# Barrientos v. Secretary of Health and Human Services

> United States Court of Federal Claims · June 11, 2024

URL: https://www.frixlaw.com/law-library/cases/10735064

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** June 11, 2024
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Nora Beth Dorsey
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10735064

## How later opinions describe it (automated extraction)

- noting that “clear, cogent, and consistent testimony can overcome such missing or contradictory medical records”
- noting that “close calls” are resolved in Petitioner’s favor
- noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”

## Opinion text

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.
*
*************************

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 diff

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10735064. Public record. Not legal advice.