# WILLIFORD v. SECRETARY OF HEALTH AND HUMAN SERVICES

> United States Court of Federal Claims · May 4, 2026

URL: https://www.frixlaw.com/law-library/cases/11320621

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** May 4, 2026
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Jennifer A. Shah
- **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/11320621

## How later opinions describe it (automated extraction)

- stating that “medical records and medical opinion testimony are favored in vaccine cases, as treating physicians are likely to be in the best position to determine whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 18-1371V
Filed: March 5, 2026

************************* *
*
JENNIFER WILLIFORD and CHARLES *
EDWARD WILLIFORD, III, parents of *
*
R.W., a minor, *
*
Petitioners, *
*
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
*
Respondent. *
*
************************* *

Nichole Glance Booker, Mast Law Firm, Smithfield, NC, for Petitioner.
James Vincent Lopez, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

Shah, Special Master:

On September 7, 2018, Jennifer and Charles “Eddie” Williford (“Petitioners” or “Mr. and
Mrs. Williford”), parents of R.W., filed a petition for compensation under the National Vaccine
Injury Compensation Program, 42 U.S.C. §§ 300aa-10, et seq.2 (the “Vaccine Act” or “Program”).
ECF No. 1 (“Pet.”). Petitioners allege that R.W. developed transverse myelitis (“TM”), neurogenic

1
This Decision will be posted on the United States Court of Federal Claims’ website, in accordance with
the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will be available to
anyone with access to the internet. As provided in 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties
may object to the Decision’s inclusion of certain kinds of confidential information. To do so, each party
may, within 14 days, request redaction “of any information furnished by that party: (1) that is a trade secret
or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files
or similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.”
Vaccine Rule 18(b). Otherwise, this Decision will be available to the public in its present form. Id.
2
National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. For ease of citation,
all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa (2012).

1
bladder, neurogenic bowel, scoliosis, and paraplegia caused by the tetanus-diphtheria-acellular
pertussis (“Tdap”) and meningococcal vaccines she received on September 11, 2015. Id. at 1.

I am very sympathetic to R.W. and the ordeal she and her family have endured. However,
for the reasons discussed in this decision, I deny entitlement. The preponderant evidence did not
establish that R.W. suffered the condition alleged, TM. The evidence also did not substantiate that
either of the subject vaccinations caused R.W.’s injury.

I. PROCEDURAL BACKGROUND

Petitioners filed medical records and medical literature with their petition. Exs. 1-12, 15-
18. They also filed affidavits from Mr. and Mrs. Williford. Exs. 13-14. Respondent filed his Rule
4(c) Report on March 13, 2019, indicating that the case was not appropriate for compensation
under the Vaccine Act. ECF No. 15 (“Report”) at 1.

Petitioners and Respondent then filed a series of expert reports. Petitioners filed two
reports from Lawrence Steinman, M.D. Ex. 23, 49. Respondent filed one report each from Neil
Romberg, M.D., and Michael Sweeney, M.D.3 Exs. A, C.

Former Special Master Katherine E. Oler held an entitlement hearing from July 26-28,
2022, at which Mr. and Mrs. Williford, R.W., and Drs. Steinman, Sweeney, and Romberg testified.
Minute Entry dated 7/28/2022; Tr. at 3, 191, 343. After the hearing, Special Master Oler directed
the parties to state whether they wished to file further expert reports from neuroradiology experts
and/or additional reports from their neurology experts. ECF No. 60.

On January 9, 2023, Petitioners filed an expert report, curriculum vitae, and literature from
David Wilson, M.D., a neuroradiologist. Exs. 88-96. On April 17, 2023, Respondent filed a
responsive report and curriculum vitae from neuroradiologist William Zucconi, D.O. Exs. D-E.

Special Master Oler held a status conference on May 2, 2023, at Respondent’s request.
Minute Entry dated 5/2/2023; ECF No. 71. Petitioners’ counsel advised that she wished to file
affidavits from R.W.’s physicians at Duke University “to clarify terminology used in the medical
record.” ECF No. 71 at 1. Respondent’s counsel stated his potential intent to object to this request
as untimely and prejudicial. Id. Several weeks later, Special Master Oler held another conference
at which the parties revealed that, before Respondent could formally state his position, Petitioners’
counsel had requested the clarifying information from Duke but had received no response. Minute
Entry dated 5/22/2023; ECF No. 73. Petitioners’ counsel agreed to withdraw the request to seek
further affidavits from Duke. ECF No. 73 at 2.

3
Petitioners filed Dr. Steinman’s curriculum vitae and the medical literature referenced in his first report
on August 24, 2020. Exs. 24-48. Shortly before the entitlement hearing, Respondent filed the medical
literature referenced in his experts’ reports, along with updated curricula vitae for his experts, and
Petitioners filed the literature referenced in Dr. Steinman’s second report. Exs. A, Tabs 1-20; Ex. B, Tab
1; Exs. C, Tabs 1-10; Ex. D, Tab 1.

2
On August 21, 2023, Petitioners filed a post-hearing brief. ECF No. 75 (“Pets.’ Post-
Hearing Brief”). On December 11, 2023, Respondent filed a responsive post-hearing brief. ECF
No. 77 (“Resp.’s Post-Hearing Brief”). On February 16, 2024, Respondent filed several pieces of
medical literature. Exs. G-M. On February 21, 2024, the parties jointly agreed the record was
complete for a decision. ECF No. 80.

On August 13, 2024, this case was reassigned to my docket. ECF No. 81. The case is now
ripe for adjudication.

II. FACT EVIDENCE

A. Medical Records

R.W. was born on September 8, 2004, and was 11 years old when she received Tdap and
meningococcal vaccines on September 11, 2015, during her well-child checkup. Ex. 2 at 166. She
did not have a significant pre-vaccination medical history.

On September 27, 2015, 16 days after receiving her vaccines, R.W. presented to Geeta
Subramaniam, M.D., an emergency medicine specialist at the Johnston Medical Center in Clayton,
North Carolina, stating “she cannot move her right leg[,] it feels like it is going to sleep.” Ex. 2 at
154, 157. R.W.’s mother reported that R.W. was “sluggish and tired” earlier that day. Id. at 154.
Dr. Subramaniam noted that R.W. had right posterior thigh pain that began at 12:00 pm that day,
which had “progressed to decreased ability to use the right leg and now inability to feel the left.”
Id. at 156. She had “a low-grade fever” that first began that day but had experienced no other
symptoms of infection. Id. at 156-57. Dr. Subramaniam noted that R.W. had received two
vaccinations “two weeks” prior. Id.

Dr. Subramaniam remarked that R.W. was “[g]enerally healthy with no significant past
medical history” and that she “[d]enied any respiratory problems or difficulty breathing presently.”
Ex. 2 at 157. She suspected Guillain-Barré syndrome (“GBS”) but noted that ascending tick
paralysis was another possibility, commenting that R.W. had been at the Benson Mule Day festival
the previous day. Id. at 158. R.W. was provisionally diagnosed with bilateral leg weakness and
transferred to the pediatric intensive care unit (“PICU”) at the WakeMed Hospital in Raleigh,
North Carolina (“WakeMed”). Id. at 161-63.

1. WakeMed Hospitalization: September 27-October 6, 2015

On arrival to the WakeMed PICU the night of September 27, R.W. was seen by pediatric
critical care physicians Bridget Donell, M.D. (attending), and Linh Tran, M.D. (resident). Ex. 4A
at 1. Dr. Tran’s exam found 1/5 strength bilaterally in the quadriceps and 0/5 strength bilaterally
in the lower legs. Id. at 3. R.W. had absent reflexes and “decreased sensation to light touch on
the distal right thigh, possibly along the L3-L4 dermatomal distribution [with] decreased 2-point
discrimination.” Id. The physicians were concerned about possible GBS or an acute spinal cord
process such as TM. Id. at 4. They noted: “Although her distribution is along the L3-L4
dermatome in the [right] thigh, there is no clearly defined sensory level, making transverse myelitis

3
a possible etiology.” Id. They ordered MRIs of the entire spine, a lumbar puncture (“LP”), and
IVIG treatment. Id.

On September 28, 2015, R.W.’s thoracic MRI revealed a “very subtle” T2 signal
abnormality of the spinal cord at the T11-12 level, with a possible second signal abnormality of
the spinal cord at the T7-8 level. Ex. 4A at 107. Her cervical spinal MRI was normal. Id. Her
lumbosacral spinal MRI showed “[s]ubtle elevation of T2 signal intensity in the conus nodularis.”
Id. Her brain MRI was normal. Id.

R.W. was seen by pediatric critical care specialists Travis Honeycutt, M.D. (attending),
and Sara Duffus, M.D. (resident), the morning of September 28, 2015. Ex. 4A at 105. They noted
R.W. had been admitted overnight and had undergone an MRI and lumbar puncture. Id. at 105,
155-58. She had been given one high-dose steroid treatment. Id. at 105. At the time, she reported
being able to feel more in her legs and was able to slightly move her toes. Id. at 106. She continued
to run low fevers intermittently overnight. Id.

On exam, R.W. had 1/5 strength in hip flexion and 0/5 strength in her knees and ankles
bilaterally. Ex. 4A at 106. She could not move her toes. Id. She did have intact sensation to soft
touch from the right knee proximally and from the left dorsum of the foot proximally, but she had
no sensation from the right knee distally or on the plantar surface of the left foot. Id. TM, multiple
sclerosis (“MS”), and less likely neoplasm or tick paralysis were included on the differential
diagnosis. Id. at 108. Dr. Honeycutt believed TM was the most likely diagnosis. Id. at 109. The
plan was to repeat the thoracic MRI with and without contrast and continue IVIG and steroid
treatments. Id. at 108. They also planned to run a respiratory viral PCR assay and an arbovirus
panel, as well as further testing of the cerebrospinal fluid (“CSF”), as recommended by infectious
disease specialists at Duke, with whom the WakeMed team had consulted. Id.

The same morning, R.W. was seen by pediatric neurologist John Wooten, M.D. Ex. 4A at
116. The history stated:

[R.W.] noticed that she started to have some pain in her [right] thigh,
located around her posterior thigh, at about 3 pm today. Shortly
thereafter, she had progressive weakness and numbness of her
[right] thigh, and she started to have some weakness spread to her
[left] thigh. She then fell over when she tried to get up from a chair
to walk. Since that time, she has had progressive numbness and
weakness in bilateral lower extremities. Mom checked temperature
. . . 100.5 (forehead). No new rashes (has had bumps behind right
knee), insect/tick bites. She did get 2 vaccines, possibly her Tdap
and HPV, approximately 2 weeks ago. She did not get her flu
vaccine[.] She did travel to some areas with pine trees a couple of
weeks ago and also attended the Benson Mule Day Festival where
she was exposed to horses and dogs.

Id. R.W. also reported experiencing urinary incontinence she could not feel and had significant
urinary retention upon arrival to the PICU. Id. On exam, she had absent reflexes in the lower
4
extremities and abdomen and flaccid lower extremities bilaterally. Id. at 118. She also had a
“gradual transition of sensation from knee to inguinal area with normal sensation of lower
abdomen (as best I can tell with sedated patient).” Id. Her upper extremities had normal strength
and reflexes. Id.

Dr. Wooten’s assessment was TM, based on her clinical presentation and MRI showing a
“demyelinating lesion of lower thoracic spine[.]” Ex. 4A at 118. He prescribed IVIG and
continued high-dose steroids. Id. He noted that R.W. had reportedly received the DTaP and
meningococcal vaccinations several weeks earlier and commented: “I find no other potential
etiology [aside from the vaccinations] in my history and exam.” Id. at 116. He recommended that
R.W.’s team clarify with her pediatrician which vaccines she received, noting her condition might
need to be reported. Id.

Later on September 28, R.W. had a repeat thoracic spinal MRI with and without contrast.
Ex. 4A at 126-27. This MRI found progression of the T2 hyperintensity between T6 and the distal
conus at T12-L1, with mild expansion and questionable patchy enhancement of the ventral cord at
T11 and T12. Id. This was interpreted to be consistent with inflammatory TM, neuromyelitis
optica (“NMO”), MS, vascular disease, or neoplasm less likely. Id.

On the morning of September 29, 2015, Drs. Honeycutt and Duffus saw R.W. again. Ex.
4A at 100. They noted that after a second dose of IVIG, R.W. reported some improvement in
sensation in the lower extremities but no improvement in motor function. Id. at 101. Her repeat
MRI with contrast was consistent with TM or acute disseminated encephalomyelitis (“ADEM”),
showing a “T2 hyperintensity between T6 and distal conus at T12-L1.” Id.

On exam, R.W. exhibited intact sensation to soft touch from the right knee proximally and
from the left mid-shin proximally. Ex. 4A at 101. She had 0/5 strength in both legs. Id. The MRI
findings were thought to be “consistent with inflammatory transverse myelitis.” Id. at 103. Her
“[h]istory of recent vaccination and a possibility of ADEM should be considered.” Id. The team
had verified R.W.’s receipt of “TDaP and meningococcal vaccinations on 09/11, possibly the
inciting event.” Id. They “w[ould] plan to report adverse vaccine event.” Id. at 104. Also, R.W.’s
Biofore rapid test for rhinovirus/enterovirus was positive, and “[t]here are reports of enterovirus
causing similar presentation.” Id. Drs. Honeycutt and Duffus believed the issue could be clarified
through measures like “[n]asal washing for viral culture” as well as “[s]erum arbovirus and RPR”
and a follow-up blood culture. Id. The plan was to continue IVIG and high-dose steroids. Id.

On October 1, 2015, R.W. was seen by neurologist Traci Sheaffer, M.D. Ex. 4A at 60.
R.W. reported that she had “tingling today all the way down to her toes.” Id. She reported
increased sensation below the knees and was able to urinate. Id. She had no improvement in
strength. Id. Dr. Sheaffer commented that R.W. reported feeling sensation when she was not
being touched, making the exam unreliable. Id. at 62.

On October 4, 2015, Dr. Honeycutt noted that R.W. was making “very slow but some
notable improvement.” Ex. 4A at 43. Her family was not ready to consider plasmapheresis
(“PLEX”) treatment. Id. By October 6, however, R.W. still had experienced “only very mild

5
improvement of sensory and motor [symptoms].” Id. at 17. After further discussions with Dr.
Honeycutt, the family opted for PLEX treatment at Duke Children’s Hospital (“Duke”). Id. at 18.

2. Duke Hospitalization: October 6-30, 2015

In an admission exam on October 6, 2015, medical resident William Fox, M.D., noted that
“[o]ther than the fever at presentation,” R.W. had not been experiencing “preceding fevers, cough,
rhinorrhea, sore throat, rash, or diarrhea” before the onset of her symptoms. Ex. 5 at 12. She did
have “mild lumbar back pain” in the two weeks prior to onset “that she attributed to her heavy
backpack.” Id.

On October 7, 2015, pediatric neurologists William Gallentine, D.O. (attending), and Sarah
Neuhaus, M.D. (fellow), had an initial consult with R.W. Ex. 5 at 15. On exam, R.W. had flaccid
lower extremities, no spontaneous movement in those limbs, and mild response to pain stimulation.
Id. at 19. She could feel cool touch but was not able to clearly distinguish vibration. Id. She had
no strength in her lower extremities and absent reflexes bilaterally in those limbs. Id. Drs.
Gallentine and Neuhaus ordered lab work and planned to review R.W.’s spinal MRI from
WakeMed with Neuroradiology. Id. at 19-20. That day, ophthalmologist Andrew Lee, M.D.,
opined that R.W. had “a normal ophthalmic exam with no evidence of current optic neuropathy,”
which ruled out NMO. Id. at 25.

R.W. saw Dr. Gallentine again on October 8, 2015. Ex. 5 at 34. Dr. Gallentine noted
Neuroradiology had reviewed the spinal MRI and it was “thought to be consistent with TM.” Id.
They did not believe R.W. had a vascular lesion or had suffered a spinal cord stroke. Id. R.W.
began the first of five PLEX treatments on October 8, 2015. Id. at 35.

On October 9, 2015, Dr. Neuhaus observed a sensory level at the T6-7 level, below which
there was decreased sensation. Ex. 5 at 39. Drs. Gallentine and Neuhaus characterized R.W.’s
condition as “Acute Flaccid Paralysis due to likely Transverse Myelitis,” which was being further
evaluated. Id.

On October 16, 2015, the results of R.W.’s nasopharynx studies were negative for
Enterovirus D68 (“D68”) and Human Parechovirus but “[p]ositive for Human Rhinovirus A-29”
(“A29”). Ex. 4A at 185. R.W.’s arboviral panel from the state lab revealed she was negative for
West Nile Virus IgM, Eastern Equine Encephalitis IgM, and La Crosse Encephalitis IgM, but
positive for West Nile Virus IgG. Id. at 185-87. The Duke physicians did not feel the positive
West Nile Virus result was clinically relevant because the labs were drawn after IVIG was given.
Ex. 5 at 40.

Also on October 16, 2015, R.W. underwent a repeat spinal MRI that revealed a “[d]iffuse
enhancement of the [ventral] cauda equina nerve roots and the ventral and dorsal aspects of the
conus medullaris.” Ex. 5 at 1725. The MRI further revealed “significant interval increase of extent
and degree of expansion of the abnormal intramedullary cord signal abnormality extending from
T3 to the conus,” suggesting “[w]orsening ascending inflammatory myelitis[.]” Id.

6
On October 17, 2015, Dr. Neuhaus and attending neurologist Edward Smith, M.D., noted
that R.W. “ha[d] not changed much other than subjective sensory finding and [was] still not able
to discriminate right from left reliably,” but she had “increased hip strength” since October 15.
Ex. 5 at 183. R.W. had undergone five sessions of PLEX “without improvement,” and her repeat
MRI revealed “evidence that long segment TM ha[d] extended further to T3; marked enhancement
of ventrally predominant nerve roots [was] also appreciated on repeat imaging, significant for
possible virally mediated process.” Id.

On October 18, 2015, R.W. was seen by pediatric infectious disease specialists Robert
Drucker, M.D. (attending), and Nazario Chaparro, M.D. (fellow). Ex. 5 at 51. R.W. and her family
“[denied] recalling any illnesses (cough, headache, diarrheas, dysuria, emesis, bloody stools)” or
“prior episode, travel, sick contacts or abdominal pain.” Id. at 52. Her parents recalled she had
rhinitis two weeks before her initial presentation. Id. They also went to a carnival where there
were horses and other animals, but R.W. denied having contact with the animals. Id. She received
her Tdap and meningococcal vaccines two weeks before her symptoms began. Id. Drs. Drucker
and Chaparro noted that R.W. did not have “significant exposure or risk factors” except rhinitis,
but “[i]nfectious causes of transverse myelitis are multiple and most of them are viral etiology
causing in most cases a post-infectious transverse myelitis.” Id. at 55-56. They recommended a
repeat LP to test the CSF for enteroviruses, herpesviruses, HIV, and other viral and bacterial
antigens. Id. at 56.

The same day, R.W. saw pediatric rheumatologist Heather Vanmater, M.D. Ex. 5 at 57.
Dr. Vanmater assessed “acute onset [long] segment transverse myelitis of unclear etiology” and
noted that R.W. received her immunizations two weeks before the onset of neurological symptoms
and had experienced some back pain in the preceding two weeks, which was not associated with
any numbness or weakness. Id. at 68-69. R.W. “ha[d] not improved and ha[d] in fact had
progression of her disease despite IV and oral steroids, IVIG and pheresis.” Id. at 69. She had no
signs or symptoms of a connective tissue disease. Id. “Her PCR was positive for rhinovirus, [and]
numerous infectious studies are pending.” Id. Dr. Vanmater ordered a complete autoimmunity
workup and stated that “[i]t [was] unclear if her progression in the size of the lesion [was] from an
infectious process not yet resolved [versus] ongoing inflammatory/autoimmune process.” Id. She
recommended a repeat brain MRI with “thin cuts of orbits for any evidence of more extensive
disease that would indicate seronegative NMO which may benefit from rituximab4.” Id.

On October 20, 2015, pediatric neurologists Carolyn Pizoli, M.D. (attending), and Suma
Das, M.D. (resident), noted R.W. had “paraplegia secondary to spinal cord findings of unknown
etiology” and stated “[a]t this point, unclear etiology, though high suspicion for virally mediated
myeloradiculopathy.” Ex. 5 at 71. They also noted that R.W. had a “low serum copper level

4
Rituximab: a chimeric murine/human monoclonal antibody that binds the CD 20 antigen; used as an
antineoplastic in the treatment of CD20-positive, B-cell non-Hodgkin lymphoma; administered
intravenously. DORLAND’S MEDICAL DICTIONARY ONLINE, https://www.dorlandsonline.com
/dorland/definition?id=43977&searchterm=rituximab (last visited Mar. 4, 2026) (“DORLAND’S”).

7
raising suspicion for copper myelopathy.” Id. They cited literature discussing copper deficiency-
mediated myelopathy. Id. at 71-72.

On October 22, 2015, Dr. Pizoli noted that R.W. would receive a five-day copper infusion
because her “repeat copper level also returned low,” and the reason for her low copper levels was
unclear. Ex. 5 at 78. The cause of R.W.’s paraplegia secondary to spinal cord findings was
unknown, but there remained a “high suspicion for virally mediated myeloradiculopathy.” Id. Dr.
Pizoli explained that a neuroradiology review from that morning revealed “concern about viral
infection” and that “[p]ropensity for ventral cauda equina enhancement was noted, raising
suspicion for viral tropism.” Id. She stated: “Given the peripheral nerve as well as spinal cord
involvement in this process, will consult neurosurgery for consideration of sural nerve biopsy.
Also recommend [electron microscopy (“EM”)] on CSF for viral particles.” Id. The EM on
R.W.’s CSF was negative. Id. at 81.

That same day, R.W. was seen by pediatric rheumatologists Jeffrey Dvergsten, M.D.
(attending), and Stephen Balevic, M.D. (fellow). Ex. 5 at 203. They noted that R.W did not have
any clinical features of an underlying rheumatologic disorder and had negative serologies for
rheumatologic/connective tissue diseases. Id. at 205. She did not have “a significant clinical
response to immunosuppression with IVIG, corticosteroids, and plasmapheresis,” and they “would
expect plasmapheresis to rapidly improve any antibody mediated inflammatory process.” Id. As
such, “it may be reasonable to consider repeat MRI now that she has finished a second course of
pulse corticosteroids,” because “there may be some thought that immunosuppression can
potentially worsen post-infectious processes.” Id. They also felt that it might be helpful for
WakeMed to run Antinuclear Antibody (“ANA”) and Extractable Nuclear Antigen (“ENA”)
panels on blood drawn before the initiation of IVIG treatment. Id.

On October 23, 2015, Drs. Drucker and Chaparro documented that R.W.’s state lab tests
were negative for enterovirus and positive for Rhinovirus A29. Ex. 5 at 207. She had been
screened for “many of the treatable causes from a viral standpoint that include most of the DNA
viruses ([Epstein-Barr virus, cytomegalovirus, herpes simplex virus]) and the bacterial causes such
as bartonella and mycoplasma pneumonia all of which are negative.” Id. at 208. They further
commented:

From the RNA viruses the most common causes [are] Enteroviruses
but she has a positive rhinovirus. Rhinovirus is of the same family
as the enterovirus (picornavirdae) and for many years Rhinovirus
wasn't diagnosed . . . thus the literature and data that have been
published state enterovirus and it isn’t clear how many of these were
actually rhinovirus since rhinovirus has been mistaken for
enterovirus. Post infectious myelitis thus can still be a possible and
the duration and recovery from this is very variable to week, months
and even years. And treatment is aimed at the inflammatory
component of the syndrome.

Id. The plan was to continue with current therapies. Id.

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On October 24, 2015, R.W. saw Dr. Gallentine for a follow-up consult. Ex. 5 at 79. Dr.
Gallentine commented that “[a]t this point, unclear etiology, though high suspicion for virally
mediated myeloradiculopathy.” Id. at 79, 81. A repeat MRI was scheduled for October 26, 2015,
to “evaluate for questionable changes in spinal cord as well as re-evaluation of nerve root
enhancement.” Id. at 81. The repeat MRI showed no changes. Id. at 88-89.

On October 27, 2015, pediatric neurologists Edward Smith, M.D. (attending), and Dr. Das
assessed “ongoing flaccid paralysis.” Ex. 5 at 88. They said R.W.’s condition had an “unclear
etiology, though high suspicion for virally mediated myeloradiculopathy.” Id. Dr. Smith advised
Mr. Williford that Duke planned to report the case to the CDC as a case of acute flaccid myelitis
(“AFM”). Id. On October 28, 2015, Drs. Smith and Das documented that the CDC report had
been completed that day. Id. at 91. However, Petitioners produced a letter from Duke’s senior
manager of health information management stating that “all efforts to locate written
communication between the CDC and [Duke] for the above captioned patient has [sic] been
unsuccessful.” Ex. 53 at 1.

At the time of R.W.’s discharge from Duke on October 30, 2015, she continued to have
“flaccid paralysis of lower extremities” but could use her “abdominal/side muscles to roll and
perform lateral transfers [with] moderate assistance.” Ex. 5 at 4. She had minimal to no sensation
to light touch at L3, L4, L5, and S1. Id. She had no patellar reflexes and reduced Achilles reflexes.
Id. She was experiencing urinary retention and sometimes had urinary or stool incontinence. Id.
The discharge summary, prepared by Ashley Naughton, M.D. (resident), and David Ming, M.D.
(attending), characterized her condition as “Post infectious/Post-inflammatory (likely virally
mediated) Myeloradiculopathy.” Id. at 5. The summary further explained:

Given [R.W.’s] lack of response to 5 plasmapheresis treatments, T
and C spinal cord were reimaged with MRI twist protocol to re-
evaluate for spinal infarction. Repeat imaging was significant for
inflammatory progression, suggesting inflammatory myelitis, with
potential etiologies including lupus, sarcoidosis, or other viral or
autoimmune causes. Rheumatology and infectious disease [were]
consulted to help further guide work up. The patient underwent
extensive lab workup for infectious and primary autoimmune
etiologies at the request of the above services, which was only
remarkable for antibodies to rhinovirus and a low serum copper of
38 ug/dl. Pertinently, patient underwent workup and imaging to rule
out SLE, seronegative NMO, and multiple esoteric infectious
etiologies. Patient underwent further therapy with high dose
methylprednisone, repeat IVIG, and 5 days of copper chloride
therapy. She underwent re-imaging with MRI following this which
showed stable T2 hyperintense lesion from T3 through the cauda
equina with multiple nerve roots. After extensive discussion
between neurology, rheumatology, and infectious disease, it was
determined that her lesion was most likely virally mediated, though
the exact etiology was never determined. She began extensive
inpatient PT/OT, and was discharged to an inpatient rehab facility
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at Levine Children's Rehabilitation hospital in Charlotte, NC with
planned follow up with neurology in roughly 6-8 weeks (they will
be coordinating with patient). Her case was reported to the North
Carolina Department of Public Health and CDC as a case of
unexplained acute flaccid myelitis.

Id. at 5-6 (emphases added). Dr. Ming also provided an addendum stating R.W. had a “lengthy
hospital course for management of acute flaccid paralysis” and noting that he “favor[ed] post-viral
as most likely etiology (of note, state lab testing was positive for rhinovirus A29 and negative for
enterovirus D068).” Id. at 10.

3. Later Treatment

On October 30, 3015, R.W. was discharged to Levine Children’s Rehabilitation Hospital
while on antibiotics for a urinary tract infection (“UTI”). Ex. 5 at 5-6, 10. She remained there
until November 24, 2015. Ex. 2 at 118. An MRI of the thoracic spine on November 21, 2015,
revealed “[m]ultiple T2 hyperintense cord signal abnormalities, compatible with demyelination,”
and an MRI of the lumbar spine showed “[a]bnormal T2 hyperintensity and enhancement of the
conus, along with enhancement of the cauda equine nerve roots,” which were thought to represent
an inflammatory process. Id. at 115-16.

On December 23, 2015, R.W. had a follow-up with Dr. Gallentine and Lyndsey Prange, a
nurse practitioner. Ex. 5 at 1726. The assessment was “transverse myelitis and demyelinating
lower extremity neuropathy,” and while she had “regained some of her truncal strength[,]” there
was not any “significant movement” in her lower extremities. Id. The records stated that R.W.
“had a clinical course and poor response to treatment that is somewhat atypical for acute transverse
myelitis” and noted “there is evidence of lumbar nerve root involvement, this can be seen [with]
more late imaging findings of enterovirus D68.” Id. at 1724. R.W.’s “lack of improvement with
[plasmapheresis], IVIG, and steroids, suggests that further immunotherapy is not indicated,”
though she “[m]ay continue to show some improvement up to 18 months.” Id. at 1726.

On April 12, 2016, R.W. presented to Dr. Smith for “[f]ollow-up [on] acquired paraparesis
10/6/15 due to myeloradiculitis (T3-conus).” Ex. 5 at 1800. She had been doing well but had
experienced no real change in lower extremity strength, function, or sensation. Id. at 1801. She
had been “experiencing what sound like brief episodes of neuropathic pain in the posterior thighs,”
and she had been self-catheterizing and using a manual wheelchair. Id.

On April 14, 2016, R.W. saw John Wiener, M.D., a pediatric urologist, “for management
of neurogenic bladder secondary to transverse myelitis” that had affected her T10 spinal level. Ex.
5 at 1836. On April 18, 2016, she saw Lloyd Hey, M.D., an orthopedic surgeon, for “scoliosis
without pain.” Ex. 2 at 71. Her physical therapist had advised she had a curvature in her spine,
which had not been observed before onset. Id. An x-ray revealed a curvature of 64 degrees. Id.
at 72. Dr. Hey commented that “[a]nything greater than 10 degrees on x-ray is scoliosis. This is
due to your Transverse Myelitis.” Id. Surgery was discussed as a treatment option. Id.

10
On April 20, 2016, R.W. saw Tobias Tsai, M.D., a physiatrist, for her “acute onset of
paraplegia in 2015, TM vs. acute flaccid paralysis, neurogenic bladder and bowel.” Ex. 2 at 70.
Dr. Tsai noted that it was unclear whether R.W.’s paraplegia “was a manifestation of TM or
(possibly more likely) acute flaccid paralysis.” Id. at 68. R.W. saw Dr. Tsai on October 5, 2016,
for a follow-up evaluation of scoliosis. Id. at 56.

On May 10, 2017, R.W. received arthrodesis5 to treat her scoliosis. Ex. 2 at 46. On
November 28, 2017, she saw physiatrist Patrick O’Brien, M.D., at Carolina Rehabilitation. Ex. 12
at 11-12. It was noted that she had tolerated her spinal fusion surgery well. Id. at 11. After the
surgery, however, she experienced increased bilateral hip contractures, for which Botox injections
were recommended. Id. at 11-12. She continued to experience neurogenic bladder and bowel. Id.
at 12. On December 15, 2017, R.W. received her first Botox treatment. Id. at 8.

On February 5, 2018, R.W. returned to Dr. Gallentine. Ex. 5 at 3910. Her diagnoses
remained acute flaccid paralysis and TM/polyradiculoneuropathy. Id. Dr. Gallentine noted that
she had regained some of her truncal strength but that there was not any significant movement in
her lower extremities. Id. at 3913. He did not believe there would be much improvement going
forward. Id.

On April 24, 2018, R.W. saw Cheryl Bennett, a physical therapist. Ex. 4D at 4692. She
was doing well and planned to continue working out with a personal trainer once or twice a week
and use a functional electrical stimulation cycle at home. Id. It was recommended that R.W.
continue to receive Botox every three months to preserve the range of motion in her hips. Id.

On August 28, 2018, Boyd Gray Howell of B3 Fitness noted that he was working with
R.W. on “stretching her hips, core strength, over all body strength, and exercise” and had seen her
50 times between November 11, 2017, and August 28, 2018. Ex. 16 at 1.

B. Affidavits and Fact Witness Testimony

1. Mrs. Williford

Mrs. Williford is R.W.’s mother and works as a paralegal. Ex. 13 (“Mrs. Williford Aff.”)
at 1; Tr. at 8-9. In her affidavit, executed October 4, 2021, she stated that R.W. was healthy prior
to the subject vaccinations, was social, excelled in school, was active in her church youth group,
and participated in various forms of dance, pageants, gymnastics, and softball. Mrs. Williford Aff.
at 1.

R.W. was in fifth grade at the time of her September 11, 2015 vaccinations. Tr. at 13. Mrs.
Williford testified that R.W. did not have a cold or rhinitis before the vaccinations, which were

5
Arthrodesis: the surgical fixation of a joint by a procedure designed to accomplish fusion of the joint
surfaces by promoting the proliferation of bone cells; called also artificial ankylosis. DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=4247&searchterm=arthrodesis (last visited Feb.
26, 2026).

11
given at a well-child visit; medical records indicating otherwise were in error. Id. at 14, 16-17.
R.W. did complain of arm pain and fatigue at the time of the vaccinations, as well as low back
pain leading up to her September 27, 2015 hospitalization. Id. at 15-16; Mrs. Williford Aff. at 1.
She had to ask to sit down during her clogging practice about four days before going to the hospital.
Tr. at 17-18.

On September 27, 2015, R.W. complained of leg pain. Mrs. Williford Aff. at 1. She asked
to take a nap after church, which was unusual. Tr. at 18-19. Shortly thereafter, she complained of
right leg pain, and she then fell trying to stand up from the bed. Id. at 19. Her parents decided to
take her to the hospital; Mr. Williford had to carry her to the car. Id. at 20.

At the local hospital, R.W. was asked to provide a urine sample, but when she attempted
to sit on the toilet, her body became “stiff,” and she had an episode of urinary incontinence that
she could not feel. Tr. at 22. After this, she was taken by private transport to WakeMed. Id. at
23-24. At WakeMed, R.W was diagnosed with TM. Id. at 26. Later, her parents were advised to
transfer R.W. to Duke for PLEX treatment, “the next step for her care.” Id. at 29. The physicians
at Duke also characterized R.W.’s diagnosis as “TM.” Id. at 30. After a conversation with a friend,
Mrs. Williford inquired with the medical team about AFM and requested that they test R.W. for
that condition. Id. at 30-31. She was told that the test was negative. Id. at 33.

R.W. remained hospitalized and in inpatient rehabilitation until November 23, 2015. Mrs.
Williford Aff. at 2. Later, she was diagnosed with scoliosis, for which surgery was recommended.
Tr. at 42. The physicians treating the scoliosis advised that the condition was secondary to R.W.’s
TM. Id. at 42-43.

At the time of hearing, R.W. continued to do exercises and personal training at home, as
well as outpatient physical therapy. Tr. at 43. She remained paralyzed from the mid-torso down
and was wheelchair bound and incontinent. Id. at 45.

2. Mr. Williford

Mr. Williford’s affidavit was materially identical to Mrs. Williford’s. See Ex. 14 (“Mr.
Williford Aff.”). He testified that, while R.W. was hospitalized, a nasal swab was taken to test her
for enterovirus and rhinovirus. Tr. at 47-48. The purpose of the test was to determine whether
R.W. had AFM or TM. Id. at 48. He recalled that the test ultimately ruled out AFM. Id. at 50-
51.

3. R.W.

R.W. testified that she was in “normal health” prior to her vaccinations. Tr. at 54. She
recalled that the day of vaccination, her arm “hurt a lot, but I just figured it was since I had gotten
the shot, so I just pushed through.” Id. at 55. Over the next few days, she had a “little bit of back
pain” but no other problems. Id. at 56. A few days before her hospitalization, she felt more tired
than usual. Id. On September 27, 2015, after church and lunch, her leg was hurting, so she lay
down. Id. at 56-57. She got up to use the restroom and felt like she was struggling to walk. Id. at
57. When she got up again, she fell. Id. She was seen by paramedics at a nearby fire station, after
12
which she was taken to the hospital. Id. at 57-58. At the time of hearing, she still could not feel
anything from her hips down, she was incontinent, and her skin had difficulty healing and was
sensitive to the sun. Id. at 61.

III. EXPERT EVIDENCE

A. Pre-Hearing Expert Reports and Affidavits

1. Petitioners’ Expert Lawrence Steinman, M.D.: First Expert Report

Dr. Steinman filed two reports in this case. Ex. 22 (“First Steinman Rep”); Ex. 49 (“Second
Steinman Rep.”). Dr. Steinman received his medical degree from Harvard University and was a
NIH Fellow in Chemical Neurobiology at Harvard Medical School. Ex. 24 (“Steinman CV”) at 1.
He completed his residency in pediatrics and pediatric/adult neurology at Stanford University
Hospital. Id. He is the GA Zimmermann Professor of Neurological Sciences, Neurology, and
Pediatrics at Stanford. Id. He is board certified in neurology and is involved in the American
Academy of Neurology as a fellow, along with the American Neurological Association, the
American Association of Immunologists, and the Clinical Immunology Society. Id. at 2. He has
published nearly 600 articles on many different topics. Id. at 5-46. He runs an active research
laboratory “investigating neuroimmunology in conditions like [TM] and [NMO].” First Steinman
Rep. at 1.

Over the course of his 40-year career, Dr. Steinman has cared for many patients, both adult
and pediatric, with neuroinflammatory diseases, including TM, NMO, GBS, optic neuritis,
multiple sclerosis, chronic inflammatory demyelinating polyneuropathy (“CIDP”), ADEM, and
others. First Steinman Rep. at 1. At the time of hearing, he had six pediatric patients with AFM
and 15-20 with TM. Tr. at 180. He has served as an expert for the Institute of Medicine of the
National Academy of Sciences (“IOM”) on matters relating to vaccines. Id. at 67; Steinman CV
at 2. He was elected to the National Academy of Sciences in 2015. Steinman CV at 2.

Dr. Steinman opined that R.W. suffered an “extensive transverse myelitis of undetermined
etiology, with competent academic teams . . . having ruled out a wide set of competing diagnoses.”
First Steinman Rep. at 6.

Dr. Steinman advanced a molecular mimicry theory to explain how the DTaP and
meningococcal vaccines could cause TM. First Steinman Rep. at 7. He described molecular
mimicry as “an evolutionary adaptation whereby viruses and bacteria attempt to fool the body into
granting them free access. Such mimicry works by showing the immune system stretches of amino
acids that look like self.” Id.

An autoimmune response can occur even where the mimicry is not exact. First Steinman
Rep. at 7. For example, Drs. Fujinami and Oldstone induced experimental autoimmune
encephalitis (“EAE”) in rabbits via immunization with proteins from the Hepatitis B virus, which
“shared a stretch of just six amino acids with myelin basic protein [‘MBP’].” Id. at 8 (quoting
Lawrence Steinman, Autoimmune Disease, 269 SCI. AM. 107, 109 (1993) (Exs. 30, 62) (“Steinman
1993”)). Other experiments similarly demonstrated that limited, nonconsecutive homologies
13
could trigger EAE in animal models. Id. at 9-11 (citing Anand M. Gautam et al., A Polyalanine
Peptide with only Five Native Myelin Basic Protein Residues Induces Autoimmune
Encephalomyelitis, 176 J. EXP. MED. 605 (1992) (Exs. 35, 67) (“Gautam 1992”); Anand M.
Gautam et al., Minimum structural requirements for peptide presentation by major
histocompatibility complex class II molecules: Implications in induction of autoimmunity, 91
PROC. NATL. ACAD. SCI. 767 (1994) (Ex. 36, 68) (“Gautam 1994”); Anand M. Gautam et al., A
Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical Signs of Experimental
Autoimmune Encephalomyelitis, 161 J. IMMUNOL 60 (1998) (Exs. 37, 69) (“Gautam 1998”)). As
a result, cross-reactivity between viral and self proteins is relatively common: one study showed
nearly 4% of antiviral monoclonal antibodies also reacted with self proteins. Id. at 7-8 (citing
Robert S. Fujinami et al., Molecular Mimicry, Bystander Activation, or Viral Persistence:
Infections and Autoimmune Disease, 19 CLIN MICROBIOL. REV. 80 (2006) (Exs. 33, 65)
(“Fujinami”); Javaraiah Srinivasappa et al., Molecular Mimicry: Frequency of Reactivity of
Monoclonal Antiviral Antibodies with Normal Tissues, 57 J. OF VIROLOGY 397 (1986) (Exs. 34,
66) (“Srinivasappa”)).

Turning to the vaccine and injury involved here, Dr. Steinman used the basic local
alignment search tool (“BLAST”) to compare the “DTaP vaccine and two myelin antigens, [myelin
oligodendrocyte glycoprotein (‘MOG’)] and MBP[,] known to be targeted in transverse myelitis.”
First Steinman Rep. at 12 (citing Oden Abramsky & Dvora Teitelbaum, The Autoimmune Features
of Acute Transverse Myelopathy, 2 ANN. NEUROL 36 (1977) (Exs. 38, 70) (“Abramsky &
Teitelbaum”); Claus G. Haase & Stephan Schmidt, Detection of brain-specific autoantibodies to
myelin oligodendrocyte glycoprotein, S100b and myelin basic protein in patients with Devic’s
neuromyelitis optica, 307 NEUROSCIENCE LETTERS 131 (2001) (Exs. 39, 71) (“Haase & Schmidt”);
Scott S. Zamvil & Anthony J. Slavin, Does MOG Ig-positive AQP4-seronegative opticospinal
inflammatory disease justify a diagnosis of NMO spectrum disorder?, 2 NEUROL.
NEUROIMMUNOL. & NEUROINFLAMM. e62 (2015) (Exs. 40, 72) (“Zamvil & Slavin”); Til Menge et
al., Neuromyelitis Optica Following Human Papillomavirus Vaccination, 79 NEUROLOGY 285
(2012) (Exs. 41, 73) (“Menge”); Steinman et al., Polypeptide Pertussis Toxin Vaccine, US PATENT
NUMBER 5,000,952 (1991) (Ex. 42) (“Steinman Patent”)). He found the tetanus toxin shared four
identical amino acids within an eight-acid sequence (KDSAGEVR) with the MBP segment. Id. at
13. This would be “sufficient to trigger an immune response with paralysis.” Id. The pertussis
toxin contained a sequence (AELRGSGDL) with five of nine identical amino acids to a sequence
in MBP. Id. at 14.

Dr. Steinman then entered the sequences he identified as homologous into the Immune
Epitope Database (“IEDB”), which lists epitopes that have been described as immunologically
relevant in the scientific literature. First Steinman Rep. at 15. He reported that the homologous
sequence in the pertussis toxin was listed in the IEDB. Id. In his opinion, this information
provided “a compelling theory that molecular mimics in the DTaP received by petitioner could
trigger immunity to myelin basic protein culminating in transverse myelitis.” Id. at 16 (emphasis
in original).

Dr. Steinman also opined there was a molecular mimic between the carbohydrate
component of the meningococcal vaccine and glycans involved in neurological disease. First
Steinman Rep. at 17-18. In particular, he claimed that mannose-containing glycans, which are in
14
the vaccine, have been shown to induce EAE in an animal model. Id. at 18 (citing Denong Wang
et al., Uncovering Cryptic Glycan Markers in Multiple Sclerosis (MS) and Experimental
Autoimmune Encephalomyelitis (EAE), 75 DRUG DEV. RES. 172 (2014) (Exs. 45, 79) (“Wang”)).

Regarding onset, Dr. Steinman opined that R.W. developed TM approximately 16 days
after vaccination. First Steinman Rep. at 18. He stated: “The best surrogates for this timing are
found in epidemiologic studies on other neuroinflammatory diseases including [GBS], ADEM. A
sixteen day delay post-immunization is concordant with these studies[.]” Id. at 19 (citing
Lawrence B. Schonberger et al., GBS Following Vaccination form the National Immunization
Program, U.S., 1976-1977, 110 AM. J. OF EPIDEMIOLOGY 105 (1979) (Ex. 46, 77)
(“Schoenberger”); L. Bennetto & N. Scolding, Inflammatory/Post-Infections Encephalomyelitis,
75 J. NEUROL NEUROSURG. PSYCHIATRY i22 (2004) (Exs. 47, 78) (“Bennetto & Scolding”),
Dimitrios Karussis & Panayiota Petrou, The spectrum of post-vaccination inflammatory CNS
demyelinating syndromes, AUTOIMMUNITY REV. (2013), http://dx.doi.org/10.1016/
j.autrev.2013.10.003 (Exs. 48, 79) (“Karussis & Petrou”)).

2. Respondent’s Expert Neil Romberg, M.D.: Expert Report

Dr. Romberg submitted one expert report in this case. Ex. A (“Romberg Rep.”). He earned
a medical degree from Pennsylvania State College of Medicine. Ex. B (“Romberg CV”) at 1. He
completed his residency at New York University and was an immunology fellow at Yale
University. Id. He has held various teaching positions in immunology and pediatrics for the past
10 years and is an Assistant Professor of Pediatrics at the Children’s Hospital of Philadelphia
(“CHOP”), which is affiliated with the University of Pennsylvania School of Medicine. Id. He
practices as an attending physician in CHOP’s Immunology Department. Id. He is board certified
in allergy/immunology and is board eligible in pediatrics. Id. at 2. He has received several awards
and grants for his work and holds membership in several immunology societies. Id. He is on the
board of three immunology journals and has published approximately 45 peer-reviewed articles.
Id. at 3-5.

Dr. Romberg opined that R.W.’s condition was consistent with “acute flaccid paralysis,”
also known as AFM. Romberg Rep. at 4. AFM is “caused by damage to the anterior cell horns.”
Id. (citing Yasaman Fatemi & Rana Chakraborty, Acute Flaccid Myelitis: A Clinical Overview for
2019, 94 MAYO CLIN. PROC. 875 (2019) (Ex. A, Tab 1) (“Fatemi”)). He explained: “Traditionally,
acute flaccid paralysis was synonymous with epidemic poliomyelitis but there are many viruses
(enterovirus D68, rhinovirus/non-D68 enteroviruses, adenoviruses and flaviviruses) that exhibit
tropism for spinal gray matter.” Id. Furthermore, rhinoviruses have genetic similarities to non-
D68 enteroviruses; thus, “routine clinical PCR-based screening tests used by hospitals” cannot
distinguish between rhinoviruses and non-D68 enteroviruses. Id. “For this reason, acute flaccid
paralysis patients are typically divided into enterovirus D68 positive cases or rhinovirus/non-D68
enterovirus positive cases.” Id. He cited a case series in which 18% of patients diagnosed with
AFM “had evidence of rhinovirus or non-D68 enterovirus.” Id. (citing Kevin Messacar et al.,
Acute Flaccid Myelitis: A Clinical Review of US Cases 2012–2015, 80 ANN. NEUROL. 326 (2016)
(Ex. A, Tab 3) (“Messacar”)). After more sophisticated testing was developed to distinguish these
viruses, another case series reported that rhinovirus had been detected in 12 of 305 pediatric AFM
patients. Id. (citing Tracy Ayers et al., Acute Flaccid Myelitis in the United States: 2015–2017,
15
144 PEDIATRICS 1 (2019) (Ex. A, Tab 4) (“Ayers”)). Dr. Romberg concluded that the fact that
R.W. was infected with rhinovirus at the outset of her symptoms suggests her case “appears to
share many typical disease features with other pediatric patients affected by this disorder.” Id.

On causation, Dr. Romberg contended that, for molecular mimicry to be considered a
“potential contributor” to an autoimmune disease, several criteria must be satisfied. Romberg Rep.
at 5 (citing Christophe Benoist & Diane Mathis, Autoimmunity provoked by infection: how good
is the case for T cell epitope mimicry?, 2 NATURE IMMUNOLOGY 797 (2001) (Ex. A, Tab 5)
(“Benoist & Mathis”); C. Wim Ang, Bart C. Jacobs & Jon D. Laman, The Guillain–Barre
syndrome: a true case of molecular mimicry, 25 TRENDS IN IMMUNOLOGY 61 (2004) (Ex. A, Tab
7) (“Ang”)). First, there must be an epidemiologic association between the vaccine antigen and
the immune-mediated disease. Id. Here, is little epidemiologic data concerning AFM and vaccines
aside from the live oral polio vaccine, which is not at issue. Id. at 5 (citing David Bearden et al.,
Enteroviruses in X-Linked Agammaglobulinemia: Update on Epidemiology and Therapy, 4 J.
ALLERGY CLIN. IMMUNOL. PRACT. 1059 (2016) (Ex. A, Tab 8) (“Bearden”)). A 2016 study in the
Morbidity and Mortality Weekly Report (“MMWR”) catalogued 10 AFM cases, none of which
were vaccine caused. Id. (citing Jesse Bonwitt et al., Acute Flaccid Myelitis Among Children —
Washington, September–November 2016, 66 MMWR 826 (2017) (Ex. A, Tab 9) (“Bonwitt”)).

Second, there must be “[i]dentification of autoreactive T cells or autoantibodies that
recognize a human structure (target antigen) that if perturbed could explain symptomology.”
Romberg Rep. at 5. R.W.’s serum did not contain any autoantibodies, nor did she have oligoclonal
banding in her CSF, suggesting she was not producing autoantibodies. Id.

Third, Dr. Romberg opined that the “vast majority” of homologies identified by BLAST
search are not immunologically relevant. Romberg Rep. at 6. He believed Dr. Steinman’s
homology metric of five of nine identical, nonsequential amino acids was too broad. Id. This is
signified by the high “E-values” assigned to the homologies Dr. Steinman identified in this case,
which were “consistent with random pairing.” Id.at 6-7. Dr. Steinman’s citation of the Gautam
articles was inapposite, because those experiments used an epitope that was “definitively known”
to cause EAE in mice. Id. at 7. Dr. Steinman, by contrast, selected peptide segments that were
not known to be immunogenic in either mice or humans. Id. Furthermore, in comparison to the
tetanus/pertussis toxins tested by Dr. Steinman, MBP has equal or greater homology with
numerous proteins that are “ubiquitous in nature.” Id. In fact, the rhinovirus A29 protein (for
which R.W. tested positive) had greater homology with MBP than the vaccine components. Id.

Dr. Romberg pointed out that the IEDB was not designed to be a “tool to prove or disprove
molecular mimicry.” Romberg Rep. at 8. The database contains information from a variety of
sources and reports findings in a simplified manner. Id. Dr. Steinman used very broad parameters
to query the IEDB, using the least stringent filter available. Id. at 9. Dr. Romberg applied a more
stringent filter based on an exact match with the sequence in question, which returned negative
results. Id. He concluded that Dr. Steinman’s methodology did not attempt to “filter” irrelevant
homologies; instead, it “explode[d] the list of possible mimics by layering the loose fit of the
Gautam references on top of a permissive 70% IEDB filter.” Id.

16
Dr. Romberg also argued that the nine-peptide sequences identified in Dr. Steinman’s
IEDB search have not been shown to have the ability to activate B or T cells. Romberg Rep. at 9.
He would find it surprising for the second sequence Dr. Steinman identified to have a role in
R.W.’s injury, because any pathogenic reaction triggered by that sequence would be expected to
primarily affect the adrenal glands. Id. R.W.’s presentation was not consistent with this type of
damage. Id.

With respect to the alleged mimics identified in the meningococcal vaccine, Dr. Romberg
noted that mannose-containing carbohydrates in the brain have a different chemical structure than
those in the vaccine. Romberg Rep. at 10 (citing Pumtiwitt C. McCarthy, Abeer Sharyan & Laleh
Sheikhi Moghaddam, Meningococcal Vaccines: Current Status and Emerging Strategies, 6
VACCINES 1 (2018) (Ex. A, Tab 18) (“McCarthy”)). Furthermore, later experiments by Dr.
Steinman have shown mice exposed to mannose-containing carbohydrates had significantly less
severe EAE, suggesting those carbohydrates do not have a role in the pathogenesis of
neuroinflammation. Id. at 10-11 (referencing Wang). Dr. Romberg concluded that if R.W. did
generate anti-mannose antibodies in response to her meningitis vaccination, these experiments
would “suggest[] those antibodies would have protected, not damaged her [central nervous
system].” Id. at 11 (emphasis in original).

Fourth, to show molecular mimicry, there must be reproduction of the relevant disease in
an animal model. Romberg Rep. at 11. Dr. Romberg could find no animal studies relating to AFM
and either of the vaccines at issue here, though he did find literature describing animal models of
AFM induced by “direct intracranial injections of live enteroviruses.” Id. (citing Alison M. Hixon
et al., A mouse model of paralytic myelitis caused by enterovirus D68, 13 PLOS PATHOGENS 1
(2017) (Ex. A, Tab 19) (“Hixon”)).

Dr. Romberg agreed that the timing of the onset of R.W.’s condition after vaccination was
consistent with the range observed between swine flu vaccination and GBS onset. Romberg Rep.
at 12. He pointed out, however, that R.W. had been given five prior doses of the DTaP vaccine
with no neurological effects, making it unlikely that her condition was caused by that vaccine. Id.

Dr. Romberg concluded that there was “no factual or scientific basis for the claim of injury
by vaccine in this case.” Romberg Rep. at 12. Furthermore, “there is an alternative, more likely
trigger for R.W.’s disease, the rhinovirus A29[.]” Id. “As rhinoviruses are detected in nasal swabs
from many acute flaccid paralysis patients, I must agree with R.W.’s discharge summary: A post-
viral etiology was the most likely cause of R.W.’s neurological disease.” Id. (citing Ayers; Ex. 5
at 10).

3. Respondent’s Expert Michael Sweeney, M.D.: Expert Report

Dr. Sweeney filed one expert report in this case. Ex. C (“Sweeney Rep.”). He earned his
M.D. from the Medical College of Wisconsin in 2010, and he is an Assistant Professor of Child
Neurology and Neuroimmunology at the University of Louisville School of Medicine. Ex. D, Tab
1 (“Sweeney CV”) at 1; Id. at 5. He completed his residency training at Cincinnati Children’s
Hospital and the University of Cincinnati, followed by a fellowship in autoimmune neurology at
the University of Utah. Sweeney Rep. at 1. He is a pediatric neurologist who is board certified in
17
neurology, with special qualifications in child neurology. Id. His clinical practice specializes in
autoimmune and inflammatory conditions affecting the nervous system, including multiple
sclerosis, NMO, anti-MOG related demyelinating disease, acute disseminated encephalomyelitis
ADEM, post-infectious/autoimmune encephalitis, and paraneoplastic syndromes. Id.

Dr. Sweeney opined that the appropriate diagnosis in R.W. was AFM. Sweeney Rep. at 3.
He explained: “Though AFM has been described as a subtype of transverse myelitis (TM), it is
largely considered a separate entity with a different pathophysiology.” Id. (citing Cynthia Wang
& Benjamin Greenberg, Clinical Approach to Pediatric Transverse Myelitis, Neuromyelitis Optica
Spectrum Disorder and Acute Flaccid Myelitis, 6 CHILDREN 1 (2019) (Ex. C, Tab 1) (“Wang &
Greenberg”)). AFM usually affects the gray matter of the spinal cord, but it can affect the white
matter in more severe cases. Id. By contrast, TM is “a demyelinating disease which affects
predominantly white matter in the spinal cord.” Id. AFM can be distinguished from TM based on
its rapid onset of symptoms, flaccid weakness, depressed/diminished deep tendon reflexes, and
predominance of gray matter involvement on imaging. Id.

Further, AFM presents with asymmetric paralysis of one or more limb “in the setting of
recent or current febrile illness.” Sweeney Rep. at 3-4. Weakness can be preceded by pain and
may progress over hours to several days. Id. at 4. The patient will have low muscle tone and
absent reflexes but often will have normal sensation. Id. (citing Ayers, Messacar, Sarah E.
Hopkins, Jay Desai & Leslie Benson, Acute Flaccid Myelitis: A Call for Vigilance and an Update
on Management, 114 PEDIATRIC NEUROLOGY 26 (2021) (Ex. C, Tab 2) (“Hopkins”)). Bowel and
bladder dysfunction are often present. Id.

Dr. Sweeney pointed out that, different from AFM, TM often presents with a specific
sensory level, along with weakness and bladder/bowel dysfunction. Sweeney Rep. at 4. Usually
reflexes are brisk, and “spasticity develops over time.” Id. Generally, TM is responsive to “acute
immunotherapies such as steroids, plasmapheresis and IVIG.” Id. Finally, about 50% of pediatric
TM patients will have a full recovery within two years of onset, though outcomes can be variable.
Id. (citing Michael Absoud, Pediatric transverse myelitis, 87 (Suppl. 2) NEUROLOGY S46 (2016)
(Ex. C, Tab 3) (“Absoud”)).

AFM is “thought to be caused by acute viral infection.” Sweeney Rep. at 4. There is
“mounting evidence that supports enterovirus D68 as the cause for biennial outbreaks” of AFM.
Id. Other enteroviruses, such as A71, and coxsackie virus have also been implicated. Id. (citing
Ryan D, Schubert, et al., Pan-viral serology implicates enteroviruses in acute flaccid myelitis, 25
NATURE MED. 1748 (2019) (Ex. C. Tab 4) (“Schubert”)). As a general matter, it is “well known
that many virus species cause AFM,” including poliovirus, West Nile virus, enteroviruses, and
Japanese encephalitis virus. Id. (citing James J. Sejvar et al., West Nile Virus–associated Flaccid
Paralysis, 11 EMERGING INFECTIONS DISEASE 1021 (2005) (Ex. C, Tab 5) (“Sejvar”); Chao-Ching
Huang et al., Neurologic Complications in Children with Enterovirus 71 Infection, 341 NEW
ENGLAND J. OF MED. 936 (1999) (Ex. C, Tab 6) (“Haung”); Tom Solomon et al., Poliomyelitis-
like illness due to Japanese encephalitis virus, 351 LANCET 1094 (1998) (Ex. C, Tab 7)
(“Solomon”)).

18
Dr. Sweeney noted there have been sporadic reports of TM preceded by rhinovirus
infection, as well as at least one case report of AFM in a patient positive for rhinovirus. Sweeney
Rep. at 4 (citing Gary R. Nelson et al., Recognition and Management of Acute Flaccid Myelitis in
Children, 55 PEDIATRIC NEUROLOGY 17 (2016) (Ex. C, Tab 8) (“Nelson”)). He pointed out that it
is very difficult to identify a specific virus from the CSF in patients with AFM, “a fact that has
contributed largely to the uncertainty in pathogenesis of AFM.” Id. Of the AFM cases reported
to the CDC in 2018, 29% were positive for enterovirus A71, 37% were positive for enterovirus
D68, and 34% were positive for other viruses, including several that were positive only for
rhinoviruses. Id. (citing Susannah L. McKay et al., Increase in Acute Flaccid Myelitis — United
States, 2018, 67 MMWR 1273 (2018) (Ex. C, Tab 9) (“McKay”)).

Dr. Sweeney acknowledged that R.W.’s case was unusual because she had sensory loss.
Sweeney Rep. at 5. Some research has shown up to 44% of AFM patients have sensory
involvement, though the evidence on this aspect of AFM is “inconclusive.” Id. (citing Messacar,
Riley Bove et al., Unmet Needs in the Evaluation, Treatment, and Recovery for 167 Children
Affected by Acute Flaccid Myelitis Reported by Parents Through Social Media, 102 PEDIATRIC
NEUROLOGY 20 (2020) (Ex. C, Tab 10) (“Bove”)).

On MRI, AFM patients can have enhancement of nerve roots, which is not typical for TM.
Sweeney Rep. at 5 (citing J.A. Maloney et al., MRI Findings in Children with Acute Flaccid
Paralysis and Cranial Nerve Dysfunction Occurring during the 2014 Enterovirus D68 Outbreak,
36 AJNR AM. J. NEURORADIOL. 245 (2015) (Ex. 93) (“Maloney”)). Such enhancement was seen
on R.W.’s imaging. Id. While the radiologists who reviewed R.W.’s imaging did not comment
on white matter versus gray matter involvement, the fact that her abnormal signal was located in
the central cord, combined with her persistent flaccid weakness, suggests “significant gray matter
involvement.” Id. Furthermore, the inflammation in R.W.’s central nervous system (“CNS”) was
limited to the lower spinal cord and did not extend to the brain or optic nerves. Id.

Finally, Dr. Sweeney commented that no causal link has been found between any
vaccination and AFM. Sweeney Rep. at 5 (citing Bonwitt). He concluded R.W. developed AFM,
as her case was consistent with other AFM cases reported in the literature. Id.

4. Dr. Steinman: Second Expert Report

Dr. Steinman first addressed Special Master Oler’s directive to address the significance of
R.W.’s rhinovirus infection, which was stated in a non-PDF order dated October 19, 2020. Second
Steinman Rep. at 1. He contended that AFM falls “under the heading” of TM. Id. He opined that
R.W.’s case was consistent with AFM except for the presence of sensory loss, but the “diagnosis
of transverse myelitis accounts for the clinical picture[.]” Id.

Dr. Steinman acknowledged that the Messacar paper identified some cases of AFM in
which the patients tested positive for “rhinovirus/enterovirus,” but the low rate of such cases makes
it “difficult to consider rhinovirus as a principal factor in the etiology of acute flaccid myelitis in
this case.” Second Steinman Rep. at 2. Also, the Ayers paper reported only 4% of AFM patients
tested positive for rhinovirus. Id. (citing Ayers). Those patients had a variety of subtypes of
rhinovirus, making it difficult to implicate any particular subtype in causing AFM. Id. It was
19
more likely that R.W.’s injury was caused by the subject vaccines than a rhinovirus, particularly
because rhinoviruses are widespread in children. Id.

Dr. Steinman disagreed that his molecular mimicry theory of causation did not meet the
criteria identified by Dr. Romberg. Second Steinman Rep. at 3. He opined that the first criterion
– “a susceptible host whose genetic background and adaptive immune responses allows emergence
of self-reactive immunity” – was likely met because R.W. suffered an injury “where the immune
system attacks the motor neuron and the spinal cord.” Id. He argued that he met the second
criterion through his methodology identifying immunologically relevant homologies between the
subject vaccines and host tissues. Id. The third criterion – a showing of a cross-reactive response
in the host to the exogenous mimic – could not be demonstrated at this point because R.W. has
already undergone immunotherapy. Id.

Furthermore, Dr. Steinman stressed that he was not attempting to scientifically prove that
the subject vaccines caused R.W.’s injury, only that they could. Second Steinman Rep. at 4-5. He
pointed out that to prove his theory, he would need to test R.W.’s blood, which would be infeasible.
Id. at 5. He asserted that his methodology reliably answered the “could” question in favor of
Petitioners. Id. at 5-7.

5. Treating Physician Travis Honeycutt, M.D.: Affidavits

R.W.’s critical care physician at WakeMed, Dr. Honeycutt, filed two separate affidavits
addressing diagnosis and causation. Exs. 10, 84. He did not file his CV. The first affidavit,
executed July 26, 2018, stated that, on September 27, 2015, he and other WakeMed physicians
diagnosed R.W. with TM, “thought to be the result of an adverse vaccine event.” Ex. 10 at 1.
Although she had a normal white blood count and was asymptomatic for a respiratory viral
infection, “viral polymerase chain reaction assay was positive for enterovirus or rhinovirus.” Id.
Her sample was sent to the state lab for further viral culture. Id.

Dr. Honeycutt noted that “[t]ransverse myelitis after vaccination is reported in medical
literature.” Ex. 10 at 2 (citing N. Agmon-Levin et al., Traverse myelitis and vaccines: a multi-
analysis, 18 LUPUS 1198 (2008) (Exs. 7, 58) (“Agmon-Levin”)). Furthermore, the National
Institutes of Health “acknowledges that vaccines appear to cause transverse myelitis when the
body’s immune system mistakenly attacks the body’s own tissue while responding to a vaccine.”
Id. (citing Traverse Myelitis, U.S. Dept. of Health & Hum. Servs., Nat. Inst. of Health (Ex. 8, 59)
(“NIH”); Traverse Myelitis Fact Sheet, Nat. Inst. of Neurological Disorders & Stroke (Ex. 9) (“TM
Fact Sheet”)). Because R.W.’s symptoms appeared 16 days after her vaccinations and because no
other cause of her condition was identified, Dr. Honeycutt concluded that her TM “resulted from
the vaccination.” Id.

The second affidavit from Dr. Honeycutt, executed July 15, 2022, noted that his first
affidavit erroneously stated that the Duke physicians diagnosed R.W. with AFM. Ex. 84 at 1. Her
actual discharge diagnosis from Duke was acute flaccid paralysis, not AFM. Id. Dr. Honeycutt’s
diagnosis of R.W. remained TM. Id.

20
B. Expert Testimony

1. Dr. Steinman’s Testimony

Dr. Steinman was recognized as an expert in neurology. Tr. at 78. He concluded R.W.
had TM, though there were “some elements” of her presentation in common with AFM. Id. at 82.
AFM is a “subset” of or overlaps with TM. Id. The Tdap and meningococcal vaccines R.W.
received were, more likely than not, a substantial factor causing her condition. Id.

TM is an inflammatory condition of the spinal cord. Tr. at 84. R.W.’s imaging showed
extensive inflammation of her spinal cord, extending to the nerve roots. Id. She also had sensory
abnormalities, “which can happen in AFM but are more a hallmark of transverse myelitis.” Id.
She had no sensation from about T10 down, which Dr. Steinman believed represented a sensory
level, a hallmark of TM, and not “just a motor neuron disease.” Id. at 85.

Dr. Steinman stated that there is a reported association between TM and vaccines, with
onset occurring from “days to months” after vaccination. Tr. at 86-88. He referenced various
literature items on this. Id. R.W.’s presentation fell within the reported timeframe. Id. The best
estimate of the date of onset was 16 days after vaccination, September 27, 2015. Id. at 86-87.

TM can also be caused by infections, metabolic deficiencies, or other factors. Tr. at 89-
90. It often involves a longitudinally extensive lesion, as was seen in R.W.’s case. Id. at 90. It
can present with gray matter involvement. Id. There is some overlap with AFM, but R.W.’s case
more closely resembled TM. Id. at 90-91.

Regarding diagnosis, Dr. Steinman discussed R.W.’s test results. Tr. at 91. Her protein
level was consistent with TM but might also be consistent with AFM. Id. at 92-94. It was unlikely
that R.W.’s condition was virally mediated because no viruses were found in her CSF, which is
near her spinal lesion. Id. at 94.

Dr. Steinman testified that a disease like AFM that affects the anterior horns of the spinal
cord, where the motor neurons are, should not “have any sensory disturbance if it’s predominantly
involving the motor neurons,” as the motor neurons are in a separate location from the sensory
neurons. Tr. at 96-97. R.W. had sensory involvement, as shown by her inability to feel her
bladder. Id. Exams where she had a T10 sensory level, meaning decreased/absent sensation below
that point, also suggested she had TM. Id. at 104-05.

The MRI taken at Duke on October 16, 2015, showed an increasing, longitudinally
extensive lesion, which would be seen in TM but likely not in AFM. Tr. at 98, 105-06. Her next
MRI on October 26, 2015, was also consistent with TM. Id. Her MRIs also showed cauda equina
nerve root enhancement and enhancement of the dorsal aspects of the conus medullaris. Id. at 99.
The inflammation of the dorsal aspects responsible for sensory function was, in Dr. Steinman’s
view, more characteristic of a diffuse myelitis than AFM. Id. at 99-100. He also felt the fact that
R.W.’s MRIs had enhancing lesions meant AFM was less likely. Id. at 101-02.

21
Dr. Steinman explained that AFM results predominantly in motor impairment and usually
affects limited parts of the body, “not usually both legs.” Tr. at 106. It does have overlapping
characteristics with other CNS disorders. Id. at 107. If he had to make a diagnosis of R.W., he
would diagnose TM. Id.

Dr. Steinman testified that enterovirus D68 has been causally linked to AFM. Tr. at 109.
Rhinoviruses and D68 do “share a lot of sequence homology.” Id. Rhinoviruses, however, are
quite prevalent and responsible for most “common” colds. Id. at 109-10. Thus, it is unsurprising
to find a rhinovirus in a person’s nose. Id. at 110. He described a study that found no statistical
association between AFM and non-D68 enterovirus or rhinovirus infections. Id. (discussing Negar
Aliabadi et al., Enterovirus D68 Infection in Children With Acute Flaccid Myelitis, Colorado,
USA, 2014, 22 EMERGING INFECTIOUS DISEASE 1387 (2016) (Exs. 6, 57) (“Aliabadi”)). Just
because rhinovirus A29 was detected in R.W. does not mean the virus caused her condition. Id.
at 113.

Turning to causation, Dr. Steinman explained that his experiments have shown a homology
of five of 12 identical amino acids can trigger an immune response in animals, when the antigen
is combined with Complete Freund’s Adjuvant to enhance the response. Tr. at 123-24.
Homologies of fewer than five identical amino acids did not cause disease in animals, even with
the adjuvant. Id.

With respect to the vaccines at issue here, Dr. Steinman used MBP and MOG as
comparators. Tr. at 129-30. He did not find any relevant homologies between the subject vaccines
and MOG, but he did with MBP, using BLAST. Id. The “E value” provided in BLAST searches
is inapplicable in this context, as it was designed to identify proteins that are genetically similar,
not molecular mimics. Id. at 125-26. Dr. Steinman acknowledged that BLAST might not be
frequently used to compare short protein sequences, as he did. Id. at 135.

Addressing the point that the MBP sequence purportedly homologous with Tdap is
primarily expressed in the adrenal glands, Dr. Steinman acknowledged that this was a legitimate
critique, but he noted that the aquaporin-4 water channel targeted in NMO is present in organs
outside the nervous system, but NMO patients do not develop disease in other organs. Tr. at 130-
31. Here, the IEDB revealed the sequence in question had been identified as an immunologically
relevant epitope. Id. at 136.

Dr. Steinman clarified that “the main weight of the evidence comes from . . . protein
similarities,” not the purported homologies between the meningococcal vaccine and mannose
clusters within the nervous system. Tr. at 144. He acknowledged that in later experiments by his
lab, “we were able to actually use those mannose clusters coupled to another protein to suppress
inflammation.” Id. at 144-45.

On Althen prong two, Dr. Steinman stated:

Well, she got the vaccine. The vaccine has a component which has
a sequence similarity to myelin basic protein. The literature tells me
that myelin basic protein is one of the targets of the immune system.
22
So that could explain how [R.W.] developed transverse myelitis
after getting the vaccine. Is there a better alternative explanation?
So I looked hard, and the reports from my colleagues showed they
looked hard too. There’s been a lot of discussion and there will be
more about D68 and rhinovirus. My argument is the vaccines were
given for sure. They are given to give you an immune response.
Whether or not a rhinovirus caused transverse myelitis, I think that’s
never been ruled in. And whether this is just flaccid myelitis and
rhinovirus is a trigger for flaccid myelitis is also controversial.

Tr. at 138. He acknowledged that there was a potential molecular mimic between rhinovirus and
MBP, suggesting that the “rhinovirus could be a substantial factor” causing R.W.’s disease. Id.at
138-39. However, “by the preponderance of evidence the vaccine is a stronger piece of evidence,
especially for transverse myelitis, than rhinovirus,” given the prevalence of rhinovirus infections.
Id. at 139.

Concerning timing, Dr. Steinman relied on the Schonberger study relating to GBS
following flu vaccination, as well as the Bennetto and Scolding study on encephalomyelitis and
the Karussis review of post-vaccination inflammatory CNS demyelinating syndromes. Tr. at 139-
40 (citing Schonberger; Bennetto & Scolding; Karussis & Petrou). The timing of the onset of
R.W.’s symptoms, 16 days after vaccination, was consistent with the latency ranges reported in
these studies. Id. at 140. Likewise, the Agmon-Levin study on TM and vaccinations found the
appropriate interval for vaccine causation was “several days to three months,” consistent with
R.W.’s case. Id. (citing Agmon-Levin).

On cross, Dr. Steinman explained that he used BLAST and IEDB searches because it would
not be feasible to experiment on actual specimens. Tr. at 150. In response to Special Master Oler’s
questioning, he said that “TM is hundreds of times more common as a diagnosis” than AFM. Id.
at 160. R.W.’s poor response to IVIG, PLEX, and steroid treatment did not rule out TM in favor
of AFM, because up to 25% of TM patients do not have a positive response to these treatments.
Id. at 161-62. He clarified that his causation theory focused on the Tdap vaccine, not the
meningococcal vaccine. Id. at 163-64.

2. Dr. Sweeney’s Testimony

Dr. Sweeney was recognized as an expert in the field of neurology with a specific focus on
clinical pediatric neurology. Tr. at 186.

Dr. Sweeney opined the correct diagnosis for R.W. was AFM. Tr. at 192. AFM is a newer
term than “acute flaccid paralysis,” which derived from the time when polio was prominent. Id.
at 193. Acute flaccid paralysis has been found to be caused by various viruses, including
enterovirus, West Nile virus, and parvovirus. Id. Beginning in 2012, there were flare-ups of cases
of acute flaccid paralysis in children, often linked to D68, and the term “AFM” began to be used
instead. Id. at 193-94. The terms are still sometimes used interchangeably. Id. To him, it appeared
the treating physicians at Duke used those terms synonymously. Id. at 194.

23
A patient with AFM typically presents with an acute, rapid onset of symptoms, including
weakness affecting one or more limbs. Tr. at 196. They will have decreased muscle tone in the
affected limb, along with decreased or absent reflexes and pain. Id. MRIs will typically show
predominantly gray matter involvement. Id. Most will have a prodromal or concurrent illness or
fever at the time of onset. Id. Pain is often the “heralding sign,” indicating the onset of weakness.
Id.

According to a CDC AFM working group article, AFM cases are classified as either
“definite,” “probable,” “possible,” or “uncertain.” Tr. at 197-98. The first symptom is “acute
onset of limb weakness where you have a period from onset to nadir, hours to 10 days.” Id. at 198.
The second sign is a “prodromal fever or illness,” which can include nonspecific respiratory
symptoms like rhinorrhea, pharyngitis, or cough, or, less commonly, gastrointestinal symptoms.
Id. Another feature is weakness “involving one or more limbs, the neck, face or cranial nerves.”
Id. Cranial nerve involvement has not been consistently reported during spikes of AFM cases. Id.
The involved limbs have decreased muscle tone and absent reflexes, different from classic
demyelinating illnesses in which reflexes and tone increase after the initial presentation. Id. at
198-99.

Nerve root enhancement sets AFM apart from other forms of myelitis. Tr. at 199. CSF
will show a white blood cell “WBC” count of greater than five cells per liter. Id. If the CSF results
show this, the case will be classified as “definite” AFM. Id.

In R.W.’s case, “she had rapid onset of weakness,” with a nadir of 4-5 hours. Tr. at 200.
From the time R.W. complained of pain to when she had flaccid limbs upon first presentation to
the hospital was a matter of hours. Id. at 200-01. She had a fever at the time of presentation,
meeting the criterion of a prodromal or concurrent illness, even though she did not have other
symptoms. Id. at 201-02. She had weakness in both legs, as well as decreased muscle tone and
absent reflexes that persisted throughout her hospitalization.6 Id. at 201-04.

Dr. Sweeney reviewed R.W.’s MRIs. Tr. at 204. Her MRIs at WakeMed showed “T2
hyperintense signal between T6 and the conus with mild expansion of the cord. And along the
ventral surface of the cord, there was patchy enhancement, which corresponds to nerve root
enhancement.” Id. at 205. Her next MRI, taken at Duke, showed “diffuse enhancement of the
cauda equina nerve root in the ventral and dorsal aspects of conus medullaris,” with “significant
interval increase in the extent and degree of expansion of the abnormal intramedullary core signal,
extending from T3 to the conus.” Id. These collectively showed the expansion of the lesion from
the T6 to the T3 level, as well as increased swelling within the spinal cord. Id. Dr. Sweeney also
pointed out that the imaging showed enhancement in the nerve roots and cauda equina, but not the
spinal cord itself, as would be expected in “classic demyelinating myelitis.” Id. at 206.

Dr. Sweeney testified that R.W.’s CSF results did not meet the criteria for “definite” AFM,
because she only had five white blood cells in her fluid. Tr. at 206, 277. Thus, he classified her

6
Dr. Sweeney could not explain why Mrs. Williford observed R.W.’s body to be very rigid in the
emergency room bathroom, but he said that true spasticity would not be transient. Tr. at 202-03.

24
case as “probable.” Id. He was not surprised a virus was not detected in the spinal fluid itself, as
that rarely occurs. Id. at 208. Her later course was also consistent with AFM, as she did not have
a favorable response to immunotherapy, which is unusual in pediatric TM. Id. at 216-17. He
would expect at least a modest response to these treatments in TM, but he would not expect a
recovery of motor function in AFM, because the causal virus destroys the anterior horn cells in the
spinal cord. Id. at 217.

Dr. Sweeney walked through the MRI images, pointing out where the gray matter
involvement was seen. Tr. at 220-22. He also identified the enhancement of the nerve roots,
showing damage to the anterior portion of the spine. Id. at 223-25. The predominant inflammation
was “more anterior and central, which is where the gray matter lives.” Id. at 227. Dr. Sweeney
interpreted R.W.’s MRIs as showing predominantly gray matter involvement. Id.

In Dr. Sweeney’s view, the general term “myelitis” encompasses a range of different
diagnoses, including AFM. Tr. at 230. Idiopathic TM typically presents with bilateral symptoms
and a sensory level. Id. There will also be evidence of inflammation within the spinal fluid, such
as an elevated WBC count, enhancement on imaging, or oligoclonal banding. Id. TM is not
applicable to R.W. because she mostly had gray matter involvement, not white matter. Id. at 232.

Asked about R.W.’s sensory involvement, Dr. Sweeney did not believe it ruled out AFM,
because the sensory symptoms were secondary to her weakness, which developed first. Tr. at 232-
33. He attributed her sensory deficits to swelling and inflammation of her spinal cord, which led
to dysfunction of the nerve cells. Id. at 233, 275-76. Nonetheless, the initial assignment of “TM”
as a diagnosis at WakeMed was appropriate, given what was known at the time. Id. at 234. TM
is a broadly used term and refers to sensory loss across the body. Id.

Given R.W.’s overall course, Dr. Sweeney disagreed that her sensory level was dispositive
against an AFM diagnosis; her flaccid weakness, fever, and absent reflexes instead signified a
viral-mediated illness like AFM. Tr. at 234-35. Also, AFM can present with sensory involvement,
as documented in the medical literature. Id. at 237-38.

On cross, Dr. Sweeney clarified that AFM and “acute flaccid paralysis” can be used
interchangeably; AFM refers to acute flaccid paralysis with a specific viral etiology. Tr. at 242-
43. TM, by contrast, is a distinct condition that does not tend to present with acute flaccid
paralysis. Id. at 243. AFM can present with secondary demyelination due to inflammation. Id.
R.W. did not have evidence of demyelination on imaging, but her sensory loss implies she had
some “demyelination or damage to the sensory tract.” Id. at 244.

Dr. Sweeney acknowledged that the physicians at Duke referred to R.W.’s condition as
“acute flaccid paralysis” due to “likely transverse myelitis” and frequently used the term
“transverse myelitis” to describe her condition. Tr. at 245. He also acknowledged that a sensory
level is “uncommon” in AFM and “more common in idiopathic or demyelinating transverse
myelitis.” Id. at 251. Bowel and bladder incontinence is common in TM but can also occur in
AFM. Id. at 252. He was asked about R.W. having tingling in her leg as an initial symptom; this,
he said, was a “positive sensory symptom.” Id. at 256. He admitted that R.W. was noted to have
“profound” sensory level loss. Id. at 257-58.
25
Dr. Sweeney explained that R.W. developed spasticity in her hips only after “she had
instrumentation of her spinal cord, so after she had surgery for her scoliosis.” Tr. at 259. However,
because it is “very unusual to develop spasticity in only one muscle group,” he believed she more
likely developed contractures, meaning the “shortening of a muscle group because of disuse,”
rather than spasticity. Id. at 259-60.

Dr. Sweeney opined that the A29 rhinovirus detected in R.W. was the principal cause of
her AFM. Tr. at 268. If she had not contracted the A29 virus, he did not believe she would have
developed AFM at that time. Id. at 271.

In response to questioning by Special Master Oler, Dr. Sweeney noted that, although R.W.
did not complain of upper respiratory symptoms before or at the time her weakness began, she had
a fever and was positive for A29, which, to him, was “enough for me to include that as a prodromal
illness.” Tr. at 280.

3. Dr. Romberg’s Testimony

Dr. Romberg was qualified as an expert in clinical immunology and pediatrics. Tr. at 299.
He testified that AFM is caused by a virus. Id. at 302. However, “[t]he Tdap or DTaP, both of
them, and Menactra are killed or dead vaccines. They are not living. They cannot reproduce, and
therefore, I cannot imagine a scenario in which they can cause AFM.” Id. Only a living pathogen
could damage the anterior horn cells and produce the damage seen in AFM. Id. at 307. There is
also no epidemiologic evidence linking the subject vaccines and AFM. Id.

With respect to the detection of A29 in R.W., Dr. Romberg explained that rhinoviruses are
part of the enterovirus family and are genetically similar to enteroviruses. Tr. at 305-06. Before
2015, rhinoviruses and enteroviruses could not be distinguished from one another through testing.
Id. at 306.

Turning to Dr. Steinman’s molecular mimicry theory, Dr. Romberg criticized Dr.
Steinman’s reliance on BLAST searches to identify potential mimics, noting that BLAST was not
designed for this purpose. Tr. at 310-11. He explained:

So I think what BLAST does is it looks at an amino acid sequence
like you or I would read letters on a page, in a linear fashion. But
the immune system can't read amino acid sequences. What it does
is it feels the surface of these peptides, both their hydrophobicity,
how attracted they are to water, and their charges, are they positively
or negatively charged, how bulky the amino acids are. And so it’s
not really reading these sequences in a linear fashion. It's really
feeling them sort of like braille. And I think for this reason, the
National Academy of Science warned against using BLAST
support[ed] theories of molecular mimicry in their IOM report.

26
Id. at 311. Also, Dr. Steinman’s method was too broad to accurately identify immunologically
relevant homologies. Id. Instead, it was likely to produce false positive results. Id. at 311-12.
Furthermore, the E-value associated with Dr. Steinman’s findings was very high, suggesting the
finding was due to chance alone. Id. at 313-14.

Dr. Romberg testified that the Gautam experiments were not relevant here, because those
experiments tested an immunologically relevant epitope in mice. Tr. at 315-16. The sequences
identified by Dr. Steinman are unrelated to those used in Gautam. Id. at 316.

Dr. Romberg further pointed out that Dr. Steinman only required a 70% sequence match
when querying the IEDB, which could produce false positive results. Tr. at 316-17. And just
because a sequence is contained in the IEDB does not mean it is immunogenic. Id. at 317. One
of the sequences Dr. Steinman searched for was an “imaginary” protein. Id. at 318. The other
primarily exists in the adrenal gland, but R.W. did not have any clinical symptoms relating to the
adrenal gland. Id.

With respect to the purported molecular mimicry between the meningococcal vaccine and
mannose 9, Dr. Romberg pointed out that the vaccine has a phosphodiester bond, “which is really
molecularly bulky and charged. So I would predict that that difference would significantly change
antibody binding and recognition.” Tr. at 320-21. Later experiments by Dr. Steinman’s group
found that the mice with anti-mannose 9 antibodies had less severe EAE, pulling against Dr.
Steinman’s theory and actually suggesting mimicry with the meningococcal vaccine would have
a protective effect. Id. at 321-22.

In response to questions from Special Master Oler, Dr. Romberg explained that he did not
believe the molecular mimicry theory could apply to AFM, but it could apply to TM because TM
is an autoimmune disease. Tr. at 335.

4. Rebuttal Testimony

a. Dr. Steinman

Dr. Steinman testified on rebuttal that, in his opinion, the data where not “anywhere near
settled for understanding whether D68 or D68 and rhinovirus are the causes of AFM.” Tr. at 345.
On the question of the expected response to immunotherapy in TM, he cited a website from the
TM Society reporting that about one-third of patients have “virtually no recovery and are left
severely functionally disabled.” Id. at 351 (referencing Rare Disease Database, Transverse
Myelitis, NORD RARE DISEASE ADVOCACY (2018) https://raredisease.org/rare-disease/transverse-
myelitis (Ex. 86) (“NORD”)). A study on treatments of TM and AFM, called the CAPTURE
study, found 24% of TM patients and 34% of AFM patients had no improvement with
corticosteroids, while 15% of TM and 11% of AFM patients were “mostly recovered” after
treatment. Id. at 355-56 (citing Benjamin Greenberg et al., Acute flaccid myelitis: long-term
outcomes recorded in the CAPTURE study compared with paediatric transverse myelitis, 3 BJM
NEUROL. OPEN 1 (2021) (Ex. C, Tab 12) (“CAPTURE”)). Similar results were reported in
response to IVIG therapy. Id. Thus, R.W.’s lack of improvement with treatment did not rule out
a TM diagnosis. Id.
27
Dr. Steinman testified that R.W.’s WakeMed MRI showed inflammation in both the motor
and sensory portions of her spinal cord. Tr. at 357. The differential diagnosis of the radiologist
included TM, but not AFM. Id. at 361. Dr. Steinman would generally defer to the radiologist to
interpret imaging like this. Id. The Duke MRI showed a longitudinally extensive lesion, which
had increased since the last imaging was done, as well as diffuse enhancement of the cauda equina
nerve root and “patchy nodular enhancement along the ventral and dorsal aspects of the thoracic
cord.” Id. at 362-63. Again, this showed involvement of both the sensory and motor neurons. Id.
at 363. The differential included inflammatory myelitis, which Dr. Steinman agreed was correct.
Id. at 364-65. However, “this case has elements of acute flaccid myelitis. It also has elements that
are transverse myelitis.” Id. at 366.

Special Master Oler asked for Dr. Steinman’s interpretation of the notation in the Duke
MRI report that there was “no abnormal enhancement of the spinal cord.” Tr. at 368-69. He
acknowledged that if he saw an TM case with no abnormal enhancement of the spinal cord, he
“would really have to scratch [his] head,” as he had never seen a TM patient without such
enhancement. Id. at 369. He pointed out, though, that another portion of the report stated there
was increased spinal cord signal at the T3-T4 level, along with mild cord enlargement “concerning
for transverse myelitis.” Id. He admitted that her imaging showed “elements of AFM with this
kind of patchy T2 hyperintensities not only in the motor areas but in the dorsal. So there’s elements
of both, but I think it’s certainly inflammatory myelitis, myelitis being a term that connects AFM
to TM anyway.” Id. at 372.

Responding to Special Master Oler, Dr. Steinman opined that the likely reason R.W. did
not develop brisk reflexes was because her disease involved inflammation of both the posterior
and anterior aspects of the lower spinal cord. Tr. at 381. He had seen that presentation in about
15-20% of his TM cases. Id. While R.W. initially had a fever, she did not have respiratory
symptoms, which “certainly goes against AFM.” Id. at 383. She had asymmetric weakness, which
can be seen in TM but weighs a bit more toward AFM. Id. at 383-84. The complaints of numbness
and paresthesia pulled toward TM. Id. at 384. The sensory level and bowel and bladder
dysfunction “[u]ndeniably” suggested TM. Id. Her WBC count remained low for TM, but the
true count might have been masked by the early treatment with steroids. Id. at 384-85.

Special Master Oler asked Dr. Steinman to comment on R.W.’s pattern of weakness. Tr.
at 386. He said that normally, AFM presents with asymmetric weakness. Id. at 387. R.W.’s
presenting complaint was right leg weakness, but over time she became weak and flaccid on both
sides. Id. However, “[c]ertainly classically she presents asymmetrically.” Id. Thus, this was an
ambiguous aspect of her condition. Id. at 387-88.

On cross, Dr. Steinman maintained that the physicians at Duke could have used the terms
“hyperintensity” and “enhancement” interchangeably in describing R.W.’s MRI. Tr. at 395-96.
He believed her pattern of weakness was consistent with TM or AFM. Id. at 396. The lack of
oligoclonal banding did not rule out TM, as it is seen in TM only in about half of cases. Id. at 400.

Dr. Steinman testified that AFM could be an autoimmune disease, as stated in the Ayers
paper. Tr. at 400 (citing Ayers). You can see fever and inflammatory cells in the CSF. Id. at 401.
28
b. R.W.

R.W. testified that when she lay down for a nap on September 27, 2015, she “started having
a little bit of numbness, but nothing extreme. But once I went to the bathroom and when I was
coming out of the bathroom, my [right] leg, it felt numb, and I was struggling to walk because I
think my leg was just numb. I really couldn’t feel much of it.” Tr. at 405. She was able to walk
back to her bed at that time. Id. at 406. When she later tried to stand up, her leg buckled. Id.
When she was first seen by paramedics, she could still feel “something,” including the touch of
metal on her foot, but the sensation was reduced. Id. at 406-07.

c. Mrs. Williford

Mrs. Williford’s recollection of events was similar to R.W.’s. Tr. at 408. By the time the
family left the house to seek medical attention, R.W. could not walk. Id. Her parents attempted
to put her on the toilet at the hospital to procure a urine sample, but “we couldn’t bend her,” and
then she urinated on herself without being able to feel it happening. Id. at 409. A nurse attempted
to mark the level where R.W. could and could not still feel. Id. at 410. By the time R.W. was
admitted to WakeMed, the demarcation was at her belly button. Id. at 411.

d. Dr. Sweeney

Dr. Sweeney testified that a T2 MRI image cannot show enhancement indicating
inflammation of the lower spinal cord. Tr. at 413. He explained that a “T2 hyperintensity” is not
synonymous with “enhancement,” which cannot be seen on a T2 sequence MRI. Id. at 414.
Enhancement is seen by comparing T1 sequences with and without contrast. Id. The “T2
hyperintensity” showed a “hyperintensity within the cord itself.” Id. This hyperintensity extended
from T6 to the distal conus, with “mild expansion, indicating that there is already significant
inflammation or swelling within the spinal cord itself.” Id. at 414-15. The enhancement pattern
on the second WakeMed MRI scan, which was given with and without contrast, was “described
as patchy and only at one to two levels. I don’t feel that the extent of her weakness, her flaccid
weakness at that point would be explained by involvement of those nerve roots alone.” Id. at 415.

Furthermore, R.W.’s very sudden onset of weakness was not consistent with a “neuropathic
process.” Tr. at 415. Instead, in his view, it was “the findings within the cord itself, which is the
T2 hyperintense signals . . . driving the weakness, the flaccid weakness at that time.” Id. He noted
that AFM has a range of “hours to days” from onset to nadir, while TM progresses over days to
weeks.” Id. at 416.

Dr. Sweeney agreed with Dr. Steinman that both AFM and TM can present with
asymmetric weakness. Tr. at 417. The lack of facial and bulbar involvement did not point away
from AFM, as those symptoms were seen in early-reported cases with cervical cord involvement.
Id. Numbness/sensory loss can occur in AFM and almost always does so in TM. Id. at 418. Both
diseases can involve bowel and bladder dysfunction. Id. R.W.’s MRI imaging showed far more
gray matter than white matter involvement, suggesting AFM. Id. at 418-19.

29
With respect to R.W.’s sensory symptoms, Dr. Sweeney cited medical records
documenting that, after her admission to Duke, she had an exam where “[s]he could feel cold on
the lateral and medial aspect of the things as well as in the feet and could feel the reflex hammer
on the bottom of her feet.” Tr. at 421. At discharge, she was noted to have “minimal to no
sensation to light touch at [the] L3, L4, L5 and S1” dermatomal distributions. Id. Other exam
notes indicated she had some degree of sensation. Id. at 421-22. However, Dr. Sweeney
acknowledged that “right around her lower abdomen there is what could be referred to as a sensory
level.” Id. at 422. He found it anomalous that she had such a low sensory level when her scans
showed signal abnormality all the way up to the T3 level. Id. at 422-23.

Concerning the causes of AFM, Dr. Sweeney stated that “we are so much further along in
understanding how enterovirus D68 causes acute flaccid myelitis than anyone could be in
describing how a potential autoimmune or molecular mimic pattern could cause acute flaccid
myelitis.” Tr. at 425. Both human epidemiology and animal models support D68 causation. Id.
at 425-26.

Commenting on the CAPTURE study, Dr. Sweeney testified that the study classified
patients as those with predominantly white matter involvement (TM) and those with
predominantly gray matter involvement (AFM). Tr. at 429 (citing CAPTURE). The study showed
that pediatric AFM was as prevalent, if not more prevalent, than TM for the timeframe reviewed.
Id. Furthermore, 30% of the AFM patients in the study had sensory symptoms and 38% had bowel
or bladder symptoms at onset. Id. at 430. Twenty-eight percent of AFM patients had “mixed”
involvement of both gray and white matter. Id. Thus, although R.W. likely had some white matter
involvement, that did not point away from AFM. Id. The authors commented that the
“epidemiologic and animal model data both support the theory that AFM is the result of a viral
infection causing the death of the anterior motor neurons.” Id. at 431. D68 likely causes the
majority of cases. Id. In “mixed” AFM patients with both white and gray matter involvement,
“the vast majority” had no or minimal improvement with steroid or IVIG treatment. Id. at 432.

In response to Special Master Oler, Dr. Sweeney opined that AFM is not currently believed
to be an autoimmune condition. Tr. at 438. It has a non-relapsing course, which is atypical for
autoimmune conditions. Id. It does not respond well to immunotherapy. Id. at 438-39. “So all
of those point against an autoimmune process.” Id.

C. Post-Hearing Neuroradiology Expert Reports

1. Petitioners’ Expert: David Wilson, M.D., Ph.D.

After the hearing, Petitioners filed an expert report from Dr. David Wilson. Ex. 88
(“Wilson Rep.”). Dr. Wilson is a professor of radiology and biomedical imaging at the University
of California, San Francisco (“UCSF”). Id. at 1. He earned his M.D. and Ph.D. at Columbia
University and completed his residency and a fellowship in neuroradiology at UCSF. Id.; Ex. 89
(“Wilson CV”) at 1. He is board certified by the American Board of Radiology in both general
radiology and neuroradiology, and he served as the Chief of Neuroradiology at San Francisco’s
VA hospital. Wilson Rep. at 1. He is active in several radiology societies and has held committee
roles in them. Id. He has published more than 60 peer-reviewed articles with an emphasis on
30
molecular imaging. Id. He has interpreted more than 3,000 images of known or suspected
demyelinating and/or autoimmune injuries. Id. at 1-2.

Dr. Wilson reviewed a series of six of R.W.’s MRIs, from both WakeMed and Duke, with
reference to a review article by Helfferich, which set forth the MRI findings typically seen in a
case of AFM. Wilson Rep. at 2 (referencing Jelte Helfferich et al., Acute flaccid myelitis and
enterovirus D68: lessons from the past and present, 178 EUR. J. OF PEDIATRICS 1305 (2019) (Ex.
90) (“Helfferich”)). According to that paper,

In AFM, the classical MRI feature is a longitudinally extensive
slight T2-hyperintense signal in the central cord, affecting the
central gray matter, often most pronounced in the cervical regions.
Initially, there is usually more diffuse spinal cord edema, evolving
over several days to T2-hyperintensity that is restricted to the
anterior horn. Enhancement of the caudal roots and sometimes of
the cranial nerves can be seen. MRI of the brain commonly reveals
an area of slight hyperintensity typically located in the dorsal pons
in the region of the nuclei of the abducens and facial nerve. The
corticospinal tracts, located ventrally, are not affected, while the
caudate nucleus may be involved. These findings may help in
securing the diagnosis, but the correlation between symptoms and
radiologic findings is usually poor, making MRI unsuitable as a
prognostic tool for AFM.

Id. at 2-3.

Dr. Wilson did not observe any evolution of the signal localization in R.W.’s MRIs to
hyperintensities limited to the anterior horn, though the variable quality of the MRIs made
comparison challenging. Wilson Rep. at 3. He stated:

Overall, all studies show a process of the distal thoracic cord
(including the end or ‘terminus’ of the cord at T12-L1 also called
the ‘conus medullaris’ or just ‘conus’) and more distally the cauda
equina nerve roots. This process spans at least 5 vertebral body
segments and involves the conus, with clear cord expansion
(increased volume) and somewhat patchy/diffuse T2 signal
abnormality.

Id. He interpreted the studies as showing “equivocal” enhancement of the cord itself, which he
did not believe was relevant to the differential diagnosis. Id. He did observe clear enhancement
of the ventral cauda equina nerve roots. Id. Overall, he agreed with the observations made by the
Duke radiologists. Id.

31
Below are the images referenced in Dr. Wilson’s report, with his comments:7

Wilson Rep. at 4.

Dr. Wilson explained the difference between “hyperintensity” and “enhancement.” Wilson
Rep. at 4. “Hyperintensity” within the spinal cord refers to bright signal on T2-weighted imaging.
Id. “Many spinal diseases (demyelinating, infectious/inflammatory, post-traumatic, degenerative,
vascular, neoplastic) have associated hyperintensities in the cord[.]” Id. Hyperintensity will
persist over time. Id. “Enhancement” refers to the breakdown of the blood-spine barrier, with
“associated bright signal on T1-weighted sequences.” Id. Enhancement generally signifies an
acute or subacute process, and it will abate over time and with treatment. Id. “Enhancement of
the cord itself can be variable especially in likely infectious/inflammatory or autoimmune cases
like [R.W.’s].” Id.

Dr. Wilson observed that

[t]he presence of cauda equina enhancement is useful, to the extent
that expert neuroradiologists and published reports can agree on its
relevance. When we see the type of cauda equina enhancement in

7
The MRI images from Dr. Wilson’s and Dr. Zucconi’s expert reports have been redacted to remove
R.W.’s identifying information.
32
[R.W.’s] case we almost always invoke [GBS] which like most
possible diseases in her case is considered [autoimmune].

Wilson Rep. at 4. With respect to AFM, “[t]he overall central nervous system findings include
brainstem and cranial nerve abnormalities, long-segment spinal involvement, non-existent or slight
cord enhancement, and in some cases cauda equina enhancement (in many cases, according to the
Okumura et al. study).” Id. at 5 (citing Akihisa Okumura et al., Serial MRI findings of acute flaccid
myelitis during an outbreak of enterovirus D68 infection in Japan, 41 BRAIN & DEV. 443 (2019)
(Exs. 95, G) (“Okumura”)). Cauda equina enhancement is not typical of TM, though it can occur.
Id.

To investigate the MRI findings in R.W. further, Dr. Wilson searched the mPower database
for cases at UCSF using the descriptors “flaccid” with either “acute” or “myelitis,” finding 20
cases of suspected AFM. Wilson Rep. at 5. None of these cases reported cauda equina
enhancement. Id. He concluded that R.W.’s MRIs were distinct from the AFM cases reported in
the literature and UCSF database, because there was no involvement of her brainstem, the
abnormalities extended to gray and white matter, the cord abnormalities were “patchy,” and the
most distinctive abnormalities were in the distal thoracic cord and conus. Id. at 6.

Dr. Wilson felt other diseases should be included on R.W.’s differential, including TM and
GBS. Wilson Rep. at 5. The MRIs most likely indicated an autoimmune process, though no
diagnosis could definitively be assigned. Id. The cord enhancement in her case was “equivocal”
and did not suggest a specific diagnosis. Id. The cauda equina enhancement observed in R.W.
has also been reported with AFM but was more consistent with GBS, in Dr. Wilson’s view. Id.

2. Respondent’s Expert: William Zucconi, D.O.

After the hearing, Respondent filed an expert report from Dr. William Zucconi. Ex. D
(“Zucconi Rep”). Dr. Zucconi earned his D.O. from the New York College of Osteopathic
Medicine in 2001, is a board-certified radiologist with a certificate in neuroradiology, and is a
professor at Dartmouth’s Geisel School of Medicine. Zucconi Rep. at 1; Ex. E (“Zucconi CV”) at
1. He previously served as an associate professor of radiology and biomedical imaging at Yale
School of Medicine and was the Neuroradiology Section Chief and Fellowship Director at Yale.
Id. Over the past five years, Dr. Zucconi has cared for numerous patients with myelopathies,
including dozens with TM. Zucconi Rep. at 1. He has treated two patients with AFM and has
considered that diagnosis in other cases. Id.

On R.W.’s MRI imaging, Dr. Zucconi commented:

The [first set of] MRIs performed on 9/28/15 demonstrate abnormal
T2 signal hyperintensity within the central gray matter of the spinal
cord, with anterior horn predominance. The anterior grey matter
involvement is most notable in the mid thoracic segments (along the
upper aspect of the abnormality). The cord involvement spans T6
through the inferior aspect of the cord (the conus medullaris). The

33
signal abnormality in the lower portion of the cord is also confined
to the central gray matter.

Zucconi Rep. at 2. The repeat thoracic and lumbar MRIs, taken 13 hours later with and without
contrast, showed a similar disease pattern, with equivocal enhancement of the ventral nerve roots
of the cauda equina. Id. That report concluded the cord abnormality had progressed, involving
levels T6-12. Id. It also noted possible enhancement of the ventral cord at T11-12, which Dr.
Zucconi interpreted to refer to the anterior nerve roots. Id.

Below are Dr. Zucconi’s annotated copies of images from R.W.’s September 28, 2015
MRIs:

Zucconi Rep. at 3.

34
Zucconi Rep. at 4.
Dr. Zucconi noted that R.W.’s October 16, 2015 MRIs were performed with and without
contrast and showed that the “T2 signal changes [remained] confined to the central cord” but had
lengthened and become more diffuse. Zucconi Rep. at 4. He opined that the contrast enhanced
images showed “prominent enhancement of the central gray matter, with anterior predominance,
and conspicuous abnormal enhancement of the cauda equina, confined to the anterior roots.” Id.
In his view, the notation in the report that there was “patchy nodular enhancement along the ventral
and dorsal aspects of the thoracic cord,” which had not previously been observed, meant there was
“enhancement in the ventral nerve roots, and dorsal horns of the central grey matter.” Id. at 4-5.

35
Dr. Zucconi’s annotated copy of the October 16, 2015 MRI is below:

Zucconi Rep. at 5.
Dr. Zucconi disagreed with Dr. Wilson’s conclusion that R.W.’s MRIs were atypical of
AFM. Zucconi Rep. at 5. First, although there were no abnormalities observed in R.W.’s
brainstem, the literature only documents brainstem lesions in AFM cases affecting the cervical
spine, which did not apply here. Id. (citing Okumura). The thoracolumbar pattern of involvement
seen in R.W.’s case was a common alternative presentation. Id. at 5-6.
Second, “[t]he case definition for AFM is not limited to cases with only gray matter
involvement.” Zucconi Rep. at 6. AFM includes cases with gray matter predominance, which
was seen here. Id. Dr. Zucconi did acknowledge R.W.’s case differed from those documented in
Okumura in that her T2 signal hyperintensity became more diffuse between the first and second
scans, “rather than becoming more discrete or localized to the anterior gray matter.” Id. However,
“[n]otably the enhancing disease seen on later exam is confined to the central gray matter and
anterior horns.” Id.
Third, the Tartaglino paper cited by Dr. Wilson “pre-dated the 2002 work of the Transverse
Myelitis Consortium Working Group, and the many developments that have since narrowed the
definitions of IATM (Idiopathic Acute Transverse Myelitis).” Zucconi Rep. at 6 (citing Lisa M.

36
Tartaglino et al., Idiopathic Acute Transverse Myelitis: MR Imaging Findings, 201 RADIOLOGY
661 (1996) (Exs. H, 96) (“Tartaglino”)).
Fourth, the combination of nerve root enhancement and gray matter lesions in the spinal
cord is “exceedingly rare” in GBS, a “very unusual” feature of TM, but a common feature of AFM.
Zucconi Rep. at 6 (citing Charidimos Tsagkas et al., Acute Polyradiculomyelitis with Spinal Cord
Gray Matter Lesions: A Report of Two Cases, 12 FRONTIERS IN NEUROLOGY 1 (2021) (Ex. I)
(“Tsagkas”); Okumura).

Dr. Zucconi opined that R.W. met the CDC diagnostic criteria for AFM, including the MRI
finding of a “spinal cord lesion largely restricted to gray matter and spanning 1 or more spinal
segments with or without ventral nerve root enhancement.” Zucconi Rep. at 6 (citing Eliza
Gordon-Lipkin et al., Comparative quantitative clinical, neuroimaging, and functional profiles in
children with acute flaccid myelitis at acute and convalescent stages of disease, 61 DEV. MED.
CHILD NEUROLOGY 366 (2019) (Ex. J) (“Gordon-Lipkin”); Benjamin Greenberg et al., Acute
flaccid myelitis, UPTODATE (last updated June 28, 2022) (Ex. K) (“Greenberg 2022”)). T2 signal
hyperintensity in the spinal cord gray matter, as was seen in R.W., is “the hallmark of AFM.” Id.
(citing Olwen C. Murphy et al., Acute flaccid myelitis: cause, diagnosis, and management, 397
LANCET 334 (2021) (Exs. C, Tab 11 & L) (“Murphy”)). Further, the delayed ventral nerve root
enhancement is a well-documented sign of AFM but is very unusual in TM. Id. (citing Okumura).
He concluded: “The imaging features of RWs case are highly suggestive of, and more likely to
reflect a virally mediated AFM given the striking central gray matter involvement and
accompanying characteristic anterior horn and ventral nerve root involvement.” Id. at 7.

IV. APPLICABLE LAW

A. Petitioner’s Burden in Vaccine Program Cases

Under the Vaccine Act, a petitioner may prevail in one of two ways. First, he may show
that he suffered a Table injury within the time provided in the Table. § 11(c)(1)(C)(i). “In such a
case, causation is presumed.” Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320
(Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed in the Table, he
may demonstrate that he suffered an “off-Table” injury that was caused-in-fact by his vaccination.
§ 11(c)(1)(C)(ii).

For both Table and non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. § 13(a)(1). That is, a petitioner must offer evidence that leads
the “trier of fact to believe that the existence of a fact is more probable than its nonexistence before
[he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010);
see also Snowbank Enter. v. United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or
speculation is insufficient under a preponderance standard). The petitioner must demonstrate that
the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing
about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs.,
165 F.3d 1344, 1352 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352,
1355 (Fed. Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his

37
assertions; rather, the petition must be supported by either medical records or the opinion of a
competent physician. § 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a
non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Secretary of Health and Human Services. 418 F.3d 1274 (Fed. Cir. 2005).
Althen requires a petitioner to establish by preponderant evidence that the vaccination caused his
injury “by providing: (1) a medical theory causally connecting the vaccination and the injury; (2)
a logical sequence of cause and effect showing that the vaccination was the reason for the injury;
and (3) a showing of a proximate temporal relationship between vaccination and injury.” Id. at
1278.

Each of the Althen prongs requires a different showing. Under Althen prong one, a
petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can
cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this
prong, a petitioner’s theory must be based on a “sound and reliable medical or scientific
explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994)
(citations omitted). Such a theory must only be “legally probable, not medically or scientifically
certain.” Id. at 548-49; Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d 867, 873 (Fed. Cir.
1991).

A petitioner may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). Despite their expertise, special masters are not empowered by
statute to conclusively resolve what are complex scientific and medical questions, and thus
scientific evidence offered to establish Althen prong one is viewed “not through the lens of the
laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. However, this does not negate or reduce a petitioner’s ultimate burden to
establish his entitlement to compensation by preponderant evidence. W.C. v. Sec’y of Health &
Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).

The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326 (stating that “medical records and medical
opinion testimony are favored in vaccine cases, as treating physicians are likely to be in the best
position to determine whether a ‘logical sequence of cause and effect show[s] that the vaccination
was the reason for the injury’”) (quoting Althen, 418 F.3d at 1280). Medical records are generally
viewed as particularly trustworthy evidence because they are created contemporaneously with the
treatment of the patient. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed.
Cir. 1993). However, the existence of medical records and/or statements of treating physician
views does not require the special master to adopt their conclusions per se. § 13(b)(1) (providing
that “[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be
binding on the special master or court”); Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706,
746 n.67 (2009) (“[T]here is nothing . . . that mandates that the testimony of a treating physician
is sacrosanct–that it must be accepted in its entirety and cannot be rebutted.”). As with expert
38
testimony offered to establish a theory of causation, the opinions or diagnoses of treating
physicians are only as trustworthy as the reasonableness of their suppositions or bases. The views
of treating physicians should also be weighed against other, contrary evidence in the record—
including conflicting opinions among such individuals. Hibbard v. Sec’y of Health & Hum. Servs.,
100 Fed. Cl. 742, 749 (2011) (it was not arbitrary or capricious for special master to weigh
competing treating physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir.
2012); Caves v. Sec’y of Health & Hum. Servs., No. 06-522V 2011 WL 1935813, *17 (Fed. Cl.
Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without
opinion, 475 Fed. App’x 765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to
the phrase “medically acceptable temporal relationship.” Id. Thus, a petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de
Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation
for what is a medically acceptable timeframe must also be consistent with the theory for how the
relevant vaccine can cause the alleged injury (Althen prong one’s requirement). Id. at 1352;
Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after
remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed. Cir.
2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec.
Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Law Governing Analysis of Fact Evidence

The process for making factual determinations in Vaccine Program cases begins with
analyzing the medical records, which are required to be filed with the petition. §11(c)(2). The
special master is required to consider “all [] relevant medical and scientific evidence contained in
the record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s
report which is contained in the record regarding the nature, causation, and aggravation of the
petitioner’s illness, disability, injury, condition, or death,” as well as the “results of any diagnostic
or evaluative test which are contained in the record and the summaries and conclusions.”
§13(b)(1)(A). The special master is then required to weigh the evidence presented, including
contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Hum. Servs., 3
F. 3d 415, 417 (Fed. Cir. 1993) (it is within the special master’s discretion to determine whether
to afford greater weight to contemporaneous medical records than to other evidence, such as oral
testimony surrounding the events in question that was given later, provided that such determination
is based on a rational analysis).

Medical records created contemporaneously with the events they describe are generally
trustworthy, because they “contain information supplied to or by health professionals to facilitate
diagnosis and treatment of medical conditions,” where “accuracy has an extra premium.” Kirby
v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (quoting Cucuras, 993
F.2d at 1528). Accordingly, if the medical records are clear, consistent, and complete, then they
should be afforded substantial weight. See generally Lowrie v. Sec’y of Health & Hum. Servs.,
No. 03-1585V, 2005 WL 6117475 at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed,
39
contemporaneous medical records are often found to be deserving of greater evidentiary weight
than oral testimony, especially where such testimony conflicts with the record evidence. Cucuras,
993 F.2d at 1528; see also Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991),
aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992), cert. den’d, Murphy v. Sullivan, 506 U.S. 974
(1992) (citing United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally
been held that oral testimony which is in conflict with contemporaneous documents is entitled to
little evidentiary weight.”)).

However, there are situations in which compelling oral testimony could be more persuasive
than written medical records, such as where records are deemed to be incomplete or inaccurate.
Campbell v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based
upon common sense and experience, this rule should not be treated as an absolute and must yield
where the factual predicates for its application are weak or lacking.”); Lowrie, 2005 WL 6117475,
at *19 (“Written records which are, themselves, inconsistent, should be accorded less deference
than those which are internally consistent.”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, the
special master should assess each witness’s credibility when determining the weight their
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum.
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

In determining the accuracy and completeness of medical records, the Court of Federal
Claims has listed four possible explanations for inconsistencies between contemporaneously
created medical records and later testimony: (1) a person’s failure to recount to the medical
professional everything that happened during the relevant time period; (2) the medical
professional’s failure to document everything reported to her or him; (3) a person’s faulty
recollection of the events when presenting testimony; or (4) a person’s purposeful recounting of
symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed. Cl. 184, 203-
04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In deciding whether to afford greater weight to
contemporaneous medical records or other evidence, such as testimony, a rational analysis must
be explicated. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory connecting the vaccine to the injury often
requires a petitioner to pr

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11320621. Public record. Not legal advice.