Barrientos v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: May 17, 2024

*************************

CINDY BARRIENTOS, * PUBLISHED

*

Petitioner, * No. 18-1899V

*

v. * Special Master Nora Beth Dorsey

*

SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine;

AND HUMAN SERVICES, * Pre-Existing Condition; Significant

* Aggravation; Transverse Myelitis;

Respondent. * Thoracic Myelopathy.

*

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Sylvia Chin-Caplan, Law Office of Sylvia Chin-Caplan, LLC, for Petitioner.

Felicia Langel, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION1

On December 10, 2018, Cindy Barrientos (“Petitioner”) filed a petition for compensation

under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42

U.S.C. § 300aa-10 et seq. (2018)2 alleging that she suffered significant aggravation of her pre-

existing transverse myelitis and thoracic myelopathy as a result of an influenza (“flu”)

1

Because this Decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it on the United States Court of Federal Claims’ website and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc in accordance with the E-

Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of

Electronic Government Services). This means the Decision will be available to anyone with

access to the Internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to

identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. If, upon review, the undersigned agrees that the

identified material fits within this definition, the undersigned will redact such material from

public access.

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). All citations in this Decision to individual sections of the

Vaccine Act are to 42 U.S.C. § 300aa.

vaccination administered to her on December 11, 2015.3 Petition at Preamble, ¶ 16 (ECF No. 1).

Respondent filed his Rule 4(c) report on February 6, 2020, asserting that Petitioner had “not met

her burden establishing entitlement to compensation under the terms of the Vaccine Act.”

Respondent’s Report (“Resp. Rept.”) at 1 (ECF No. 26).

After carefully analyzing and weighing the evidence presented in this case in accordance

with the applicable legal standards, the undersigned finds that Petitioner has failed to provide

preponderant evidence that her pre-existing condition was significantly aggravated by the flu

vaccination she received on December 11, 2015. Thus, Petitioner has failed to satisfy her burden

of proof under Loving v. Secretary of Health & Human Services, 86 Fed. Cl. 135, 142-44 (2009).

Accordingly, the petition shall be dismissed.

I. ISSUES TO BE DECIDED

The parties stipulate that Petitioner was born on November 24, 1973, and that she

received a flu vaccine on December 11, 2015. Joint Prehearing Submission (“Joint

Submission”), filed Oct. 26, 2022, at 1 (ECF No. 93). They also stipulate that “prior to the

administration of the flu vaccine on December 11, 2015, [Petitioner] suffered from a pre-existing

thoracic myelopathy.” Id. Further, they stipulate that after she received the flu vaccination on

December 11, 2015, Petitioner’s condition worsened as noted on her magnetic resonance

imaging (“MRI”) and by her treating physicians. Id. at 2. The parties stipulate that Petitioner

suffered from her condition for more than six months and that she timely filed her petition within

the applicable statute of limitations. Id.

The parties dispute the nature of Petitioner’s condition before and after her flu vaccine.

Joint Submission at 2. Petitioner “asserts that the flu vaccine that she received on December 11,

2015, resulted in a significant aggravation of her underlying [longitudinally extensive transverse

myelitis].” Id. at 3. Respondent disputes that she suffered transverse myelitis and/or

longitudinally extensive transverse myelitis “before or after the administration of the flu vaccine

on December 11, 2015.” Id. at 2. Respondent also disputes that the vaccine was the cause of her

significantly worsened pre-existing condition. Id. Instead, Respondent attributes Petitioner’s

worsening to the “evolution of [her] pre-existing condition.” Id.

3

In the preamble of her petition, it was not clear that Petitioner’s claim was significant

aggravation, but in paragraph 16, she specifically asserted her claim based on significant

aggravation. Petition at ¶ 16 (ECF No. 1). Additionally, in their joint submission, the parties

specified that Petitioner was alleging significant aggravation. Joint Prehearing Submission

(“Joint Submission”), filed Oct. 26, 2022, at 1-3 (ECF No. 93). The undersigned agrees that the

facts presented raise a claim of significant aggravation.

2

II. PROCEDURAL HISTORY

Petitioner filed her petition and medical records on December 10 and December 12,

2018. Petition; Petitioner’s Exhibits (“Pet. Exs.”) 1-9. On January 22, 2020, the case was

4

reassigned to the undersigned. Notice of Reassignment dated Jan. 22, 2020 (ECF No. 23).

Respondent filed his Rule 4(c) report arguing against compensation on February 6, 2020. Resp.

Rept. at 1.

On September 9, 2020, Petitioner filed an expert report from Dr. Carlo Tornatore. Pet.

Ex. 13. Respondent filed an expert report from Dr. Adil Javed on April 14, 2021. Resp. Ex. A.

The undersigned held a Rule 5 conference on June 22, 2021. Rule 5 Order dated June 22, 2021

(ECF No. 47). The undersigned did not reach a preliminary opinion as to causation. Id. at 2.

Given the complexity of the clinical course and MRI findings, a hearing was recommended. Id.

On September 30, 2022, Petitioner submitted her pre-hearing brief. Pet. Pre-Hearing

Brief (“Br.”), filed Sept. 30, 2022 (ECF No. 78). Respondent filed a pre-hearing brief on

October 21, 2022. Resp. Pre-Hearing Br., filed Oct. 21, 2022 (ECF No. 86). An entitlement

hearing was held November 16 and November 17, 2022. Order dated Nov. 17, 2022 (ECF No.

98); Transcript (“Tr.”) 1, 148. Following the hearing, the undersigned requested the parties to

file supplemental expert reports commenting on Petitioner’s treating physician Dr. Elliot

Frohman’s diagnostic statement from 2019 and explaining how this statement affects their

respective opinions as to diagnosis and causation. Order dated Nov. 17, 2022.

Respondent filed a supplemental expert report from Dr. Javed on December 16, 2022.

Resp. Ex. C.5 Instead of a supplemental expert report,6 Petitioner responded to the Court’s

request by citing medical records submitting a brief. Pet. Status Rept., filed Mar. 6, 2022 (ECF

No. 110); Pet. Br. Addressing the Court’s Order (“Pet. Supplemental Br.”), filed Mar. 13, 2023

(ECF No. 112). On June 5, 2023, Petitioner filed a post-hearing brief. Pet. Post-Hearing Br.,

filed June 5, 2023 (ECF No. 117). On August 7, 2023, Respondent filed a post-hearing brief.

Resp. Post-Hearing Br., filed Aug. 7, 2023 (ECF No. 118).

The matter is now ripe for adjudication.

4

Petitioner continued to file medical records throughout the course of litigation.

5

Respondent labeled this as exhibit B however, Respondent already had an exhibit B and it is

Dr. Javed’s CV. Therefore, the undersigned will refer to Dr. Javed’s supplemental expert report

as exhibit C.

6

In February 2023, Petitioner filed a status report indicating her expert was on medical leave

until June/July 2023 and would be unable to draft a supplemental report. Pet. Status Rept., filed

Feb. 2, 2023 (ECF No. 108).

3

III. MEDICAL TERMINOLOGY

A. Transverse Myelitis

Transverse myelitis “is a rare clinical syndrome in which an immune-mediated process

causes neural injury to the spinal cord, resulting in varying degrees of weakness, sensory

alterations[,] and autonomic dysfunction.” Pet. Ex. 18 at 1.7 The Transverse Myelitis

Consortium Working Group proposed diagnostic criteria including “bilateral sensory, motor, or

autonomic dysfunction attributable to the spinal cord, a clearly defined sensory level[,] and

peaking of symptoms within [four] hours and 21 days.” Id. “In addition, evidence of an

inflamed spinal cord (e.g. cerebrospinal fluid (CSF) pleocytosis,[8] elevated [immunoglobulin G

(“IgG”)] index[9] or gadolinium enhancement[10] by [MRI] and exclusion of [] compressive

etiology by neuroimaging should be observed.” Id.

Petitioner’s expert, Dr. Tornatore, opined that transverse myelitis is “a generic term for

inflammation of the spinal cord.” Tr. 11. Transverse myelitis does not indicate an etiology, “just

that the [spinal] cord is inflamed.” Tr. 127. It can be caused “by a host of different things,”

including medication toxicity, tumors, compression myelopathy, and autoimmune diseases. Tr.

11. Transverse myelitis is diagnosed by MRI findings which show “characteristic [] signal

changes in the spinal cord suggesting inflammation or edema” of the spinal cord. Tr. 127, 163-

64. MRI findings related to transverse myelitis include “spinal cord enlargement,

7

N. Agmon-Levin et al., Transverse Myelitis and Vaccines: A Multi-Analysis, 18 Lupus 1198

(2009).

8

Pleocytosis is the “presence of a greater than normal number of cells in the [CSF].”

Pleocytosis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=39556 (last visited Apr. 25, 2024).

9

“Serum protein quantification is used to detect and monitor the course of [certain] diseases

[including] autoimmune diseases.” Kathleen Deska Pagana & Timothy J. Pagana, Blood

Studies, in Mosby’s Manual of Diagnostic and Laboratory Tests 10, 279 (6th ed. 2018).

“Proteins within the blood are made up of albumin and globulin. Several types of globulin

exists, one of which is gamma globulin. Antibodies are made up of gamma globulin protein and

are called immunoglobulins. There are many classes of immunoglobulins (antibodies).” Id. at

280. IgG “constitutes approximately 75% of the serum immunoglobulins; therefore[,] it

constitutes the majority of circulating blood antibodies.” Id.

10

“A contrast medium called gadolinium is a paramagnetic enhancement agent that crosses the

blood-brain barrier. It is especially useful for distinguishing [certain] abnormalities.”

Miscellaneous Studies, in Mosby’s Manual of Diagnostic and Laboratory Tests, supra note 9, at

1024, 1060.

4

intramedullary[11] increased T2 signal lesions,[12] and variable enhancement.” Pet. Ex. 13 at 28

(quoting Pet. Ex. 39 at 1).13 These abnormalities may be “diffuse and extend over several spinal

levels.” Id. (quoting Pet. Ex. 39 at 1). In addition to MRI, a lumbar puncture or “spinal tap” is

“done to try to sort out what the source of [] inflammation” is by analysis of the CSF. Tr. 11-12.

Respondent’s expert, Dr. Javed, opined that compression of the spinal cord can cause

inflammation. Tr. 301. When the spinal cord is squeezed, “some of the fibers die, [and] some of

the fibers [] inflame.” Id. Inflammation can also occur in response to infection. Tr. 190, 245,

263. An infection can stimulate the immune response which causes transverse myelitis. Tr. 245.

In transverse myelitis, “[w]hen the inflammatory lesion extends across more than three

vertebral segments longitudinally, it is commonly referred to as longitudinally extensive

transverse myelitis.” Pet. Ex. 13 at 27 (citing Pet. Ex. 16 at 2).14

B. Transverse Myelopathy

Transverse myelopathy is a “myelopathy[15] that extends across the spinal cord.”

Transverse Myelopathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=91256 (last visited Apr. 25, 2024).

According to Respondent’s expert, Dr. Javed, compressive myelopathy occurs when

there is “compression from [an] outside structure, the bone, the calcification, the disc material.”

Tr. 160. There is water inside and around and the center of the spinal cord. Id. As the spinal

cord is compressed by the outside (disc material), it “squeezes,” and “stifles the spinal cord, and

the spinal cord’s blood supply is also stifled, and the area where the blood supply is occurring

Intramedullary means “within the spinal cord.” Intramedullary, Dorland’s Med. Dictionary

11

Online, https://www.dorlandsonline.com/dorland/definition?id=25811 (last visited May 8, 2024).

12

T1 and T2 are technical terms applied to different MRI methods used to generate magnetic

resonance images.” T1 and T2 Lesions, MS Austl., https://www.msaustralia.org.au/glossary/t1-

t2-lesions/ (last visited May 8, 2024). Different methods are “used to detect different structures

or chemical in the central nervous system. . . . A T2 MRI image provides information about

disease burden or lesion load (the total amount of lesion area, both old and new).” Id.

13

Rohit Bakshi & John C. Mazziotta, Acute Transverse Myelitis After Influenza Vaccination:

Magnetic Resonance Imaging Findings, 6 J. Neuroimaging 248 (1996). This is also cited as

Resp. Ex. A3.

14

Wafa Akkad et al., Longitudinally Extensive Transverse Myelitis Following Vaccination with

Nasal Attenuated Novel Influenza A(H1N1) Vaccine, 67 Archives Neurology 1018 (2010).

15

Myelopathy is “any of various functional disturbances or pathologic changes in the spinal

cord, often referring to nonspecific lesions in contrast to the inflammatory lesions of myelitis.”

Myelopathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/

definition?id=32732 (last visited Apr. 25, 2024).

5

starts to become ischemic and dies off.” Tr. 160-61. For example, if you “squeeze a water bottle

or a[] balloon, there is ballooning, congestion, upwards and downwards. . . . This is compressive

myelopathy. And if it’s not relieved then it gets worse and worse over time.” Tr. 161.

Compressive myelopathy and spinal cord ischemia are related. Tr. 303. When the spinal

cord is compressed, the “blood supply is [] stifled . . . [and] become[s] ischemic and dies off.”

Tr. 160-61. Compressive myelopathy “decrease[s] the [perfusion] of blood in that site.” Tr. 304.

IV. FACTUAL SUMMARY

A. Summary of Medical Records16

1. Pre-Vaccination Records

Petitioner was born on November 24, 1973. Pet. Ex. 1 at 7. Petitioner received at least

two other flu vaccinations prior to the one at issue: one on September 27, 2013, and another on

October 2, 2014. Id. at 556. Prior to the vaccination at issue, Petitioner had an extensive and

complicated medical history.

Relevant to the issues raised in this case, on March 24, 2014, Petitioner saw Kathryn

Drake Hart, M.D., her primary care provider (“PCP”) for thoracic back pain that had reportedly

started in early February 2014. Pet. Ex. 1 at 227. She reported pain “all across the thoracic back

area, [] tingling radiating down [her] rib cage down to hips and all the way down to the feet on

both sides. [She] [a]lso ha[d] decreased sensation under both breasts at the lower rib cage all

around the torso into the back.” Id. Petitioner was assessed with thoracic back pain, lumbar

radicular pain, hypertension, chest discomfort, and an abnormal urinalysis. Id. at 228-29. Dr.

Hart ordered thoracic and lumbar spine x-rays, and prescribed meloxicam, tramadol, and

cyclobenzaprine for Petitioner’s back pain. Id.

Petitioner returned to Dr. Hart on April 1, 2014. Pet. Ex. 1 at 289. Petitioner reported

that her back pain was improving, but “[s]he still [had] achiness in her thoracic back area, and

tingling down her flanks, lateral thighs and down to her feet. Also with numbness in the same

area intermittently,” and she “frequently [felt] cold.” Id. It was noted that Petitioner “relate[d]

all of the symptoms to having had a Mirena placed,” and which was removed “about a month

ago.” Id. Dr. Hart noted that Petitioner’s thoracic back pain was a “somewhat puzzling

presentation.” Id. at 290. The X-rays showed mild arthritis but were otherwise normal. Id. Dr.

Hart noted that she had a lengthy discussion with Petitioner and that Petitioner “[c]ould consider

MRI given the paresthesias that she’s had in her legs, but she [was] having steady improvement

of her symptoms.” Id. Dr. Hart suggested a follow-up visit in two to three weeks, and if her

symptoms did not improve, they would “consider MRI and neurology referral.” Id.

16

Sections of this summary are largely taken from Respondent’s Rule 4(c) report and Dr.

Tornatore’s initial expert report. See Resp. Rept. at 2-14; Pet. Ex. 13 at 2-27. Additional factual

summaries are set forth in the parties’ briefs. See Pet. Pre-Hearing Br. at 1-16; Resp. Pre-

Hearing Br. at 3-10; Pet. Post-Hearing Br. at 1-19; Resp. Post-Hearing Br. at 3-11.

6

On April 9, 2014, Petitioner sent an e-mail to Dr. Hart, stating that she was having pain

“on [her] left back side” and “some numbness in [her] mid[-]section and some in [the] outer part

of [her] legs.” Pet. Ex. 1 at 304. Petitioner wrote that she “[at] times . . . found [herself] unstable

while starting to walk.” Id. On April 10, 2014, Dr. Hart ordered an MRI of Petitioner’s lumbar

spine due to lumbar radicular pain, paresthesia of both legs, and weakness of both legs. Id. at

307. A note from April 16, 2014, indicated that Petitioner’s insurance had “denied the MRI

orders.” Id. at 304.

Petitioner saw Dr. Hart again on April 21, 2014. Pet. Ex. 1 at 320. Regarding

Petitioner’s thoracic back pain, Dr. Hart noted it had been present for the last two months and

that it had “[u]nusual presentation [and] puzzling symptoms.” Id. at 321. Dr. Hart referred

Petitioner to neurology, noting she had “[t]horacic back pain for [two] months, ha[d] paresthesia

of flanks, legs, feet. Ha[d] occasional sensation of weakness in legs. Exam[ination] show[ed]

decreased sensation in legs, strength OK. Insurance ha[d] declined MRIs.” Id. at 319.

Two days later, on April 23, 2014, Petitioner saw neurologist Jeffrey Tramonte, M.D.

Pet. Ex. 1 at 326. Dr. Tramonte summarized Petitioner’s history as follows:

[Petitioner] is a 40-year-old woman who works in the call center for Lone Star

Circle of Care. . . . In early February 2014, she developed severe upper-mid

thoracic back pain with tingling from about her bra line down to her toes. Since

that time her pain and tingling have been constant. Symptoms are worse with

heat exposure (Uhtoff phenomenon). In addition, she has urinary urgency and

problems with initiating urination. She also complains of weakness in her legs,

unsteadiness when standing and walking, and she complains of vaginal numbness

and sexual dysfunction.

Id. at 334. Neurological examination was abnormal in that Petitioner’s reflexes were

“pathologically brisk” in both lower limbs and plantar response was “toe[s] upgoing bilaterally.”

Id. at 337. Sensation was “decreased to light touch to [] T4 spinal level bilaterally,” and gait and

balance were “notable for [] mild spastic paraparesis.” Id. Dr. Tramonte assessed Petitioner

with T4 thoracic myelopathy, with onset in early February 2014. Id. He also listed differential

diagnoses including multiple sclerosis (“MS”), thoracic transverse myelitis, thoracic cord tumor,

herniated thoracic disc, and infection. Id. He ordered an MRI of the thoracic spine, cervical

spine, and brain “all with [gadolinium] per MS protocol.” Id. Dr. Tramonte noted that he

“[a]nticipate[d] this is most likely MS and discussed with patient.” Id.

Petitioner underwent an MRI of the brain on April 29, 2014. Pet. Ex. 1 at 377. The MRI

showed “[s]cattered punctate white matter foci, greater than expected for the patient’s age.” Id.

It was noted that the finding was “nonspecific and may be seen with microangiopathic disease,

vasculopathy, demyelination[,] and migraines.” Id. An MRI of the cervical spine revealed

“[s]pondylotic changes with multilevel cord contact; otherwise unremarkable evaluation of the

cervical cord.” Id. at 385. The MRI of Petitioner’s thoracic spine was abnormal and showed a

7

“[p]artially calcified central/right paracentral ventral epidural mass at T5/T6.[17] Given its

proximity to the disc space, this may represent a calcified extrusion; a meningioma may have a

similar appearance. Associated myelopathic signal change [was] noted.” Id. at 392. A surgical

consultation was recommended due to the mass. Id.

On May 19, 2014, Petitioner saw neurologist Ekokobe Fonkem, D.O. Pet. Ex. 3 at 22.

Dr. Fonkem noted that the differential diagnosis for Petitioner’s T5-6 spinal mass was

“meningioma versus schwannoma.” Id. Dr. Fonkem advised Petitioner that she could have

surgery or have serial monitoring with spine MRIs, and Petitioner stated she would like to see a

spinal surgeon. Id.

On May 23, 2014, Petitioner saw David Garrett, Jr., M.D., a neurosurgeon. Pet. Ex. 3 at

28. Petitioner reported thoracic back pain since February 2014, and reported feeling “a band

around her just under the area of her breasts” and “numb from this area to her feet.” Id. Dr.

Garrett noted that Petitioner had “markedly diminished proprioception in toes of both feet” and

hyperreflexia in her knee and ankle joints. Id. at 31. Dr. Garrett noted that regardless of whether

Petitioner’s spinal mass was calcified disc or meningioma, “it need[ed] to be resected due to her

myelopathy.”18 Id. at 32.

Petitioner underwent spinal surgery on June 27-28, 2014. Pet. Ex. 3 at 195-200. It was

noted that the time spent in the operating room and difficulty of the case was increased “by at

least 50%” due to Petitioner’s “extreme obesity with a body mass index of 58.” Id. at 200. The

post-operative diagnosis indicated that Petitioner had suffered a calcified herniated thoracic disc

at T5-T6. Id. at 195. During surgery, “the motor-evoked potential signal was lost from the right

leg area. The left leg area remained intact with signal throughout.” Id. at 200.

On June 29, 2014, the date after her surgery, Dr. Garrett noted that Petitioner had “some

movement in her right foot, but no ability to move [her] right leg.” Pet. Ex. 3 at 200.

A physical therapy (“PT”) record from June 29, 2014 noted that Petitioner was on bed

rest due to a CSF leak. Pet. Ex. 3 at 206. Her initial PT evaluation took place on July 1, 2014.

Id. at 902. It was noted that Petitioner was still on bed rest, but she may be ready to begin the

17

The spinal cord is the “part of the central nervous system that is lodged in the vertebral canal.

It extends from the foramen magnum, where it is continuous with the medulla oblongata, to the

upper part of the lumbar region, ending between the twelfth thoracic and third lumbar vertebrae,

often at or near the first and second lumbar vertebrae.” Medulla Spinalis, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=88447 (last visited

Apr. 30, 2024). The spinal cord is referenced by its location within the spinal column, which is

divided into parts, cervical, thoracic, lumbar, sacral, and coccygeal. Id. Abbreviations are used

throughout this Decision. For example, T5/T6 or T5-T6 stand for the level of the spinal cord at

the thoracic vertebral level 5 and 6.

18

MRI of thoracic spine showed at T5/T6 a “central/right paracentral ventral epidural mass

deforming the ventral cord occupying approximately 50% of the cross-sectional area of the

canal.” Pet. Ex. 3 at 31.

8

following day. Id. At PT on July 3, 2014, Petitioner reported that her right leg did “not work

well.” Id. at 901. It was also noted that Petitioner was beginning to mobilize but could not lift

her right leg for transfers. Id. at 902. She began ambulating on July 5, 2014. Id. at 898.

Petitioner decided that she wished to complete her PT at an outpatient facility, and she was

discharged home on July 6, 2014. Id. at 146. She was instructed to follow-up with Dr. Garrett in

two weeks for a post-operative wound check. Id.

On July 9, 2014, three days after discharge, Petitioner called reporting that she had “lost

all balance and mobility again to the right leg since yesterday,” stating it was “like before

surgery.” Pet. Ex. 3 at 7779. Petitioner reported that she could feel touch to her leg but she was

unable to move her leg or wiggle her toes. Id. She was instructed to go to the emergency

department (“ED”) immediately. Id. Petitioner subsequently had an extensive inpatient

admission, from July 9 to August 1, 2014. See generally Pet. Ex. 3. MRI of the thoracic spine

done July 9, 2014 showed “postoperative changes of discectomy” at T5-T6. Id. at 2083.

“Within the adjacent lung [was] a loculated rim-enhancing fluid collection representing an

abscess.” Id. There was “abnormal enhancement in the right paraspinal soft tissues at T5-T6

concerning for infection. Additionally, there [was] abnormal enhancement in the epidural space

of the thoracic spine extending from T2-T3 inferiorly. There [was] a rim-enhancing fluid

collection in the dorsal epidural space extending from T4-T11 representing an epidural abscess.”

Id. At T5-T6, there also appeared to be “a recurrent central and right paracentral disc herniation

which results in moderate to severe spinal canal stenosis where there [was] significant cord

compression and cord deformity without cord signal abnormality.” Id. at 2083-84. The

impression was

1. Extensive epidural abscess extending from T4-T11 which primarily involves

the dorsal epidural space and results in multilevel mild and moderate spinal canal

stenosis.

2. Large rim-enhancing loculated fluid collection in the right thoracic cavity

representing an empyema.[19] There [was] extension of abnormal enhancement

into the right paraspinal soft tissues at T5 and T6 likely representing infection.

3. Recurrent T5-T6 right paracentral disc herniation which results in moderate to

severe spinal canal stenosis.

Id. at 2084.

19

An empyema is an abscess (“a localized collection of pus within tissues, organs, or confined

spaces”) or pleural effusion (“the presence of fluid in the pleural space”) containing pus.

Empyema, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=16115 (last visited May 9, 2024); Abscess, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=185 (last visited May 9, 2024);

Pleural Effusion, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=72555 (last visited May 9, 2024).

9

Petitioner underwent a number of surgical procedures and suffered significant post-

operative complications, including but not limited to sepsis, epidural abscess20 from T4-11, right

lung loculated empyema, possible right paraspinal abscess at T5-6, paraplegia, and urinary

incontinence. See generally Pet. Ex. 3. Petitioner’s post-operative course was complicated by

methicillin-resistant Staphylococcus aureus (“MRSA”)21 bacteremia, MRSA epidural abscess,

right chest empyema with chest tube placement, atrial fibrillation, and persistent CSF leak

requiring intubation and intensive care unit (“ICU”) admission. Id. at 2021-29, 7865-66.

Records note “she became paraplegic on August 26, 2014.” Id. at 7850. On or about August 1,

2014, Petitioner was discharged to inpatient rehabilitation. See id. at 7865.

On August 26, 2014, Petitioner presented to the ED with worsening lower extremity

weakness since August 25, 2014. See Pet. Ex. 3 at 7865. An MRI of the thoracic spine done

that same day found

[i]nterval development of cord expansion and associated increased intramedullary

signal essentially throughout the thoracic spine without significant enhancement.

This appearance is nonspecific and may [be] the result of venous

congestion/edema, cord ischemia or potentially infectious myelitis. . . . Interval

increase in T5 and T6 vertebra (to include the posterior elements) marrow signal

and enhancement with further endplate destruction [] with now both anterior and

posterior disc herniations compressing the spinal cord compatible with discitis

osteomyelitis.[22]

20

An epidural abscess is “a collection of pus located between the dura mater and surrounding

bone.” Epidural Abscess, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=54350 (last visited Apr. 30, 2024). Dura mater is “the outermost,

toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal

cord.”). Dura Mater, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=15060 (last visited May 9, 2024).

21

Staphylococcus aureus is “a species comprising the yellow-pigmented, coagulase-positive

pathogenic forms of the genus; it causes serious suppurative infections and systemic disease, . . .

and has developed resistance to nearly all classes of antibiotics.” Staphylococcus Aureus,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?

id=108211 (last visited May 8, 2024). Methicillin is “a semisynthetic penicillin, used

intravenously or intramuscularly as an antibacterial in resistant staphylococcal infections.”

Methicillin Sodium, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=30916 (last visited May 9, 2024).

22

Osteomyelitis is “inflammation of bone caused by infection, usually by a pyogenic organism,

although any infectious agent may be involved. It may remain localized or may spread through

the bone to involve the marrow, cortex, cancellous tissue, and periosteum.” Osteomyelitis,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?

id=35862 (last visited May 9, 2024).

10

Id. at 7812. An MRI of the lumbar spine also done the same day found “[i]nterval development

of loculated subdural fluid collection likely representing effusion anteriorly displacing the cauda

equina[23] nerve roots throughout the lumbar spine.” Id. There was a “drainable fluid collection

to suggest epidural abscess.” Id.

Also on August 26, a neurosurgical consultation noted that Petitioner had presented to the

ED “this evening with complaint of bilateral lower extremity weakness.” Pet. Ex. 3 at 7803.

Petitioner had “minimal movement of her bilateral [lower extremities] with intact minimal ankle

plantarflexion/dorsiflexion on the left. She [was] unable to perform this against resistance.

[Petitioner] ha[d] very subtle movement of her right lower extremity.” Id. at 7805. The MRI

findings were reviewed and it was noted that since the prior examination, there had been

“interval development of [c]entral increased cord signal and expansion extending from the C7-

T1 level to the T11-T12 level without discrete associated intramedullary enhancement.” Id. at

7806. “Discitis osteomyelitis ha[d] progressed centered at T5-T6 with associated endplate

destruction, marrow signal abnormality and both anterior and posterior disc herniation [was]

compressing the spinal cord at the T5-T6 level,” and “[a]bnormal signal enhancement,”

involving the right more than the left, at “T5-T6 neural foramina.” Id. The impression was

1. Interval development of cord expansion and associated increased

intramedullary signal essentially throughout the thoracic spine without significant

enhancement. This appearance is nonspecific and may the result of venous

congestion/edema, cord ischemia[,] or potentially infectious myelitis.

2. Overall interval decrease in size of the epidural abscess seen on 7/9/2014

exam[ination] with residual signal abnormality and enhancement most compatible

with phlegmon within the predominantly posterior epidural space.

3. . . .

4. Interval increase in T5 and T6 vertebra (to include the posterior elements)

marrow signal and enhancement with further endplate destruction [] with now

both anterior and posterior disc herniations compressing the spinal cord

compatible with discitis osteomyelitis.

Id. at 7806-07.

On September 9, 2014, Petitioner was seen by Sangeetha Ranganath, M.D., an infectious

disease specialist. Pet. Ex. 3 at 7865. Dr. Ranganath noted that Petitioner had suffered

disseminated MRSA infection, MRSA bacteremia, and that her CSF cultures were positive for

MRSA. Id. at 7865. Dr. Ranganath noted,24

23

Cauda equina is “the collection of spinal roots that descend from the lower part of the spinal

cord and are located within the lumbar cistern of the caudal dural sac.” Cauda Equina, Dorland’s

Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=63754 (last

visited May 9, 2024).

24

For a complete discussion of Petitioner’s post-operative course, see Pet. Ex. 3 at 7865-66 (an

extensive note authored by Dr. Ranganath).

11

1. Spinal epidural abscess due to MRSA, thoracic, [status post] decompression on

7/10/14

2. T5-6 discitis/osteomyelitis, interval progression on the imaging but improving

clinical markers

3. Right lung empyema, [status post] decortication on 7/10, with pleural fluid

[culture] positive for MRSA

4. MRSA bacteremia in July 2014 due to above all

5. Bilateral lower ext[remity] weakness

6. Bowel/bladder incontinence due to above

7. Morbid obesity.

Id. at 7870. Petitioner was able to move her left foot toes but not her right foot. Id. at 7866. She

remained incontinent. Id. On September 16, 2014, Petitioner requested that she be discharged to

home. Id. at 7884.

On September 26, 2014, Petitioner saw Dr. Ranganath in follow-up. Pet. Ex. 3 at 7914.

At this time Petitioner had “sensations in her left foot and [was] able to move [her] left foot but

[she was] still not able to move her right foot.” Id. She had urinary retention and required a

catheter. Id.

On September 29, 2014, computed tomography (“CT”) scan of Petitioner’s chest

continued to show “osteomyelitis discitis of T5 and T6 and central stenosis and compression of

the spinal cord.” Pet. Ex. 1 at 483.

At an October 2, 2014 follow-up visit with Dr. Ranganath, Petitioner had sensations in

her left foot but was still unable to move her right foot. Pet. Ex 3 at 7928. She was told to

follow up in one week for labs and a CT chest scan. Id. at 7931. A flu shot was administered.25

Id. She had a urology follow-up the same day. Id. at 7943. It was noted she was in a wheelchair

and did “not walk at all” and had “numbness from her waist down.” Id. She could not “feel to

void or defecate.” Id.

On October 14, 2014, at a neurosurgical follow-up examination, assessment was

“[p]araplegia due to poorly controlled osteomyelitis, though the epidural abscess component has

improved.” Pet. Ex. at 7981. Dr. Garrett discussed with Petitioner that

[s]he could experience further improvement in neurologic function, as the

infection is non-detected. . . . Return of function is favored as her spinal cord

shows more congestion rather than compression. [Dr. Garret] fe[lt] that the risk

of further CSF-cutaneous fusion makes it unlikely that she would benefit from

further decompressive surgery. She has risk of instability with further surgery []. .

25

Petitioner is not alleging any injury related to this flu shot.

12

. . Her pattern of spinal cord injury [was] a Brown-Sequard[26] type, which carries

a more favorable prognosis.

Id.

An MRI of the thoracic spine done October 21, 2014 demonstrated a “[d]estructive

process centered in the T5/T6 disc space with associated endplate erosion and patchy marrow

edema involving the adjacent vertebral bodies [were] similar to the prior exam[ination].” Pet.

Ex. 1 at 535. Associated mild anterolisthesis was unchanged. Id. “Residual T5/T6 endplate

ridging [was] again noted, contacting the ventral cord. Epidural and paraspinal enhancement at

this level [was] similar representing residual phlegmon and/or granulation. Intramedullary T2

prolongation with associated mild cord expansion [had] improved from the prior exam[ination],

extending to the T9/T10 level, previously to T11/T12.” Id. No discrete peripheral enhancing

fluid collection was seen within the paraspinal or epidural soft tissues and the previously noted

loculated right pleural fluid collection was no longer seen. Id. The impression was “[s]imilar

configuration of spondylo-discitis at T5/T6. No discrete drainable fluid collection [was] seen.

Improved intramedullary T2 prolongation as described.” Id.

Petitioner saw her PCP, Dr. Hart, in follow-up on November 3, 2014. Pet. Ex. 1 at 562.

Dr. Hart noted that Petitioner had back surgery with multiple complications. Id. Petitioner

reported that she was discharged from rehabilitation “[ab]out a month ago.” Id. She reported

that she initially had no movement or sensation in her lower extremities and she was currently

unable to stand or walk, but she was beginning to be able to pull to stand with assistance. Id.

Petitioner had outpatient PT evaluation on March 24, 2015. Pet. Ex. 1 at 604. It was

noted that Petitioner had paraplegia following a spinal cord injury, bilateral leg weakness,

spasticity, and difficulty walking. Id. Petitioner reported that she was ambulatory after her

surgery in June 2014; however, she had complications after surgery, and had subsequent surgery

on July 9, 2014. Id. at 605. She had been wheelchair bound since that time. Id. She had about

six weeks of inpatient rehabilitation. Id. Assessment showed that Petitioner had “[right] [lower

extremity] extensor spasticity and [left] [lower extremity] flexor spasticity, . . . limiting her full

knee [range of motion] bilaterally.” Id. at 608. Petitioner was “unable to ambulate even short

household distances.” Id. Petitioner also had weakness and poor endurance limiting her ability

to walk. Id. at 611. She required assistance transferring out of the wheelchair and with bed

mobility due to upper extremity and core weakness. Id. at 608, 619.

On March 26, 2015, Petitioner’s assessments included “[s]pasticity.” Pet. Ex. 1 at 628.

Petitioner stated she had good days and bad days, when she was “less confident in use of her

legs.” Id. When standing “fully erect[,] the spasticity ma[de] her knees buckle.” Id. The

therapist noted “spasticity in her left [lower extremity] decreas[ed] [her] ability to tolerate

standing for more than [two] minutes.” Id. at 629.

26

Brown-Sequard is “a syndrome due to damage of one half of the spinal cord, resulting in

ipsilateral paralysis and loss of discriminatory and joint sensation, and contralateral loss of pain

and temperature sensation.” Brown-Séquard Syndrome, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=110337 (last visited May 9, 2024).

13

Petitioner underwent urodynamic testing on June 1, 2015 “to characterize her neurogenic

bladder, urinary leakage, and incomplete bladder emptying.” Pet. Ex. 3 at 8178. Petitioner was

currently “catheterizing [three] to [four] times per day and leaking between catheterization[s].”

Id.

On July 24, 2015, Petitioner was using a wheelchair and a rolling walker. Pet. Ex. 1 at

955. It was noted she had become independent with many of her activities of daily living and

had begun to walk unassisted with her walker. Id. Petitioner was going to continue therapy

independently at her home, and the therapist noted that Petitioner would be reevaluated in

November 2015. Id.

Petitioner saw her PCP on September 17, 2015. Pet. Ex. 1 at 1032. She reported that she

was followed closely by her neurosurgeon, infectious disease specialist, physical therapist, and

urologist. Id. Petitioner reported “very slow but steady improvement in her strength and

walking ability.” Id. Dr. Hart noted that Petitioner was still wheelchair-bound at this time. Id.

at 1033. Petitioner had follow-up visits with her neurosurgeon on October 7, 2015, and her

physical therapist on November 5 and December 2, 2015, and she was discharged from PT on

December 10, 2015. Id. at 1078, 1104; Pet. Ex. 3 at 8215.

2. Vaccination and Post-Vaccination Records

On December 11, 2015, Petitioner saw her PCP for a follow-up visit. Pet. Ex. 1 at 1126.

Petitioner reported very slow but steady improvement, but she reported that over “the last several

weeks,” her “legs [were] getting tight and stiffening at night” and she was having “noticeable

spasms.” Id. Dr. Hart referred Petitioner to Dr. Tramonte for an evaluation of muscle spasms of

her lower legs. Id. at 1129, 1180. Petitioner received a flu vaccination at this visit. Id. at 1129;

Pet. Ex. 9 at 9.

On December 18, 2015, seven days after the flu vaccine, Petitioner had a PT

appointment, reporting that her left extremity “spasticity [was] worse today than previous[ly].”

Pet. Ex. 1 at 1148. Petitioner reported she had “been unable to stand all day due to her ‘good

leg’ being unreliable and not tolerating weight bearing.” Id.

Petitioner reported similar problems at PT on December 30, 2015. Pet. Ex. 1 at 1170.

Petitioner reported “continued inability to rely on [left lower extremity] for weight bearing” and

“overall increase in spasticity making it difficult to transfer as independently as she had []

before.” Id. She reported her husband had been helping her with stretching. Id. During the

session, Petitioner was able to transfer, stand, and pivot, whereas previous session she was

unable to. Id. at 1171. “Significant increase in extensor spasm tone” over the last two sessions

was noted. Id.

On December 30, 2015, Petitioner saw neurologist Dr. Tramonte due to worsening

weakness and spasticity. Pet. Ex. 1 at 1181. Dr. Tramonte noted that Petitioner had “worsening

left leg weakness, spasticity, and sensory loss since the middle of December 2015.” Id. Dr.

Tramonte noted that Petitioner had “chronic urinary incontinence and has not noticed any recent

14

change to bowel or bladder control” and “chronic back pain that [was] unchanged.” Id. MRIs of

the thoracic and lumbar spine were ordered to further evaluate her condition. Id. at 1185. In his

order for MRIs, Dr. Tramonte noted that the reason for the imaging was “worsening left lower

extremity weakness. Eval[uate] for new compression.” Id. at 1179. Dr. Tramonte’s assessment

was

T4 thoracic myelopathy due to calcified dis[c] herniation, [status-post]

decompression, followed by a complicated course of infection with empyema,

abscess[,] and compression of the conus medullaris and cauda equina in 2014.

Her chief complaint at this time is worsening weakness, spasticity, and sensory

loss in the left leg since the middle of Dec[ember] 2015. This could be the natural

evolution of thoracic cord compression with resolving infection/compression of

the conus and cauda equina versus a new compressive lesion. . . . If there are no

new lesions/compression [seen on MRI], then treatment will include referral for

aquatic therapy and Baclofen for spasticity.

Id. at 1185.

An MRI of the thoracic spine was performed on January 8, 2016. Pet. Ex. 1 at 1211. It

revealed “[i]nterval development of expansile T2 prolongation/edema within the thoracic cord

extending between T1/T2 and T10. Associated intramedullary syringohydromyelia[27] [was]

noted at T6 and T7 without enhancement.” Id. It was noted that the findings were “nonspecific

and may be secondary to altered CSF flow dynamics, transverse myelitis[,] and cord ischemia.”

Id.

On January 13, 2016, Petitioner saw neurosurgeon Dr. Garrett. Pet. Ex. 3 at 8249. Dr.

Garrett’s impression was “[t]horacic transverse myelitis due to either prior compression of spinal

cord, meningitis, or even as autoimmune phenomenon from flu vaccine.” Id. at 8250. He further

noted that surgical intervention was not warranted and that “[t]his process may be inflammatory

and [could] resolve with time, possibly.” Id. He advised Petitioner to have another MRI in six

months and to discontinue her antibiotics because her osteomyelitis appeared to have resolved.

Id.

Petitioner returned to Dr. Tramonte for follow-up on January 20, 2016. Pet. Ex. 1 at

1250. Dr. Tramonte noted Petitioner’s MRIs “showed worsening pre-existing signal abnormality

27

Syringohydromyelia or syringomyelia “a slowly progressive syndrome of cavitation in the

central segments of the spinal cord, generally in the cervical region, but sometimes extending . . .

down into the thoracic region; it may be of developmental origin, arise secondary to tumor,

trauma, infarction, or hemorrhage, or be of unknown cause.” Syringomyelia, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=48639 (last visited

May 8, 2024). “It results in neurologic deficits, usually segmental muscular weakness and

atrophy with a dissociated sensory loss (loss of pain and temperature sensation, with preservation

of the sense of touch), and thoracic scoliosis is often present.” Id. It is sometimes referenced as

a “syrinx.” Id. The undersigned uses syringohydromyelia and syringomyelia interchangeably

throughout this Decision.

15

in the thoracic spinal cord from T1-T10, a change that initially was present after developing a

T4-T11 epidural abscess, along with new syringomyelia at T6/7. [He] suspect[ed] the changes

[were] ischemic in nature.” Id. at 1254.

Petitioner had a follow-up MRI of her thoracic spine on July 1, 2016. Pet. Ex. 3 at 8321.

The MRI revealed the following:

1. Interval progression of abnormal signal and expansion of the mid thoracic cord

with abnormal signal extending caudally through the T11 level. This has

progressed since the prior study at which time the abnormal signal extended

through the midportion of T10. These findings are consistent with mild

progression of long segment myelomalacia.[28]

2. Focal kyphosis[29] at T5-T6 with chronic anterior wedging of T6. T5-T6

interbody fusion.

3. Moderate C5-C6 spinal canal stenosis due to posterior projecting osteophytes.

4. The cystic myelomalacia at T6 has slightly decreased in size when compared to

the prior exam[ination].

5. Moderate multilevel spondylosis in the lower thoracic spine consisting of facet

hypertrophy and ligamentum flavum thickening.

6. No abnormal enhancement in the thoracic spine.

Id.

Dr. Garrett next saw Petitioner on July 12, 2016. Pet. Ex. 3 at 8348. He noted that

Petitioner “received a flu shot about [six] weeks prior to her onset of progressive loss of [lower

extremity] strength.” Id. His impression was that Petitioner was suffering a “[t]horacic

myelopathy.” Id. at 8349. He noted that the “recent regression in lower extremity strength

correlates with the prolonged T2 signal within the spinal cord but cannot tell if it is new ischemia

or myelitis. Process undergoing is unclear to me, but no surgical intervention is warranted at this

point. Her disc area operated on is now fused. Kyphosis should not progress.” Id.

On July 25, 2016, Petitioner saw Dr. Tramonte who noted that the new MRI “findings are

thought to represent expected progression of long segment myelomalacia. [He] suspect[ed] the

initial changes were ischemic in nature.” Pet. Ex. 1 at 1308.

On November 15, 2016, Petitioner returned to Dr. Garrett (neurosurgery). Pet. Ex. 3 at

8373. His assessment was “[t]horacic myelopathy - recent regression in lower extremity strength

correlates with the prolonged T2 signal within the spinal cord but cannot tell if it is new ischemia

28

Myelomalacia is the “morbid softening of the spinal cord.” Myelomalacia, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=32720 (last visited

May 9, 2024).

29

Kyphosis is “an area of the vertebral column that is dorsally convex” or “abnormally increased

dorsal convexity in the curvature of the thoracic vertebral column.” Kyphosis, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=27290 (last visited

May 3, 2024).

16

or myelitis.” Id. at 8374. He further noted that he was “not sure why her spinal cord developed

inflammatory changes and she began to lose ability[,] primarily motor strength in her legs about

one and a half years after her initial decompression surgery.” Id. at 8375.

On February 1, 2017, Petitioner saw Dr. Tramonte in follow-up. Pet. Ex. 1 at 1359. Dr.

Tramonte noted that Petitioner had a calcified mass at T5/6 that was surgically removed, and that

her post-surgery health was “complicated by an epidural abscess, empyema, meningitis, with

compression of the conus medullaris[30] and cauda equina.” Id. Petitioner “also developed a

CSF leak needing a thoracotomy for resection of the dis[c] as well as dural repair.” Id. Dr.

Tramonte noted that Petitioner’s prior MRI in July 2016 showed a syringomyelia that had

progressed from T6/7 in December 2015 to T11 in July 2016. Id. at 1366. He noted that “[t]he

findings are thought to represent expected progression of long segment myelomalacia,” and he

suspected that “the initial changes were ischemic in nature.” Id.

On March 10, 2017, Petitioner saw neurologist Darin Okuda, M.D., at University of

Texas (“UT”) Southwestern Medical Center MS clinic. Pet. Ex. 7 at 7. Dr. Okuda noted that

Petitioner’s “initial difficulties began in February 2014 when she experienced complaints of

numbness and tingling.” Id. He described her surgery and hospital course, noting that she was

unable to walk at the time of discharge. Id. He further noted that Petitioner received a flu

vaccine in December 2015, after which she reported being non-ambulatory. Id. Dr. Okuda

diagnosed Petitioner with myelopathy, noting that “etiology [was] currently unclear based on the

available data.” Id. at 9. He elaborated: “Based on the existing data, it is unclear if an

intramedullary process was present only after exposure to a vaccination or if the described

changes within the thoracic spinal cord were related to her prior neurosurgical procedures (i.e.,

presence of an infection followed by an aberrant immune behavior).” Id. Dr. Okuda wanted to

see more of Petitioner’s medical records related to her neurosurgical procedures and post-surgery

treatments, and to schedule a follow-up appointment. Id.

Petitioner returned to the UT Southwestern Medical Center MS Clinic on May 16, 2017.

Pet. Ex. 7 at 26-27. Impression was

[m]yelopathy (etiology currently unclear based on available data). . . . Based on

the available information from Baylor Scott and White, it appears [that] an

intramedullary process was present following her neurosurgical procedures with

evolution over time. However, this cannot be confirmed without the

corresponding [] images.

Id. at 27. Petitioner was asked to obtain additional images for further evaluation and to sign a

waiver so that the MS clinic could request the images directly. Id. While the record contains

notes of email and telephone exchanges, it does not appear that Dr. Okuda saw Petitioner in

follow-up. See, e.g., id. at 38, 45-47, 51-52, 66, 70, 74, 79-80.

30

The conus medullaris or conus is “the cone-shaped lower end of the spinal cord, at the level of

the upper lumbar vertebrae.” Conus Medullaris, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=66882 (last visited Apr. 25, 2024).

17

On October 18, 2017, Petitioner saw Elliot Frohman, M.D., at UT Health Austin. Pet.

Ex. 10 at 35. Dr. Frohman noted that Petitioner’s symptoms in February 2014 were “reminiscent

of a sensory transverse myelitis.” Id. at 40. He suspected that Petitioner “did in fact have

transverse myelitis, although the pathoetiologic underpinning of this process remain enigmatic.”

Id. Dr. Frohman recommended a further work-up for the causes of her myelitis, ordered plasma

exchange treatment, and stated that Rituxan treatment would be considered. Id. at 41.

After further testing, Petitioner saw Dr. Frohman in follow-up on November 1, 2017.

Pet. Ex. 10 at 29. Dr. Frohman counseled Petitioner that he believed her syndrome in February

2014 was consistent with myelitis, but “the underlying etiology remain[ed] elusive,” which he

emphasized was “NOT [an] uncommon circumstance in a significant proportion of myelitis

patients.” Id. at 31. He recommended a number of treatments, which he stated may lead to some

improvement in Petitioner’s condition, even though the treatment was so remote from the initial

episode of myelitis in February 2014. Id. at 31-32. Diagnosis was “idiopathic transverse

myelitis.” Id. at 32.

On March 7, 2018, Petitioner had a follow-up visit with Dr. Frohman. Pet. Ex. 10 at 15.

Petitioner had completed some treatment, but Dr. Frohman stated it was “too early to tell

whether there ha[d] been a meaningful exchange.” Id. at 18.

Petitioner saw Dr. Frohman again on July 9, 2018. Pet. Ex. 10 at 11. She had been

attending PT twice weekly and felt she was making great progress. Id. at 14. Dr. Frohman noted

that he wanted to see her back “in the next three months to review her progress.” Id. Her

diagnosis remained idiopathic transverse myelitis. Id.

Petitioner returned to the UT Health Austin on October 4, 2018. Pet. Ex. 10 at 4. Her

diagnosis remained “idiopathic transverse myelitis by evidence to date.” Id. at 8.

MRI studies of the cervical, thoracic, and lumbar spine showed “extension of expansile

cord signal abnormality” throughout the entire spinal cord from the C2 level in the cervical spine

extending to the conus. Pet. Ex. 12 at 23. There was “[n]o definitive abnormal enhancement

appreciated,” however, evaluation was limited due to motion. Id. The studies also showed

“[m]ultilevel cervical spondylosis and facet arthropathy with varying degrees of mild foraminal

narrowing and mild to moderate spinal stenosis.” Id. Petitioner had the same findings in her

thoracic spine, most notably at T10-T11 and T11-T12. Id. In the lumbar spine, she also had

“spondylosis and facet arthropathy with superimposed pronounced dorsal epidural fat (epidural

lipomatosis) which significantly narrows the thecal sac throughout the mid to lower lumbar

spine.” Id.

18

In a 2019 visit with Dr. Frohman to develop a plan of care, Dr. Frohman stated that

“given [Petitioner’s] worsening and fluctuating symptoms, we will treat her as having

[neuromyelitis optica (“NMO”)31 spectrum disorder (“NMOSD”)].”32 Pet. Ex. 12 at 88.

3. Detailed Review of Physical Therapy Records: March 2015 –

December 2015

PT records show that in March 2015, prior to the vaccination at issue, Petitioner was

paraplegic following a spinal cord injury, with bilateral leg weakness, spasticity, and difficult

walking. Pet. Ex. 1 at 604, 608. She was unable to ambulate even short distances with a rolling

walker. Id. Petitioner attended over 40 outpatient PT visits from March through July 2015. See

id. at 614, 954. During that time, she developed the ability to stand, pivot, perform transfers, and

ambulate using a rolling walker. Id. at 955. Detailed PT notes establish that Petitioner had good

days when she was able to accomplish her goals of walking, and other days when she was unable

to do so due to spasticity, tone, and fatigue. Id. at 628-29. For example, on May 15, 2015,

Petitioner was unable to walk from the bed to the bathroom with her walker due to increased

muscle tone and fatigue. Id. at 770-71. On May 26, 2015, she had difficulty ambulating due to

tone. Id. at 782. Three days later, on May 29, 2015, Petitioner had difficulty standing upright

without initiating more tone. Id. at 789.

In June 2015, Petitioner had increased spasticity resulting in difficulty with transfers and

ambulation. Pet. Ex. 1 at 793. She also complained of increased low back pain. Id. at 821, 830.

She was able to ambulate with her rolling walker, but for shorter distances. Id. at 830, 837, 866-

67. On July 6, 2015, Petitioner complained that her left lower extremity felt like it was going to

buckle, and she continued to have increased spasticity that limited the distance she could use her

walker. Id. at 884. On July 24, 2015, Petitioner was discharged from PT. Id. at 954. Her

discharge notes indicated that Petitioner required a rolling walker and that her maximum gait in

one session was 28 feet. Id. at 955. She did not meet her goal of walking 50 feet with her rolling

walker. Id. She tolerated treatment but was limited due to increased spasticity in her lower

extremities. Id. at 945.

After being discharged from PT at the end of July 2015, Petitioner returned to outpatient

therapy on November 5, 2015. Pet. Ex. 1 at 1073. At this time, she complained of difficulty

ambulating distances greater than 25 feet intervals. Id. at 1074. She also had central upper back

31

Neuromyelitis optica is the “combined, but not usually clinically simultaneous, demyelination

of the optic nerve and the spinal cord; it is marked by diminution of vision and possibly

blindness, flaccid paralysis of the extremities, and sensory and genitourinary disturbances.”

Neuromyelitis Optica, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition? id=92610 (last visited May 3, 2024).

32

The undersigned asked the parties’ experts to address Dr. Frohman’s reference in 2019 to

NMOSD. Order dated Nov. 17, 2022. Respondent filed an expert report by Dr. Javed

addressing the question. Resp. Ex. C. Petitioner filed a brief addressing the Court’s order. Pet.

Supplemental Br. Both agreed that Petitioner did not meet the requirements for the diagnosis of

NMOSD. Therefore, the undersigned does not discuss Dr. Frohman’s diagnosis of NMOSD.

19

pain, aching, and burning, and bilateral lower extremity parasthesias. Id. When she walked, she

experienced pain and her knees were described as spastic. Id. at 1076. On November 12, 2015,

Petitioner had a “good day” and walked 40 to 45 feet with her rolling walker. Id. at 1088. But at

the next visit, she reported a “bad day,” when she was unable to walk at all. Id. at 1098. On

December 2, 2015, she had significant fatigue, resulting in her knee buckling with ambulation.

Id. at 1105-06. On December 3, 2015, she had difficulty walking with increased tone and lack of

control of her right lower extremity. Id. at 1110. At the visit on December 10, 2015, she

reported being unable to walk after her last therapy session. Id. at 1110-20.

Post-vaccination, on December 18, 2015, Petitioner had left lower extremity spasticity

making it difficult to stand because her “good leg” was unreliable. Pet. Ex. 1 at 1148. On

December 29, 2015, her increased spasticity made it difficult to transfer independently. Id. at

1170. She had a significant increase is extensor spasm and tone over two therapy sessions, and

the therapist notified Petitioner’s physician of the change in her condition. Id. at 1171.

B. Petitioner’s Declaration33

Petitioner wrote that prior to receiving the flu vaccine at issue, she developed a wound

infection from spinal surgery in July 2014. Pet. Ex. 33 at ¶ 1. She required readmission for

surgery to clear out the infection and became paralyzed from the waist down. Id. Her

neurosurgeon, Dr. Garrett, told her she had a 70-80% chance of walking again. Id.

After intensive therapy and rehabilitation, Petitioner regained “considerable strength”

prior to the fu vaccine on December 11, 2015. Pet. Ex. 33 at ¶ 2. She was able to stand; take

some steps with a walker; and pivot to sit on chairs, couches, the shower chair, the toilet, and

into the car. Id. at ¶¶ 2, 7. She could also transfer from her wheelchair, pivot onto the workout

table in PT, walk from one end of the parallel bars to the other, and ride a stationary bike for 10

minutes. Id. at ¶ 2. She had regained the ability to walk 50 feet with her walker. Id. She stated

that for the six months prior to the flu vaccine, she did not use a Hoyer lift, or personal lift, to get

in and out of bed, chairs, the shower, or the toilet. Id.

At a PCP appointment on December 11, 2015, Dr. Hart told Petitioner she needed the flu

vaccine because “she was confined to a wheelchair and could not afford to get ill.” Pet. Ex. 33 at

¶ 3. “Within days” of receiving the flu vaccine, Petitioner’s family noticed Petitioner was losing

control of her legs and “they were becoming weaker[] and would buckle causing [her] to lose

[her] balance and fall.” Id. She lost the ability to stand, use the walker, and pivot. Id. at ¶¶ 3, 7.

She now required a Hoyer lift to get her in and out of bed, her wheelchair, and the toilet. Id. at ¶

7. She had to use a sliding board to get in and out of the car because she could no longer stand

and take the few steps needed to pivot into the car. Id. Petitioner’s therapist recommended she

contact her neurologist, Dr. Tramonte. Id. at ¶ 3.

Dr. Tramonte scheduled an MRI that was performed January 8, 2016. Pet. Ex. 33 at ¶ 3.

Thereafter, Dr. Tramonte’s office advised Petitioner to go back to see Dr. Garrett about having

33

The exhibit is labeled as an “affidavit” however, it is not notarized and therefore the

undersigned will refer to it as a declaration.

20

another surgery on her back. Id. at ¶ 4. Upon contacting Dr. Garrett, Petitioner was told the

MRIs “showed fluid near the site of [her] previous operation.” Id. Dr. Garrett told her he would

not operate on her again because it would hurt more than it would help her. Id. He diagnosed

her with TM and told Petitioner that the symptoms she was describing to him were “similar to

Swine Flu. [She] told Dr. Garrett that [she] had received the flu shot earlier in December.” Id.

Petitioner continued with PT twice per week. Pet. Ex. 33 at ¶ 5. After a few weeks,

Petitioner’s physical therapist noticed “very little improvement.” Id. Petitioner’s left leg, which

had been her stronger leg before the flu vaccine, “was now weak and [she] could not stand on it.

[Her] right leg, the weaker leg before the flu vaccine, would lift up and bend when [she]

attempted to use it to stand.” Id. at ¶¶ 5, 12. Petitioner had little feeling in her left leg besides

numbness. Id. at ¶ 12. She could not stand without using a standing frame and soft locks to

prevent her knees from buckling. Id. Petitioner later found out muscle spasms were the reason

she could not stand. Id. at ¶¶ 5, 12. After the flu vaccine she also developed more spasms in her

right leg. Id. at ¶ 13. “The spasms cause[d] [her] right foot to lift when [she] attempt[ed] to

place it on the ground to stand and walk.” Id. She could no longer lift her “right ankle

automatically.” Id. at ¶ 14. Petitioner then began outpatient PT where she used a sliding board

to get on and off the table and the therapist stretched her legs to help with muscle spasms. Id. at

¶ 6. She did not notice much improvement. Id.

In addition to leg muscle spasms, Petitioner also suffered bladder spasms after the flu

vaccine. Pet. Ex. 33 at ¶ 8. “While [she] required intermittent urinary catheterization every [four

to six] hours, before the flu shot, catheterization every [six] hours kept me dry. After the flu

shot, the bladder spasms would cause [her] to leak urine.” Id. at ¶ 10. She averred she did not

have bladder spasms or urinary leakage prior to the flu vaccine. Id. Petitioner’s “bowels have

also been affected by the flu shot.” Id. at ¶ 11. “Before the flu shot, [she] was beginning to

sense when a bowel movement was going to occur. After the flu shot, [she] lost that sensation.”

Id. Since she is now paraplegic, she cannot move or bend her legs for personal hygiene such as

dressing below the waist, toileting, catharizing, or showering below the waist. Id. ¶¶ 8, 11, 15.

Because Petitioner cannot move below the waist, she has developed pressure sores. Pet.

Ex. 33 at ¶ 19. The first pressure sore was on her left ankle in August 2020. Id. By 2021,

Petitioner had developed pressure sores in her left buttock and right hip. Id. at ¶¶ 22-23.

Petitioner required extensive treatment of her multiple pressure wounds including cleaning and

dressing the wounds, use of VeraFlo Vacuum, an ED visit with IV antibiotics for infection, use

of Hyperbaric oxygen chamber, and a flap surgery. Id. at ¶¶ 22-28. In addition to pressure sores,

Petitioner is at higher risk of developing infections and kidneys stones because she is wheelchair

bound. Id. at ¶¶ 21-22. In 2021, Petitioner had a stent inserted for kidney stones. Id. at ¶ 22.

When Petitioner started seeing Dr. Frohman at UT Austin MS Clinic, he ordered

plasmapheresis for treatment of her transverse myelitis at UT Southwestern Dallas. Pet. Ex. 33

at ¶ 9. She also received Rituxan. Id. With these treatments, Petitioner averred she regained

some sensation in her lower legs and could stand in a standing frame but was not able to move

her legs on her own. Id. She stopped the Rituxan when she developed pressure sores. Id. Dr.

Frohman also referred her for Botox injections to treat her muscle spasms, but she reported

Botox did not make much of a difference in her condition. Id. As of the date of her declaration

21

(May 31, 2022), she was taking Baclofen and Levetiracetam for her leg spasms which decreased

the number of them but did not completely prevent them from occurring. Id. She stated she did

not require medications for muscle spasms prior to the flu vaccine. Id.

C. Expert Reports

1. Petitioner’s Expert, Dr. Carlo Tornatore34

a. Background and Qualifications

Dr. Tornatore is a board-certified neurologist. Pet. Ex. 13 at 2; Pet. Ex. 40 at 2. He

received his M.D. from Georgetown University School of Medicine where he subsequently

completed a neurology residency at Georgetown University Hospital. Pet. Ex. 40 at 2-3.

Thereafter he completed a post-doctoral fellow at the National Institutes of Neurologic Disorders

and Stroke at the National Institutes of Health. Id. at 3; Pet. Ex. 13 at 2. Since then, he has been

on the faculty at Georgetown. Pet. Ex. 13 at 2; Tr. 6. He is currently a Professor and Chairman

of the Neurology Department at Georgetown University Medical Center where he oversees

“research endeavors of 15 laboratories, consisting of 19 Principal Investigators and over 90 post-

doctoral fellows, doctoral candidates, graduate students[,] and lab technicians. These labs focus

on various aspects of the neuroscience, including neuroplasticity, neuroimaging, cognitive

neuroscience[,] and language disorders.” Pet. Ex. 13 at 1. He is also the Neurologist-in-Chief

and Chairman of Medstar Georgetown University Hospital. Id.; Tr. 7. Additionally, Dr.

Tornatore is the Director of the MS Center at Georgetown where sees and treats patients with

MS and other neuroimmune system disorders including transverse myelitis. Pet. Ex. 13 at 2; Tr.

7-8. Dr. Tornatore testified he has about 400 patients with transverse myelitis that exclude MS.

Tr. 8. Dr. Tornatore has authored or co-authored numerous publications. Pet. Ex. 40 at 8-19.

b. Opinion

i. Loving Factor One: What Was Petitioner’s Condition

Prior to Administration of the Vaccine?

Dr. Tornatore opined that Petitioner had a “very complicated course.” Pet. Ex. 13 at 26.

As a brief overview, in March 2014, Petitioner developed spinal cord-related neurologic

symptoms caused by a mass compressing the T5/T6 level of the spinal cord. Id. She had

significant stenosis in her thoracic cord due to degenerative disc disease. Tr. 10. The stenosis

caused edema (swelling) and inflammation of the spinal cord seen on MRI. Pet. Ex. 13 at 26.

She had decompressive surgery June 27, 2014. Id. Post-operatively, Petitioner developed a

“very profound post-operative infection around her spinal cord” along with a thoracic abscess

that required a second operative procedure on July 10, 2014. Tr. 10. As a result of the infection,

Dr. Tornatore opined that about six weeks after her second surgery, Petitioner developed

longitudinally extensive transverse myelitis, shown on the MRI August 26, 2014. Pet. Ex. 13 at

26. Two months later, on October 21, 2014, an MRI was done and showed improvement. Id.

34

Dr. Tornatore submitted one expert report and testified at the hearing. Pet. Ex. 13; Tr. 3, 150.

22

After providing an overview, Dr. Tornatore reviewed Petitioner’s clinical course in more

detail and provided his opinions of significant MRI findings. See Pet. Ex. 13 at 2-25; Tr. 12-18.

Petitioner’s MRI on April 29, 2014 showed a partially calcified paracentral ventral epidural mass

(calcified extrusion or meningioma) at T5 and T6. Tr. 12. Petitioner had surgery on June 27,

2014. Tr. 14-15. Post-operatively, she had a very complex clinical course. Id. She had a

pleural effusion (fluid on the lungs), was hospitalized in ICU, and was discharged from the

hospital on July 6, 2014, only to return on July 9, with significant weakness of the right lower

extremity and bladder incontinence. Id. Her MRI on July 9, 2014, showed an extensive epidural

abscess from T4 to T11 (above the nipples to below the belly button level). Tr. 16.

Additionally, there was a “large loculated fluid collection in the thoracic cavity” described as an

empyema or “collection of pus in the chest wall.” Tr. 16-17. Thus, the MRI done July 9, 2014,

showed pus in and around the spine and thoracic area. Id. Petitioner also had a “recurrent []

paracentral disc herniation [] result[ing] in moderate to severe spinal cord stenosis.” Tr. 17. She

also had an abscess from the top of her right lung at the level of her collar bone down to the level

of T11/T12, below her belly button level, described by Dr. Tornatore as a “huge infection in the

chest.” Tr. 18.

Relative to the spinal cord, the July 2014 MRI showed focal inflammation of the spinal

column bones and epidural space at T2 to T3. Tr. 18. Next to the dura, or covering of the spinal

cord, was a collection of pus indicating there was a bacterial infection from T4, above the nipple

line, and downward to below the level of the belly button. Tr. 18-19. The covering of the spinal

cord, called the dura, showed enhancement on MRI “all up and down the spinal cord.” Tr. 19.

Dr. Tornatore explained that during the surgery, the dura was nicked, causing leakage of the

spinal fluid and creating a pathway for bacteria to get to the spinal cord. Tr. 20. Analysis of the

spinal fluid showed “[a]bsolutely astounding” results. Tr. 21. Petitioner’s white blood cell count

was elevated to 56,000 indicating “profound inflammation in the spinal fluid.” Id. According to

Dr. Tornatore, this indicated that Petitioner had “inflammatory myelitis, no question.” Tr. 22.

The next MRI, done August 26, 2014, showed worsening with “interval development of

central cord signal and expansion from C7 to T11,” and it was very evident that Petitioner had

inflammation of the spinal cord. Tr. 23 (quoting Pet. Ex. 3 at 7812). This inflammation was

probably a result of venous congestion, cord ischemia (due to lack of blood flow), or infection.

Tr. 24-25. Although Petitioner was still on antibiotics, it is very difficult to treat infection in the

soft tissues. Tr. 26. Ongoing infections take months and months to treat, and during this time, it

is not surprising for a patient to have “ups and downs” during their clinical course. Tr. 24.

By September 9, 2014, the infectious disease specialist noted that Petitioner had

“disseminated MRSA.” Pet. Ex. 3 at 7865. MRI done October 20, 2014 showed a destructive

process at T5 and T6 with patchy bone marrow edema, and significant inflammatory changes in

the spinal cord, and Petitioner’s spine at this level was in a bent-over position. Tr. 30. At this

point, Petitioner had a “really chronic issue in her spinal cord.” Tr. 32. Dr. Tornatore opined

that Petitioner’s condition put her at risk for subsequent inflammatory events. Id. Petitioner

remained on antibiotics. Id. From November 2014 to April 2015, Petitioner made slow

improvement. Tr. 33-37. By April 2015, Petitioner still had significant weakness in her lower

extremities, but was able to walk 30 feet with a walker, and she was beginning to feel her feet.

She had foot drop in her right lower extremity. Tr. 36.

23

Moving forward to October 7, 2015, Dr. Tornatore opined that Petitioner could walk with

a walker, that she was beginning to feel her legs, and she was still on antibiotics. Tr. 38-39.

However, Dr. Tornatore opined that there was something continuing to happen in her spinal cord

because Petitioner was not able to walk normally. Id. The records show that Petitioner had a

“good day” on November 12, 2015, evidenced by her ability to walk 40 to 45 feet with her

walker. Tr. 40 (quoting Pet. Ex. 1 at 1888). But she had difficulty placing her right foot with

sitting, standing, or walking. Id. She also complained that day of stiffness in her legs, although

she had less tightness or spasticity. Id.

On December 3, 2015, Petitioner had more stiffness and increased muscle tone in both

legs, right greater than left, and fatigue. Tr. 42 (citing Pet. Ex. 1 at 1110). Dr. Tornatore opined

that Petitioner was experiencing “more spasticity at this point.” Tr. 43. Additionally, the note on

December 3 raised the question of whether something else was going on in Petitioner’s spinal

cord or suggested that whatever was happening was “getting a little more prominent.” Id.

Petitioner remained on the antibiotic doxycycline. Id.

At her PT visit on December 11, 2015, Petitioner reported that she was “unable to walk”

the day after her last session. Tr. 44 (quoting Pet. Ex. 1 at 1119). Dr. Tornatore said “there’s a

little something here” and he again questioned whether “something else [was] going on.” Tr. 45.

At her appointment with Dr. Hart on December 11, 2015, the records stated that in the “last

several weeks,” Petitioner’s legs were getting tight and she had stiffening at night. Tr. 46

(quoting Pet. Ex. 1 at 1126). She was also having noticeable spasms. Id. Dr. Hart referred

Petitioner to her to neurologist. Id. Dr. Tornatore opined there was “some change” in

Petitioner’s tone in her lower extremities. Tr. 47. Petitioner received her flu vaccination at this

visit. Id.

ii. Loving Factor Two: What Is Petitioner’s Current

Condition (or Her Condition Following the Vaccination,

If Also Pertinent)?

According to Dr. Tornatore, shortly after receiving a flu vaccination on December 11,

2014, Petitioner had a significant aggravation of her transverse myelitis with worsening

neurologic symptoms and recurrent edema and inflammation of the thoracic spinal cord,

demonstrated by her January 8, 2016 MRI. Pet. Ex. 13 at 26. Dr. Tornatore opined that

Petitioner’s diagnosis was transverse myelitis, initially caused by infection, and subsequently

aggravated by the flu vaccination. Id.; Tr. 10.

On December 18, 2015, Petitioner reported that her spasticity was worse and she was

unable to stand. Tr. 47-48 (citing Pet. Ex. 1 at 1148). This was also noted at her PT visit on

December 30, 2015, when Petitioner’s increased spasticity made it difficult for her to bear

weight. Tr. 48 (citing Pet. Ex. 1 at 1170). Petitioner saw her neurologist, Dr. Tramonte, on

December 30, and he noted that she had worsening weakness since mid-December. Tr. 50

(citing Pet. Ex. 1 at 1181). Petitioner did not have changes to her bladder or bowel, and she had

no increase in her chronic pain. Tr. 51 (citing Pet. Ex. 1 at 1181).

24

Petitioner had an MRI on January 8, 2016, 15 months after her last one. Tr. 52. Dr.

Tornatore opined that it showed edema of the spinal cord from T1 to T10 with an intramedullary

syringohydromyelia at T6/T7 (an abnormal collection of fluid in the central canal of the spinal

cord). Tr. 53 (citing Pet. Ex. 1 at 1211). According to Dr. Tornatore, this finding indicated

persistent inflammation. Tr. 54. He agreed that Petitioner initially had inflammation of the

spinal cord due to compression, and then there was more ischemia, lack of blood flow, and death

of tissue, “related back to . . . inflammation and irritation at that site.” Tr. 56. However, he also

agreed that the MRI findings could be due to cord ischemia and altered CSF flow dynamics. Tr.

56-57.35

Petitioner saw her neurosurgeon, Dr. Garrett, on January 13, 2016. Pet. Ex. 3 at 8249.

Dr. Tornatore interpreted Dr. Garrett’s notes from that visit to mean that Dr. Garrett agreed that

the MRI findings were “due to spinal cord compression that antedated the abscess and edema . . .

but [Dr. Garrett] acknowledge[d] that the MRI could be [] an autoimmune phenomenon, and he[]

invoke[ed] the flu vaccine.” Tr. 58 (citing Pet. Ex. 3 at 8249). Although Dr. Garrett noted that

Petitioner could have an autoimmune condition, Dr. Tornatore agreed that Dr. Garrett did not

treat Petitioner for transverse myelitis. Tr. 58.

On January 20, 2016, Petitioner returned to see her neurologist, Dr. Tramonte. Pet. Ex. 1

at 1250. Dr. Tornatore interpreted the note from that visit to mean that Dr. Tramonte thought the

changes in the MRI were “ischemic in nature,” caused by a “lack of blood flow in that area of the

spinal cord.” Tr. 62 (citing Pet. Ex. 1 at 1254). Although Dr. Tornatore disagreed with Dr.

Tramonte’s opinions in this regard, he agreed that there could be a “slow[ly] diminish[ing]

decrease in blood flow to the spinal cord” caused by swelling. Tr. 62-63. And he agreed that

there was “probably some lack of blood flow contributing” to Petitioner’s condition. Tr. 63.

The next MRI was done July 1, 2016, and again it was markedly abnormal. Tr. 64 (citing

Pet. Ex. 3 at 8320). Dr. Tornatore observed that Dr. Tramonte now interpreted the results as

transverse myelitis. Tr. 65. However, Dr. Tornatore agreed that Petitioner was not treated for

transverse myelitis. Id.

Dr. Tornatore was questioned about Petitioner’s visits to Dr. Frohman, a

neuroimmunologist. See Tr. 72. In a note dated November 11, 2017, Dr. Frohman attributed

Petitioner’s initial syndrome, beginning in 2014, to be consistent with inflammation and myelitis

of the spinal cord, but he concluded that the “underlying etiology remain[ed] elusive.” Tr. 75

(quoting Pet. Ex. 10 at 31). At Petitioner’s next visit with Dr. Frohman on October 4, 2018, Dr.

Frohman noted that Petitioner’s chief complaint was “idiopathic transverse myelitis.” Tr. 76

(quoting Pet. Ex. 12 at 92).

At the hearing, after reviewing Petitioner’s 2018 MRI of the spine, Dr. Tornatore

supplemented his opinions. He opined that Petitioner’s 2018 MRI, as compared to the prior

MRI done in January 2016, showed Petitioner had an “inflammatory process” extending from

C1 (with chronic compression at T6 and across the T5/T6 disc space and kyphosis at T5/T6)

with an “increased extensive abnormal expansile cord signal seen throughout the thoracic

35

For a more complete discussion of the January 8, 2016 MRI, see Tr. 52-57.

25

cord, extending . . . all the way to the bottom of the spinal cord.” Tr. 283-284 (citing Pet. Ex.

12 at 140). Dr. Tornatore characterized Petitioner’s 2018 MRI as the “worst” of all of

Petitioner’s MRI studies, showing an “area of increased signal going from C1 all the way

down to the very bottom. It’s the whole spinal cord now.” Tr. 285.

After review of all of Petitioner’s MRI studies, including the one done in 2018, Dr.

Tornatore opined that in 2014, Petitioner had transverse myelitis due to active inflammation.

Tr. 288-89. He then addressed the question of why Petitioner was worse in 2018, even

though at that time she was being treated with immunosuppressants. Tr. 285-87. Dr.

Tornatore agreed that given the findings on the 2018, it was time to consider other etiologies

for Petitioner’s condition, because her “inflammatory myelitis” had been ongoing for four

years, along with scarring (glial formation). Tr. 291-92. He also agreed that based on the

2018 MRI study, that Petitioner’s illness was not monophasic, but progressive. Tr. 292-93.

Dr. Tornatore opined that the onset of Petitioner’s myelitis was July 2014. Tr. 293.

He opined that one and one-half year later, she had the vaccination at issue, and according to

Dr. Tornatore, Petitioner relapsed and never recovered. Tr. 293-94. Dr. Tornatore agreed

there was “canal stenosis” and that the stenosis was “contributing, you know, to some of

this.” Tr. 296. He also agreed that the stenosis was present “at the very beginning, before she

had the surgery.” Id.

Ultimately, Dr. Tornatore agreed with Respondent’s expert Dr. Javed, stating “we

can’t distinguish what is [caused by] canal stenosis versus what is inflammatory disease of the

cord.” Tr. 296-97. He further agreed that the vaccine did not cause the “subsequent

progression that [Petitioner] experienced.” Tr. 298. He opined that the vaccine “had one

moment in time where it made things worse, causing exacerbation, and then the natural

history of her myelitis [] just continued on from that point . . . forward.” Id.

iii. Loving Factor Three: Does Petitioner’s Current

Condition (or Condition After Vaccination) Constitute a

“Significant Aggravation” of Her Condition Prior to

Vaccination?

As stated above, Dr. Tornatore opined that the vaccine “had one moment in time

where it made things worse, causing exacerbation, and then the natural history of

[Petitioner’s] myelitis [] just continued on from that point . . . forward.” Tr. 298.

When asked to quantify Petitioner’s alleged vaccine-related injury, given her complex

clinical history, his acknowledgement that canal stenosis was a contributing factor present

before surgery, and that it contributed to the subsequent progression of disease, Dr. Tornatore

26

used the Kurtzke extended disability status (“EDS”) score36 to compare Petitioner’s condition

before and after vaccination. Tr. 299. Before her vaccination on December 11, 2015,

Petitioner, on her best day, could walk with a walker, and thus, Dr. Tornatore assigned her an

EDS score of 6.5. Tr. 300. After vaccination, she was wheelchair-bound, which placed her at

a score of 7.0 or 7.5. Id. He concluded that Petitioner’s vaccination worsened her disability

by roughly 20%. Id.

iv. Loving Factor Four/Althen Prong One: Medical Theory

of Causation

Dr. Tornatore explained that acute transverse myelitis “has been reported following

certain vaccinations, including, specifically, the seasonal [flu] vaccination.” Pet. Ex. 13 at 27.

He referenced the National Institute of Neurological Disorders and Stroke (“NINDS”) fact sheet

on transverse myelitis which stated that the condition can be a “post-vaccinal” event. Tr. 78

(citing Pet. Ex. 38 at 2).37 He also cited a paper about acute disseminated encephalomyelitis

(“ADEM”) by Huynh et al.,38 which stated that ADEM (“of which transverse myelitis is part of”)

has been associated with vaccines, including the flu vaccine. Tr. 79-80 (citing Pet. Ex. 20 at 1).

He cited mechanisms proposed by Huynh et al., including molecular mimicry39 and the

“inflammatory cascade process.” Tr. 81 (citing Pet. Ex. 20 at 6). Dr. Tornatore described a

“first hit” that occurs with an antecedent infection and molecular mimicry, followed by a

“second infection with an unrelated infection result[ing] in sufficient reactivation of the primed

autoreactive T-cells to eventually end in demyelination of the central nervous system,”

constituting the “second hit.” Id. With molecular mimicry, Dr. Tornatore explained that there is

exposure to an antigen and “the immune system recognizes the antigen and processes it, but then

because the antigen has homology to self-protein, the immune response is directed not only to

36

The Kurtzke EDS scale “was developed by Dr. John Kurtzke in the 1950s to measure the

disability status of people with MS.” Kurtzke Expanded Disability Status Scale, Multiple

Sclerosis Ctrs. of Excellence, U.S. Dep’t of Veterans Affs., https://www.va.gov/MS/

Professionals/diagnosis/Kurtzke_Expanded_Disability_Status_Scale.asp (last updated Mar. 18,

2021). Dr. Tornatore testified that the Kurtzke EDS scale is used for other inflammatory

disorders and is relevant here. Tr. 299.

37

Transverse Myelitis Fact Sheet, NINDS, https://www.ninds.nih.gov/health-information/

disorders/transverse-myelitis (last reviewed July 25, 2022).

38

William Huynh et al., Post-Vaccination Encephalomyelitis: Literature Review and Illustrative

Case, 15 J. Clinical Neuroscience 1315 (2008).

39

For further discussion of molecular mimicry and transverse myelitis, see Pet. Ex. 13 at 30; Pet.

Ex. 36 (Kai W. Wucherpfenning & Jack L. Strominger, Molecular Mimicry in T Cell-Mediated

Autoimmunity: Viral Peptides Activate Human T Cell Clones Specific for Myelin Basic Protein,

80 Cell 695 (1995)) (discussing molecular mimicry, viral pathogens, and reactivity to myelin

basic protein).

27

the protein that was presented, the antigen, but also to the host protein which was already there.”

Tr. 83. The vaccine is “misdirected at those antigens in the host . . . in the spinal cord.” Id.

The paper by Huynh et al. does not relate to transverse myelitis, but instead is about post-

vaccination ADEM. Pet. Ex. 20 at 1. The authors state that ADEM is “an inflammatory

demyelinating disease of the central nervous system that is usually considered a monophasic

disease.” Id. ADEM has been associated with several vaccines, including the flu vaccine. Id.

The article discusses the presumptive mechanisms of ADEM, including molecular mimicry and

the immune-inflammatory model. Id. at 6. The immune-inflammatory model “combines the

concept of molecular mimicry with the inflammatory cascade process.” Id. “A ‘first hit’ is

experienced after an antecedent infection with a virus that expresses determinants allowing

molecular mimicry. This need not be clinically eventful or significant.” Id. “A second infection

with an unrelated virus results in sufficient reactivation of the primed autoreactive T cells to

eventuate in demyelination of the [central nervous system]. This constitutes the ‘second hit.’”

Id. The authors also noted that some patients “have a certain underlying genetic predisposition

[and] may be more prone to developing ADEM post-vaccination.” Id.

Central to Dr. Tornatore’s opinions as to causation is the concept of “fertile field.” Tr.

83; Pet. Ex. 13 at 30. He explained that this mechanism presumes there is “already tissue

injury.” Tr. 83. According to Dr. Tornatore, in the fertile field model, “activation of an immune

response by an immunogen with sequence homology to self-proteins may prime autoreactive T-

cells in the host, but might lack the momentum to initiate an adverse autoimmune reaction

independently.” Pet. Ex. 13 at 30. “However, a later immune stimulation or coincidental

immune stimulation event by a vaccine or other immunogen, even one without cross-reactive

antigens or sequence similarity, could initiate an autoimmune reaction in a susceptible host that

could lead to inflammatory demyelination.” Id. He explained that the combination of molecular

mimicry, fertile field, and genetic predisposition all play a role. Tr. 83.

In support of his opinions about “fertile field,” Petitioner filed a paper by Fujinami et al.40

Pet. Ex. 13 at 30 (citing Pet. Ex. 25). They wrote that “[i]nfection of the host and the interactions

between the immune response and virus set the stage for a ‘fertile field’ where the host and/or

target organ is ‘primed’ for subsequent immunopathology.” Pet. Ex. 25 at 1. Three potential

mechanisms are discussed: molecular mimicry, bystander activation, and persistent viral

infection. Id. The authors discuss how autoimmunity could develop in the context of a viral

infection. Id. at 2. “Persistent viral infections can lead to immune-mediated injury due to the

constant presence of viral antigen driving the immune response.” Id. An example given of a

persistent viral antigen was Theiler’s encephalomyelitis in mice that causes a central nervous

system infection. Id. After the mice recover from an acute infection in the neurons, they

40

Robert S. Fujinami et al., Molecular Mimicry, Bystander Activation, or Viral Persistence:

Infections and Autoimmune Disease, 19 Clinical Microbiology Revs. 80 (2006).

28

develop persistent infection in glial cells41 and the infection can be detected throughout the

lifetime of the animal. Id. The authors suggested that while a person may be “repeatedly

exposed to a potential immunogen without any untoward consequences . . . , if the person had a

viral infection at the time of exposure, infection would alter the immunological environment in

which the antigen was encountered, leading to a profound immune response.” Id. at 4.

Fujinami et al. identified MS, myocarditis, and diabetes as three illnesses where the

fertile field model is being studied in animal models. Pet. Ex. 25 at 5. One question is whether a

viral infection “having mimicry with self [central nervous system] proteins could prime for

autoimmune disease later in life.” Id. The first step is a “priming infection (setting up the fertile

field) [that] increases the number of autoreactive T cells but not sufficiently to cause disease.”

Id. at 6. The next step is that a “critical number or mass of autoreactive T cells must be

generated in order for [the illness] to develop.” Id. The authors suggested bystander activation

and molecular mimicry as possible ways to explain how exacerbations or secondary events

occur. Id. at 5-6. The authors concluded that “[v]iruses have been shown to be one of the

environmental factors that are capable of precipitating autoimmune disease by a variety of

possible mechanisms discussed” and noted the challenges in obtaining evidence to develop

application of the fertile field model, including, for example, the need to obtain the “total

infectious history of each individual” in order to assess whether they contribute to autoimmune

diseases. Id. at 12.

In addition to molecular mimicry, the immune-inflammatory model, and the fertile field

model, Dr. Tornatore opined that another mechanism, bystander activation, can contribute to the

development of transverse myelitis in the context of the facts and circumstances relevant here.

Tr. 85-86; Pet. Ex. 13 at 29. He defined bystander activation as a “nonspecific antiviral response

to inflammation” resulting in T-cells releasing cytokines and chemokines that cause tissue

damage. Tr. 86. In support of bystander activation, Dr. Tornatore cited an article by Smatti et

al.42 about viruses and autoimmunity. Tr. 84 (citing Pet. Ex. 37 at 2 fig.1). The authors used

“bystander activation” to describe a mechanism “whereby a non-specific and over-reactive

antiviral immune response creates a localized pro-inflammatory environment along with the

release of self-antigens from the damaged tissue. These self-antigens are subsequently taken up

and presented by antigen presenting cells [] to stimulate the previously non-responsive, yet

autoreactive T cells in the vicinity triggering autoimmunity.” Pet. Ex. 37 at 2. The authors

discussed flu viruses and noted that viral replication of these viruses have been reported in the

respiratory tract, pancreas, and other internal organs. Id. at 4. One of the studies referenced by

the authors reported an association between the flu virus and ADEM. Id. at 8 tbl.1. However,

vaccines were not discussed in Smatti et al. and neither was transverse myelitis.

41

Glial cells are “the cells of the supportive tissue of the central nervous system.” Neuroglia

Cells, Dorland’s Online Med. Dictionary, https://www.dorlandsonline.com/dorland/

definition?id=64287 (last visited May 9, 2024).

42

Maria K. Smatti et al., Viruses and Autoimmunity: A Review on the Potential Interaction and

Molecular Mechanisms, 11 Viruses 762 (2019).

29

Lastly, Dr. Tornatore discussed epitope spreading, “whereby invading antigens accelerate

an ongoing autoimmune process by local activation of antigen presenting cells and over

processing of antigens.” Pet. Ex. 13 at 29; see also Tr. 86. Dr. Tornatore explained that in the

backdrop of a viral infection, there is antigen presentation. Tr. 86. Due to disruption of tissue,

“there are more epitopes . . . released from the tissue.” Id. He likened this process to the fertile

field, “where you have not only epitopes, but you also have a lot of inflammation.” Id.

According to Dr. Tornatore, all these mechanisms “feed on one another . . . especially given [the

context of] a previous underling inflammatory event in the spinal cord and then a subsequent one

with the [flu] vaccination.” Tr. 86-87. The Smatti et al. paper also discussed epitope spreading,

describing it as a mechanism “in which a viral infection triggers the release of more self-antigens

and the de novo activation of autoreactive cells, which consequently spread to target additional

self-epitopes.” Pet. Ex. 37 at 2.

Specific to molecular mimicry, Dr. Tornatore described hemagglutinin, “an important

viral protein of [flu] A” and the “current [flu] A virus [in] vaccines.” Tr. 87. He explained that

it is “an antigen present on [flu] A” in the flu vaccine. Id. He cited a paper by Li et al.43 which

showed that an antigen in the flu vaccine reacts against brain tissue and parts of the nervous

system. Tr. 88 (citing Pet. Ex. 35). Dr. Tornatore stated that Li et al. identified “two broadly

cross-reactive epitopes on hemagglutinin A.” Tr. 88. The “antibodies against these epitopes

react with hemoglobin and numerous types of important normal tissues and organs.” Id. One of

the antibodies discussed in Li et al. “reacted against neuronal cells.” Tr. 89 (citing Pet. Ex. 35 at

5 tbl.II). Immunoreactivity testing showed that the antibodies “attached to [] brain tissue . . .

[and] parts of the nervous system.” Id. Dr. Tornatore concluded that Li et al. supported the

mechanism of molecular mimicry because they identified “the antigen, [] the antibody, the

immune system . . . and the fact that it will attach to [] part of the nervous system, causing

injury.” Id.

Dr. Tornatore also cited Agmon-Levin et al. which discussed transverse myelitis and

vaccines. Pet. Ex. 18. The authors described the mechanisms of molecular mimicry and epitope

spreading, as well at the mechanisms associated with post-infectious transverse myelitis. Id. at 4.

Regarding vaccines, they also discussed the role of adjuvants. Id. at 5. They noted that “[t]he

association of [transverse myelitis] with so many different vaccines alludes to the idea that a

common denominator might be responsible, such as a common adjuvant.”44 Id. In Agmon-

Levin et al., the authors conducted a literature search identifying 37 cases45 of transverse myelitis

following vaccinations. Id. at 2, 3 tbl.1. Two of the cases occurred after the flu vaccine. Id.

The authors concluded, “[t]he rarity of post-[flu] vaccination neurological complications

reported in recent years makes it impossible to establish a definite causal relation.” Id. at 4.

43

Yuan Li et al., Identification and Characterization of Epitopes from Influenza A Virus

Hemagglutinin that Induce Broadly Cross-Reactive Antibodies, 41 Int’l J. Molecular Med. 1673

(2018).

44

There is no evidence to suggest that Petitioner’s flu vaccine contained an adjuvant.

45

Forty-three cases were found but six were excluded due to lack of clinical or demographic

information. Pet. Ex. 18 at 2.

30

In addition to citing the papers discussed above, Dr. Tornatore referenced case reports of

transverse myelitis after the H1N1 vaccination. Pet. Ex. 13 at 28. The first case report

(published in 2011) described a patient with a cervical lesion at C6 and C7 that had “mild

expansion of the cord and enhancement.” Id. (quoting Pet. Ex. 17 at 1).46 The patient was

previously healthy. Pet. Ex. 17 at 1. About one month after vaccination, he developed fever,

followed two days later by decreased sensation on his abdomen and urinary urgency. Id.

Neurology examination showed brisk reflexes and sensory impairment of the right leg. Id. CSF

showed mild pleocytosis and was positive for oligoclonal bands. Id. Cervical MRI revealed a

lesion at the C6/C7 level with gadolinium enhancement, consistent with transverse myelitis. Id.

Steroid treatment for five days resulted in almost complete recovery. Id. The authors

specifically noted that there was “no spinal cord compression, other neurological disease, . . . or

progression over [four] weeks.” Id. at 2. Regarding vaccine causation, the authors suggested

that the adjuvant in the vaccine47 may have played a role in an immune-mediated process. Id.

The second case was reported by Akkad et al. (published in 2010) and described a patient

with longitudinally extensive transverse myelitis in association with receiving an attenuated virus

nasal48 H1N1 vaccine.49 Pet. Ex. 16 at 1. Akkad et al. described a patient who developed

symptoms of transverse myelitis four days after vaccination. Id. MRI showed a non-enhancing

lesion extending from the cervical spine thought the entire thoracic spinal cord (longitudinally

extensive transverse myelitis). Id. No oligoclonal bands were present. Id. at 2. After steroids

and plasmapheresis, the patient had significant improvement. Id.

Nakamura et al.50 also reported a case of a patient who developed transverse myelitis (C6

to T3) seven days after the flu vaccine. Pet. Ex. 19 at 1-2. Treatment with gamma globulin

afforded a partial recovery. Id. at 2-3. Bakshi and Mazziotta also described a case of acute

transverse myelitis with onset four weeks after receipt of a flu vaccination. Pet. Ex. 39 at 1.

MRI showed spinal cord enlargement from the C3 level to the upper thoracic levels. Id. at 1. No

enhancement was seen. Id. at 3. No antecedent infectious or alternative causes were noted. Id.

46

Isabelle Korn-Lubetzki et al., H1N1 Vaccine-Related Acute Transverse Myelitis, 13 Isr. Med.

Ass’n J. 249 (2011).

47

Again, there is no evidence to suggest that Petitioner’s flu vaccine contained an adjuvant.

48

Petitioner here did not receive a nasal vaccine.

49

Ambrose et al. noted that the patient reported in the Akkad et al. paper received treatment for

mycoplasma pneumonia 20 days before the onset of her transverse myelitis, and therefore, it was

also a potential cause. Pet. Ex. 15 at 1 (Christopher S. Ambrose, A Case Report of Transverse

Myelitis Following Influenza Vaccination, 68 Archives Neurology 1085 (2011)).

50

Naoko Nakamura et al., Neurologic Complications Associated with Influenza Vaccination:

Two Adult Cases, 42 Internal Med. 191 (2003).

31

Other articles filed by Petitioner have been reviewed, but they are not discussed because

the substance was covered by other articles, or they are less relevant. See, e.g., Pet. Ex. 21 (case

report describing encephalitis, not transverse myelitis);51 Pet. Ex. 22 (an older article discussing

vaccine-induced autoimmunity);52 Pet. Ex. 23 (describing Guillain-Barré Syndrome (“GBS”), a

peripheral neuropathy, not transverse myelitis, a central nervous system disorder).53

v. Loving Factor Five/Althen Prong Two: Logical

Sequence of Cause and Effect

Dr. Tornatore opined that Petitioner initially developed transverse myelitis in July 2014,

when she was readmitted to the hospital after surgery. Tr. 128. Her MRI on July 9, 2014 was, in

his opinion, consistent with transverse myelitis. Id. The immune response to infection (caused

by the surgery and its complications) led to the transverse myelitis that occurred in July 2014.

Id. In summary, he opined that Petitioner’s initial trigger of transverse myelitis was post-

operative infection. Tr. 127.

In December 2015, after the flu vaccination, Dr. Tornatore opined that Petitioner’s

transverse myelitis worsened. Tr. 129. He attributed the worsening to the flu vaccination via the

mechanisms described above. Id. However, when asked to do so, he advanced two non-vaccine

related possibilities to explain Petitioner’s worsening in December 2015. The first was that he

acknowledged that Petitioner had “good days and bad days.” Id. Thus, the worsening in her

clinical condition could reflect the ups and downs that occur with the disease. See Tr. 24.

The second possibility was that something re-triggered Petitioner’s transverse myelitis

even before she received her flu vaccination. Tr. 129. Dr. Tornatore stated there was no

explanation as to what the trigger was since Petitioner did not have a fever or new infection. Id.

He suggested that Petitioner may have had a deep seeded infection and so although she was on

an antibiotic, it was possible that the treatment was “really not adequate,” and “maybe that’s

what triggered the December changes prior to the vaccine.” Tr. 131. If Petitioner still had a

lingering infection, he suggested that it was “most likely the discitis, the bone infection, because

that’s the hardest to get rid of. If there was any bacteria that had lingered . . . the immune system

would . . . fight that off . . . lead[ing] to [] inflammation all over again in the spinal cord.” Tr.

132. He further explained that “any infection will stimulate the immune system . . . and then it’s

going to overshoot because it’s already had this happen one time and then it’s going to cause the

myelitis to develop as a spillover. It’s a fertile field effect.” Tr. 132-33. He explained that it is

the “[s]ame concept as if the antigens came in from the vaccine.” Id.

51

Isabelle Van Ussel et al., Encephalitis Related to a H1N1 Vaccination: Case Report and

Review of the Literature, 124 Clinical Neurology & Neurosurgery 8 (2014).

52

Arnon Dov Cohen & Yehuda Shoenfeld, Vaccine-Related Autoimmunity, 9 J. Autoimmunity

699 (1996).

53

Reinhard Kiefer et al., Immune-Mediated Neuropathies, in 88 Advances in Neurology,

Neuromuscular Disorders 11 (Rahman Pourmand & Yadollah Harati eds., 2001).

32

Dr. Tornatore generally agreed with the interpretation of Petitioner’s MRI studies

provided by the treating radiologists and her physicians. Tr. 133-35. He noted that she had

inflammation, congestion, and edema. Tr. 134. The MRIs showed that Petitioner had

destruction of the discs and bone itself, which caused her to be “tilted,” which could cause

changes in her ambulation. Tr. 135. While he agreed that destruction of bone can lead to

instability and inflammation, he believed that in Petitioner’s case, it was the effect of the vaccine

because of “the tempo of her change in December.” Tr. 138. Regarding Petitioner’s spasms,

spasticity, and muscle tightness, Dr. Tornatore agreed that these problems can be caused by

“anything that hits the spinal cord.” Tr. 136. And on cross-examination, Dr. Tornatore

acknowledged that Petitioner had compressive myelopathy and that from the onset she had

severe stenosis that was never resolved. Tr. 115.

vi. Loving Factor Six/Althen Prong Three: Proximate

Temporal Relationship

Dr. Tornatore opined that the initial onset of Petitioner’s transverse myelitis was in the

post-operative period when she was readmitted to the hospital on July 9, 2014. Tr. 128. He

based this opinion on the MRI done July 9, 2014, which he believed is consistent with transverse

myelitis. Id.

Generally, Dr. Tornatore testified that the time frame for development of transverse

myelitis after vaccination is one to 63 days. Tr. 90. He opined that the mechanisms of molecular

mimicry and fertile field “happen pretty quickly.” Id. He testified that Petitioner’s significant

aggravation of transverse myelitis occurred within a week of vaccination, although “there was

even a hint that there was something maybe that happened just before the vaccination.” Tr. 91.

However, he believed that the vaccine “really triggered everything.” Id.

2. Respondent’s Expert, Dr. Adil Javed54

a. Background and Qualifications

Dr. Javed is a board-certified neurologist. Resp. Ex. A at 1; Resp. Ex. B at 3. He

received his M.D. from Southern Illinois University School of Medicine. Resp. Ex. B at 1.

Thereafter he completed a neurology residency at Yale University School of Medicine and a

neuroimmunology fellowship at the University of Chicago. Id. He is currently an Associate

Professor in the Department of Neurology at the University of Chicago School of Medicine. Id.;

Resp. Ex. A at 1. He also leads a “multi-disciplinary autoimmune clinic” where he diagnoses

patients with transverse myelitis, MS, NMO, and other autoimmune diseases. Resp. Ex. A at 1;

Tr. 153, 155-57. Dr. Javed has authored or co-authored multiple publications. Resp. Ex. B at 4-

6. His research focuses on “evaluating MS lesions and brain/spine atrophy using advanced MRI

techniques.” Resp. Ex. A at 1; Tr. 153-54, 156.

b. Opinion

54

Dr. Javed submitted two expert reports and testified at the hearing. Resp. Exs. A, C; Tr. 150.

33

i. Loving Factor One: What Was Petitioner’s Condition

Prior to Administration of the Vaccine?

Prior to vaccination, Dr. Javed’s opinion was that Petitioner had compressive

myelopathy. Resp. Ex. A at 3; Tr. 159-60. In reviewing Petitioner’s medical records, he

cautioned that the terminology was confusing. Tr. 210. He agreed that Petitioner had

inflammation or myelitis, but it was caused by compressive myelopathy. Id. He explained that

“compressive myelitis can be confused . . . with either [an] infectious or autoimmune . . .

myelitis.” Tr. 210. To distinguish the cause, Dr. Javed explained that a spinal tap to analyze

CSF for the presence of inflammation is required. Tr. 209-10. When Petitioner’s records stated

“transverse myelitis” as a chief complaint, or otherwise referenced transverse myelitis, he stated

that conclusions as to the cause could not be reached absent a proper “vet[ting]” or workup. Tr.

210-12.

Dr. Javed provided the following opinions relevant to Petitioner’s condition before

vaccination. Petitioner’s relevant clinical course began prior to June 2014, when her pre-

operative MRIs showed that she had a moderate central canal stenosis at the T5 level and mild

central canal stenosis at T6. Resp. Ex. A at 3; Tr. 159-60. Dr. Javed explained that Petitioner

had a disc or calcification pressing into the ventral (back) side of the spinal cord, compressing it

by 50%. Tr. 161. This resulted in a 6.5 mm “spinal cord area being pressed significantly to

almost [] half that.” Id. He added the ventral part of the spinal cord supplies power and strength

“to the legs, control of bladder, [and] sensation to the legs.” Id.

Surgery to remove the disc or calcification pressing the spinal cord was not successful.

Tr. 160-62. Instead of being relieved by surgery, Petitioner’s compressive myelopathy was

“worsened by surgery,” and then worsened even more by her post-operative infections. Id. Dr.

Javed opined that the appearance of compressive myelopathy looked like longitudinally

extensive transverse myelitis, but the cause was compression. Tr. 162 (citing Resp. Ex. A1).55

Moving forward to October 2014, Petitioner’s MRI showed intramedullary T2 prolongation with

mild cord enhancement to T9/T10 and T11/T12. Tr. 172; Pet. Ex. 1 at 535.

During Petitioner’s post-operative course, Dr. Javed opined that there were dynamic

changes in her clinical condition due to her infections and treatment for the infections. Tr. 173.

In other words, Petitioner’s clinical course was not linear, but dynamic. Tr. 174. However,

moving forward to December 2015, Petitioner experienced an increase in muscle tone and

spasticity evidencing a progression of her compressive myelopathy. Tr. 174-75. This

continuous and worsening compression caused more damage to nerve fibers and more venous

congestion. Id.

55

Eoin P. Flanagan et al., Teaching NeuroImages: “Pancake-Like” Gadolinium Enhancement

Suggests Compressive Myelopathy Due to Spondylosis, 80 Neurology e229 (2013)

34

ii. Loving Factor Two: What Is Petitioner’s Current

Condition (or Her Condition Following the Vaccination,

If Also Pertinent)?

After vaccination, Dr. Javed opined that Petitioner continued to have transverse myelitis

secondary to a mechanical obstruction caused by her herniated disc. Tr. 263. As stated earlier,

the surgery was not successful and did not relieve the obstruction. Tr. 160-62. Then she had a

post-operative infection that caused inflammation and transverse myelitis. Tr. 263-65. The

infection was treated with antibiotics. See Pet. Ex. 1 at 562. Although there was no

inflammation or evidence of infection on the MRI done January 8, 2016, Petitioner had “ongoing

symptoms of compressive myelopathy which mimic[ked] . . . infection. So it is very hard to

tease [] out” what was caused by infection and what was caused by compression. Tr. 266.

Regardless, Dr. Javed testified that the MRI done in January 2016 did not show active infection.

Tr. 264. Dr. Javed opined that the MRI findings and Petitioner’s clinical course were the result

of progressive compressive myelopathy not vaccination. Tr. 200.

To illustrate his opinions, Dr. Javed reviewed two images from Petitioner’s MRIs: one

taken before surgery on April 29, 2014, and the other taken after vaccination on July 1, 2016.

Resp. Ex. A at 13.

Id. The arrow on the left image shows “severe compression of the spine from the surrounding

tissue” on the MRI dated April 29, 2014, prior to vaccination. Id. The MRI done July 1, 2016

again shows the “severe bony defect” (arrow on the right image) and “more diffuse white signal

change . . . due to altered CSF flow.” Id. Dr. Javed opined these findings were not due to

inflammatory or “vaccine induced transverse myelitis,” but the result of severe compression. Id.

Dr. Javed next discussed the MRI done January 8, 2016 (done after Petitioner’s flu

vaccination on December 11, 2015). Tr. 186 (citing Pet. Ex. 1 at 1211). He opined it showed

worsening myelopathy due to compression. Id. Clinically, this MRI is consistent with

35

“[p]aralysis of the legs, weakness, spasticity, urine retention,” and all the other symptoms that

Petitioner was experiencing. Id. The MRI report stated the finding was “nonspecific and may be

secondary to altered CSF flow dynamics, transverse myelitis [,] and cord ischemia. Correlation

with clinical history [was] recommend.” Pet. Ex. 1 at 1211. Dr. Javed opined that the most

likely cause of the findings was “stenosis and venous congestion.” Tr. 187.

When asked to differentiate between symptoms caused by infection/inflammatory

myelitis from those caused by compressive myelopathy, Dr. Javed explained that was not

possible because “[t]hey’re the same. They present the same way.” Tr. 266. Thus, it is not

possible to tease out signs and symptoms caused of transverse myelitis caused by infection and

inflammation from ongoing symptoms of compressive myelopathy. Id.

Moving forward in Petitioner’s clinical course, Dr. Javed offered his interpretation of

Petitioner’s 2018 MRI. Tr. 304-05. He observed that the stenosis or “kink” in Petitioner’s spinal

cord at T5/T6 was worse, causing kyphosis. Tr. 305. There was dilation or swelling of the

spinal cord above and below the lesion (stenosis), and the worsening observed on the MRI was

probable due to that finding. Tr. 305-06. Dr. Javed further opined that Petitioner’s spinal

stenosis (and compressive myelopathy) caused the syrinx and further extension of disease. Tr.

306. He explained that transverse myelitis is a monophasic illness, but the 2018 MRI shows

progressive worsening, over four to five years after initial onset. Id. Dr. Javed opined that this

progression is not consistent with transverse myelitis, but it is consistent with worsening due to

progressive compressive myelopathy. Tr. 306-07.

iii. Loving Factor Three: Does Petitioner’s Current

Condition (or Condition After Vaccination) Constitute a

“Significant Aggravation” of Her Condition Prior to

Vaccination?

The parties stipulated that after Petitioner received the flu vaccine on December 11, 2015,

that her condition worsened as noted on her MRI imaging and by her treating physicians. Joint

Submission at 1-2. While the parties agreed that Petitioner’s worsened, they disagreed on the

nature or cause of the worsening. Id. at 2. As described above, Dr. Javed opined that

Petitioner’s worsening after vaccination was caused by progressive compression myelopathy and

not an autoimmune reaction to the flu vaccine. Tr. 306-07.

iv. Loving Factor Four/Althen Prong One: Medical Theory

of Causation

Dr. Javed opined that the weight of the evidence does not support a finding that the flu

vaccine can cause transverse myelitis. Tr. 189. He cited the 2012 Institute of Medicine (“IOM”)

report, which stated that the “epidemiologic evidence is insufficient or absent to assess an

association between [the] [flu] vaccine and transverse myelitis.” Resp. Ex. A6 at 3.56 The IOM

56

Inst. of Med., Influenza Vaccine, in Adverse Effects of Vaccines: Evidence and Causality 293,

309 (Kathleen Stratton et al. eds., 2012).

36

committee reviewed six papers that reported “the development of transverse myelitis after

administration of a[] [flu] vaccine” and they concluded that aside from a temporal association,

there was no other evidence of causality. Id. at 3-4. The committee also observed that the

natural flu infection is “rarely” associated with transverse myelitis. Id. at 3. They concluded that

while “[a]utoantibodies, T cells, and molecular mimicry may contribute to the symptoms of

transverse myelitis,” the papers “did not provide evidence linking these mechanisms to [the] [flu]

vaccine.” Id. Thus, they concluded that any association “based on knowledge about the natural

infection” was “weak.” Id. Dr. Javed further noted that the flu vaccine at issue here was an

inactivated vaccine, not a live viral vaccine, and he inferred that the causal association was

lacking due to that fact. Tr. 190.

Next, Dr. Javed opined that here, there is no evidence to support the hypothetical

mechanism of a fertile field due to the lack of MRI findings showing autoimmune or infectious

inflammation after vaccination. This opinion is discussed more below Loving factor five/Althen

prong two.

Regarding Petitioner’s theory of molecular mimicry, Dr. Javed opined that to invoke this

mechanism “as a likely cause of autoimmune disease, several criteria need to be met.”57 Resp.

Ex. A at 16. These include “1) proof that flu antigens are similar to human myelin antigens; 2)

proof antibodies or T cells generated against the flu antigens cross react with human myelin

antigens; [and] 3) a reliable scientific [link] in the real word that exposure to flu antigen causes

human disease.”58 Id. at 16-17. Because there is insufficient evidence to meet these three

criteria, Dr. Javed concluded that the flu vaccine does not cause “inflammatory, longitudinal,

transverse myelitis.” Id. at 17; see also Tr. 193-94.

Dr. Tornatore also discussed the theory of epitope spreading, “whereby invading antigens

accelerate an ongoing autoimmune process by local activation of antigen presenting cells and

over processing of antigens.” Pet. Ex. 13 at 29. In response, Dr. Javed opined that there was no

evidence of an ongoing autoimmune response prior to vaccination. Resp. Ex. A at 17. Dr. Javed

also disagreed that there was support for the bystander activation theory since there was no

evidence that Petitioner had “auto-reactive immune cells prior” to her vaccination. Id.

Dr. Javed discussed the medical literature cited by Dr. Tornatore. See Resp. Ex. A at 13,

15; Tr. 195-96, 238-42. He disagreed that Mealy et al.59 provided support that vaccinations can

57

The undersigned does not apply the criteria discussed by Dr. Javed. Instead, the undersigned

uses the Loving/Althen criteria and the legal standards set forth below in the legal standards and

analysis sections.

58

During the hearing, Dr. Javed referenced the IOM in support of this criteria; however, he did

not cite the portion of the text that contains this criteria. Tr. 244. Again, the undersigned does

not adopt this criteria or use it in her analysis as it is not consistent with Loving/Althen.

59

Maureen A. Mealy et al., Vaccines and the Association with Relapses in Patients with

Neuromyelitis Optica Spectrum Disorder, 23 Multiple Sclerosis & Related Disorders 78 (2018).

37

cause relapses in patients with transverse myelitis because the patients in that paper had

NMOSD, which Petitioner did not have. Id. (citing Pet. Ex. 41). The Van Ussel et al. paper

reviewed 22 cases of central nervous system demyelinating illnesses associated with either the

H1N1 flu vaccine and/or natural infection. Pet. Ex. 21 at 1; see Tr. 238. Five patients had

transverse myelitis following vaccination and one after infection. Pet. Ex. 21 at 4 tbl.1.

Although Dr. Javed acknowledged the case reports, he compared them to thousands of patients

who get natural infections and vaccinations and who do not experience transverse myelitis. Tr.

239, 241. Further, he noted that vaccines are recommended to those with transverse myelitis. Id.

Discussing Agmon-Levin et al., Dr. Javed opined that transverse myelitis is rare, and that rare

cases can be temporally associated with vaccination, but he disagreed that a temporal association

alone could establish cause and effect. Tr. 240-42 (citing Pet. Ex. 18).

Dr. Javed also reviewed the transverse myelitis fact sheet, published by NINDS, which

stated that transverse myelitis can be a “post-infectious autoimmune phenomenon.” Pet. Ex. 38

at 3. He noted that the statement contrasted with the 2012 IOM findings relative to vaccines and

transverse myelitis. Tr. 245. He acknowledged that autoimmune disease causation is

multifactorial, and may include “genetic, hormonal, endocrine, infectious, and environmental

factors.” Tr. 251.

When asked what evidence he would need before he could find that transverse myelitis

was caused by a vaccine, Dr. Javed acknowledged that he had “very high standards.”60 Tr. 242.

He stated that case reports were insufficient, particularly in this case, because Petitioner here had

“ongoing pathology,” with very different circumstances than those described in the case reports.

Tr. 243. Ultimately, Dr. Javed reiterated that in order to find causation, he would want to see

evidence meeting the three-pronged criteria to assess vaccine causation, as discussed earlier. Tr.

242-44.

v. Loving Factor Five/Althen Prong Two: Logical

Sequence of Cause and Effect

Dr. Javed opined that the flu vaccine was not the cause of Petitioner’s worsening

condition after vaccination. Tr. 159. “Inherent in [Petitioner’s] claim is first the

acknowledgement that she had [] ongoing thoracic myelopathy from another cause unrelated to

the vaccine, i.e., spinal cord compression.” Resp. Ex. A at 2. Dr. Javed explained that Petitioner

had an ongoing myelopathy from spinal cord compression caused by a mechanical obstruction

due to a herniated disc. Id.; Tr. 263. She underwent surgery and had a post-operative infection.

Tr. 263. Dr. Javed agreed that Petitioner’s post-operative infection did cause inflammation

correctly identified as transverse myelitis. Id. Petitioner’s infection was treated with antibiotics,

and it was cleared up by the time of her flu vaccine on December 11, 2015. Tr. 264. Dr. Javed

testified that there was no evidence of inflammation/myelitis seen in Petitioner’s MRI done

January 8, 2016. Id. There was no evidence of T2 prolongation representing inflammation, no

enhancement, and no evidence of osteomyelitis or discitis. Tr. 178, 264. Although enhancement

on MRI is not always present, it is often present, and if she had infection, Dr. Javed would have

Again, Dr. Javed’s standards and criteria are not used by the undersigned. Dr. Javed’s expert

60

medical opinions are evaluated using the applicable legal framework.

38

expected to see enhancement. Tr. 264. Thus, while he agreed that Petitioner had a post-

operative infection that caused transverse myelitis, he strongly disagreed that there was evidence

of transverse myelitis after her vaccination, specifically on the MRI done post-vaccination

(January 8, 2016). Id.

In reviewing the Petitioner’s records, Dr. Javed noted confusion with the use of the word

inflammation. Tr. 301-02. He explained that there is inflammation caused by compression as

well as that due to an autoimmune cause. Id. The word myelitis does not distinguish between

these causes. Tr. 302. He explained, “[w]hen you squeeze the [spinal] cord, some of the fibers

die [and] some of the fibers [] inflame.” Tr. 301.

Dr. Javed explained that Petitioner’s treating physicians did not perform a lumbar

puncture after vaccination to determine whether there was inflammation in the CSF. Tr. 192.

He suggested that a lumbar puncture was not done because Petitioner’s physicians did not see

inflammation suggestive of transverse myelitis on her MRI, and so they did not think the

procedure was warranted. Id. Moreover, Petitioner’s MRI showed no diffuse enhancement to

indicate inflammation consistent with transverse myelitis. Tr. 198-99.

In support of his opinion that if Petitioner’s treating physicians had suspected acute

transverse myelitis after her flu vaccination, they would have ordered diagnostic testing and

treatment with steroids, Dr. Javed filed a case report by Bakshi and Mazziotta. Resp. Ex. A at

13-14; Pet. Ex. 39. There, the MRI showed enlarged spinal cord from C3 to the upper thoracic

cord and CSF showed elevated inflammatory markers. Pet. Ex. 39 at 1. The patient was treated

with intravenous steroids which led to “a marked recovery by [two] weeks.” Id.

According to Dr. Javed, Petitioner was able to walk after her initial back surgery because

the surgery may have relieved some of the pressure on her spinal cord. Tr. 202-03.

Additionally, she received pain medications, therapy, and other treatment. Id. Although she

may have had some improvement, Dr. Javed opined that she “never really [had] progressive

improvement” after surgery. Tr. 203. Her course was complicated by infection and an abscess

which caused inflammation. Id. After treatment (with antibiotics), the inflammation subsided,

and as a result there may have been some improvement. Tr. 202-03.

Further, Dr. Javed observed that the physician who interpreted Petitioner’s post-

vaccination MRI on January 8, 2016, noted “[i]nterval development of expansile T2

prolongation/edema within the thoracic cord extending between T1/T2 and T10. Associated

intramedullary syringohydromyelia [was] noted at T6 and T7 without enhancement. Finding

[was] nonspecific and may be secondary to altered CSF flow dynamics, transverse myelitis and

cord ischemia.” Resp. Ex. A at 2 (quoting Pet. Ex. 1 at 1211). Based on this report, Dr. Javed

opined that the radiologist mentioned three possible causes for the findings.61 Id. at 3. It was Dr.

Javed’s opinion that the “progression of [Petitioner’s] symptoms and changes in the MRI are

related to the progressive of her pre-existing compressive myelopathy.” Id.

61

Two of these included altered CSF flow dynamics and cord ischemia (which Dr. Javed opined

was caused by compression). Tr. 227-28.

39

On cross-examination at the hearing, Dr. Javed was questioned about many of

Petitioner’s medical records. When questioned about PT records from December 2015,

documenting changes in Petitioner’s condition, Dr. Javed agreed that Petitioner had complaints,

but he opined that her symptoms were fluctuating because her “underlying process . . . was

worsening.” Tr. 216.

During this period of questioning, Dr. Javed was asked about Petitioner’s treating

neurologist, Dr. Tramonte, and his records dated January 20, 2016, when he saw Petitioner for

“worsening weakness, sensory loss, and spasticity . . . since the middle of December 2015.”62

Tr. 218; see Pet. Ex. 2 at 864. Dr. Javed noted that Dr. Tramonte recounted Petitioner’s “history

of thoracic spondylitic myelopathy.” Tr. 218 (quoting Pet. Ex. 2 at 863). Dr. Javed noted that in

December 2015, Dr. Tramonte concluded that Petitioner had “T4 thoracic myelopathy due to

calcified dis[c] herniation.” Tr. 219 (quoting Pet. Ex. 2 at 864).

Dr. Javed was also questioned about Dr. Garrett’s records from January 2016 and

specifically about the assessment which stated, “thoracic transverse myelitis due to prior

compression of spinal cord, meningitis, or even as autoimmune phenomenon from flu vaccine.”

Tr. 224; see Pet. Ex. 3 at 8250. Dr. Javed explained that an autoimmune reaction from the flu

vaccine was only one of the possibilities mentioned by Dr. Garrett. Tr. 224-26. Dr. Javed

testified that in July 2016, Dr. Garrett also documented an assessment stating that Petitioner’s

worsening “correlate[d] with a prolonged T2 signal within the spinal cord but [could not] tell if

[it was] a new ischemia or myelitis.” Tr. 227 (quoting Pet. Ex. 3 at 8349). Dr. Javed opined that

the reference to ischemia meant lack of oxygen due to worsening compression. Tr. 227-28.

Dr. Frohman’s medical records documented a history taken in November 2017, which

state that Petitioner had a “slow but steady improvement” after surgery until December 2015.

Pet. Ex. 10 at 37. When questioned about the note, Dr. Javed explained that it was written one-

and-one-half years after the events at issue. Tr. 204-05. Dr. Javed also agreed that Petitioner did

have improvement after surgery, although he characterized this period as Petitioner having “good

days and bad days.” Tr. 204. As her infection improved, she probably “had slow, steady

improvement.” Tr. 205. However, Petitioner’s progressive compressive myelopathy was not

62

Dr. Tramonte’s records from this visit on January 20, 2016, include his assessment that

Petitioner had a “T4 thoracic myelopathy due to calcified dis[c] herniation, [status post]

decompression, followed by a complicated course of infection with empyema, abscess and

compression of the conus medullaris and cauda equina in 2014.” Pet. Ex. 2 at 867. Her chief

complaint at the time of her December 30, 2015 visit with Dr. Tramonte “was worsening

weakness, spasticity, and sensory loss in the left leg since the middle of Dec[ember] 2015. Her

MRIs showed worsening pre-existing signal abnormality in the thoracic spinal cord from T1-

T10, a change that initially was present after developing a T4-T11 epidural abscess, along with

new syringomyelia at T6/7.” Id. Dr. Tramonte suspected “the changes were ischemic in nature”

and “referred her for aqua therapy, and scheduled repeat MRIs . . . in [six] months.” Id. It does

not appear that Petitioner had the repeat MRI six months later. Dr. Tramonte’s referral order for

aqua therapy stated “[e]val[uate] and treat weakness in legs due to thoracic myelopathy.” Id. at

862.

40

being treated. Id. And Dr. Javed again emphasized that a lumbar puncture was not performed

and there was no workup to diagnose transverse myelitis. Tr. 209.

Regarding the references in the medical records to Petitioner’s allergies and the flu

vaccine being identified as an allergy, Dr. Javed disagreed that this was evidence of vaccine

causation. Tr. 212, 230-31 (referencing Dr. Frohman’s and Dr. Tramonte’s records). Dr. Javed

explained that allergies are usually charted by nursing staff, not physicians. Tr. 213.

Additionally, with regard to the records which state that Petitioner developed TM after a flu

vaccine, Dr. Javed also opined that these records were not evidence of vaccine causation. Tr.

221-23 (citing Pet. Ex. 2 at 864); see also Pet. Ex. 1 at 1293 (“[T]here was consideration that the

changes could be vaccine relate myelitis from the flu shot.”).

While some of Petitioner’s treating physicians questioned the role of Petitioner’s flu shot,

Dr. Javed opined that they did not conclude that it was the cause of her illness, or that it caused

an aggravation of her condition. Tr. 227-31; Resp. Ex. A at 10-11. Dr. Javed further explained

that Dr. Garrett questioned whether Petitioner’s symptoms were due to cord compression,

although he concluded that surgical intervention was not warranted. Tr. 232-33, 236-38.

Dr. Javed also disagreed with Dr. Frohman’s diagnosis of transverse myelitis. Tr. 197-

98. He emphasized, however, that Dr. Frohman did not attribute Petitioner’s transverse myelitis

to vaccination. Pet. Ex. 10 at 40. Dr. Frohman wrote that he “suspect[ed] that [Petitioner] did in

fact have transverse myelitis, although the pathoetiological underpinnings of this process remain

enigmatic.” Id. Based on this note, Dr. Javed opined that Dr. Frohman did not attribute the

cause of Petitioner’s condition to the flu vaccine. Tr. 198-99.

Another fact important to Dr. Javed’s opinion that Petitioner did not have post-

vaccination transverse myelitis was that her MRI on January 8, 2016 showed an intermedullary

syringohydromyelia at T6 and T7. Resp. Ex. A at 13. He defined syringohydromyelia as a

“syrinx, a fluid filled cavity in the spinal cord from chronic and slow blockage of CSF fluid

caused by subarachnoid space [] flow blockage, i.e., from spinal stenosis.” Id. He asserted that

“[a]cute transverse myelitis does not cause syringohydromyelia/syrinx.” Id. The following

image shows the syrinx at T8-9:

41

Resp. Ex. A4 at 2 fig.1.63

In support of his opinion, Dr. Javed cited Arai et al., which reported a case of spinal

stenosis that caused an intramedullary syringohydromyelia. Resp. Ex. A at 14 (citing Resp. Ex.

A4 at 1). The authors of the paper explained that “[l]ong-standing blockade of [CSF] circulation

is considered to be one of the main causes of syringomyelia associated with degenerative

diseases of the cervical spine.” Resp. Ex. A4 at 1. In the case reported, the patient had a disc

herniation at T9 and T10, and the syringomyelia occurred in that part of the spine. Id. The

authors discussed CSF flow dynamics and the improvement which can be achieved by

decompression of the spinal cord compression. Id. at 2-3. They concluded that although rare,

“long-standing compression of the spinal cord due to spinal spondylosis could . . . be one of the

main causes of syringomyelia.” Id. at 3.

In further support of his opinion that Petitioner suffered from compressive myelopathy

and not post-vaccination transverse myelitis, Dr. Javed cited several other articles. See Resp. Ex.

A at 10-13. A paper by Kelley et al.64 described five patients with compressive myelopathy that

mimicked transverse myelitis. Tr. 184 (citing Resp. Ex. A2). All five patients were suspected to

have transverse myelitis but were ultimately diagnosed with spinal stenosis. Resp. Ex. A2 at 1.

The authors explained that “[c]ompressive myelopathy is occasionally associated with [] T2

signal changes on [MRI]. When this occurs, the radiologic appearance can result in misdiagnosis

of transverse myelitis.” Id. Specific to the facts here, the authors stated that in the case of

longitudinally extensive transverse myelitis appearance on MRI, there are other causes that are

important to recognize, including “in the setting of myelopathy . . . symptomatic spinal stenosis.”

Id. at 2. All five of the patients with “compressive myelopathy experienced progressive

neurological dysfunction over months, as reflected in the mean duration from onset to symptom

nadir or interventions, whereas patients with transverse myelitis characteristically reach[ed] a

nadir of deficit within [two] weeks.” Id.

Flanagan et al. described a 41-year old male with progressive hand weakness and

paraparesis. Resp. Ex. A1 at 1. The patient deteriorated in spite of steroid treatment. Id. One

year later, he underwent cervical decompression and his clinical condition stabilized. Id. The

authors explained that MRI enhancement “due to focal disruption of the blood brain barrier at the

point of maximal stenosis strongly suggest[ed] cervical stenosis as the cause of myelopathy.” Id.

Regarding Petitioner’s theory that there was a “fertile field” which allowed for an

immune response to cause transverse myelitis, Dr. Javed disagreed that there was evidence to

support a fertile field mechanism. Tr. 191-92. He explained that the MRI done in January 2016

did not show evidence of infection, discitis, enhancement, or meningitis. Tr. 175-77. The MRI

did show a lot of bony destruction. Tr. 178. Dr. Javed opined that the MRI showed worsening

compressive myelopathy. Tr. 177, 186. The pressure on Petitioner’s spine looked worse. Id.

63

Atsushi Arai et al., Syringomyelia Due to Thoracic Spinal Stenosis with Ossified Ligamentum

Flavum, 51 Neurologia medico-chirurgica 157 (2011).

64

Brendan J. Kelley et al., Compressive Myelopathy Mimicking Transverse Myelitis, 16

Neurologist 120 (2010).

42

According to Dr. Javed, Petitioner’s compressive myelopathy got worse because her spinal cord

nerves were damaged, causing more venous congestion, and worsening of her condition. Tr.

175.

In addition to the lack of findings to support a “fertile field” for the development of an

autoimmune reaction, Dr. Javed also explained that none of Petitioner’s treating physicians

treated her for transverse myelitis after her vaccination. See Tr. 167, 198-99, 231, 305. If

Petitioner’s treating doctors thought she had autoimmune transverse myelitis, Dr. Javed asserted

that she would have received diagnostic testing (a lumbar puncture and CSF analysis) to confirm

the diagnosis. Tr. 163-64, 171, 207, 209. And if the diagnosis of transverse myelitis was

confirmed by the presence of inflammation in the CSF, treatment would have been initiated. Tr.

266-71. But neither Petitioner’s neurosurgeon (Dr. Garrett) nor her neurologist (Dr. Tramonte)

performed diagnostic testing or treated her for transverse myelitis. Tr. 164, 271.

Dr. Javed disagreed with Dr. Tornatore that treatment for transverse myelitis, including

IVIG and plasma exchange, were contraindicated due to Petitioner’s condition or clinical course.

Tr. 303. Even in patients with high risk of developing complications, like clotting, Dr. Javed

opined that the risk of clots was very low. Id.

Lastly, Dr. Javed opined that it was “extremely unlikely” that the vaccine caused

autoimmune inflammation of the spinal cord that continued for a period of four or five years (as

evidenced by Petitioner’s MRI in 2018). Tr. 306. He emphasized that transverse myelitis is a

monophasic illness, not a progressive one. Id. Thus, he opined that it is more probable that

Petitioner’s worsening was caused by compressive myelopathy. Tr. 307.

vi. Loving Factor Six/Althen Prong Three: Proximate

Temporal Relationship

Dr. Javed agreed that given Petitioner received the vaccination at issue on December 11,

2015, and approximately one week later complained of weakness, there was an appropriate time

period for onset of an autoimmune reaction (transverse myelitis). Tr. 261. However, he believed

that Petitioner was “already declining prior to vaccination.” Resp. Ex. A at 16. “Given that

[Petitioner] had very low reserve in the spinal cord to begin with (i.e., added injuries from spinal

cord damage from stenosis + injury from abscess + injury from discitis), a slowly developing

process may have a sharp inflection point in terms of clinical decline.” Id. He opined

“[v]accination in this case would be [] a mere temporal association (coincidental) and not a

causal association.” Id.

V. LEGAL FRAMEWORK

A. Standard of Adjudication—Factual Issues

A petitioner must prove, by a preponderance of the evidence, the factual circumstances

surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh

the evidence presented, which may include contemporaneous medical records and testimony.

See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a

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special master must decide what weight to give evidence including oral testimony and

contemporaneous medical records). Contemporaneous medical records, “in general, warrant

consideration as trustworthy evidence.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d

1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378,

1382 (Fed. Cir. 2021) (rejecting the presumption that “medical records are accurate and complete

as to all the patient’s physical conditions”); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed.

Cl. 532, 538 (2011) (“[T]he absence of a reference to a condition or circumstance is much less

significant than a reference which negates the existence of the condition or circumstance.”

(quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,

968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d

mem., 503 F. App’x 952 (Fed. Cir. 2013).

There are situations in which compelling testimony may be more persuasive than written

records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of

Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the

factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.

Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)

(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than

those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a

determination regarding a witness’s credibility is needed when determining the weight that such

testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379

(Fed. Cir. 2009); Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir.

1993).

Despite the weight afforded to medical records, special masters are not bound rigidly by

those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &

Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see

also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.

Spec. Mstr. Feb. 18, 1994) (“[Section 13(b)(2)] must be construed so as to give effect also to §

13(b)(1) which directs the special master or court to consider the medical records (reports,

diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special

master or court to be bound by them.” (emphasis omitted)).

B. Standards for Adjudication—Causation

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

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 & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting

H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,

44

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health

& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of

evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic predisposition, or general acceptance in the scientific or medical communities

to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by

presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of

the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321

(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));

see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The

received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d

at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent

can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors

unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to

establish a prima facie case, the burden does not shift. Bradley, 991 F.2d at 1575.

“Regardless of whether the burden ever shifts to the [R]espondent, the special master

may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner

has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,

162-63 aff'd, 586 F. App’x 588 (Fed. Cir. 2014); see also Stone v. Sec’y of Health & Hum.

Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (“[E]vidence of other possible sources of injury can

be relevant not only to the ‘factors unrelated’ defense, but also to whether a prima facie showing

has been made that the vaccine was a substantial factor in causing the injury in question.”); de

Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The

government, like any defendant, is permitted to offer evidence to demonstrate the inadequacy of

the [P]etitioner’s evidence on a requisite element of the [P]etitioner’s case-in-chief.”); Pafford,

451 F.3d at 1358-59 (“[T]he presence of multiple potential causative agents makes it difficult to

attribute ‘but for’ causation to the vaccination. . . . [T]he Special Master properly introduced the

presence of the other unrelated contemporaneous events as just as likely to have been the

triggering event as the vaccinations.”).

To receive compensation through the Program, Petitioner must prove either (1) that she

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a

vaccine that she received, or (2) that she suffered an injury that was actually caused by a

vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Because Petitioner

does not allege she suffered a Table Injury, she must prove a vaccine she received caused her

injury. To do so, Petitioner must establish, by preponderant evidence: “(1) a medical theory

causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect

showing that the vaccination was the reason for the injury; and (3) a showing of a proximate

temporal relationship between vaccination and injury.” Althen v. Sec’y of Health & Hum.

Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005).

The causation theory must relate to the injury alleged. Petitioner must provide a sound

and reliable medical or scientific explanation that pertains specifically to this case, although the

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explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Hum. Servs., 35 F.3d 543, 543, 548-49 (Fed. Cir. 1994). Petitioner cannot

establish entitlement to compensation based solely on his assertions; rather, a vaccine claim must

be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In

determining whether Petitioner is entitled to compensation, the special master shall consider all

materials in the record, including “any . . . conclusion, [or] medical judgment . . . which is

contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh

the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s

favor when the evidence weighs in her favor. See Moberly, 592 F.3d at 1325-26 (“Finders of

fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence

presented to them and, if appropriate, as to the credibility of the persons presenting that

evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s

favor).

Testimony that merely expresses the possibility—not the probability—is insufficient, by

itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &

Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and

noting that a possible causal link was not sufficient to meet the preponderance standard). The

Federal Circuit has made clear that the mere possibility of a link between a vaccination and a

petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at

1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and

the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon

v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is

by no means required, a possible mechanism does not rise to the level of preponderance.

Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

C. Standards for Adjudication—Significant Aggravation

The elements of an off-Table significant aggravation case are set forth in Loving. See

Loving, 86 Fed. Cl. at 142-44; see also W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352,

1357 (Fed. Cir. 2013) (holding that “the Loving case provides the correct framework for

evaluating off-table significant aggravation claims”). The Loving court combined the Althen

test, which defines off-Table causation cases, with a test from Whitecotton. Whitecotton v.

Sec’y of Health & Hum. Servs., 17 F.3d 374 (Fed. Cir. 1994), rev’d sub nom., Shalala v.

Whitecotton, 514 U.S. 268 (1995) (concerning on-Table significant aggravation cases). The

resultant test has six components, which are:

(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 significant 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.

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Loving, 86 Fed. Cl. at 144.

The statute defines “significant aggravation” as “any change for the worse in a pre-

existing condition which results in markedly greater disability, pain, or illness accompanied by

substantial deterioration in health.” § 33(4).

VI. ANALYSIS

A. Significant Aggravation

1. Loving Factor One: What Was Petitioner’s Condition Prior to

Administration of the Vaccine?

The first step in the Loving test is to determine Petitioner’s condition prior to the

administration of her flu vaccine on December 11, 2015. The parties agree and stipulate that

prior to receiving the flu vaccine at issue on December 11, 2015, Petitioner “suffered from a pre-

existing thoracic myelopathy.” Joint Submission at 1. Petitioner’s medical records establish,

and both experts generally agree, that in March/April 2014 Petitioner developed spinal cord-

related neurologic symptoms caused by a herniated disc/mass compressing the spinal cord at T5

and T6. Both experts agree that Petitioner had significant stenosis in her thoracic spinal cord.

Dr. Javed opines that the disc was compressing the spinal cord by about 50%. The stenosis

caused edema (swelling) and inflammation of the spinal cord seen on MRI. Petitioner underwent

decompressive surgery on June 27, 2014.

The medical records show, and the experts agreed, that post-operatively, Petitioner

developed a very profound post-operative infection around her spinal cord along with an epidural

and thoracic abscess. This infection required a second operative procedure and lengthy treatment

with antibiotics. Dr. Tornatore opined that about six weeks after her second surgery, Petitioner

developed longitudinally extensive transverse myelitis, as seen on her MRI August 26, 2014.

Ultimately, Dr. Javed agreed that due to the infection, Petitioner developed transverse myelitis.

Two months later, on October 21, 2014, an MRI showed improvement. Both experts

acknowledged that Petitioner improved some after surgery and antibiotics.

Both experts agreed that the initial back surgery did not result in decompression of the

stenosis in Petitioner’s spinal cord. Both experts agreed that there was a component of

compressive myelopathy causing Petitioner’s condition. Thus, the undersigned finds that prior to

her vaccination, Petitioner had thoracic myelopathy with compression and

inflammatory/infectious myelitis; that Petitioner had a spinal cord injury and paraplegia; and that

she had a limited ability to walk with a rolling walker, although she had difficulty with use of her

right foot and problems with spasticity and tone that limited her ability to stand, pivot, and walk.

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2. Loving Factor Two: What Is Petitioner’s Current Condition (or Her

Condition Following the Vaccination, If Also Pertinent)?

The second part of the Loving test is to discuss “the person’s current condition (or

condition following the vaccination if that is also pertinent).” Loving, 86 Fed. Cl. at 144. Here,

Petitioner’s condition following vaccination through 2018 is most pertinent.

To the extent that Petitioner’s affidavit or histories noted in the medical records are

inconsistent with and contradicted by the physicians’ objective physical examinations or

diagnostic testing, the undersigned defers to the contemporaneous physician findings as the most

reliable source of information. See Cucuras, 993 F.2d at 1528 (noting that “the Supreme Court

counsels that oral testimony in conflict with contemporaneous documentary evidence deserves

little weight”); Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed. Cl. 598, 608 (2010); Stevens

v. Sec’y of Health & Hum. Servs., No. 90-221V, 1990 WL 608693, at *3 (Cl. Ct. Spec. Mstr.

Dec. 21, 1990) (noting that “clear, cogent, and consistent testimony can overcome such missing

or contradictory medical records”); Vergara v. Sec’y of Health & Hum. Servs., No. 08-882V,

2014 WL 2795491, at *4 (Fed. Cl. Spec. Mstr. May 15, 2014) (“Special Masters frequently

accord more weight to contemporaneously-recorded medical symptoms than those recorded in

later medical histories, affidavits, or trial testimony.”).

Petitioner received her flu vaccine on December 11, 2015. On December 18, 2015,

Petitioner reported that her spasticity was worse and she was unable to stand. This was also

noted at her PT visit on December 30, 2015, when Petitioner’s increased spasticity made it

difficult for her to bear weight. Based on the records filed, Petitioner has not been able to

ambulate, even for short distances, since December 2015.

Subsequent MRI studies, done in 2016 and 2018, show progressive worsening. On

January 8, 2016, the MRI showed expansile prolongation/edema and intramedullary

syringohydromyelia within the thoracic spinal cord that “may be secondary to altered CSF flow

dynamics, transverse myelitis[,] and cord ischemia.” Pet. Ex. 1 at 1211. A July 1, 2016 MRI

showed “progression of abnormal signal and expansion” of the thoracic cord. Pet. Ex. 3 at 8321.

On November 9, 2018, the MRI showed “extension of expansile cord signal abnormality” and

multilevel cervical spondylosis with “varying degrees of mild foraminal narrowing and mild to

moderate spinal stenosis.” Pet. Ex. 12 at 23. The undersigned finds that since vaccination,

Petitioner has experienced a progressive worsening of her clinical course and MRI findings.

3. Loving Factor Three: Does Petitioner’s Current Condition (or

Condition After Vaccination) Constitute a “Significant Aggravation”

of Her Condition Prior to Vaccination?

The next factor of the Loving test is to determine whether there is a “significant

aggravation” of Petitioner’s condition by comparing her condition before vaccination to her

condition after vaccination. The statute defines “significant aggravation” as “any change for the

worse in a pre-existing condition which results in markedly greater disability, pain, or illness

accompanied by substantial deterioration in health.” § 33(4). Using this definition, the

48

undersigned finds that, based on all of the facts and circumstances here, Petitioner did have a

significant aggravation of her underlying condition.

The parties stipulated that Petitioner’s condition worsened post-vaccination. Joint

Submission at 2. The undersigned agrees that prior to her vaccination on December 11, 2015,

Petitioner had a limited ability to ambulate with a rolling walker and that after vaccination she no

longer could do so.

As explained by Dr. Tornatore, Petitioner’s condition worsened after her vaccination.

Prior to December 11, 2015, Petitioner could ambulate short distances with a rolling walker.

Beginning mid-December 2015, approximately December 18, she developed increasing

spasticity, particularly in her left leg. This increase in spasticity limited her ability to stand,

pivot, and ambulate. She was unable to walk with her walker. The increase in spasticity was

concerning enough that it was reported to her physician.

Based on the parties’ joint submission, the PT records, Petitioner’s affidavit, and the

opinions of Dr. Tornatore, the undersigned finds that the Petitioner developed a worsening of her

condition in mid-December 2015, which constituted a significant aggravation of her condition as

compared to her condition before vaccination on December 11, 2015.

4. Loving Factor Four/Althen Prong One: Medical Theory of Causation

The fourth Loving factor has its origins in Althen prong one, and Petitioner must set forth

a medical theory explaining how the received vaccine co

This text is long and has been trimmed here. Open the source document for the complete record.