This sequence of cause and effect is usually supported by facts derived from petitioner’s

medical records. Althen, 418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at

1326; Grant, 956 F.2d at 1148. In this case it was also significantly supported by the opinion

and testimony of his primary treating MS specialist. The Federal Circuit has held, “A special

master should consider the causation opinions of 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.” Capizzano, 440 F.3d at 1280.

A. Petitioners’ Experts’ Opinions Regarding Loving Prong Five (Althen Prong Two)

Dr. Steinman opined that the flu vaccine more likely than not significantly aggravated

petitioner’s MS. After demonstrating his theory of molecular mimicry, Dr. Steinman testified

that petitioner’s significant aggravation occurring rapidly and progressively was likely due to a

recall response to the influenza vaccine that he received in December 2014 which had an

identical H1N1 component as was contained in the 2010 vaccine which petitioner also received.

Pet. Ex. 4 at 3; Pet. Ex. 16; Tr. 252-53. He testified that the theory of molecular mimicry with a

recall response fit in petitioner’s case because “recall immunity is very fast…sometimes it’s hard

to measure…sometimes the very fast response is not necessarily in a neutralizing antibody

[but]…in a memory killer T cell.” Id. at 252.

The history of the time period from December 1, 2014 forward is detailed above and is

summarized here. There is no question that petitioner had an episode of optic neuritis in June of

2014, which appeared to have mostly resolved over the next couple months. In June, he had an

MRI of the brain which demonstrated no evidence of demyelination in the brain but did show

enhancement solely at the globe of the optic nerve. Pet. Ex. 3 at 8-9. He had no medical

encounters between a follow-up at the Moran Eye Center in August and the December 1, 2014

appointment with Dr. Richards. There was no evidence of prior viral or bacterial infections

during the months prior to December 1.

Mrs. Gardner testified that her employer was offering incentives for employees to do a

full physical exam with their doctors at that time. She said that she had petitioner make an

appointment and she did for herself as well because of this program. Tr. 10. Thus the

appointment was made not because of any particular troublesome symptom, but simply for an

annual physical. At that appointment on December 1, Mr. Gardner told Dr. Richards that in the

last week he had experienced a sensation almost like pins and needles, mostly in his left foot but

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extending up on the left to his abdomen which comes and goes and at times there is a heat

sensation on the left thigh. Pet. Ex. 4 at 6. He received the flu vaccine at that appointment. A

couple days later, he began to experience flu like symptoms. He continued to work until

December 7, when he called in sick as he was feeling cold and achy and was barely able to use

his right leg. Dr. Richards had apparently ordered blood work. Mr. Gardner came in on

December 8, for the bloodwork, and the medical assistant noticed he was having difficulty

walking at that appointment. She set him up to see Dr. Richards again. He saw Dr. Richards on

Wednesday, December 10, when he told the doctor that his right leg felt worse since this past

Monday (December 8). The note indicated that while standing there he could hardly lift his right

leg up, his memory had not been as good as before and his brain was feeling foggy. Pet. Ex 4 at

9. He said the tingling in his left side was still present and he had a limp. He told Dr. Richards

that two or three days after his last appointment his right leg went numb from his foot to his

thigh. Dr. Richards suggested that he see a neurologist, but he did not decide to hospitalize him

or make urgent arrangements to see a neurologist. Mr. Gardner went home.

When the Gardners awoke on December 12, Mrs. Gardner testified that her husband

could not get out of bed. She had responsibilities at work, so she pushed him out of bed onto the

floor. She went to work but returned an hour and a half later and found that he was still on the

floor in the bathroom, and he could not urinate. She had to pull him down the stairs and put him

in the car. She drove him to the Intermountain Medical Center emergency room. Tr. 18. He was

admitted to the hospital through the ER. Upon admission, the initial MRIs were done

demonstrating the tumefactive lesion in the brain and the extensive lesion in the spinal cord.

Dr. Foley explained that petitioner had only some pins and needles sensation on

December 1, 2014. Within several days he was having some type of what appeared to be a

systemic reaction to the flu vaccine. After a few days, he started to notice more neurological

symptoms and then later in the time period he starts to get much worse to the point where his

wife has to put him in the car to drive him to the hospital on December 12. At that point he had

right leg paralysis, severe weakness and bladder dysfunction. Tr. 124.

Dr. Foley testified that an acute inflammatory lesion in the spinal cord that is gadolinium

enhancing is going to manifest very, very rapidly as clinical symptoms. He correlated at least the

onset of the cervical spine lesion with the rapid development of symptoms over the course of 12

days. He said that this rapid development of symptoms combined with the MRI demonstration

of an enhancing tumefactive lesion in the brain and an extensive enhancing lesion in the cervical-

thoracic spine suggests an open blood-brain barrier and blood-cord barrier. As such he thought

that there was likely an open blood-brain barrier that exposed the CNS to the antigenic stimulus

generated by the vaccine. He testified 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. He testified that the space in

which the cervical-thoracic cord passes is less than the size of a half dollar. He said his theory

would be 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.

While petitioner had not had an MRI in the months immediately before December, he did

have one in June which showed no evidence of MS lesions in the brain. He had at most mild

39

symptoms on December 1, which rapidly became worse beginning a few days later. Dr. Sriram

agreed that these lesions were massively enhanced on December 12, but he said it was his best

guess that they probably began to develop in October or November. Tr. 342.

Dr. Foley testified, as petitioner’s treating physician, that petitioner’s current diagnosis is

“atypical MS.” Tr. 105. He explained in his second expert report that petitioner’s “MS was

significantly exacerbated by the influenza vaccination, leaving him with permanent, severe

disability following the vaccination.” Pet. Ex. 63 at 1. Dr. Steinman agreed that petitioner had

“an atypical case that had a lot of features of ADEM – that there was intense inflammation that

caused horrible damage.” Tr. 279. Both experts agreed that, within a few days of the flu

vaccination, petitioner experienced flu-like symptoms, and after that began to experience more

neurological symptoms as he complained of cognitive difficulties, vision changes, and persistent

left leg numbness with the most prominent symptom becoming right leg dysfunction leading to

paralysis by December 12, when his signs and symptoms had become severe. Dr. Foley

classified this progression as an “acute event.” He said petitioner’s course “did not have the

typical hallmark of a tumefactive MS event in that it developed so dramatically, had no

oligoclonal bands in the CSF and was essentially monophasic which is why he initially called it

ADEM. Tr. 106. The lack of oligoclonal bands is much more common in ADEM than in an

acute tumefactive MS situation.” Id. Dr. Foley also noted that he “elected to call it ADEM at the

time,” of diagnosis, “knowing that [he] was going to follow [petitioner] over time and that we

would treat him as if he had ADEM.” Id. Both Dr. Foley and Dr. Steinman indicated that there

were no other identifiable causes of petitioner’s significant aggravation. Tr. 144, 212. On cross

examination, Dr. Foley stated that petitioner “met the McDonald criteria certainly on the basis of

the optic neuritis and the acute ADEM-like event.” Id. at 151. He said, it was not clear if

petitioner would have met the criteria solely on the basis of the pins and needles at the beginning

of the month, as this would not “count…as a bona fide event.” Id.

Dr. Foley also testified that while mild cognitive complaints were expressed such as word

finding difficulty, Mrs. Gardner testified that early in the time period she did not recall any

cognitive issues and basically that his left leg was tingly. She thought that petitioner’s symptoms

at the time might have been stress related. Tr. 10. Dr. Foley explained that, consistent with the

tumefactive lesion in the brain, the cognitive symptoms appeared to manifest more distinctly

later in the course once petitioner was in rehab, which he thought was also consistent with his

theory. Tr. 125.

Dr. Foley was asked how he interpreted the MRIs and correlated them with the symptom

development. He said that when Mr. Gardner lost function in his legs by December 12, the

doctors ordered MRIs of the brain and of the cervical and thoracic spine. Both the brain and

spinal films were massively contrast enhancing. So, the process radiographically suggested a

“major inflammatory storm kind of situation which clearly played out clinically.” Tr. 108.

Petitioner was then treated with high dose steroids which brought his legs back some. Id. at 107.

They did a second MRI on December 22, which demonstrated slightly decreased edema and

enhancement in the brain. The radiologist noted that the findings would be consistent with

tumefactive MS with treatment response. Mild enhancement of the intraorbital optic nerve was

seen, similar to the prior scan. An asymmetric atrophy of the right intraorbital optic nerve was

also identified. On the spinal cord they noted an enhancing intramedullary lesion now extending

40

from C6 to T2 that measured 4.3 by .9 by .9 centimeters which was significantly increased from

2.8 by .8 by .6 on the prior scan. Dr. Foley indicated that we were seeing some improvement in

the brain MRI as a result of the initial steroid treatment but some worsening in the spinal cord

lesion burden during this time frame. Tr. 110-11. He testified that this was consistent with

petitioner’s legs becoming worse in the hospital. He was essentially paralyzed in the legs and the

doctors then went to plasmapheresis. He said that this imaging presentation was significantly

worse than a standard presentation of multiple sclerosis. With the background of no lesions in

the brain in the June MRI, and the significant development of enhancing lesions corresponding

with the rapid onset of symptoms in December, he characterized these lesions as more acutely

reactive. Tr. 111-12.

A third set of MRIs was done on January 26, 2015 which showed a large left temporal

lobe area of white matter T2 signal hyperintensity, with resolution of the previously seen

associated edema and mass effect. There was slight volume loss on this scan which Dr. Foley

explained would relate to neuronal cell death caused by the initial lesion burden. On the spinal

cord films a mild fusiform cord lesion from C6 to T2 with mild residual post-contrast

enhancement was seen, but no cord expansion, which had previously been seen on the prior two

scans. The lesion was similar in extent but without the previous mass effect and demonstrated

mostly resolved contrast enhancement. Tr. 113

Dr. Foley said that gradual resolution that was seen and this kind of symptom course

“would be more typical of a real severe ADEM which is why [he is] calling it…an atypical MS.”

Tr. 115. The lesions have remained relatively stable with a little bit of variability with resolution

of the swelling which allowed his spinal cord to take effect again and allow him to walk. He

still has multiple problems but at least he can walk. Id.

He was asked if the lesions in ADEM and tumefactive MS can look the same and Dr.

Foley said that they can. He said this was a rare and “real severe form of MS,” described as

tumefactive MS, which can have “significant amounts of edema with significant open blood-

brain or blood-cord barrier dysfunction.” Tr. 116. Thus, the first thing that comes to mind on

this presentation is ADEM with these images, the clinical course and the monophasic large

attack. Id. Dr. Foley further testified that petitioner obviously had optic neuritis before, but that

this event is what left petitioner disabled. Id.

When asked to explain physiologically what was going on in the central nervous system,

Dr. Foley said that there is an opening in the blood brain and blood cord barrier that occurs due

to an antigenic stimulus and then circulating immune cells will rush in and if they aggregate will

start to do several things. One is that they can swell the spinal cord and put pressure on the

corticospinal tract going to the legs and it can compromise bowel and bladder function. These

inflammatory aggregates can also start exerting a negative effect on the neuronal pools around

them and start killing cells, killing neurons which ultimately led to the atrophy that we see in his

scans years later. Tr. 121-22.

Dr. Foley was asked about the time course of what occurred in petitioner. He said that

because we don’t have an MRI immediately before the vaccination, we cannot say for sure.

However, if you take from the time of the injection when petitioner had some mild

41

paresthesias—shortly thereafter he has some sort of reactive symptoms that suggest some

systemic reaction to the flu shot. Then, after a few days, petitioner really starts to notice more

and more neurological symptoms. Tr. 124. Dr. Foley explained that the spinal cord, especially

the anterior cord where corticospinal tracts are very small – less than a half dollar around –

lesion formation there is rapidly transmitted into clinical symptoms. Id. So, at the beginning we

have only pins and needles paresthesias prior to the injection, and then after a couple of days it

seems like he has reacted negatively to the flu shot, but not necessarily worsened neurologically.

Then after that he really starts with this whole progression described in the testimony by Mr. and

Mrs. Gardner where it takes her an hour to get him into the car to go to the hospital on December

12. Id. Dr. Foley continued, stating that an inflammatory lesion in the spinal cord will manifest in

symptoms very rapidly, so it was his view that sometime in the first week after having the flu

shot petitioner developed at least a spinal cord lesion that was rapidly and severely symptomatic.

Id.

When asked about the role of the tumefactive brain lesion in the development of this

disease, Dr. Foley said the lesion was primarily in the temporal lobe into the frontal lobe which

would induce speech dysfunction, cognitive dysfunction, processing slowing, probably

emotional abnormalities. Tr. 125. As we heard Mrs. Gardner testify, petitioner could hardly

speak by the end of his admission. He said that we saw more of the brain symptoms come out

during the rehabilitation stay, which is what he would expect as the time course for the

development of cognitive symptoms secondary to the tumefactive brain lesion. Id.

Regarding petitioner’s previous bout with optic neuritis in June 2014, Dr. Steinman noted

that there was no clinical or radiographic evidence of disease activity elsewhere in his nervous

system. Pet. Ex. 66 at 20. Further, on cross examination, Dr. Foley stated that, “the eloquent

tissue in the spinal cord and…the progression of his clinical construct during the hospitalizations

would be entirely consistent with new and enlarging lesions in eloquent tissue that had very little

reserve areas…there would be a tight correlation between onset of clinical symptoms and the

new and enlarging lesions and edema related to those lesions, especially in the spinal cord.” Tr.

163-64.

Dr. Foley testified that petitioner’s clinical presentation and MRIs “suggest a very open

blood-brain barrier or blood cord barrier, and so there’s just a lot of inflammatory process, and

generally in MS, there will be a lot of oligoclonal bands generated with that.” Tr. 107. Petitioner

received high dose intravenous steroids and was transferred to a rehabilitation unit and “became

completely paraplegic with no use of either leg,” and continued bowel and bladder problems. Tr.

120-21.

On questioning by the Court, Dr. Steinman endorsed the concept that if petitioner had

some level of MS at the time of the vaccination it is likely that the blood brain barrier was open

and “even if it weren’t open, the immune cells, once they’re activated, they can go across the

blood brain barrier, and if they get across and they recognize, for instance, MOG, they could

stick there and cause damage.” Tr. 308. Dr. Foley noted that respondent had a nice article by

DeKeyser, 32 which for the most part he agreed with, in which they say in the following six weeks

32

Jaques De Keyser et al., Effects of influenza vaccination and influenza illness on exacerbations in multiple

sclerosis, 159 J. Neurol. Sci. 51 (1998).3 [Resp. Ex. A-3].

42

after an influenza illness, there was roughly a 33% incidence of relapse and that relapse after

influenza vaccination is much less common—only about 5%. Tr. 128; Resp. Ex. A-3. So, he

said, 5% is less common but it still occurs and obviously becomes 100% if it happens to you. He

said that, fortunately, we see relapse secondary to the antigenic stimulus of vaccination much

less frequently than after infection, but his busy neuroimmunology clinic sees one approximately

every couple of months. Tr. 128.

B. Respondent’s Experts’ Opinions Regarding Loving Prong Five (Althen prong

two)

Dr. Forsthuber and Dr. Sriram opined that petitioner’s MS was already symptomatic at

the time of the vaccination on December 1, 2014. Resp. Ex. A; Resp. Ex. B; Resp. Ex. F. Dr.

Forsthuber wrote in his second expert report that “there is no reliable evidence that the influenza

epitope claimed by Dr. Steinman as a ‘molecular mimic’ induces immunity, or that this sequence

could generate and/or activate MOG reactive T cells,” in pe

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