Court Opinion

ID: 4674286
Source: CourtListenerOpinion
Date Created: 2021-04-02 20:01:42.627023+00
Date Added: 2024-06-11T08:03:19.882448
License: Public Domain

In the United States Court of Federal Claims
                                    OFFICE OF SPECIAL MASTERS
                                             No. 16-864V
                                           (to be published)

*************************
I.J.                        *
                            *                                            Filed: January 4, 2021
                Petitioner, *
                            *
          v.                *                                            Entitlement Decision; Transverse
                            *                                            Myelitis; Spinal Cord Infarction;
SECRETARY OF HEALTH AND     *                                            Tetanus Diphtheria acellular
HUMAN SERVICES,             *                                            Pertussis; Causation; Althen
                                                                         Prong One
                        *
            Respondent. *
                        *
*************************

Robert J. Krakow, Law Office of Robert Krakow, P.C., New York, NY, for Petitioner.

Catherine Stolar, U.S. Dep’t of Justice, Washington, DC, for Respondent.

                                       ENTITLEMENT DECISION 1

        I.J.         filed a petition on July 21, 2016, seeking compensation under the National
Vaccine Injury Compensation Program (“Vaccine Program”). 2 Petition (“Pet.”) at 1 (ECF No. 1).
Mr. I.J. has alleged that he developed transverse myelitis (“TM”) due to the Tetanus Diphtheria
acellular-Pertussis (“Tdap”) vaccine he received on July 22, 2013. Id.

        An entitlement hearing was held in this matter on October 22-23, 2019. After consideration
of the record and testimony provided at hearing, I deny an entitlement award in this case. As

1
  This Decision will be posted on the Court of Federal Claims’ website in accordance with the E-Government Act of
2002, 44 U.S.C. § 3501 (2012). This means that the Decision will be available to anyone with access to the
internet. As provided by 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. Specifically, under Vaccine Rule 18(b), each party has fourteen days
within which to 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, the
whole Decision will be available to the public in its current form. Id.
2
 The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§ 300aa-
10–37 (2012) (hereinafter “Vaccine Act” or “the Act”). Individual section references hereafter shall refer to § 300aa
of the Act.
discussed in more detail below, Petitioner has preponderantly established that he likely
experienced TM, prevailing over Respondent’s proposed alternative diagnosis of a spinal cord
infarction. But insufficient preponderant evidence offered in this case stands for Petitioner’s
contention that the Tdap vaccine can cause TM, or that it did so in this case.

I.      Factual Background

        A. Medical History Prior to Vaccination

        Prior to his vaccination in July 2013, Mr. I.J. was a healthy and active thirty-four-year-
old man with no history of neurological problems or clotting disorders. Tr. at 22–24. Earlier that
year, Mr. I.J. had undergone a surgical procedure to repair a torn anterior cruciate ligament
(“ACL”) in his left knee. Ex. 2, filed July 26, 2016 (ECF No. 8-2); Ex. 15, filed Apr. 3, 2017 (ECF
No. 28-1). However (and relevant to the claim at hand), Mr. I.J.'s family history was significant
for thrombophilia. 3 Ex. 2. at 18, 21, 225.

        B. Onset of Injury

       On July 22, 2013, Mr. I.J. received the Tdap vaccine. Vaccination Record, filed July 26,
2016 as Ex. 1 (ECF No. 8-1); Tr. at 7. No immediate complication or reactions were documented.
See Ex. 1. A little over two weeks later, on August 6-7, 2013, Mr. I.J. reported feeling ill with
what he believed was a minor cold, but he quickly recovered. Ex. 2 at 8. The following day (August
8, 2013), however, Mr. I.J. was reaching into the back pocket of his pants (to retrieve a Metro
card needed for public transportation in New York City) when he experienced a “pinch” in his
shoulder, broadening to sudden sharp pain and burning sensation in the back of his neck that ran
down from both shoulders and arms into his left leg. Id. at 7; Tr. at 14–15. These symptoms
continued to worsen, and within minutes he began to experience pain, tingling, and numbness that
spread throughout his arms and legs. Ex. 2 at 7.

        Mr. I.J. walked to NYU Medical Center, where he was immediately admitted to the
emergency department. Tr. at 14–15. Within hours, Mr. I.J. lost the ability to use his arms and
legs and began to exhibit urinary retention. Id. at 20. An MRI of Mr. I.J.'s cervical spine revealed
increased signal “predominantly within the central gray matter of the cervicothoracic cord
extending from C3 to the T1-2 level, most prominent from the C6 to the T1 level.” Ex. 8B at 1,
filed Jan. 4, 2019 (ECF No. 50-2). These results were deemed to be compatible with a diagnosis
of TM. Id. at 1–2.

3
  Thrombophilia is the tendency to form blood clots. Thrombophilia, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=49901&searchterm=thrombophilia (last visited Nov. 23,
2020);            Thrombus,             Dorland’s           Medical           Dictionary               Online,
https://www.dorlandsonline.com/dorland/definition?id=49919&searchterm=thrombus (last visited Nov. 23, 2020).

                                                      2
        On August 9, 2013, treating neurologist Dr. Stephen Galetta noted that Mr. I.J.'s
symptoms had developed over the course of six hours. Ex. 2 at 20. He also observed that the MRI
of Mr. I.J.'s cervical spine showed “high signal extending down the anterior part of the cord,”
and the signal intensity seemed to be concentrated in the ventral horns of the spinal cord. Id. Based
on Mr. I.J.'s presentation and MRI results, Dr. Galetta proposed several differential diagnoses,
including TM, West Nile Virus, Neuromyelitis Optica (“NMO”), and Acute Disseminated
Encephalomyelitis (“ADEM”). Id.

        From August 9 to 15, 2013 Mr. I.J. was treated with Solumedrol, intravenous
immunoglobulin (“IVIG”), and plasma exchange (“PLEX”), and he underwent a series of
diagnostic laboratory studies to refine his diagnosis. Ex. 2 at 183, 373–444. One such test was an
antinuclear antibodies (“ANA”) test, which was performed on August 9, 2013, and resulted in a
positive showing (thus suggesting the possible existence of an autoimmune process). 4 Id. at 139.
Because Mr. I.J. did not have a family history of rheumatologic disease, however, this result
was only deemed suggestive of the presence of primary rheumatologic disease. Id. at 50.
Mycoplasma pneumoniae 5 antibody levels were also elevated, but the significance of these
findings was not immediately clear given the possibility that they were attributable to the IVIG
treatment Mr. I.J. was receiving at the time. Id. at 167, 172. Mr. I.J. was also found to be
positive for other antibodies, but treaters concluded that such results did not likely explain his
condition. Id. at 55–56, 61, 139, 169–70, 172. Tests for Rhinovirus and enterovirus were also
positive. Id. 2 at 49. Additionally, Thrombophilia studies revealed that Mr. I.J. had elevated
Factor VIII levels and an activated partial thromboplastin time 6 of 23. Id. at 162, 166, 170, 392.

       A repeat MRI was performed on August 17, 2013. Ex. 9F, filed Jan. 4, 2019 (ECF No. 51-
1). The results of this MRI showed

4
  An ANA test is typically used to assess the presence of systemic lupus erythematosus, as well as other autoimmune
diseases (e.g., mixed connective tissue disease, scleroderma, rheumatoid arthritis, Sjögren’s syndrome, and
polymyositis). However, because otherwise-healthy individuals also often test positive for ANA, follow-up testing is
necessary to confirm the existence of an autoimmune condition. See K. Pagana, et al., Mosby’s: Manual of Diagnostic
and Laboratory Tests 80, 82 (6th ed. 2018) (“Mosby’s”).
5
  Mycoplasma pneumoniae is a bacterial species responsible for mild respiratory tract disease. Mycoplasma
pneumoniae,                 Dorland’s                 Medical             Dictionary               Online,
https://www.dorlandsonline.com/dorland/definition?id=91174&searchterm=Mycoplasma+pneumoniae (last visited
Nov. 23, 2020).
6
  Activated partial thromboplastin time (“aPTT”) is the period required for clot formation in recalcified blood plasma
after contact activation and the addition of platelet substitutes (e.g. brain cephalin or similar phospholipids); used to
assess the intrinsic and common pathways of coagulation. Activated partial thromboplastin time, Dorland’s Medical
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=113783 (last visited Nov. 24, 2020). A
prolonged aPTT can indicate a deficiency of a number of factors, including prekallikrein, high-molecular-weight
kininogen, factors XII, XI, IX, VIII, I, V and II, and fibrinogen. Id. The PTT (partial thromboplastin time) test is used
to assess the intrinsic system and the common pathway of clot formation. See Mosby’s at 344–45. Normal findings
for aPTT are 30-40 seconds and 60-70 seconds for PTT. Id. at 344.

                                                           3
         …a long segment of T2/FLAIR hyperintensity extending from C2 to T3, largest
         between C4 and C7 where most of the transverse diameter of the cord is noted . . .
         At T2 and T3, the inferior aspect of the lesion, the T2-bright signal involves
         predominantly the central gray matter. Patchy enhancement is noted scattered
         throughout portions of the spinal cord between C4 and T1, with conspicuous
         enhancement of the anterior horns of the central gray matter at C4. The DWI pulse
         sequence reveals some small foci of restricted diffusion.

Ex. 9F at 1–2. Based on these results, Mr. I.J.'s differential diagnosis was narrowed to
encompass only TM and spinal cord infarction—though the diagnosis of TM was identified as
favored due to “the age of [Mr. I.J.      the repeat occurrence, and the holocord 7 involvement, and
the cervical location” of the lesion. Id. at 2.

        That same day, Mr. I.J. was evaluated by an infectious disease specialist, Dr. Eddie
Louie, M.D., who (mistakenly believing Mr. I.J. had received the Hepatitis B rather than Tdap
vaccine) noted that a causal connection between the Hepatitis B vaccine and TM has been
identified. Ex. 2 at 61. Dr. Louie dismissed the possibility that the rhinovirus played in the onset
of Mr. I.J.'s condition, noting that this sort of viral infection is not associated with
neuromuscular diseases in which there is damage to the anterior horn of the spinal cord. Id. He
also observed that Petitioner’s symptoms were improving with steroid and IVIG treatment. Id.
Because there were some lingering concerns, however, that Mr. I.J.'s condition could partially
be the result of mycoplasma myelitis, 8 he was started on intravenous azithromycin. Id. at 61, 213.

        Dr. Albert Favate—a member of the hospital stroke team—provided a neurology
consultation on August 19, 2013, and his assessment differed from the prior proposals that TM
explained Petitioner’s condition. Instead, Dr. Favate noted that “[i]n view of presentation cord
signal on MRI vascular etiology-thrombosed anterior spinal artery origin with prese[r]vation of
posterior collu[m]n function. [A]s possible sources are Vertebral artery thrombotic formation
w/Hypercoagulable state…Note AVM may be compressed and not seen on cord MRI in initial
phase of cord infarct.” Ex. 2 at 62. Dr. Favate recommended that Mr. I.J. undergo a coagulopathy
work-up with hematology, as well as an MRI and spinal angiogram to visualize spinal circulation.
Id. He also recommended repeat serological testing to further refine Mr. I.J.'s diagnosis. Id.

7
  Holocord presentation denotes involvement of the entire spinal cord, extending from the cervicomedullary junction
to the tip of the conus. Y. Sheikh et al., Holocord Presentation, Radiopaedia, https://radiopaedia.org/articles/holocord-
presentation?lang=us (last visited Dec. 14, 2020).
8
  Mycoplasma myelitis is a rare form of TM resulting from a Mycoplasma pneumoniae infection. An M. pneumoniae
infection is an exclusionary criterion under the proposed diagnostic criteria for TM. See, e.g., Transverse Myelitis
Consortium Working Group, Proposed Diagnostic Criteria and Nosology of Acute Transverse Myelitis, 59 Neurology
499, 500 (2002), filed as Ex. 35 on July 21, 2019 (ECF No. 63-4) (“Working Group”).

                                                           4
         Following Dr. Favate’s evaluation, and at his recommendation, Kenneth Hymes, M.D., a
hematologist, evaluated Mr. I.J. for thrombophilia. Ex. 2 at 62–65. Dr. Hymes acknowledged
that while Mr. I.J.'s first MRI was interpreted as being most consistent with TM, he also noted
that a repeat MRI conducted a few days after Mr. I.J.'s admission appeared to be more consistent
with a spinal cord infarction. Id. at 62. Mr. I.J.'s family history of lethal pulmonary emboli 9 was
also quite concerning to Dr. Hymes. Id. at 62, 65 (“[t]he positive family history of thrombophilia
is noteworthy, and a thrombophilic disorder with venous thrombosis and paradoxical embolization
might explain clinical findings”). He concluded that Mr. I.J. had experienced “[a]cute onset of
back pain and extremity weakness, possibly due to vascular injury to the spinal cord. A spinal
artery dissection or embolic lesion might explain these symptoms.” Id. at 65. Thus, Dr. Hymes
suggested Mr. I.J. undergo thrombophilia studies. Id. He allowed, however, that a diagnosis of
TM was still also a reasonable explanation for Petitioner’s condition. Id.

        Dr. Stephanie Sterling also provided a follow-up infectious disease consultation with Mr.
I.J. on August 19, 2013. Ex. 2 at 66–68. Mr. I.J. told Dr. Sterling at this time that he had
received “a bunch of vaccines” approximately two to three days prior to the onset of his condition.
Id. at 66. Based on such (incorrect) reporting, Dr. Sterling proposed that vaccination could be
related to Petitioner’s subsequent development of TM. Id. at 68. Dr. Sterling, however, reviewed
Mr. I.J.'s most recent MRI results, noting that newly-recorded abnormalities were focused
predominantly in the anterior horns of the central gray matter of the spinal cord, and might
therefore be more consistent with a spinal cord infarction. Id. at 68. She also acknowledged that
Petitioner’s condition was improving with steroids, IVIG, and PLEX treatments. Id. Dr. Sterling
did agree with Dr. Louie’s decision to rule out a rhinovirus infection as causal, since existing
literature did not support such a relationship. Id. And she expressed some skepticism regarding the
role mycoplasma pneumoniae might have played in Mr. I.J.'s condition, though she agreed to
continue treatment with azithromycin. Id.

        On August 20, 2013, Mr. I.J. was evaluated by yet another neurology specialist, Dr.
Miguel Litao. Ex. 2 at 213. Mr. I.J. had now developed a fever, exhibited elevated white blood
cell counts, and was experiencing difficulty breathing. Id. He was prescribed Zosyn and
Vancomycin, but his azithromycin treatment was discontinued due to the low likelihood of
mycoplasma infection. Id. at 213–14. Dr. Litao also observed that the August 17th MRI results
were (in his view) most consistent with a spinal cord infarction in the anterior spinal artery area.
Id. at 213.

       Shortly thereafter, Mr. I.J. was transferred to the medical intensive care unit. Ex. 2 at
230–31. A progress note was prepared by critical care physician, Dr. Jessica Leland Taff, at the
time of Mr. I.J.'s transfer. Id. Dr. Taff observed that Mr. I.J.'s age, holocord involvement,

9
 A pulmonary embolism is the closure of the pulmonary artery or one of its branches by an embolism. Pulmonary
Embolism,                  Dorland’s                 Medical                  Dictionary               Online,
https://www.dorlandsonline.com/dorland/definition?id=72763&searchterm=pulmonary+embolism (last visited Nov.
23, 2020).

                                                      5
and cervical location of the spinal cord lesion favored a TM diagnosis. Id. She also expressed a
desire to obtain Mr. I.J.'s immunization history due to reports of TM following receipt of the
Hepatitis B vaccine. Id. at 231. Dr. Taff acknowledged, however, that the restricted diffusion seen
in the August 17th MRI was suggestive of a spinal cord infarction. Id.

        At the recommendation of several treating physicians, Mr. I.J. underwent a spinal
angiogram 10on August 21, 2013. Ex. 5 at 41 (filed on compact disc); Ex. 9D at 3, filed Jan. 4, 2019
(ECF No. 50-9). The angiogram demonstrated “a lower cervical watershed corresponding to the
region of maximum abnormality…on the spinal MRI.” Ex. 9D at 3. The anterior spinal artery was
also described as “segmentally narrowed,” though it was acknowledged that this narrowing could
be due to an earlier thrombotic event. Id. But given the extensive distribution of the lesion, passive
compression or active inflammation were also considered. Id.

        A follow-up hematology consultation provided by Dr. Hymes noted evidence of spinal
artery occlusion in the angiogram, but he indicated that the results of Mr. I.J.'s thrombophilia
studies could also be seen in inflammation and were not likely to have caused an aggressive
thrombotic event. Ex. 9D at 76. Additionally, an echocardiogram did not reveal a right-to-left
shunt—circumstances commonly associated with an increased risk of embolism. Id. at 75; see also
N. Gomperts et al., A Broken Heart: Right-to-Left Shunt in the Setting of Normal Cardiac
Pressures, 24 Can. J. Cardiology. 227, 227 (2008), filed on July 21, 2019 as Ex. 32 (ECF No. 63-
1). Though he could not yet identify the etiology for his findings, and despite the caveats previously
mentioned, Dr. Hymes remained confident that the most likely diagnosis was an embolic lesion.
Ex. 2 at 76.

        On August 23, 2013, Mr. I.J. was released from the medical intensive care unit and was
transferred back to the neurology department. Ex. 2 at 245. Efforts to conclusively diagnose Mr.
I.J. were summarized by Dr. Taff, who noted:
         Initial MRI C[ervical] and T[horacic] spine on 8/8 showed long segment, central
         increased signal [within] cervicothoracic spinal cord [without] enhancement
         compatible [with] transverse myelitis . . . Repeat MRI done on 8/17 showed
         decreased diffusion thought to be [consistent with] a spinal cord infarction within
         the Anterior Spinal Artery territory . . . On 8/22 he had a spinal angiograph showing
         a mid-cervical filling defect of the Anterior Spinal artery congruent [with]
         suspected spinal infarct in the cervical watershed region…Hematology was
         consulted for concern of pro-thrombotic state, but felt that labs were not consistent
         with Antiphospholipid Ab syndrome or another pro-coagulant state . . . clarify
         patient’s immunizations at occupational health, as there are case reports of TM

10
  A spinal angiogram is a diagnostic procedure in which a contrast dye is injected into the arteries supplying the spinal
cord and x-ray images are obtained in order to study blood flow to the area. NYU Langone Health, Spinal Angiogram,
https://med.nyu.edu/radiology/about-us/subspecialties/neuro-interventional/our-services/patient-information-spinal-
angiogram (last visited Dec. 14, 2020).

                                                           6
        following Hep[atitis] B immunization, although this appears a much less likely
        scenario given angio[gram] and MRI findings.

Ex. 2 at 245–47. Dr. Taff thus acknowledged that the etiology of Mr. I.J.'s condition was still
unclear, and hematology specialists felt that the thrombophilia panel results were not likely to have
caused such an aggressive thrombotic event—even though she overall seemed to favor infarction
as the proper diagnosis. Id. at 248.

       On August 26, 2013, Mr. I.J. was again evaluated by neurology in anticipation of his
being discharged to a rehabilitation facility. Ex. 2 at 276. His active problem list at that time
included TM and thrombophilia. Id. It was also noted that Mr. I.J. exhibited an Anterior Spinal
Artery blockage at the C5 level, but it was again observed that this occlusion could be due to
swelling within the spinal cord. Id. at 281. This conclusion was echoed the very next day during a
neurology follow-up. Id. at 291.

        Mr. I.J. was discharged from NYU Hospital on August 29, 2013, and was transferred to
Rusk Rehabilitation for intensive physical therapy. Ex. 2 at 6, 13. Mr. I.J.'s discharge diagnoses
included tetraplegia, spinal cord infarction, and thrombophilia, but notably did not include a TM
diagnosis. Id. at 7. Dr. Foo, a neurologist, mentioned Mr. I.J.'s recent vaccinations, and he
indicated that vaccination records should be obtained for further consideration. Id. at 8, 12. But he
also observed the overall conflict in the medical record between possible diagnoses, noting as
follows:

        The differential diagnosis is between spinal cord infarct and transverse myelitis.
        The age of the patient, the repeat occurrence, and the holocord involvement, and
        the cervical location favor transverse myelitis. Spinal cord infarction is suggested
        by the evidence of restricted diffusion in portions of the lesion, the focal gray matter
        T2-bright lesions noted on the current examination as well as on the prior
        examination, and the focal gray matter enhancement in portions of lesions.

Id. at 10.

        C. Follow-up Treatment

        For the next several months, Mr. I.J. participated in intensive inpatient rehabilitation.
See generally Ex. 6, filed Nov. 30, 2016 (ECF No. 17-1); Ex. 11, filed on Feb. 23, 2017 (ECF No.
22-1). Mr. I.J. was later transferred to Brandywine Nursing Home where he received
rehabilitation therapy for approximately six months. Ex. 11 at 3–4. On August 22, 2014, Mr. I.J.
was again transferred—this time to Lindenwood Nursing facilities for continued nursing and
rehabilitative care. See Ex. 6. His diagnosis at the time of admission was described as “spinal cord
infarction vs. transverse myelitis, paraplegia, thrombophilia….” Id. at 380. After seven months at
Lindenwood, he was discharged home on March 20, 2015. Id. at 380–82. At the time of his

                                                   7
discharge, Mr. I.J.'s diagnosis was characterized as an “unspecified spinal cord disease.” Id. at
380. There are no records documenting medical or rehabilitative services since March 2015.

II.    Witness Testimony

       A.   I.J.
        Mr. I.J. submitted an affidavit and provided testimony at the entitlement hearing.
Petitioner’s affidavit, filed as Ex. 4 on July 25, 2016 (ECF No. 6-1) (“Affidavit”); Tr. at 7–40. Mr.
I.J. first described his past medical history as healthy with no significant problems—having only
experienced gall stones in 2006 or 2007 and an ACL tear in his left knee that required arthroscopic
surgery in early 2013. Affidavit at 1–2; Tr. at 11–12.

        Mr. I.J. explained that in 2013, he was offered a job as a patient advocate at NYU
Medical Center, and was required to receive the Tdap vaccine as a condition of his employment.
Affidavit at 2; Tr. at 13. He received the Tdap vaccine on July 22, 2013. Affidavit at 2; Tr. at 13.
Approximately two weeks later, Mr. I.J. was boarding a bus when he reached into his back, right
pants pocket to retrieve his bus pass and felt a sharp, burning pain that ran from the back of his
neck to his right shoulder and arm. Affidavit at 2; Tr. at 14. The pain and burning sensation
progressed and spread to his left shoulder and arm and down his leg, and he began to experience a
tingling sensation and weakness in his limbs. Affidavit at 2; Tr. at 14–16. He reported that at one
point, while walking to the hospital, he collapsed to one knee and struggled to get up. Affidavit at
3; Tr. at 17. When Mr. I.J. arrived at NYU Medical Center, he was admitted to the emergency
department where he continued to experience progressive weakness, numbness, and a needle-like
pain sensation that was predominantly focused in his back and extending into his left arm. Tr. at
20–21. He also experienced urinary retention that required catheterization. Id. at 29–30.

        Shortly after his emergency department admission, Mr. I.J. underwent an MRI scan. Tr.
at 24. Prior to his scan, Mr. I.J. recalled being fully mobile. Id. Immediately following his MRI
scan, however, Mr. I.J. lost all mobility from the neck down. Id. at 25–27. He also exhibited
urinary retention, for which he required catheterization, as well as difficulty regulating his body
temperature. Id. at 28–30. Following treatment with IVIG and plasmapheresis, Mr. I.J. regained
some mobility in his arms. Id. at 28.

        Mr. I.J. then described his extended rehabilitation at Rusk Rehabilitation. Tr. at 31. He
was eventually able to push back with his arms and support his own bodyweight with his arms. Id.
He was then transferred to Brandywine Nursing Home for additional therapy. Affidavit at 3; Tr.
at 32. He emphasized that this facility was located two hours away from his home, which made it
difficult for his family to visit him regularly. Tr. at 32. Mr. I.J. described his time at Brandywine
as lonely and emotionally difficult. Id. After approximately six months, Mr. I.J. was again
transferred—this time to Lindenwood Nursing Facility. Affidavit at 3–4; Tr. at 33. He was
eventually discharged home, but he continues with physical therapy at Rusk Rehabilitation and a

                                                 8
community access program. Tr. at 35–37. He has recovered some strength in his legs and mobility
in his upper extremities, but he does not have the dexterity he possessed prior to the onset of his
injury. Id. at 35–36.

       B. Petitioner’s Experts

               1.      Dr. Scott Zamvil, M.D., Ph.D.

        Dr. Zamvil, a neuroimmunologist, provided testimony at the hearing and offered a single
expert report. Tr. at 41–160; Report, filed as Ex. 16 on Sept. 11, 2017 (ECF No. 31-1) (“Zamvil
Rep.”). Dr. Zamvil opined that the Tdap vaccine can cause TM and did so in Petitioner’s case.

       Dr. Zamvil received his bachelor’s degree in chemistry from Claremont Men’s College.
Dr. Zamvil Curriculum Vitae, filed as Ex. 17 on Sept. 11, 2017 (ECF No. 35-1) (“Zamvil CV”) at
1. He then obtained a Ph.D. in medical microbiology along with a medical degree from Stanford
Medical School. Id. Dr. Zamvil completed an internship in internal medicine at Pacific
Presbyterian Medical Center before completing residencies in internal medicine and neurology at
Stanford University Medical Center and Brigham and Women’s Hospital respectively. Id. He is
board certified in neurology. Id. Dr. Zamvil has served as a professor of both neurology and
immunology at Harvard Medical School and the University of California, San Francisco, and he
has published numerous journal articles on these subjects. Id. at 1, 14–21.

        Some of Dr. Zamvil’s research has specifically considered T cell recognition of
autoantigens on myelin and central nervous system demyelination. Tr. at 43–44. He does not,
however, have expertise in vascular medicine or neuroradiology. Id. at 108. Dr. Zamvil has clinical
duties at the Multiple Sclerosis clinic at the University of California, and he often sees patients
suffering from demyelinating conditions, including multiple sclerosis (“MS”) and NMO, but he
has only recently started seeing patients with TM when they are concurrently experiencing NMO.
Tr. at 42, 48, 107. He explained, however, that TM overlaps with other demyelinating conditions
with which he is more familiar. Id. at 42, 45, 106. Though he was not able to personally evaluate
Mr. I.J. Dr. Zamvil relied on the submitted medical records—including the treating physician
opinions and diagnostic test results contained therein. Tr. at 50. He did not, however, review either
the MRI studies or angiogram in forming his opinion, and instead deferred to Petitioner’s
neuroradiology expert, Dr. Watanabe, for her interpretation of those studies. Id. at 109–10.

        Based on the medical record and the reports contained therein, Dr. Zamvil concluded that
Mr. I.J. more likely than not experienced TM. Tr. at 51, 90, 110. He supported this conclusion
by noting that the initial onset of Mr. I.J.'s condition—which progressively worsened over the
course of six to eight hours—was “stuttering” rather than an acute onset with near immediate
maximal deficit. Tr. at 52. This, Dr. Zamvil opined, was consistent with the diagnostic criteria for
TM set forth by the Transverse Myelitis Consortium Working Group. Id. at 60; Working Group,
at 500.

                                                 9
         Dr. Zamvil began his testimony with a discussion focused on the diagnostic criteria and
 pathophysiology of TM, in light of the TM Working Group criteria. Tr. at 49–50, 76–84; Working
 Group at 500. He described TM as an inflammatory autoimmune response within the spinal cord.
 Tr. at 44–45. TM may follow an infectious disease process and its pathogenesis is likely the result
 of specific autoantigens. Id. at 44–45, 123–24. In this vein, Dr. Zamvil acknowledged that TM is
 diagnostically distinct from other demyelinating conditions such as ADEM. Id. at 116. Dr. Zamvil
 next addressed the first inclusionary criterion outlined by the Working Group paper: the
 development of sensory, motor, and autonomic dysfunction. Tr. at 51, 76–78 (referencing Working
 Group at 500). Dr. Zamvil concluded that Mr. I.J. satisfied this criterion because the weakness
 and paralysis he experienced was an obvious example of motor dysfunction. Tr. at 77. Petitioner
 also had documented spinothalamic 11 sensory dysfunction and autonomic dysfunction resulting in
 urinary retention. Id. at 77–78.

         The second criterion—bilateral signs and/or symptoms—was also satisfied in Dr. Zamvil’s
estimation, because Mr. I.J. exhibited sensory and motor dysfunction bilaterally. Tr. at 78. Dr.
Zamvil did acknowledge that these symptoms were worse on Mr. I.J.'s right side than on his
left, but noted that this diagnostic criterion did not require precisely symmetrical presentation, just
bilateral. Id.; Working Group at 500. The third criterion discussed was that of a defined sensory
level. Id. at 78–80. Based on the record alone, Dr. Zamvil was unable to conclude whether Mr.
I.J.'s clinical presentation satisfied this criterion. Id. at 79–80. Some evidence, such as the loss
of sensory perception below the level of T4, favored it, but evidence like the loss of motor function
in Petitioner’s arms (a level greater than T4), did not. Id. at 79. Thus, Dr. Zamvil admitted that
additional information was required to determine if this diagnostic criterion had been established.
Id. at 79–80. But he expressed more confidence that the criterion requiring “the exclusion of extra-
axial compressive etiology by neuroimaging” was satisfied, since the MRI imaging in this case did
not reveal evidence of a compressive etiology such as spinal stenosis or blood. Id. at 80; Working
Group at 500.

        Next, Dr. Zamvil addressed the criterion requiring evidence of inflammation, as established
by pleocytosis 12 or elevated IgG index or Gadolinium enhancement. Tr. at 80–82. Mr. I.J.'s
cerebrospinal fluid (“CSF”) analysis, Dr. Zamvil admitted, was negative for pleocytosis—yet in
his opinion this was an insufficient reason to rule out a TM diagnosis. Id. at 68, 81. According to
Dr. Zamvil, only fifty-seven percent of patients experiencing TM will exhibit pleocytosis, meaning
nearly half do not. Id. at 67, 82; P. Barreras et al., Clinical Biomarkers Differentiate Myelitis from

11
  The term “spinothalamic” refers to the region extending between the spinal cord and the thalamus. Spinothalamic,
Dorland’s                           Medical                           Dictionary                           Online,
https://www.dorlandsonline.com/dorland/definition?id=46603&searchterm=spinothalamic (last visited Nov. 23,
2020).
12
  Pleocytosis describes an elevated white blood cell count in the cerebrospinal fluid. Pleocytosis, Dorland’s Medical
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=39556&searchterm=pleocytosis (last
visited Nov. 23, 2020).

                                                        10
 Vascular and Other Causes of Myelopathy, 90 Neurology 12, 17 (2018), filed as Ex. 86 on Oct.
 21, 2019 (ECF No. 98-1) (“Barreras”). Dr. Zamvil also agreed that Mr.I.J.   did not demonstrate
 an elevate IgG index or Gadolinium enhancement on his initial August 8, 2013 MRI. Tr. at 81.
 However, given such a presentation, the TM Working Group diagnostic criteria recommends the
 performance of repeat MRI and lumbar punctures, between two to seven days following onset.
 Working Group at 500. In this case, the repeat MRI performed on August 17, 2013 did reveal
 enhancement consistent with TM, but a repeat CSF study was not performed (based on the filed
 medical record). Tr. at 69–70. Thus, Dr. Zamvil allowed that this criterion was not technically
 satisfied—though he speculated that pleocytosis would have been evident in subsequent CSF
 studies had they been performed. Id. at 69–70, 80–82.

        The last inclusionary criterion to be addressed was the timeframe in which Mr. I.J.
experienced progression to nadir. Tr. at 59–60, 64–66, 82–83. This factor, according to Dr. Zamvil,
is the most important in differentiating between myelitis and vascular etiologies. Id. at 58 (citing
Barreras at 12). The TM Working Group criteria indicates that a patient with TM would be
expected to reach nadir no sooner than four hours after the initial onset of symptoms. Working
Group at 500. Mr. I.J.'s symptoms progressed over the course of six hours, and Dr. Zamvil
concluded that he did not reach nadir until somewhere between eight to nine hours after the onset
of his symptoms. Tr. at 60. Thus, this time course was sufficient to meet the last inclusionary
criterion. Id. at 82–83.

        Dr. Zamvil next discussed the exclusionary criteria set forth in the TM Working Group
paper—those factors that, if present, argue against a TM diagnosis. Tr. at 83–84. He easily
concluded that Mr. I.J. did not satisfy most of the exclusionary criteria, but he ultimately
deferred to Dr. Watanabe, an expert in neuroradiology, regarding the second exclusionary
criterion—clear arterial distribution clinical deficit consistent with thrombosis of the anterior
spinal artery. Id. at 83–84. Based on his own preliminary review, however, he did not find evidence
of embolism or thrombosis despite the “standard” workup that was performed. Id. at 90.

        Besides vouching for TM as the proper diagnosis, Dr. Zamvil expressed the opinion that
the spinal cord infarction diagnosis included in the differential did not accurately characterize the
constellation of symptoms Mr. I.J. experienced. Tr. at 55–57. Because a spinal cord infarction
was a suspected cause of Mr. I.J.'s condition, he underwent a “bubble study.” 13 Id. at 55. The
results of that study showed that Mr. I.J. did not suffer from a right-to-left shunt—strong
evidence contradicting the conclusion that Petitioner’s injuries were vascular in nature. Id. at 56–
57. Additionally, the prolonged, “stuttering” onset Mr. I.J. experienced was more consistent
with TM than spinal cord infarction. Id. at 60. Mr. I.J. did not reach nadir until at least six hours
after the initial onset of his first symptom. Id. at 57. This, according to Dr. Zamvil, would be highly

13
  A “bubble study” or a contrast echocardiography is performed most commonly to evaluate heart wall motion (a
measure of heart wall function) and to detect valvular disease, evaluate the heart during stress testing, and identify and
quantify pericardial fluid. Mosby’s at 820.

                                                           11
 unusual for a spinal cord infarction, which more commonly presents in an “apoplectic” manner,
 with patients reaching nadir within minutes of onset. Id. at 59–60, 64–66; Barreras at 12, 16
 (finding that nearly ninety percent of study participants experiencing spinal cord infarction reached
 nadir in less than six hours while only four percent of participants experiencing spinal cord
 inflammation reached nadir within the same timeframe); Working Group at 500 (noting
 progression to nadir between four hours and twenty-one days following onset of symptoms is an
 inclusionary criterion for the diagnosis of TM). He acknowledged, however, that members of the
 stroke team who evaluated Mr.I.J.        did characterize the onset of his symptoms as “apoplectic,”
 and although he disagreed with this reading of the record, he acknowledged that he lacked expertise
 in vascular medicine. Tr. at 141–42.

        Dr. Zamvil further supported his opinion by distinguishing the effects TM has on dorsal 14
spinal column function versus the impact of an anterior spinal artery infarction. Tr. at 71–72, 87–
88. As he explained, infarction in the anterior 15 spinal artery (located on the front facing portion
of the spinal cord) will in turn impact the anterior and lateral portions of the cord itself, thereby
affecting motor function and spinothalamic perceptions while preserving dorsal column function.
Id. at 72. As a result, a patient experiencing an anterior spinal artery infarction would exhibit
problems with motor function, temperature, pain, and gross touch sensations, but would not
experience any changes to dorsal column functions such as proprioception, vibratory sense, and
fine touch perception. Id. Dr. Zamvil admitted that he could not definitively conclude whether Mr.
I.J. retained dorsal column function because the clinical testing for these functions was either
not performed or was done but not recorded. Id. at 72–73, 88. Instead, Dr. Zamvil relied on MRI
findings indicating posterior cord involvement to exclude a spinal cord infarction diagnosis. Id. at
86.

       Similarly, Dr. Zamvil acknowledged that Mr. I.J. was diagnosed with a “longitudinally
extensive myelopathy”—a condition that he agreed is more often the result of a vascular myopathy
(such as ischemic stroke) than inflammatory myopathies. Tr. at 148–49 (citing Barreras at 15).
Further still, Barreras found that twenty percent of study participants were initially misdiagnosed
with TM and were later found to have vascular abnormalities. Tr. at 145–46; Barreras at 15.

       Dr. Zamvil did, however, stress that other record evidence generally supported TM as the
more likely diagnosis. MRI results were consistent with TM, and treating physicians overall
seemed to embrace the TM diagnosis. Tr. at 53–54. Additionally, Mr. I.J. experienced some
improvement following treatment with Solumedrol, IVIG, and plasmapheresis—common

14
  The term “dorsal” refers to the back of or a position that is more towards the back surface than some other object of
reference.            Dorsal,              Dorland’s               Medical              Dictionary             Online,
https://www.dorlandsonline.com/dorland/definition?id=14794&searchterm=dorsal (last visited Nov. 23, 2020).
15
  The term “anterior” refers to the front of or more forward position of an organ. Anterior, Dorland’s Medical
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=3163&searchterm=anterior (last visited
on Nov. 23, 2020).

                                                         12
 treatments for neuroinflammatory conditions 16—though Dr. Zamvil was unable to discern the
 extent of that improvement. Tr. at 54. Dr. Zamvil also emphasized that in acute TM, both gray and
 white matter may be involved, and thus the involvement of gray matter does not preclude a TM
 diagnosis, further reducing the significance of MRI findings suggesting lesion involvement as
 encompassing both. Id. at 74.

         Dr. Zamvil next opined on the issue of causation. He testified to two potential mechanisms
 by which the Tdap vaccine could theoretically cause TM: molecular mimicry and innate immune
 activation through adjuvant activity. Tr. at 92, 101; Zamvil Rep. at 9–12. Dr. Zamvil explained
 that while not all vaccines can cause TM, vaccines containing the tetanus toxoid, such as Tdap,
 contain protein sequences that share structural homology with those of myelin-targeting
 autoantigens, and have been the subject of epidemiological studies seeking to identify relationships
 between vaccination and neurological conditions. Tr. at 92, 112–13 (citing R. Baxter et al., Acute
 Demyelinating Events Following Vaccines: A Case Centered Analysis, 63 Clinical Infectious
 Diseases 1456, 1456 (2016), filed as Ex. 16 Ref. 12 on Sept. 11, 2017 (ECF No. 32-3) (“Baxter”));
 Zamvil Rep. at 9.

         In the presence of sufficient homology, T cells and antibodies may (due to similarity
 between vaccine components and myelin proteins) engage in cross-reactivity against central
 nervous system myelin. Tr. at 92; Zamvil Rep. at 11. To ascertain if such homology existed, Dr.
 Zamvil conducted his own BLAST search 17 in which he reviewed the National Institutes of
 Health’s protein sequence database, comparing protein sequences contained within the Tdap
 vaccine with those commonly found in human myelin. Tr. at 92; Zamvil Rep. at 10–11. He found
 that there was significant sequential homology between these sequences, supporting the possibility
 of molecular mimicry as the pathogenic impetus. Zamvil Rep. at 11. However, though he described
 how molecular mimicry can lead to the development of other conditions such as experimental

16
    Solumedrol is an anti-inflammatory synthetic glucocorticoid. Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=89219 (last visited Dec. 14, 2020). Plasmapheresis is a
procedure in which plasma is removed from blood and is then transfused back into the body with added donor
components such as frozen plasma or albumin. Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=39455&searchterm=plasmapheresis (last visited Dec. 14,
2020). IVIG therapy is used to treat immune system disorders. During an IVIG treatment, immunoglobulin (a
combination of antibody proteins) is injected into the body to help the immune system fight off infections. See Primary
Immunodeficiency:     Treatment,       Mayo       Clinic,    https://www mayoclinic.org/diseases-conditions/primary-
immunodeficiency/diagnosis-treatment/drc-20376910 (last visited Dec. 14, 2020).
17
   Basic Local Alignment Search Tool (“BLAST”) is a medical/scientific internet resource that assists researchers in
finding regions of similarity between biological sequences of amino acids. The program compares nucleotide or
protein sequences to sequence databases and calculates the statistical significance. BLAST, U.S. National Library of
Medicine, https://blast ncbi nlm nih.gov/Blast.cgi (last visited Nov. 19, 2020). Research undertaken to identify such
homology has been previously described as an “in silica” study—meaning that the research is conducted via a desktop
or personal computer, and access to scientific databases, to identify the comparable amino acid sequences that is
referenced to establish homology. See, e.g., Blackburn v. Sec. of Health & Hum. Servs., No. 10-410V, 2015 WL
425935, at *10 (Fed. Cl. Spec. Mstr. Jan. 9, 2015). This kind of research is clearly case-oriented, and is not equivalent
to lab or clinical research that an expert might perform and/or rely upon for an opinion.

                                                          13
 autoimmune encephalomyelitis and narcolepsy, Dr. Zamvil admitted that he could not identify any
 studies concluding that Tdap can cause TM via this proposed mechanism. Tr. at 97, 136–37, 139,
 152.

         To further bulwark his proposed causal theory, Dr. Zamvil offered a study in which the
 incidence of TM and ADEM (a different neurologic disease with a likely autoimmune etiology or
 mechanism) following vaccination was studied. Tr. at 113–16; Zamvil Rep. at 7 (citing Baxter at
 1456). Baxter found that after nearly 64 million vaccine doses, only seven cases of TM and eight
 cases of ADEM were reported within 5 to 28 days post-vaccination. Baxter at 1456. While a
 relationship between vaccination and the development of TM could not be established, Baxter
 concluded that there was a statistically significant association between the Tdap vaccine and the
 subsequent development of ADEM. Id. at 1460. Dr. Zamvil opined that the causal relationship
 between Tdap and ADEM would be parallel to the expected relationship between Tdap and TM—
 Baxter’s express finding pertaining to TM to the contrary. Tr. at 116.

         Dr. Zamvil also relied on a series of case reports documenting instances of TM following
 vaccination. Tr. at 119–121; Zamvil Rep. at 7 (citing N. Agmon-Levin et al., Transverse Myelitis
 and Vaccines: A Multi-Analysis, 18 Lupus 1198, 1198–1204 (2009), filed as Ex. 16 Ref. 9 on Sept.
 11, 2017 (ECF No. 31-10) (“Agmon-Levin”)). Agmon-Levin highlighted forty-three case reports
 of TM following vaccination. Agmon-Levin at 1199. Of these, only four involved TM after
 receiving either the diphtheria-tetanus-pertussis vaccine or the diphtheria-tetanus vaccine. Id.
 Agmon-Levin also found that seventy-three percent of TM cases were reported within one month
 of vaccination, consistent with the timeframe Ms.I.J.     experienced. Id.

        Another case report cited by Dr. Zamvil documented acute transverse myelitis in a seven-
month-old child following receipt of the DTaP vaccine (a slightly different formulation of the same
vaccine that is administered to children). R.M.S. Riel-Romero, Acute Transverse Myelitis in a 7-
Month-Old Boy After Diphtheria-Tetanus-Pertussis Immunization, 44 Spinal Cord 688, 688–91
(2006), filed as Ex. 16 Ref. 11 on Sept. 11, 2017 (ECF No. 32-2) (“Riel-Romero”). Though the
treating physicians discussed in Riel-Romero noted several documented instances of TM following
receipt of the Tdap or other diphtheria-tetanus containing vaccine, they found that the temporal
association was not sufficient to establish a causal association and noted the possibility of mere
coincidence. Riel-Romero at 690. In relying on case reports generally, Dr. Zamvil acknowledged
the inherent limitations of such evidence, accepting that they could at bottom only show a temporal
relationship between vaccination and injury rather than provide scientifically-reliable causal proof.
Tr. at 120.

       Regarding the timeframe in which Mr. I.J. experienced the onset of his condition, Dr.
Zamvil opined that an autoimmune reaction would be expected to occur two to three weeks
following vaccination. Tr. at 98–100. Mr. I.J.'s symptoms began seventeen days after receipt of
the Tdap vaccine. Id. at 98. Thus, Dr. Zamvil concluded that the onset of Mr. I.J.'s condition
was consistent with an autoimmune reaction to his Tdap vaccination. Id.

                                                 14
         Dr. Zamvil also testified to the role adjuvants, such as alum, have in promoting pro-
 inflammatory responses. Tr. at 101. He explained that such a pro-inflammatory response may
 exacerbate autoimmune responses already initiated through cross-reactivity. Id.; S. Eisenbarth,
 Crucial Role for the Nalp3 Inflammasome in the Immunostimulatory Properties of Aluminum
 Adjuvants, 453 Nature 1122, 1122–25 (2008), filed as Ex. 16 Ref. 29 on Sept. 11, 2017 (ECF No.
 33-10) (“Eisenbarth”). This theory proposes that the alum adjuvant stimulates proinflammatory
 cytokine production via the Nalp3 innate immune response system. Eisenbarth at 1122. The
 proinflammatory cytokines such as interleukin-1β and interleukin-18 that are produced are
 associated with various aspects of adaptive immunity and antibody production. Id. at 1125.

       Lastly, Dr. Zamvil addressed whether the onset of Mr. I.J.'s symptoms seventeen days
post-vaccination was medically appropriate. He explained that the Tdap vaccine Mr. I.J.
received was a booster, and thus would have initiated a faster, amnestic response. Tr. at 98–100.
Thus, cellular and immune responses within one or two weeks would be expected. Id. He did not,
however, reconcile this proposed timeline (7-14 days) with Mr. I.J.'s onset seventeen days post-
vaccination. 18

            2. Dr. Alyssa Watanabe

        Dr. Watanabe, a neuroradiologist, provided testimony at the hearing and offered three
expert reports. Tr. at 161–225; Report, filed as Ex. 21 on Jan. 4, 2019 (ECF No. 52-1) (“Watanabe
Rep.”); Supplemental Report, filed as Ex. 63 on Oct. 10, 2019 (ECF No. 85-1) (“Watanabe Supp.
Rep.”); Supplemental Report, filed as Ex. 89 on April 24, 2020 (ECF No. 111-1) (“Third Watanabe
Rep.”). Dr. Watanabe opined that Mr. I.J. more likely than not suffered from TM as a result of
his Tdap vaccination. Watanabe Rep. at 22.

        Dr. Watanabe received her bachelor’s degree (biological sciences) from Stanford
University before receiving her medical degree from the University of California, San Francisco.
Curriculum Vitae of Dr. Watanabe, filed as Ex. 27 on Jan. 8, 2019 (ECF No. 53-1) (“Watanabe
CV”). She completed an internship in internal medicine at Huntington Memorial Hospital before
completing her residency in diagnostic radiology at the University of California, Los Angeles. Id.
at 1. Dr. Watanabe then completed several fellowships in neuroradiology and interventional
neuroradiology at the University of Washington and the University of Southern California, though
she elected to withdraw from her final fellowship in order to pursue a position in private practice.
Id.; Tr. at 203. She is board certified in radiology and has additional certifications in
neuroradiology. Watanabe CV at 1. Dr. Watanabe has held several positions as an instructor and
clinician in the fields of radiology and neuro imaging, although her most recent educational and
clinical activity at the University of Southern California has been in a volunteer capacity. Id. at 2;

18
   In his report, Dr. Zamvil again relied on a comparison to ADEM (a neurological condition that he agrees is
diagnostically distinguishable from TM), noting that it can occur within the proposed seventeen-day timeframe
proposed by Petitioner. Zamvil Rep. at 13.

                                                     15
 Tr. at 200–02. 19 She has also published numerous articles regarding radiology. Watanabe CV at
 4–11.

         Dr. Watanabe began by discussing angiography and the results of the August 8, 2013
 angiogram Mr.I.J.      underwent during his initial hospitalization. Tr. at 171. As she explained, the
 process of angiography includes rapidly injecting contrast dye during a CT scan in order to
 visualize the patient’s arteries. Id. Though some of the literature offered by Petitioner questioned
 the efficacy and reliability of angiography in diagnosing ischemic events such as infarction, Dr.
 Watanabe opined that such tools could still be helpful when the clinical picture is unclear. Id. at
 216–18; M. Vargas et al., Spinal Cord Ischemia: Practical Imaging Tips, Pearls, and Pitfalls, 36
 Am. J. Neuroradiology 825, 828 (2015), filed as Ex. 24 on Jan. 4, 2019 (ECF No. 52-4). Mr.I.J.
 underwent a CT angiogram on August 8, 2013, and according to Dr. Watanabe, its results did not
 reveal any vascular abnormalities. Tr. at 171–72; Watanabe Rep.at 6–7. These findings thus
 eliminated some of the most common etiologies of spinal cord infarction from consideration. Tr.
 at 171–72.

         Dr. Watanabe next addressed the MRI imaging results that were obtained throughout the
three-week period of Mr. I.J.'s hospitalization. Tr. at 173. The first MRI image to be addressed
was obtained on August 8, 2013. Id.; Watanabe Rep. at 7–8; Ex. 8D, filed Jan. 4, 2019 (ECF No.
50-4). In Dr. Watanabe’s view, it revealed “a very long segment of abnormal signal enhancement
throughout his cervical and going down into the thoracic cord,” which was initially interpreted to
be compatible with a diagnosis of TM. Id. at 173. Dr. Watanabe agreed with this interpretation,
though she acknowledged that these results were also compatible with other disease processes such
as stroke and polio. Id. at 173, 175. She also agreed that there was no evidence of enhancement in
this initial MRI (which would have suggested the presence of an active inflammatory process). Id.
at 209, 218. She later noted, however, that up to forty percent of patients experiencing TM will
have no MRI findings with initial enhancement, diminishing the significance of its absence. Id. at
211; Watanabe Supp. Rep. at 2 (citing G. Scotti & S. Gerevini, Diagnosis and Differential
Diagnosis of Acute Transverse Myelopathy. The Role of Neuroradiological Investigations and
Review of the Literature, 22 Neurological Sci. Supp. 69, 69–73 (2001), filed as Ex. 64 on Oct. 10,
2019 (ECF No. 85-2).

        The second MRI images reviewed by Dr. Watanabe were obtained on August 17, 2013. Id.
at 177; Ex. 9B, filed Jan. 4, 2019 (ECF No. 50-7). These follow-up images revealed Gadolinium
enhancement—consistent with an inflammatory process and a breakdown of the blood-brain-

19
   Dr. Watanabe’s credibility was somewhat diminished during cross examination, when she revealed that she is not
a listed faculty member on the University of Southern California Medical School’s website despite identifying herself
as a USC “Clinical Instructor” on her CV. Tr. at 201; Watanabe CV at 2. She also admitted that the work she does
there is done primarily on a “volunteer” basis—a detail that was not included in either her CV or her direct testimony.
Tr. at 201; Watanabe CV at 2. While these admissions somewhat undermined the probative value of Dr. Watanabe’s
testimony, I do not find that they established a firm basis for questioning the honesty or accuracy of her testimony or
opinions, which (except for the points she attempted to make about causation) largely stemmed from her professional
radiologic expertise.

                                                         16
 barrier—that had not been present in the initial August 8th MRI. Tr. at 177–78, 193. Dr. Watanabe
 explained this absence from the initial MRI study as the likely result of the MRI being conducted
 so close in time to the onset of the disease process. Id. at 178. She also noted that the abnormal
 signal was limited to the posterior portion of the spinal cord—opposite from the location of the
 anterior spinal artery. 20 Id. at 178–79. In her view, an anterior spinal artery infarction would not
 affect the posterior segment of the spinal cord. Id. In addition, TM often features signal
 abnormalities distributed throughout both the anterior and posterior segments of the cord, in a
 pattern of two round bright spots known as “owl eyes” or “snake eyes,” though similar features
 may be present after a spinal cord infarction. Id. at 179–80, 194–95. This abnormality establishes
 damage to the anterior horn cells. Id. at 194. In 2016, three years after the initial onset of his
 symptoms, follow-up MRI imaging continued to reveal this pattern of damage in Mr.I.J.'s
 spinal cord, further supporting TM over infarction. Id.; Ex. J, filed Sept. 17, 2019 (ECF No. 78-1).

         The MRI imaging studies overall also revealed holocord involvement and mild diffusion
restriction. Tr. at 182–84, 190; Ex. 9F at 2. As Dr. Watanabe explained, holocord involvement
means that both the gray and white matter of the spinal cord are affected. Tr. at 182–83. She opined
that this pattern of involvement is typical of TM. Id. at 181, 183–84. She also explained that
diffusion restriction is a process in which the diffusion of water between cell membranes of tissue
in the body becomes impaired. Id. at 190. Although diffusion restriction is associated with TM, it
can also be seen in other conditions such as tumors, and abscesses, and she further explained that
it is “one of the most distinctive findings that one would expect for a stroke.” Id. at 190, 219; Y.
Kim et al., The Role of Diffusion-Weighted MRI in Differentiation of Ideopathic Acute Transverse
Myelitis and Acute Spinal Cord Infarction, 65 J. Kor. Soc’y Radiology 101, 101–08 (2011), filed
as Ex. 25 on Jan. 4, 2019 (ECF No. 52-5).

        Because mild restriction diffusion was noted in Petitioner’s August 17th MRI, a spinal
angiogram was ordered and was performed on August 21, 2013. Tr. at 184, 189. That angiogram,
Dr. Watanabe concluded, provided no evidence of vessel cutoff, 21 with the anterior spinal artery
appearing to her to be intact. Id. at 185. Though she acknowledged treater documentation of a
“cutoff,” Dr. Watanabe attributed this misinterpretation to how the results of the angiogram were
communicated by the treating radiologist. Id. at 224. Thus, notes regarding a cutoff do not support
a diagnosis of spinal cord infarction, but they likely mislead treaters to that conclusion. Id. at 189.

       Dr. Watanabe also noted that there was no evidence of a blood clot at the time the
angiogram was performed, but she acknowledged the possibility that a previously existing clot

20
   Dr. Watanabe acknowledged, however, that dorsal column involvement was not documented by any of Mr. I.J.'s
treating physicians, but she nonetheless maintained that her review of the MRI images revealed posterior cord
involvement. Id. at 222–23.
21
  Dr. Watanabe used the term “cutoff” to describe an occlusion within the anterior spinal artery—something that she
did not see in Mr. I.J.'s spinal angiogram. Tr. at 186–87. If an occlusion is present, the dye that is injected into the
artery will abruptly stop, or “cutoff,” within the vessel. Id. at 187.

                                                          17
        (that could have precipitated Petitioner’s symptoms) had dissolved. Tr. at 188. The absence of a
        clear cutoff or blood clot within the anterior spinal artery was further proof to Dr. Watanabe that
        a spinal cord infarction was an unlikely explanation for the radiological findings. Id. She did
        observe a narrowing of the anterior spinal artery in the angiogram, but attributed it to inflammation
        of the cord. Id. at 192. This opinion was supported by evidence of patchy enhancement—a finding
        consistent with inflammation—on the August 17th MRI. Id. at 193.

                Based predominantly on the August 17th MRI imaging, Dr. Watanabe concluded that Mr.
       I.J.    more likely than not experienced TM rather than a spinal cord infarction. Tr. at 197. Her
        overall impression was that the subsequent imaging did not evidence an embolism or thrombotic
        event. Id. She admitted, however that the Working Group diagnostic criteria requires that all
        inclusionary criteria are met while all exclusionary criteria are eliminated before a TM diagnosis
        can be accepted. Id. at 208 (citing Working Group at 500). She similarly acknowledged that Mr.
I.J.     did not strictly meet these criteria, given the absence of pleocytosis and the lack of
        enhancement on his initial MRI—though she argued that the MRI performed nine 22 days after the
        onset of his symptoms did show evidence of the required enhancement. Tr. at 209–10. To
        substantiate her position in light of these criteria (and Mr.I.J.'s  clinical picture), Dr. Watanabe
        opined that clinical judgment is not bound by rigid restrictions set forth on paper. Tr. at 210. This
        argument was undercut by the medical record itself, however, because treating physicians did not
        unequivocally conclude that Mr.I.J.       suffered from TM. See, e.g., Ex. 2 at 7 (listing discharge
        diagnoses as tetraplegia, spinal cord infarction, and thrombophilia).

               On rebuttal, Dr. Watanabe explained her process for reviewing MRI images, including a
       description of the computer program and monitors that allowed her to review the images obtained
       during Mr. I.J.'s initial hospitalization. Tr. at 390–91. Utilizing such technology, Dr. Watanabe
       observed that the majority of slides showed posterior cord involvement—contrary to the
       contentions of Respondent’s expert. Id. at 316–18, 391–92. She again reiterated that posterior cord
       involvement is not consistent with the “well defined geographic distribution” seen in anterior
       spinal artery infarcts. Id. at 393. Dr. Watanabe also noted that the initial MRI performed on Mr.
       I.J. on August 8, 2013 (approximately eight hours after onset) was conducted with diffusion-
       weighted imaging (“DWI”) 23, though she acknowledged that this was unusual, and she was unable
       to explain why DWI had been performed. Id. at 394, 396. According to Dr. Watanabe, that August
       8th study did not show diffusion restriction—a characteristic that both she and Respondent’s expert
       agreed would have been present if Mr. I.J. had in fact suffered a spinal cord infarction. Id. at

       22
         Dr. Watanabe did concede that the Working Group diagnostic criteria require that repeat imaging studies, such as
       an MRI, be repeated 2-7 days following onset, and that Mr. I.J.'s second MRI was performed outside of this
       recommended timeframe. Tr. at 210.
       23
          The DWI technique uses water movement within the body to create a diagnostic image. See M. Thurnher & R.
       Bammer, Diffusion-Weighted MR Imaging (DWI) in Spinal Cord Ischemia, 48 Neuroradiology 795, 799 (2006), filed
       as Ex. 70 on Oct. 10, 2019 (ECF No. 86-4).

                                                              18
394–96. These observations bulwarked Dr. Watanabe’s opinion that Mr. I.J.          more likely than
not had experienced TM rather than a spinal cord infarction.

        Dr. Watanabe’s reports and testimony also touched in part on whether the Tdap vaccine
can cause TM, and she offered some additional case reports to support the contention. See, e.g.,
Tr. at 214–15, 221 (citing N. Gregg et al., Tdap Vaccination and Acute Demyelinating Events, 88
Neurology 1, 1–6 (2017), filed as Ex. 66 on Oct. 10, 2019 (ECF No. 85-4) (“Gregg”)). However,
such opinions greatly exceeded her professional expertise or knowledge, and since Dr. Zamvil was
by contrast well qualified to offer testimony and opinions on these matters, I have not given the
opinions she offered on this aspect of Petitioner’s case much, if any, weight.

       3.      Dr. Mark Levin

       Dr. Levin, a hematologist, provided testimony and submitted a single expert report. Tr. at
231–90; Report, filed as Ex. 39 on Aug. 22, 2019 (ECF No. 68-1) (“Levin Rep.”). Following a
review of the medical record and the reports filed by Drs. Zamvil, Watanabe, and Alexander, Dr.
Levin concluded that Mr. I.J.'s overall hematologic condition was insufficient to support a
diagnosis of spinal cord infarction. Levin Rep. at 5; Tr. at 236.

        Dr. Levin received his bachelor’s degree from Yeshiva University, followed by a medical
degree from SUNY – Downstate Medical College. Dr. Levin Curriculum Vitae, filed as Ex. 62 on
Sept. 26, 2019 (ECF No. 81-1) (“Levin CV”). He subsequently obtained his master’s in business
administration from Herriott-Watt University in Scotland. Id. at 1. After obtaining his medical
degree, Dr. Levin completed his internship and residency in internal medicine at New York
Downtown Hospital and Hahnemann University Medical Center. Id. He also completed post-
doctoral training in hematology and oncology at the Long Island Jewish Hillside Hospital Medical
Center. Id. Dr. Levin is board certified in internal medicine and oncology. Id. While he has
previously held board certification in hematology, he has not sought recertification since 2000. Id.;
Tr. at 232, 258. Throughout his career, Dr. Levin has served as an associate professor of medicine
at several academic institutions in addition to his role as an attending clinician. Levin CV at 2. On
average, Dr. Levin sees approximately 400 patients a year, and has experience in evaluating
patients for stroke, though he indicated that such evaluations only happened “on occasion.” Tr. at
234. Beyond his clinical duties, Dr. Levin has also published numerous journal articles and
abstracts on topics within the fields of oncology and hematology. Levin CV at 6–11.

        The first hematologic factor addressed by Dr. Levin was Mr. I.J.'s family history of
venous thromboembolism (“VTE”), and whether it was significant in this case for diagnostic
purposes. Tr. at 237–39, 263; Levin Rep. at 2–3. Dr. Levin opined that a family history of VTE
alone was an insufficient basis for concluding that Mr. I.J. had an increased prothrombotic risk.
Tr. at 237–38; Levin Rep. at 2. He explained that genetic risk alone is quite low—Mr. I.J.'s
records did not contain any evidence for genetic risk beyond the family history notation—and
environmental factors may play a large role in the development of VTE. Tr. at 237–39; Levin Rep.

                                                 19
 at 2–3 (citing F. Couturaud et al., Factors that Predict Thrombosis in Relatives of Patients with
 Venous Thromboembolism, 124 Blood 2124, 2129 (2014), filed as Ex. 40 on Aug. 22, 2019 (ECF
 No. 68-2)). In addition, Dr. Levin noted that he lacked background evidence regarding the
circumstances and context in which Mr. I.J.'s relatives experienced VTE, making it impossible
for him to determine whether Mr. I.J. was at an increased risk for a prothrombotic condition.
Levin Rep. at 3. He also clarified that in his view Mr. I.J. did not suffer from VTE or a deep
vein thrombosis (“DVT”), adding that a venous clot such as VTE or DVT is “essentially the same
phenomenon” as an arterial clot such as what could be seen in an anterior spinal artery infarction.
Tr. at 264–45.

       Dr. Levin next addressed clotting risk and its relationship to Factor VIII levels (given the
findings of elevated Factor VIII levels for Mr. I.J.   Tr. at 239. As he explained, Factor VIII is
one of several hematologic requirements for blood clotting. Id. at 239–40. Factor VIII levels
average at about 100—and if too low can result in hemophilia, or the inability to clot. Id. at 240.
By contrast, when Factor VIII levels are too high, dangerous excessive clotting can occur. Id.

        Mr. I.J. presented with an elevated Factor VIII level of 196, consistent with the risk
factors associated with greater clotting like thrombosis or infarction. Id.; Ex. 2 at 166. While
treating physicians found this clinically significant, Dr. Levin attributed this elevation to
Petitioner’s alleged TM (and hence consistent with the diagnosis favored in Petitioner’s overall
claim). As he noted, inflammation—such as that seen within the spinal cord of a patient suffering
from TM—commonly leads to a secondary increase in Factor VIII. Tr. at 240–42, 282; Levin Rep.
at 4. This explanation thus relies on the assumption that spinal cord inflammation would have
systemic effects, but Dr. Levin did not provide any medical literature to support this supposition,
and he conceded that elevated Factor VIII levels can also occur after an infarction (and hence be
evidence of a propensity for the circumstances leading to infarction). Tr. at 283–84, 288–90.

        The next risk factor addressed by Dr. Levin was that of obesity. Tr. at 243–44; Levin Rep.
at 3. At the time of his hospital admission, Mr. I.J. had a body mass index (“BMI”) 24 of 32. 25
Ex. 2 at 942. Dr. Levin explained that while a BMI over 30 meets the clinical requirement for
obesity, Mr. I.J. just barely met that criterion, and this (coupled with his relatively young age)
would reduce the significance of this finding. Tr. at 243–44. Thus, it was Dr. Levin’s opinion that
Petitioner’s at worst mild obesity did not make it any more likely that he suffered from a spinal
cord infarction despite acknowledging that obesity is typically associated with an increased risk of

24
  An individual’s BMI is a measure of body fat that gives an indication of nutritional status. Body Mass Index,
Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=82333 (last visited
Nov. 23, 2020).
25
   In his report, Dr. Zamvil noted that Mr. I.J.'s BMI at the time of admission was 31.6. Zamvil Rep. at 3. The
medical record indicates, however, that Mr. I.J.'s BMI on August 8, 2013 was actually 32. Ex. 2 at 942. The
distinction between the two numbers is not large enough to give it great evidentiary significance.

                                                      20
stroke. Id. at 244, 276–78.

        Dr. Levin also discussed the role marijuana use 26 may have played in Mr. I.J.'s clinical
presentation. Tr. at 244–45; Levin Rep. at 3. He acknowledged that marijuana is a risk factor for a
number of cardiovascular problems, but he did not find it to be significant for an increased
prothrombotic risk. Id. at 244. His review of the relevant literature revealed only one report that
described two cases of marijuana-induced VTE—a condition Mr. I.J. did not suffer from. Id. at
244; D. Salhan et al., Cannabis-Induced VTE: Is it a Safe Recreational Drug?, 150 Chest Supp.
909A, 909A (2016), filed as Ex. 41 on Aug. 22, 2019 (ECF No. 68-3) (“Salhan”). Dr. Levin
acknowledged, however, that Salhan cited marijuana consumption as a risk factor for ischemic
stroke. Tr. at 275–76. He concluded nonetheless that marijuana consumption did not increase the
likelihood that Mr. I.J. had experienced a spinal cord infarction. Id. at 244–45.

        Finally, Dr. Levin compared incidence rates between TM and spinal cord infarction,
finding that while both conditions are relatively rare, TM is more common, occurring in 3 per
100,000 person-years, 27 while primary and secondary spinal cord infarction occurs at a rate of 1.5
and 1.6 per 100,000 person-years respectively. 28 Tr. at 242; Levin Rep. at 3–4; A. Qureshi et al.,
A Population-Based Study of the Incidence of Acute Spinal Cord Infarction, 9 J. Vascular
Interventional Neurology 44, 44 (2017), filed as Ex. 43 on Aug. 22, 2019 (ECF No. 68-5); T. West
et al, Acute Transverse Myelitis: Demyelinating Inflammatory, and Infectious Myelopathies, 32
Seminars Neurology 97, 97 (2012), filed as Ex. 44 on Aug. 22, 2019 (ECF No. 68-6). This, he
seemed to suggest, further made it more likely that Mr. I.J.'s injury was TM (although opining
on statistical/epidemiologic issues like illness risk exceeded Dr. Levin’s expert qualifications).

           C.       Respondent’s Expert - Dr. David Alexander

        Dr. Alexander, a neurologist, acted as Respondent’s sole expert, providing testimony at the
entitlement hearing in addition to preparing three reports. Tr. at 291–389; Report, filed as Ex. A
on Feb. 28, 2018 (ECF No. 41-1) (“Alexander Rep.”); Supplemental Report, filed as Ex. N on
Sept. 20, 2019 (ECF No. 79-1) (“Alexander Supp. Rep.”); Supplemental Report, filed as Ex. O on
Jan. 2, 2020 (ECF No. 107-1) (“Third Alexander Rep.”). Dr. Alexander opined that Mr. I.J.

26
     Medical records from Mr. I.J.'s   initial admission note marijuana use in his social history. Ex. 2 at 38, 64, 79, 312.
27
   The person years metric identifies the actual amount of time—in years—that an individual is at risk. See L.
Alexander et al., Calculating Person-Time, ERIC Notebook – University of Chapel Hill Department of Epidemiology,
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwiSwcb1_c3tAhUlxVkKHt
AhUlxVkKHWlmCsoQFj&url=https%3A%2F%2Fsph.unc.edu%2Ffiles%2F2015%2F07%2Fnciph_ERIC4.pdf&us
u=AOvVaw0KRjpRECJsQZt-9DhcmkuQ (last visited Dec. 14, 2020).
28
  At hearing, Dr. Levin represented that TM occurs at a rate of three percent while spinal cord infarction occurs at a
rate of 0.6 percent. Tr. at 242. This statement was likely made in error. Dr. Levin’s report, however, is consistent with
the literature, and accurately reflects that secondary spinal cord infarction occurred in 0.0016 percent of study
participants, while TM occurred in 0.003 percent of study participants. Levin Rep. at 3–4.

                                                            21
more likely than not experienced an anterior spinal artery infarction, as opposed to TM, and that
his condition was caused by factors other than the Tdap vaccine. Tr. at 299.

        Dr. Alexander received his bachelor’s degree (neuroscience) from Amherst College before
obtaining his medical degree from the University of Minnesota Medical School. Updated Dr.
Alexander Curriculum Vitae at 1, filed as Ex. Q on Jan. 2, 2020 (ECF No. 107-3) (“Alexander
CV”). He then completed an internship in internal medicine at Boston University Medical Center
followed by a residency in neurology at Columbia Presbyterian Medical Center’s Neurological
Institute of New York. Id.; Tr. at 292. Dr. Alexander is board certified in neurology with
subspecialties and certifications in vascular neurology, neurorehabilitation, and spinal cord
medicine. Alexander CV at 2. He has held several academic positions at the University of
California, Los Angeles Medical School’s department of neurology, and he has held the position
of full-professor there since 2008. Id. at 2–3; Tr. at 292.

        Dr. Alexander presently serves as the medical director and vice chief of staff for the
California Rehabilitation Institute—an in-patient facility that is primarily focused on neurological
rehabilitation. Alexander CV at 3; Tr. at 293. Throughout his career, Dr. Alexander has treated
between twenty and fifty patients with TM, but has treated thousands of patients who suffered
from a stroke. Tr. at 294. In addition to his clinical and academic duties, Dr. Alexander has
published several articles on subjects within the field of neurology and neurorehabilitation, though
he primarily focuses on his clinical practice and academic responsibilities rather than research.
Alexander CV at 11–14; Tr. at 295–96.

       Dr. Alexander began by reviewing relevant definitions and the TM diagnostic criteria set
forth in the TM Working Group paper. Tr. at 302–05. TM describes general spinal cord
inflammation, and can be secondary to other conditions such as NMO, MS, and/or Lupus. Id. at
301–02. If a pre-existing causal infection cannot be identified, then the TM is deemed idiopathic.
Id. He emphasized that, overall, “it is pretty easy to be wrong about [TM],” and agreed that
Barreras found that up to fifty percent of TM diagnoses are wrong, with a large number of those
misdiagnosed patients actually suffered from a vascular abnormalities. Id. at 341–42 (citing
Barreras at 15).

        Dr. Alexander largely echoed the testimony of Dr. Zamvil regarding the proper criteria for
a TM diagnosis (as embraced by the TM Working Group), but differed drastically in how to
understand or apply those criteria. In particular, while Dr. Zamvil advocated for their flexible
application, Dr. Alexander proposed they be utilized in a more stringent manner. See Tr. at 300,
302–05, 375. He also took issue with Dr. Zamvil’s testimony regarding gray matter involvement.
Id. at 304. According to Dr. Alexander, TM primarily targets white matter, and will not typically
affect gray matter. Id. at 304.

       Next, Dr. Alexander explained the process of diagnosing spinal cord infarction (in
connection with his overall contention that the record best supports that as the proper diagnosis

                                               22
 over TM). Tr. at 305–06. Spinal cord infarction—which accounts for only one percent of all
 strokes—is characterized by sudden onset of bilateral signs and symptoms. Id. at 305, 313. These
 symptoms may develop over the course of hours, but timely administration of treatment can
 reverse ischemic damage. Id. at 329.

         Dr. Alexander also focused on the extent of gray matter involvement, which he explained
 tends to be more extensive following a spinal cord infarction, because it is more sensitive to
 ischemia. Tr. at 305. Gray matter involvement in the anterior horn cell area following a spinal cord
 infarction may manifest as snake or owl eyes sign on MRI imaging studies. Id. at 309–10;
 Alexander Rep. at 8. He also disputed the efficacy of angiography in diagnosing spinal cord
 infarction, noting that although it is an imaging test commonly used to diagnose vascular problems
 (such as arteriovenous malformations or arteriovenous dural fistulas), it is rarely used for purposes
 of diagnosing a suspected spinal cord infarction. Tr. at 312, 366. The usefulness of angiography is
 further reduced by the fact that clots are often resorbed, broken down, or embolized before an
 angiogram can be performed. Id. Dr. Alexander estimated that approximately seventy-five percent
 of all spinal cord infarctions have no identified etiology, and he thus did not find it unusual that
 Mr.I.J.'s
       treating physicians did not propose an etiology for his suspected infarction—though
 some documentation was made in the record regarding his procoagulant state. Id. at 313–14, 336–
 37.

        MRI imaging in a patient who has suffered a spinal cord infarction is typically negative for
enhancement, but DWI—what he deems the “gold standard” measure for stroke assessment—may
be positive within fifteen minutes of ischemic changes. Tr. at 307–08, 323, 379–80. DWI
positivity, however, will fade within a couple of days. Id. at 379–80. He also allowed that DWI
positivity can be seen in some instances of TM, though he disputed the probative value of case
studies documenting this phenomenon. Id. at 383–84 (citing Kim at 103). Similarly, the presence
of “watershed” abnormalities, which reflect and are attributable to reduced circulation and
diminished vascular supply, are also consistent with spinal cord infarction. Id. at 310–11. But Dr.
Alexander also noted that CSF and dorsal column function are not typically affected in the event
of an anterior spinal artery infarction. Id. at 305–06.

       Another point of dispute raised by Dr. Alexander was Petitioner’s experts’ use of the term
“holocord” to describe transverse involvement of the spinal cord. Tr. at 308; Alexander Rep. at 8.
In his view, “holocord” more accurately defines longitudinal involvement of the spinal cord,
beginning at the cervicomedullary junction in the neck and extending all the way down to the
conus, or tail, of the spinal cord. Tr. at 308; Alexander Rep. at 8. Dr. Alexander’s review of the
record did not reveal evidence of the extensive longitudinal involvement contemplated by his
proposed definition. Tr. at 308.

        Based on his review of the medical record, Dr. Alexander concluded that Mr. I.J. more
likely than not suffered an acute spinal cord infarction in the cervical region. Tr. at 314. This
determination began with the discharge diagnosis, in which treating physicians who had attended

                                                23
 to Petitioner throughout his illness documented tetraplegia, spinal cord infarction, and
 thrombophilia, but shied away from TM in the final differential. Id. at 314, 340; Ex. 2 at 4, 7. He
 further bulwarked his conclusion by referring to the results of Mr.I.J.'s          MRI studies. Dr.
 Alexander noted that the “long linear white streak down . . . the more anterior portion of the cord”
 seen in the MRI conducted on August 8, 2013, was consistent with the “typical pencil-shaped
 lesion that you see in spinal cord infarction,” along with evidence of ventral cord preservation. Tr.
 at 300–01, 316 (citing Ex. 87 at 2). More specifically, Dr. Alexander opined that in cases of TM,
 one would expect to see “more involvement of the cord” (evidenced by enhancement) rather than
 a discreet stripe or contained anterior horn involvement. Tr. at 318.

        Though the MRI images obtained on August 17, 2013 showed some evidence of dorsal
 column involvement, Dr. Alexander noted that this finding had only been emphasized during Dr.
 Watanabe’s hearing testimony. Tr. at 321. But even if accurate, Dr. Alexander considered this
 finding to be not particularly noteworthy, because the anterior horn cells of the central gray matter
 remained the area of greatest involvement. Id. at 321–22, 361–63. Similarly, the patchy
 enhancement seen in the second MRI, though admittedly a potential sign of TM-related
 inflammation, can also evidence spinal cord infarction in thirty to forty percent of cases. Id. at 324,
 382–83. Ultimately, while he did not dispute the finding of dorsal cord involvement, Dr. Alexander
 concluded that the overall presentation was more consistent with a spinal cord infarction. Id. at
 379.

         Dr. Alexander also raised the possibility that the “enhancement” documented in the second
 August 2013 MRI (but not seen in the first) may not actually have reflected enhancement
 attributable to cord inflammation, but rather a phenomenon known as “luxury perfusion,” whereby
 blood flow is increased to an area previously affected by an infarction. Tr. at 324–25. Additionally,
 Dr. Alexander opined that the DWI positivity seen in the second MRI was further evidence of an
 acute spinal cord infarction, given the importance of that finding in diagnosing infarction
 generally. Id. at 323. He did acknowledge, however, that if viewing the August 17, 2013 MRI in
 isolation, it could support a diagnosis of TM (although he still maintained the overall record leaned
 against that conclusion). Id. at 322, 325. He furthered this contention by noting that the MRI study
 conducted on November 15, 2016—three years after the onset of Mr.I.J.'s                   condition—
 evidenced a “primarily ventral change” (which he interpreted as a pencil-shaped lesion in the
 anterior horn) and an owl’s eyes abnormality, both of which he argued supported a diagnosis of
 spinal cord infarction. Id. at 323–24.

        Besides the above, Dr. Alexander disputed Dr. Watanabe’s findings regarding the
watershed abnormality seen on the August 17, 2013 MRI. Tr. at 325–26. Whereas Dr. Watanabe
interpreted the abnormality to extend beyond the area of expected involvement following an
anterior spinal artery infarction, Dr. Alexander expressed the opinion that the longitudinal position
of the abnormality, plus its posterior cord involvement, were more consistent with an acute spinal
cord infarction, and the extent of these abnormalities actually evidenced the central area of
maximum infarction and ischemia. Id. at 196, 311–12, 325–26.
                                                 24
          Dr. Alexander also deemed the August 21, 2013 spinal angiogram as supportive of his
  theory. Tr. at 333; Ex. 2 at 451–52. The attenuation, filling defect, and segmental narrowing of the
  anterior spinal artery that Dr. Watanabe agreed it revealed were consistent with a thrombotic event
  such as an ischemic stroke. Tr. at 333–34. Even though a clot was not visible in the angiogram, he
  explained that clots often dissolve, leaving behind residual arteriole narrowing. Id. at 334–35. Dr.
  Alexander also addressed the “cutoff” discussed by Dr. Watanabe. Id. at 333. After reviewing the
  angiogram report, he highlighted the note regarding an abrupt attenuation and filling defect at the
  C6 level. Id. at 334; Ex. 2 at 452. He admitted, however, that the term “cutoff” was not used in the
  record. Tr. at 367. Nonetheless, he concluded that a vessel abnormality existed, and he agreed with
  the radiological interpretation noting “discontinuity” within the vessel. Id. at 368. And even if Dr.
Watanabe was correct that Mr. I.J. had not experienced a cutoff of the vessel, treating physicians
on the stroke team still believed Mr. I.J. suffered an infarction. Id. at 334. Further still, Dr.
Alexander emphasized that strokes do not require complete vessel occlusion, and the same
treatment would likely be rendered regardless. Id. at 334, 369–70.

        Ultimately, after applying the TM Working Group diagnostic criteria, Dr. Alexander
concluded that a diagnosis of TM was not supported by the medical record. Tr. at 317. The initial
August 2013 MRI study did not reveal enhancement, and neither the MRI nor CSF studies 29
produced evidence of inflammation that would occur in the presence of a central nervous system
demyelinating event. Id. at 317–18, 331. Additionally, the total area of cord involvement was fairly
limited, and was confined to the anterior horn cells thus preserving posterior column functions—
though the total area of involvement was sufficient to cause the neurological symptoms Mr. I.J.
experienced. Id. at 318, 335–36. Dr. Alexander found such limited cord involvement to be more
consistent with a spinal cord infarction than TM. Id. at 316.

       The thrombophilia studies—and more specifically the finding of elevated Factor VIII
levels—also supported Dr. Alexander’s proposed diagnosis. Though Dr. Zamvil attributed this
finding to the inflammatory processes specific to TM, Dr. Alexander argued that the limited
amount of tissue involved in TM is not enough to provoke systemic inflammation. Tr. at 343. Dr.
Alexander’s argument was further substantiated by the lack of evidence showing either local or
systemic inflammation. Id. at 343–44. Regardless of whether Mr. I.J. suffered from TM or spinal
cord infarction, Dr. Alexander believed that he would have exhibited elevated Factor VIII levels
given the overall nature of his physical condition. Id. at 344.

        Dr. Alexander further distinguished the competing diagnoses based on the timeframe in
which Mr. I.J. experienced the initial onset of his symptoms. He opined that a sudden onset and
rapid deterioration like that experienced by Mr. I.J. when he was boarding the bus and reaching
for his wallet was indicative of an apoplectic event such as vascular infarction, and not consistent

29
  Dr. Alexander did allow for the possibility that immediate steroid treatment could mask pleocytosis, but he did not
believe this point was applicable because his understanding was that Mr. I.J. did not receive steroid treatment until
after the CSF study was completed. Tr. at 358.

                                                        25
 with how an inflammatory myelitis, such as TM, would present. Id. at 306–07, 319, 326–31, 372.
 Dr. Alexander also articulated that if Mr.I.J.had been suffering from TM, and the inflammatory
 process had started two weeks post-vaccination as proposed by Petitioner, then the acute nature of
 his symptoms onset was made even less likely. Id. at 327, 372. But Dr. Alexander also pointed out
 that treaters characterized the onset of Mr.I.J.'s      condition as “apoplectic,” thus undermining
 Petitioner’s proposed timeline of events. Id. at 373.

        Further, the stepwise, stuttering progression of Mr. I.J.'s symptoms was consistent with
collateral circulation following the initial onset of a spinal cord infarction. Id. at 329–30. This is
due to the body’s attempt to compensate and avoid ischemic damage by increasing blood flow to
the spinal cord. Id. This process, however, is not sustainable, and the failure of this system results
in ischemic damage to the cord. Id. at 330. Dr. Alexander also explained that back pain like that
experienced by Mr. I.J. at the initial onset of his symptoms is typical of a spinal cord infarction,
but not of TM. Id. at 319, 327. On cross examination, however, Dr. Alexander did admit that the
overall timeline of symptom progression did fit the accepted temporal period for onset of TM
(between four hours and twenty-one days), and that treaters seemed to recognize, consistent with
Petitioner’s testimony, that Mr. I.J. had experienced progressive symptoms over the course of
six to eight hours. Id. at 375–76. He maintained, however, that patients suffering from a spinal
cord infarction could also reach nadir within the same timeframe. Id. at 342.

       Dr. Alexander next addressed how the treatments Mr. I.J. received factor into
determining a proper diagnosis. While Dr. Zamvil emphasized the role of treatments Mr. I.J.
received and his subsequent improvement in forming his opinions, Dr. Alexander disputed the
diagnostic significance of these points. Tr. at 338–39. He noted that the improvements Mr. I.J.
experienced were mostly sensory in nature, and he opined that those improvements could have
been spontaneous. Id. He further explained that steroid treatment is non-specific and is not
necessarily indicated when TM is suspected. Id. Similarly, Dr. Alexander argued that the IVIG
treatment Mr. I.J. received is also non-specific and has not been demonstrated to be an effective
treatment for TM—though it is widely administered to TM patients and Mr. I.J. was noted as
having “marked improvement” following IVIG treatment. Id. at 352–56. He did ultimately admit
that Mr. I.J.'s improvement subsequent to his IVIG treatment could evidence an inflammatory
condition. Id. at 352–55, 357.

       After the entitlement hearing, Dr. Alexander submitted a second supplemental report
addressing Dr. Watanabe’s interpretation of the DWI MRI obtained on August 8, 2013, as well as
her conclusion (based on a comprehensive review of all relevant images) that the MRI performed
on August 13, 2013 demonstrated dorsal/posterior cord involvement—a conclusion he notes did
not appear in any of Dr. Watanabe’s pre-hearing reports. See generally Third Alexander Rep.

        In this report, Dr. Alexander took issue with Dr. Watanabe’s interpretation of the DWI
MRI obtained on August 8, 2013. Third Alexander Rep. at 1–2. Whereas Dr. Watanabe concluded
that the images were negative for indicia of a spinal cord infarction, Dr. Alexander noted that the

                                                 26
 DWI revealed increased signal intensity in the anterior portion of the spinal cord—the same area
 that demonstrated signal intensity in the T2 weighted MRI—consistent with an acute ischemic
 stroke. Id. at 2. He noted, however, that the quality of the images was not typical for diagnostic
 purposes, and there was no accompanying radiologic report for these images within the medical
 record. Id. He nonetheless concluded that the DWI MRI obtained just a few hours after Mr.I.J.
 first began experiencing symptoms was most consistent with a spinal cord infarction. Id.

        Dr. Alexander did agree with Dr. Watanabe’s conclusion that Mr. I.J.'s August 17th MRI
showed posterior/dorsal spinal cord involvement. Third Alexander Rep. at 5. But unlike Dr.
Watanabe, Dr. Alexander attributed these findings to a spinal cord infarction rather than TM. Id.
at 6–7. As he explained, posterior cord involvement is not uncommon in patients who have
experienced an anterior spinal artery infarction because both the anterior and posterior spinal
arteries are fed by the radiculomedullary artery. Id. at 3–5. In support of this contention, Dr.
Alexander cited several items of literature, including a study in which more than half of all
participants who experienced an anterior spinal artery infarction exhibited posterior cord
involvement. Id. at 4 (citing C. Masson et al., Spinal Cord Infarction: Clinical and Magnetic
Resonance Imaging Findings and Short Term Outcome, 75 J. Neurology Neurosurgery Psychiatry
1431, 1434 (2004), filed as Ex. D on Aug. 2, 2019 (ECF No. 67-2)); see also J. Novy et al., Spinal
Cord Ischemia: Clinical and Imaging Patterns, Pathogenesis, and Outcome in 27 Patients, 63
Archives Neurology 1113, 1117 (2006), filed as Ex. F on Aug. 2, 2019 (ECF No. 67-4); S.
Weidauer et al., Spinal Cord Ischemia: Aetiology, Clinical Syndromes and Imaging Features, 57
Neuroradiology 241, 244 (2015), filed as Ex. H on Aug. 2, 2019 (ECF No. 67-6) (“Weidauer”).

        Thus, Dr. Alexander maintained that a clot in the radiculomedullary artery can result in
ischemic changes to both the anterior and posterior spinal cord. Third Alexander Rep. at 5–6 (citing
Weidauer at 244). Dr. Alexander supported his proposed interpretation by noting that the signal
distribution within the posterior column was limited to the area surrounding the left posterior spinal
artery and did not cross the cord midline as would be expected in TM. Third Alexander Rep. at 7.
Lastly, he noted that these findings would not have appeared on the initial MRI obtained just hours
after the onset of Mr. I.J.'s symptoms because ischemic changes to the tissue would have
developed over time and only after secondary blood supplies to the cord were exhausted. Id. at 7–
8.

III.    Procedural History

        This matter commenced with the filing of the Petition on July 21, 2016. Over the following
months, Petitioner filed medical records in support of her claim. Respondent thereafter filed a Rule
4(c) Report on April 24, 2017, asserting that compensation was not appropriate in this case.
Respondent’s Report, filed April 14, 2017 (ECF No. 29). Petitioner subsequently filed expert
reports from Drs. Zamvil, Watanabe, and Levin along with supporting literature between the
summer of 2017 and fall 2019. Respondent filed a responsive report by Dr. Alexander on February
28, 2018, along with literature in opposition to Petitioner’s position. The parties filed their

                                                 27
 respective pre-hearing briefs over the summer of 2019, and a two-day entitlement hearing took
 place on October 22-23, 2019. The parties elected to file post-hearing briefs, doing so on April 24,
 2020. Petitioner’s Brief (ECF No. 112) (“Petitioner’s Post-Hearing Br.”); Respondent’s Brief
 (ECF No. 113). The matter is now fully ripe for resolution.

IV.     Applicable Legal Standards

        A. Petitioner’s Overall Burden in Vaccine Program Cases

        To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.
Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). 30
In this case, Petitioner does not assert a Table claim.

         For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). 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, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a 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,
1352–53 (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 assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 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. Sec’y of Health & Hum. Servs., 418 F.3d 1274, 1278 (2005): “(1) a medical
theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and

30
   Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,
2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

                                                        28
effect showing that the vaccination was the reason for the injury; and (3) a showing of proximate
temporal relationship between vaccination and injury.”

        Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
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). Such a theory must
only be “legally probable, not medically or scientifically certain.” Id. at 549.

        Petitioners 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). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny 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. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury.

        In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.
Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum. Servs.,
746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof.” (citing Moberly, 592 F.3d at 1322)). Petitioners otherwise always have the ultimate burden
of establishing their overall Vaccine Act claim with preponderant evidence, regardless of what
evidentiary level of evidence on the “can cause” prong is required. W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted); Tarsell v. United States, 133 Fed.
Cl. 782, 793 (2017) (noting that Moberly “addresses the petitioner’s overall burden of proving
causation-in-fact under the Vaccine Act” by a preponderance standard).

        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; Grant v. Sec’y of Health & Hum. Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“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

                                               29
 ‘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, since 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).

         Medical records and statements of a treating physician, however, do not per se bind the
 special master to adopt the conclusions of such an individual, even if they must be considered and
 carefully evaluated. Section 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) (“there 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 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 be weighed against other, contrary
 evidence also present in the record—including conflicting opinions among such individuals.
 Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (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); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
 Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 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. 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 align with the theory of how the relevant vaccine can
cause an 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, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 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), mot. for rev. denied (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

       B. Legal Standards Governing Factual Determinations

        The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 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,

                                                  30
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.” Section 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 at a later date, provided that such determination is evidenced by
a rational determination).

        Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed.
Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”), aff’d sub nom. Rickett v. Sec’y of Health
& Hum. Servs., 468 F. Appx. 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption
is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people
honestly report their health problems to those professionals; and (iii) medical professionals record
what they are told or observe when examining their patients in as accurate a manner as possible,
so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez
v. Sec’y of Health & Hum. Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.
Apr. 10, 2013); Cucuras v. Sec’y of Health & Hum. Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993
F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to
accurately report the onset of their daughter’s symptoms”).

        Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are generally 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 Dep’t of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991) (citing United States
v. United States 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.”)).

        There are, however, situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like 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 (“’[w]ritten

                                                31
 records which are, themselves, inconsistent, should be accorded less deference than those which
 are internally consistent’”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination
 regarding a witness’s credibility is needed when determining the weight that such testimony should
 be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,
 1575 (Fed. Cir. 1993).

         When witness testimony is offered to overcome the presumption of accuracy afforded to
 contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
 compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Hum. Servs.,
 No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). 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 making
 a determination regarding whether to afford greater weight to contemporaneous medical records
 or other evidence, such as testimony at hearing, there must be evidence that this decision was the
 result of a rational determination. Burns, 3 F.3d at 417.

       C. Analysis of Expert Testimony

        Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,
1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the
factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,
Inc., 509 U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328,
1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed.
Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a
theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592–95).

         The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health

                                                 32
 & Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have
 been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
 expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
 persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
 Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
 been employed at the threshold, to determine what evidence should be admitted, but instead to
 determine whether expert testimony offered is reliable and/or persuasive.

         Respondent frequently offers one or more experts in order to rebut a petitioner’s case.
 Where both sides offer expert testimony, a special master’s decision may be “based on the
 credibility of the experts and the relative persuasiveness of their competing theories.”
 Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
 Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion
 “connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
 great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health &
 Hum. Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot.
 for rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 999 (Fed. Cir. 2013) (citing Cedillo,
 617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
 a particular expert’s credibility, is part of the overall reliability analysis to which special masters
 must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
 (“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
 see also Porter v. Sec’y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this
 court has unambiguously explained that special masters are expected to consider the credibility of
 expert witnesses in evaluating petitions for compensation under the Vaccine Act”).

          Expert opinions based on unsupported facts may be given relatively little weight. See
 Dobrydnev v. Sec’y of Health & Hum. Servs., 556 F. Appx. 976, 992–93 (Fed. Cir. 2014) (“[a]
 doctor’s conclusion is only as good as the facts upon which it is based”) (citing Brooke Group Ltd.
v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993) (“[w]hen an expert assumes
facts that are not supported by a preponderance of the evidence, a finder of fact may properly reject
the expert’s opinion”)). Expert opinions that fail to address or are at odds with contemporaneous
medical records may therefore be less persuasive than those which correspond to such records. See
Gerami v. Sec’y of Health & Hum. Servs., No. 12-442V, 2013 WL 5998109, at *4 (Fed. Cl. Spec.
Mstr. Oct. 11, 2013), aff’d, 127 Fed. Cl. 299 (2014).

       D. Consideration of Medical Literature

        Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all the medical literature submitted
in this case, I discuss only those articles that are most relevant to my determination and/or are

                                                 33
 central to Petitioner’s case—just as I have not exhaustively discussed every individual medical
 record filed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016)
 (“[w]e generally presume that a special master considered the relevant record evidence even
 though he does not explicitly reference such evidence in his decision”) (citation omitted); see also
 Paterek v. Sec’y of Health & Hum. Servs., 527 F. Appx. 875, 884 (Fed. Cir. 2013) (“[f]inding
 certain information not relevant does not lead to—and likely undermines—the conclusion that it
 was not considered”).

          E. Consideration of Comparable Special Master Decisions

        In reaching a decision in this case, I have considered other decisions issued by special
 masters (including my own) involving similar injuries, vaccines, or circumstances. I also reference
 some of those cases in this Decision, in an effort to establish common themes, as well as
 demonstrate how prior determinations impact my thinking on the present case.

         There is no error in doing so. It is certainly correct that prior decisions from different cases
 do not control the outcome herein. 31 Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351,
 1358–59 (Fed. Cir. 2019); Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998).
 Thus, the fact that another special master reasonably determined elsewhere, on the basis of facts
 not in evidence in this case, that preponderant evidence supported the conclusion that vaccine X
 caused petitioner’s injury Y does not compel me to reach the same conclusion in this case.
 Different actions present different background medical histories, different experts, and different
 items of medical literature, and therefore can reasonably result in contrary determinations.

         However, it is equally the case that special masters reasonably draw upon their experience
 in resolving Vaccine Act claims. Doe v. Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328, 338–39
 (2007) (“[o]ne reason that proceedings are more expeditious in the hands of special masters is that
 the special masters have the expertise and experience to know the type of information that is most
 probative of a claim”) (emphasis added). They would therefore be remiss in ignoring prior cases
 presenting similar theories or factual circumstances, along with the reasoning employed in
 reaching such decisions. This is especially so given that special masters not only routinely hear
 from the same experts in comparable cases but are also repeatedly offered the same items of
 medical literature regarding certain common causation theories. It defies reason and logic to
 obligate special masters to “reinvent the wheel”, so to speak, in each new case before them, paying
 no heed at all to how their colleagues past and present have addressed similar causation theories
 or fact patterns. It is for this reason that prior decisions can have high persuasive value—and why

31
   By contrast, Federal Circuit rulings concerning legal issues are binding on special masters. Guillory v. Sec’y of
Health & Hum. Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y
of Health & Hum. Servs., No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014). Special
masters are also bound within a specific case by determinations made by judges of the Court of Federal Claims after
a motion for review is resolved.

                                                        34
 special masters often explain how a new determination relates to such past decisions. 32 Even if the
 Federal Circuit does not require special masters to distinguish other relevant cases (Boatmon, 941
 F.3d at 1358), it is still wise to do so.

                                                     ANALYSIS

I.       Petitioner Has Established TM as His Likely Injury

        In many Vaccine Program claims, prior to applying the Althen analytic framework it is
proper first to determine the nature of the petitioner’s injury, especially if the claimant’s causal
theory is dependent on the establishment of a specific injury. Broekelschen, 618 F.3d at 1345;
LaPierre v. Sec’y of Health & Hum. Servs., No. 17-227V, 2019 WL 6490730, at *16–17 (Fed. Cl.
Spec. Mstr. Oct. 18, 2019). That is the case here, since the parties strenuously dispute the proper
diagnosis—TM or spinal cord infarction—and since Petitioner’s causation theory wholly assumes
that the former is the correct one. Petitioner has not alleged that a spinal cord infarction could be
vaccine-caused, so a determination that this best characterized his injury would be fatal to his
claim.

        Resolving this question is difficult. Both sides offered credible, reliably-bulwarked points
for their respective positions, supported in turn by fair and persuasive expert testimony. In addition,
the medical record is ultimately equivocal on the matter. Unquestionably Mr. I.J.'s initial
treaters included both TM and infarction in their preliminary diagnostic differentials, noting the
testing and imaging results that supported both. Although by the time of Petitioner’s discharge it
could reasonably be concluded that treaters were leaning against TM as a final diagnosis, the record
is ambiguous enough on the subject to leave more than a little room for doubt, and Mr. I.J.'s
post-hospitalization record offers no clarification of the matter. Dr. Watanabe’s reading of the
MRIs in this case also provided perspectives on the nature of Petitioner’s injury that were not fully
rebutted by Respondent (even after being provided the opportunity post-trial to do so).

        The parties seemed to agree that the TM Working Group criteria were a good general
yardstick for evaluating if TM was present in this case—and it appears that not all were met fully.
Yet Petitioner successfully established either that certain of the criteria (for example, proof of
inflammation) had not completely been eliminated, or more generally that a TM diagnosis should
not be held to the literal standard set by the criteria. Tr. at 77–78, 80–83. And it is not my function
as special master to propose a “correct” diagnosis. Rather, my task is to weigh whether the

32
  Consideration of prior determinations is a two-way street that does not only inure to the benefit of one party. Thus,
I would likely take into account the numerous decisions finding no association between vaccination and autism when
confronted with a new claim asserting autism as an injury and have informed such claimants early in the life of their
case that the claim was not viable for just that reason. But I would also deem a non-Table claim asserting GBS after
receipt of the flu vaccine as not requiring extensive proof on Althen prong one “can cause” matters, for the simple
reason that the Program has repeatedly litigated the issue in favor of petitioners.

                                                         35
 evidence preponderantly supports one conclusion over another—an analysis that leaves ample
 room for doubt to remain in either direction, regardless of the final determination.

         Petitioner did persuasively establish that he experienced sensory, motor, and autonomic
 dysfunction consistent with TM. Tr. at 77. Similarly, he presented evidence that established the
 bilateral nature of his symptoms despite the initial unilateral presentation. Id. at 78. Petitioner’s
 position was further bulwarked by the absence of connective tissue disease, infectious disease,
 abnormal void flows, and spinal radiation. Id. at 83–84. Other etiologies, such as optic neuritis and
 MS were also eliminated as potential causes for Mr.I.J.'s condition. Id. at 84. The progression
 of Petitioner’s symptoms over the course of approximately eight or nine hours satisfied the
 Working Group’s proposed diagnostic criteria and further distinguished Petitioner’s course from
 that which is typical of spinal cord infarction. Id. at 57, 63, 83. And there is treater support for his
 proposed diagnosis, and (unlike in other cases) a review of the medical record beyond his initial
 onset does not suggest, based on the accumulation of additional information over time, that treaters
 later abandoned TM as an explanation. On the other hand, Respondent’s expert Dr. Alexander
 provided a number of reasonable points for why an infarction was more likely.

       Overall, this issue is close, with the evidence largely in equipoise. The experts were equally
credible, making some points that were unrebutted while ceding others. Under such circumstances,
persuasive Vaccine Program caselaw counsels me to decide the matter in the Petitioner’s favor.
See Purtill v. Sec’y of Health & Hum. Servs., No. 18-832V, 2019 WL 7212162, at *6 (Fed. Cl.
Spec. Mstr. Nov. 12, 2019) (citing Roberts v. Sec’y of Health & Hum. Servs., No. 09-427V, 2013
WL 5314698 (Fed. Cl. Spec. Mstr. Aug. 29, 2013)). I do so here, and thus find that preponderant
evidence has been offered to establish that Petitioner more likely than not suffered from TM.

II.    Petitioner Has Not Demonstrated that the Tdap Vaccine “Can Cause” TM

       A.      Relevant Case Law Regarding Vaccine Causality of TM

        Claims alleging acute, nerve-demyelinating conditions like TM following vaccination are
common in the Vaccine Program. While some petitioners have obtained damages based on a
successful showing that TM was caused by the Tdap vaccine, most such cases have been resolved
through stipulations and proffers, leaving very few reasoned decisions addressing the issue of
causation—and even those that exist are not particularly recent. See, e.g., Raymo v. Sec’y of Health
& Hum. Servs., 11-654V, 2014 WL 1092274 (Fed. Cl. Spec. Mstr. Feb. 24, 2014) (petitioner
established entitlement to compensation for a claim alleging TM following receipt of the HPV,
Hepatitis A, meningococcal, and Tdap vaccines); Roberts, 2013 WL 5314698 (petitioner was
entitled to compensation for a claim alleging TM following receipt of the Tdap vaccine); Helman
v. Sec’y of Health & Hum. Servs., No. 10-813V, 2012 WL 1607142 (Fed. Cl. Spec. Mstr. Apr. 5,

                                                  36
 2012) (petitioner was entitled to compensation for a claim alleging TM and NMO following receipt
 of the Tdap vaccine). 33

          By contrast, several more recent, well-reasoned decisions have found that petitioners failed
 in their effort to establish that the flu vaccine “can cause” TM, as required by the first Althen prong.
 See Pearson v. Sec’y of Health & Hum. Servs., No. 16-09V, 2019 WL 3852633, at *13–14 (Fed.
 Cl. Spec. Mstr. July 31, 2019); Forrest v. Sec’y of Health & Hum. Servs., No. 14-1046V, 2019
 WL 925485 (Fed. Cl. Spec. Mstr. Jan. 28, 2019). Although such determinations are somewhat less
 on point given the different vaccine at issue, they cast light on deficiencies in the reasoning that
 led prior special masters to conclude that the Tdap vaccine could be causal of the same injury (and
 also the theories offered in this particular case).

          In Pearson, for example, an adult petitioner alleged that his receipt of the flu vaccine in
 October 2012 precipitated TM, with onset within three months (although it took treaters
 considerably longer to arrive at the diagnosis, which was not wholly supported by the record).
 Pearson, 2019 WL 3852633, at *3–4. The Pearson petitioner made many arguments parallel to
 those advanced in this case, e.g., that TM has an autoimmune-driven pathogenesis with molecular
 mimicry as its mechanism. Id. at *6. Molecular mimicry was also relied upon in the Tdap-TM
 cases mentioned above. See Roberts, 2013 WL 5314698, at *6; Helman, 2012 WL 1607142, at *3.
 And the Pearson Petitioner relied specifically on Agmon-Levin’s review of post-vaccine TM cases
 to support his causation showing. Pearson, 2019 WL 3852633, at *7. In reaction, Respondent’s
 expert pointed out that Agmon-Levin in totality identified only two instances of TM post-flu
 vaccine, and then only after a review of more than 35 years of literature to cull possible examples—
 thus implicitly demonstrating how little evidence existed for an association. Id. at *9. The special
 master denied compensation, observing (among other things) the low probative value of case
 reports generally, as well as the error in overreliance on Agmon-Levin, given the facial limitations
 of its findings. Id. at *14.

         Forrest also featured an adult petitioner arguing that the flu vaccine caused TM, albeit with
 a far shorter onset timeframe (within a day or more of vaccination). Forrest, 2019 WL 925495, at
 *1. But there (as here) the petitioner also proposed molecular mimicry as the mechanism. Id. at

33
   I issued a decision approximately two years ago denying entitlement for a claim alleging TM following receipt of
the DTaP vaccine (among others) in an infant child who experienced onset between thirty and thirty-six hours after
vaccination. Palattao v. Sec’y of Health & Hum. Servs., No. 13-591V, 2019 WL 989380 (Fed. Cl. Spec. Mstr. Feb. 4,
2019). The DTaP vaccine is the variant of the Tdap administered to infants and children. Notably, however, the
petitioners in Palattao expressly rejected the theory of molecular mimicry espoused in this case, and instead relied
solely on an aberrant proinflammatory cytokine response as the vaccine-instigated disease driver. Id. at *8. I found
that the onset had occurred too close in time to the vaccination, and that the petitioners had failed to “demonstrate that
cytokine upregulation in the periphery attributable to a vaccine can also trigger TM.” Id. at *36 (emphasis in original).
Thus, because of the difference in causation theory and overall circumstances, I find Pallattao to be less useful as a
guide to resolution of this matter.

                                                           37
*3. In addition, Respondent (not Petitioner, as in this case) offered Baxter to undermine
Petitioner’s causation theory, highlighting that the very large-scale study saw no increased
incidence of TM after administration of the flu vaccine—parallel to the same finding Baxter
reached with respect to the Tdap vaccine (a finding Dr. Zamvil acknowledged at trial of this
matter). Id. at *5. Although the special master’s denial of entitlement in Forrest turned partially
on some matters not relevant herein (in particular, the short onset timeframe and its inconsistency
with the causal theory), the decision took special note of Baxter, observing the extent to which the
study undermined the claimant’s case (while acknowledging the “general rule” that petitioners are
not required to submit affirmative epidemiologic evidence as part of their prima facie case). Id. at
*5.

       As I have already stated in my overview of the applicable legal standards to this case, none
of these prior decisions control the outcome herein. However, they do provide guidance in
evaluating the strength of the evidence offered by Petitioner herein in attempting to show that TM
can be vaccine-caused—and the evidentiary weakness of certain items relied upon to do so.

       B.      Petitioner’s Althen One Showing was Insufficient

        Petitioner’s showing for the first Althen prong was only credibly supported by the
testimony and report of Dr. Zamvil (since neither Drs. Watanabe or Levin possessed the necessary
training or background to offer a reliable opinion on the “can cause”/causation prong).
Unquestionably, Petitioner has offered a variety of evidence in addition to Dr. Zamvil’s report to
support this prong. And, as noted above, there are reasoned decisions from the Program’s past that
support Petitioner’s case. I nevertheless find (based on consideration of Dr. Zamvil’s report,
testimony, the filed literature, and other, more recent decisions) that it has not been preponderantly
established that the Tdap vaccine can cause TM—and this determination, unlike my resolution of
the disputed injury question, is not close at all.

        As a threshold matter, I note that Petitioner has mischaracterized the evidentiary standard
that is applied to the first Althen prong. See generally Petitioner’s Post-Hearing Br. at 46. Thus,
Petitioner incorrectly maintains that “reliable scientific evidence” is not required to meet his
preponderant burden—although perhaps in so asserting he confuses the fact that no particular class
of evidence (i.e. medical literature; research studies; expert reports; peer-reviewed articles; etc.)
need be offered with the overall obligation of Program petitioners to offer a reliable theory,
regardless of what specific items of evidence are gathered to support it. Knudsen, 35 F.3d at 548.
If certain individual components of evidence critical to a theory’s success are not themselves
reliable, that finding reasonably impacts the overall theory’s evidentiary preponderance. Petitioner
also erroneously suggests a theory’s mere plausibility is enough to meet the preponderant
standard—a contention that the Federal Circuit clearly rejected in the recent Boatmon decision.

                                                 38
 Boatmon, 941 F.3d at 1359. 34 Petitioner thus fashions evidentiary standards for evaluating his
 claim that are far easier to meet than the actual preponderant standard governing the claim.

         Beyond this, the primary elements of Petitioner’s theory have several deficiencies. First,
 scientific evidence not previously available when the TM/Tdap cases I mention above (and which
 Petitioner references favorably) were decided six or more years ago does not support a causal
 association between the Tdap vaccine and the development of TM. Compare Baxter
 (epidemiologic study published in 2017) with Raymo, 2014 WL 1092274, at *19 (“[t]here are no
 epidemiologic studies . . . linking or refuting a link between [TM] and vaccination”). Baxter is a
 large-scale, comprehensive epidemiological study aimed at examining the risk of demyelinating
 event following vaccination generally, and evaluated instances of the occurrence of two acute
 demyelinating diseases (TM and ADEM) within a field of nearly 64 million vaccinations
 (including almost six million Tdap recipients) derived from data maintained by the Vaccine Safety
 Datalink. Baxter at 1456–57. Only seven cases of TM were reported between 5-28 days post-
 vaccination—the very timeframe applicable herein. Id. at 1456–57. Baxter concluded that there
 was no reliably-demonstrated association between vaccination and the subsequent development of
 TM. Id. at 1456, 1461 (“[i]n conclusion, TM and ADEM are rarely, if ever, associated with
 vaccines”).

         Although it is unquestionably the case that Vaccine Program litigants are not required to
 offer epidemiological evidence to prevail, special masters may take note of its existence and
 consider it when determining if a claimant has met his burden of proof. See Palattao, 2019 WL
 989380, at *37 (citing D’Toile v. Sec’y of Health & Hum. Servs., 726 F App’x 809, 811–12 (Fed.
 Cir. 2018)). While I cannot state whether pre-Baxter decisions more favorable to Petitioner’s
 theory, like Raymo or Roberts, would have been decided differently had the article existed when
 they were issued, I can take Baxter into account in this unquestionably later case—and find that it
 greatly damages Petitioner’s causation theory.

         Ironically, in this case Baxter was offered by the Petitioner as an exhibit to Dr. Zamvil’s
 report—making it difficult for Petitioner to argue herein (as many petitioners do when attempting
 to rebut damaging epidemiologic proof) that my consideration of it amounts to “requiring”
 Petitioner to have found positive epidemiologic evidence to prevail. Indeed, Dr. Zamvil expressly
 relied on the Baxter article to support an association between TM and receipt of the Tdap vaccine.

34
   Petitioner also maintains that special masters need not “apply gatekeeping standards of reliability pursuant to
Daubert,” citing Boatmon for this proposition as well. Petitioner’s Post-Hearing Brief at 46, citing Boatmon, 941 F.3d
at 1359. This is correct—but only in the narrow sense that it would not be legal error if a special master fails to apply
those standards. As I have already noted above, however, there is ample Federal Circuit support (cited even in
Boatmon) for embracing and applying the Daubert standards in Vaccine Act cases, for purposes of evaluating the
reliability of scientific and medical evidence (and thus what weight to give it). In the Program (unlike a federal district
court), Daubert does not function to limit what evidence is considered by a special master—but it does provide a way
to assess the trustworthiness of medical and scientific evidence, and hence the weight to give such evidence. I
consistently follow Daubert in this manner when I decide Vaccine Act cases—and it is my conclusion that I would
not be performing my function adequately if I did not do so.

                                                           39
Tr. at 113–16; Zamvil Rep. at 7. But his assertions regarding its findings essentially ignored what
is so glaringly unfavorable about them. Thus, Dr. Zamvil attempted to redirect attention to the fact
that Baxter’s authors did find a slightly increased risk of ADEM following vaccination. Baxter at
1456 (noting eight reported cases of ADEM within 5-28 days of receiving the Tdap vaccine); Tr.
at 116. But ADEM is not the claimed injury (and Petitioner could not establish it on the present
record even if he so alleged). TM is the relevant injury—and therefore the findings in Baxter
specific to TM cannot simply be ignored.

        Second, the applicability of prior decisions like Raymo, Roberts, and Helman—all of which
rely on literature similar to that offered herein, or more broadly involve theories parallel with
Petitioner’s theory of autoimmunity attributable to molecular mimicry—is limited by other
specific aspects of their respective holdings, or diminished by more recent determinations
involving the same causal theories producing TM. See Forrest, 2019 WL 925495, at *3 (citing
Caves v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 119, 135 (2011), aff’d without opinion, 463
F. App’x 932 (Fed. Cir. 2012)). In Raymo, for example, the petitioners prevailed based on a theory
that the tetanus toxoid component of the Tdap vaccine can cause TM via molecular mimicry and
bystander activation of IL-6—a proinflammatory cytokine which is associated with the
development of TM. Raymo, 2014 WL 1092274, at *18, 20. The special master noted, however,
that although molecular mimicry was an accepted medical/scientific explanation for many
autoimmune diseases, in acute TM “homology has not been demonstrated between any suspected
precipitating agent and the spinal cord nerve sheaths or axons.” Id. at *20. The special master thus
based her liability determination on the finding that the theory of bystander activation—a
mechanism not proposed by Petitioner’s experts in this case—was also a reasonable causal
explanation under the circumstances. Id. at *20; see also Dr. Zamvil Rep. at 9.

        The petitioners in Roberts similarly relied on the theory of molecular mimicry to explain
how the Tdap vaccine could cause TM. Roberts, 2013 WL 5314698, at *6. The special master
deciding that case acknowledged that petitioners’ theory was supported by an expert opinion, but
included no further analysis to explain why the theory was persuasive. Id. And in Helman, only
two sentences of the special master’s analysis in total are dedicated at all to the first Althen prong.
Helman, 2012 WL 1607142, at *3. The special master concluded therein that the petitioner had
met his burden merely by providing expert testimony referencing causal mechanisms such as
molecular mimicry in addition to substantiating literature, though the special master did not
explain what literature was provided. Id. No analysis explained how the Tdap vaccine can cause
TM, thus greatly limiting the persuasive quality of such a determination. By contrast, and despite
the fact that the decisions do not involve Tdap, more recent determinations like Forrest and
Pearson constitute far more reliable guidance. These decisions in particular note the comparative
weakness of case study-oriented literature like Agmon-Levin, especially when weighed against
the value of Baxter.

      Finally, and with the above as framework, I do not conclude that Petitioner’s specific
showing on the association between Tdap vaccine and TM was itself and on its own terms reliable
                                                40
 or robust enough to preponderantly establish the first Althen prong. 35 Thus, Dr. Zamvil relied on
 molecular mimicry—a generally accepted scientific explanation for many autoimmune diseases,
 to be sure, but one that cannot simply be invoked in every Vaccine Act claim to support causation.
 Forrest, 2019 WL 925495, at *3 (citing Caves, 100 Fed. Cl. at 135). Rather, petitioners must
 demonstrate (where they raise molecular mimicry as a possible mechanism) that it likely does link
 the vaccine in question to the relevant injury. See Yalacki v. Sec’y of Health & Hum. Servs., No.
 14-278V, 2019 WL 1061429, at *34 (Fed. Cl. Spec. Mstr. Jan. 31, 2019), mot. for review den’d,
 146 Fed. Cl. 80 (2019). No such showing was made in this matter. Moreover, merely
 demonstrating some homology between vaccine components and relevant self-structures based on
 computer database searches does not carry the day. See Pek v. Sec’y of Health & Hum. Servs., No.
 16-736V, 2020 WL 1062959, at *16 (Fed. Cl. Spec. Mstr. Jan. 31, 2020) (citing Blackburn, 2015
 WL 425935, at *7 n.14)).

        Dr. Zamvil’s assertions about the role the vaccine’s alum adjuvant could play in activation
 of an aberrant innate response were even less reliable or persuasive. This argument relies mostly
 on what is known as a general matter about the performance of adjuvants in promoting an immune
 response—a noncontroversial assertion as far as it goes. But he has not shown, nor offered
 evidence in addition to his testimony, that reliably suggests or establishes that vaccines containing
 an aluminum adjuvant can, independent of anything else, cause a pathologic response not
 otherwise shown to be vaccine-attributable. I have previously criticized similar arguments in other
 cases, where petitioners try to convert what is known about a functioning immune process into
 something pathologic. See, e.g., Olson v. Sec’y of Health & Hum. Servs., No. 13-439V, 2017 WL
 3624085, at *20–21 (Fed. Cl. Spec. Mstr. July 14, 2017), mot. for review den’d, 135 Fed. Cl. 670
 (2017), aff’d, 758 Fed. App’x 919 (2018). The argument is no better structured or advanced in this
 case.

         Petitioner also offered a few case reports, either collated in Agmon-Levin or contained in
 independent items of literature, to bulwark his causal showing. But these too also were ultimately
 of limited probative value—and not just for the reason that case reports generally are not given
 significant weight when deciding Program cases, since they do not establish causation per se. See
 Knorr v. Sec’y of Health & Hum. Servs., No. 15-1169V, 2018 WL 6991548, at *30 (Fed. Cl. Spec.
 Mstr. Dec. 7, 2018) (citing W.C. v. Sec’y of Health & Hum. Servs., No. 07-456V, 2011 WL
 4537887, at *13 (Fed. Cl. Spec. Mstr. Feb. 22, 2011), aff’d, 704 F.3d 1352 (Fed. Cir. 2013)). Riel-

35
   Petitioner has argued that Respondent’s expert, Dr. Alexander did not himself rebut Dr. Zamvil’s theory, taking
specific issue with Dr. Alexander’s invocation of an Institute of Medicine report that purports to find no evidence
associating TM with tetanus toxoid-containing vaccines like Tdap. Petitioner’s Post-Hearing Br. at 49–50; Ex. A Ref.
1. My finding on the first Althen prong, however, is derived from a determination that Petitioner’s showing was itself
not preponderant—and that showing included especially damaging evidence like Baxter. I thus do not devote time
herein to weighing the competing strengths and weaknesses of each side’s expert contributions on this prong.
Petitioners must themselves meet their preponderant burden, no matter the relative strength of Respondent’s counter-
efforts—and this was not a case where a robust showing by the Petitioner merited consideration of Respondent’s
success in rebutting it.

                                                         41
Romero, for example, not only involved a young child rather than adult like Mr. I.J. but also
acknowledged that its observation of an association could simply be coincidental. Riel-Romero at
690. Agmon-Levin provided only four instances of association, and the weight this piece of
literature should receive overall has reasonably been questioned. Pearson, 2019 WL 3852633, at
*14. Other articles similarly offered limited numbers of case study instances. See, e.g., Gregg at 1
(describing two case reports of TM post-vaccination); F.S. Pidcock et al., Acute Transverse
Myelitis in Childhood, 68 Neurology 1474, 1476, 1479 (2007), filed as Ex. 55 on Sept. 13, 2019
(ECF No. 74-6) (“Pidcock”) (documenting thirteen instances of TM post-vaccination). But both
Pidcock and Gregg emphasize that the documented reports of post-vaccination TM could be
coincidental, and neither article claims to establish a causal relationship between vaccination and
the subsequent development of TM. Gregg at 4 (noting a possible association, but not
distinguishing between temporal and causal association types); Pidcock at 1479. These case reports
overall had some evidentiary value, and I have taken them into account (as my analysis should
demonstrate). But they are not enough to meet the preponderant burden, especially given the far
more comprehensive, contrary evidence provided by Baxter. 36

        All in all, the theory that the Tdap vaccine could cause TM was reasonably advanced in
this case, as the theory has found some success in the past—but it was not preponderantly
supported herein by sufficient reliable evidence, whatever the form, to find the first Althen prong
was met.

III.     Althen Prongs Two and Three

       Petitioner’s claim cannot succeed, given his failure to meet at least one of the three Althen
prongs. See Deshler v. Sec’y of Health & Hum. Servs., No. 16-1070V, 2020 WL 4593162, at *21
(Fed. Cl. Spec. Mstr. July 1, 2020) (citing W.C., 704 F.3d at 1356)). However, for purposes of
completion of my overall analysis, I will also discuss his success in meeting the other two.

         Regarding the second, “did cause” prong, I find an absence of evidence that would allow
me to conclude that the Tdap vaccine likely produced Petitioner’s TM. Here, the inability to satisfy
certain of the TM Working Group criteria (acknowledged expressly by Dr. Zamvil), while not fatal
to Petitioner’s diagnosis contentions, was much more harmful to this Althen prong showing. Thus,
not only is there little evidence that Petitioner had experienced something amiss in the two week
post-vaccination period, but there was hardly any testing evidence (whether from serologic
sampling or MRI imaging) that would establish the existence of inflammation—a telltale sign
confirming the presence of the autoimmune process that Petitioner’s causation theory proposes

36
  The fact that TM specifically, or vaccine injuries generally, are rare occurrences also is no defense to the insufficient
preponderant evidence offered in this case on causation. As a general matter, the Program is premised on the policy
consideration that vaccination is safe for the majority of individuals, but that in order to encourage use of vaccines
compensation for injuries should be permitted under specific defined circumstances. The Act thus inherently accepts
that vaccine injuries are uncommon—but their rarity is not a shield protecting petitioners from their evidentiary
obligations. Were it otherwise, claimants could prevail merely by pointing to their own individual “case study.”

                                                           42
would have been instigated by the Tdap vaccine. The aspect of Dr. Zamvil’s opinion relying on
the pro-inflammatory characteristics of the alum adjuvant especially required some record
confirmation of excessive or unusual inflammation post-vaccination—evidence not found in this
record. There was also no evidence of any autoantibodies that might arguably be associated with
the asserted TM cross-reaction. And no treaters ever proposed that Petitioner’s injury, however
defined, was likely caused by his prior Tdap vaccine. At most, the record reveals instances in
which treaters assumed Petitioner had received a different vaccine (Hepatitis B) that they believed
could be associated with TM—but in some of these instances went on to opine that vaccine
causation was less likely than infarction given the diagnostic study results. See, e.g., Ex. 2 at 8, 61,
92, 230–31, 245–47. There is thus insufficient support in the record for the conclusion that the
Tdap vaccine could have caused Petitioner’s TM.

        I additionally observe that the medical record suggests the existence of a pre-onset
intercurrent respiratory infection. Ex. 2 at 8. It is recognized that infection can be the instigating
cause of TM—and the presence of such an infection has in other cases been held to possibly
explain various demyelinating conditions. See, e.g., Deshler, 2020 WL 4593162, at *18 (two-thirds
of GBS cases follow an antecedent infection); Palattao, 2019 WL 989380, at *38 (evidence that
infant had upper respiratory infection prior to onset of TM undercut vaccine causality). The
evidence to support this alternative explanation is not itself particularly robust (certainly no
infectious agent was identified in testing), and I do not propose that it establishes a stronger
explanatory case than what Petitioner offered, or that (had the burden shifted to Respondent) it
was preponderantly established as an alternative cause. But it is additional evidence that was not
fully explained or distinguished by Petitioner, and thus it also undermined somewhat Petitioner’s
claim. See Deshler, 2020 WL 4593162, at *22.

        By contrast, I find the record and evidence offered in this matter does support the
conclusion that Petitioner’s TM occurred in a medically acceptable timeframe, consistent with his
causation theory. As noted above, Petitioner asserts that his symptoms began just over two weeks
after his receipt of the Tdap vaccine—a timeframe which has consistently been deemed medically
appropriate in cases involving demyelinating conditions, including TM, following vaccination.
See, e.g., Raymo, 2014 WL 1092274, at *23 (onset of TM three to four days after receipt of the
Tdap vaccine); Schmidt v. Sec’y of Health & Hum. Servs., No. 07-020V, 2009 WL 5196169, at
*14 (Fed. Cl. Spec. Mstr. Dec. 17, 2009) (onset of TM one month after receiving the flu vaccine
falls within a medically acceptable timeframe). The onset timeframe was also consistent with Dr.
Zamvil’s persuasive testimony about the time it would take for a molecular mimicry-driven
process to manifest neurologic harm. But because Petitioner’s causation theory in this case was
not sufficiently supported with preponderant evidence, the consistency of the onset timing in this
case with Petitioner’s theory does not aid Petitioner.

                                                 43
                                                 CONCLUSION

        Mr. I.J. was an engaging and highly sympathetic witness, and he plainly brought this
case in the good-faith belief that the Tdap vaccine he had received might be related to his
subsequent and sudden debilitating symptoms. He deserves praise for his aplomb in handling the
deficits his condition has imposed on him. Petitioner unquestionably has marshalled credible
support for his claim. And although it remains uncertain what his actual diagnosis should be, he
has carried his burden (albeit in a close case) of establishing that he more likely than not
experienced TM.

        But the Vaccine Act permits me to award compensation to a petitioner alleging a “non-
Table Injury” only if he can show by medical records or competent medical opinion that the injury
could be, or was, vaccine-caused. And on these matters, the evidence is far less close, as even some
of the proof Petitioner himself offered undercuts his Althen prong one showing. Thus, there is
insufficient evidence to support an award of compensation, leaving me no choice but to hereby
DENY this claim.

       In the absence of a motion for review filed pursuant to RCFC Appendix B, the clerk of the
court SHALL ENTER JUDGMENT in accordance with the terms of this decision. 37

         IT IS SO ORDERED.
                                                                          /s/ Brian H. Corcoran
                                                                           Brian H. Corcoran
                                                                           Chief Special Master

37
  Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices
renouncing their right to seek review.

                                                          44