Henningsen v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 21-1101V

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ALICE HENNINGSEN, * Chief Special Master Corcoran

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Petitioner, * Filed: May 8, 2026

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v. *

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SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

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Respondent. *

*

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Anne C. Toale, Mctlaw, P.A., Sarasota, FL, for Petitioner.

Meghan Murphy, U.S. Department of Justice, Washington, DC, for Respondent.

ENTITLEMENT DECISION 1

On March 23, 2021, Alice Henningsen filed a petition for compensation under the National

Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petition (ECF No. 1) (“Pet.”).

Petitioner alleges that she experienced transverse myelitis (“TM”) due to an influenza (“flu”)

vaccine she received October 31, 2019. Pet. at 1.

The matter went to hearing on May 12–13, 2025, with the parties’ dispute focused on the

issue of diagnosis: TM versus a spinal cord infarct. Now, based on review of the record and filed

briefs, I deny entitlement in this tragic case. It has not been preponderantly established that

Petitioner likely experienced TM—and even if she had, it is also not likely the flu vaccine caused

her injury.

1

Under Vaccine Rule 18(b), each party has fourteen (14) 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 present form. Id.

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3755 (codified as amended at 42 U.S.C. §§ 300aa-10–34 (2012)) (hereinafter “Vaccine Act” or “the Act”).

All subsequent references to sections of the Vaccine Act shall be to the pertinent subparagraph of 42 U.S.C. § 300aa.

I. Factual Background

Petitioner was 26 years old when she received a flu vaccine on October 31, 2019. See Ex.

2 at 5. Significantly, there is no record evidence that Ms. Henningsen experienced any immediate

vaccine reaction. And nothing in the record establishes that in the weeks prior to the emergency

hospitalization described below, Petitioner was experiencing an autoimmune process likely

leading to illness. Rather, the record is devoid of any concerning outward symptoms for well over

a month.

On December 8, 2019 (thirty-nine days post-vaccination), Ms. Henningsen arrived at the

emergency department (“ED”) of Ascension Via St. Christi Francis in Wichita, Kansas, around

1:15 – 1:20 pm, complaining of tightness and pain in her back, numbness and tingling in her

bilateral lower extremities, and altered sensation in her lower and upper extremities. Ex. 5 at 12,

19–20. She explained at the hospital that she had experienced pain in her right shoulder blade the

previous day which seemed to have resolved on its own, but that the pain had returned, and had

begun radiating up her neck to the base of her skull, as well as down her spine. Id. at 37.

Petitioner also informed emergency treaters that progression of her symptoms was notably

rapid. In an intake medical record from December 8th (containing a time stamp of 2:32 pm),

Petitioner reported the onset of the acute pain and sensations that lead her to seek emergency care

as beginning two hours prior, or around 12:30 pm. Ex. 5 at 12. In addition, at the time of her arrival

at the hospital, Petitioner was still able to walk, but not long after she could no longer lift her left

leg, and had decreased ability to move her right leg. Id. Thus, a clear and downward progression

of Petitioner’s symptoms was occurring—within a two to three-hour timeframe, measured from

the moment of onset.

That very day, treaters began their efforts to ascertain an explanation for Petitioner’s

sudden debilitating symptoms. An initial MRI of petitioner’s cervical, thoracic, and lumbar spine

was performed without contrast 3 around 3:00 pm that day. See Ex. 5 at 15–17. The results were all

deemed unremarkable, however (beyond some evidence of preexisting degenerative changes). Id.

In particular, this first set of MRI images did not appear to reveal the presence of any signal

corroborating the existence of spinal cord lesions (although at this time Petitioner was plainly

experiencing significant and alarming clinical symptoms—and as noted below, both radiologic

3

“Enhancement” refers to “any method of exaggerating the visible difference between adjacent structures on imaging

by administering contrast media/agents.” Curry v. Sec’y of Health & Hum. Servs., No. 22-729V, 2025 WL 1693655,

at n.5 (Fed. Cl. Spec. Mstr. Apr. 28, 2025). Gadolinium is a contrast agent injected into an imaged patient’s blood,

and it causes images to appear brighter where damage to the central nervous system’s “blood brain barrier” is sufficient

to allow leakage into it (thus permitting the gadolinium agent to enter the central nervous system). Osenbach v. Sec'y

of Health & Hum. Servs., No. 16-419V, 2023 WL 5714809, at *17 n.32 (Fed. Cl. Spec. Mstr. Aug. 8, 2023), aff'd, No.

2024-1663, 2025 WL 2387944 (Fed. Cir. Aug. 18, 2025).

2

experts who testified in this matter agreed that the conclusions drawn from the first MRI by

contemporaneous treaters were in error).

That afternoon, Petitioner continued to feel weaker. Ex. 5 at 18. Ms. Henningsen was

subsequently admitted to the Intensive Care unit (“ICU”) for further evaluation. Id. at 32. By this

time (which the ICU record suggests was close to 5:30 pm—the same day her symptoms had begun

a few hours earlier), she could no longer move her extremities. Id. at 37. On exam, Petitioner had

a weak cough and was breathing deeply, but she stated that swallowing was becoming more

difficult. Id. The admitting physician noted that Petitioner reported receiving a flu vaccine about

three weeks prior, and removal of her birth control implant about a month prior. Id.

Petitioner’s onset was again noted to have occurred around noon on December 8, 2019,

based on her history recollections. Ex. 5 at 55. The ICU physician assessed Ms. Henningsen with

acute flaccid quadriplegia, but was still considering whether the correct diagnosis was cervical

myelopathy, myelitis, acute inflammatory demyelinating polyneuropathy, or spinal cord ischemia.

Id. at 40. Labs taken the same day were unremarkable, though testing for antibodies to a West Nile

virus was positive. Id. In addition, a lumbar puncture to assess cerebrospinal fluid (“CSF”)

occurred around 8:00 pm that evening, but it revealed normal protein, a normal white blood cell

count of 1 (out of a range of 1-10), and no other evidence of spinal cord inflammation. Id. at 1401.

On the evening of December 8th, a second round of MRIs (this time of Petitioner’s brain

and cervical spine) were performed, with contrast plus diffuse weighted imaging (“DWI”). 4 Ex. 5

at 1509–10. DWI was employed based on the treating neurologist’s view that it could potentially

“rule out” cervical cord ischemia—although the treater noted as well that an exam of Petitioner

had not revealed sparing of her vibration sensation, which in his view made ischemia “less likely.”

Ex. 5 at 55. The brain MRI yielded normal results. Id. at 1510. The repeat cervical imaging

established no abnormal enhancement (which would be evidence of active inflammation) or

degenerative concerns. Id. The record of this cervical MRI does not mention findings pertinent to

DWI.

Early the next morning (December 9, 2019), during a critical care consultation continued

issues with Petitioner’s breathing were observed. Ex. 5 at 2731, 2736. Treaters had trouble

confirming Petitioner’s reports of breathing issues with clinical evidence of a deficiency, however,

and seemed to deem breathing concerns something to watch. See, e.g., Id. at 2735-36 (“[n]o acute

4

DWI is an MRI technique that permits observation of the motion of water molecules within tissue, providing contrast

based on cellular density and microstructure, and has special utility when attempting to diagnose stroke/infarct. Highly

cellular tissue restricts water movement, appearing bright, while free-moving water appears dark. Ross v. Sec’y of

Health & Hum. Servs., No. 22-136V, 2025 WL 3531575, at n.4 (Fed. Cl. Spec. Mstr. Nov. 14, 2025).

3

cardiopulmonary process, - monitor closely with low threshold for NIPPC 5 or intubation if

needed”) (emphasis added), 2737 (“[r]esp: FVC was 300 today but clinically she doesn't appear to

be that weak as that value is incredibly low. Will repeat and trend q8h. In the meantime, will

change to HFNC to decrease her WOB as subjectively she says she’s having issues but clinically

I don't appreciate it”). But Petitioner was later intubated in the early morning of December 10th.

Id. at 5203. She also now had a rash on her extremities, hands, chest and back, so antibiotic

management was requested, and she was prescribed prednisone. Id. at 43–44.

On the afternoon of December 10, 2019, another MRI was performed (this time of

Petitioner’s brain) but it also yielded normal results, although a dedicated orbit MRI was

recommended. Ex. 5 at 1506–07. A second cervical spine MRI occurred the same day (performed

with and without contrast). Id. at 1507–08. Although this imaging again yielded no evidence of

degenerative issues, “extensive T2 hyperintensity has developed throughout much of the cervical

cord extending from the level of C2 to at least the level of T3,” along with “mild scattered

enhancement,” and evidence of edema throughout the cord that had progressed since the imaging

from December 8th. Id. at 1507, 1508. The radiologist who performed the MRI specifically noted

that “[g]iven the long segment involvement, rapid progression and diffuse cross-sectional

involvement, findings most likely represent transverse myelitis or a demyelinating process such as

neuromyelitis optica.” Id. at 1507.

Petitioner remained hospitalized throughout mid-December. She underwent yet another

MRI on December 18, 2019, this time of her cervical and thoracic spine, and it was performed

with and without contrast. Ex. 5 at 1086–87. The imaging showed further progression of T2 signal

changes, into upper thoracic cord, extending from medulla to the level of T5-6, with the latter

progression deemed “convincing evidence of a gray matter process.” Id. at 1086. But there was

also evidence of “abnormal diffusion-weighted imaging within the mid cervical cord,” plus “new

irregular patchy enhancement throughout the cervical cord.” Id. Overall (and with some emphasis

on the finding of gray matter thoracic involvement), the radiologist who performed the MRI

deemed the results to be suggestive of a subacute cord infarct.” Id. (A progress note prepared by

one of Petitioner’s treaters later that month characterized the results of this particular MRI to “favor

ischemia rather than inflammatory process.” Ex. 5 at 67).

A follow-up lumbar puncture to test Petitioner’s CSF occurred on December 18, 2019. Ex.

5 at 1401. It again revealed normal protein levels, but a white blood cell count of eleven, one over

the lab’s range of normal (1-10). Id. (as discussed below, the parties dispute the medical validity

of this range). Notably, this CSF sample was taken ten days after Petitioner’s onset. The next day

(December 19, 2019), a spinal angiogram was performed, and compared to the results of the

5

“NIPPC” stands for “Noninvasive Positive Pressure Ventilation”—a medical treatment that delivers breathing

support using a mask, rather than via an invasive breathing tube (endotracheal tube). Noninvasive Ventilation, National

Library of Medicine, https://www.ncbi.nlm.nih.gov/books/NBK578188/ (last visited May 8, 2026).

4

December 18th cervical/thoracic MRIs. Id. at 1516–18. (The preamble section of the report clearly

identifies Petitioner’s differential at this time as “suspected transverse myelitis versus possible

cord infarct”). Id. at 1516. The angiogram showed “patency of the anterior spinal artery,” as well

as segmental medullary arteries bilaterally, with normal appearing capillary and venous blush of

the cervical cord. Ex. 5 at 1518. No other interpretation of the findings is contained in the imaging

report.

On December 25, 2019, Petitioner began receiving IVIG therapy, which she completed

four days later. Ex. 5 at 67. On the 26th, she was evaluated for transport to a rehabilitation facility

for further care. Id. Petitioner continued to receive care in the ICU until January 7, 2020, when she

was discharged and transferred to Craig Hospital for in-patient rehabilitation. Id.; Ex. 1 at 45.

Treatment in First Half of 2020

Petitioner remained at Craig Hospital from early January to late March 2020. Ex. 1 at 45.

Upon admission, it was noted that she had been diagnosed with pneumonia while in the ICU and

treated for it with an antibiotic. Id. Petitioner now reported blurry vision for the first time, and she

continued to have shortness of breath, for which she was still on a ventilator. Id. at 46. The

admitting physician assessed Ms. Henningsen with tetraplegia with cranial nerve involvement of

unknown etiology, and her differential diagnosis at that time included TM, neuromyelitis optica

spectrum disorder (“NMOSD”), or a vascular event. Id. She was evaluated for respiratory failure

deemed secondary to quadriplegia. Id. at 49.

After arriving at Craig Hospital in January, Petitioner was evaluated by Kori Lehman PA-

C and neurologist Maysun Ali, M.D. Ex. 1 at 67. At this point, Ms. Henningsen had no spontaneous

movement in all four extremities on exam, flaccid tone throughout and decreased sensation distal

to C4. Id. at 66. It was also noted the December 8th MRI performed with diffusion seemed to point

toward a spinal cord infarct, although TM could still not be fully excluded (and further imaging

was not deemed to be warranted). Id. at 67. Petitioner was prescribed a low dose of acetylsalicylic

Acid (aspirin) “for potential spinal cord infarct,” although PA Lehman deemed this “less likely”

since there was not evidence of “multiple areas infarct at once.” Id.

On January 27, 2020, a lumbar puncture revealed that Petitioner’s CSF proteins were

within range and other laboratory testing yielded normal results. Ex. 13 at 1516. In early February,

Petitioner was seen by another neurologist, who took note of the fact that her onset had occurred

over a matter of hours, suggesting cord ischemia, but that MRIs showed cord signal abnormality

that increased with edema and enhancement, supportive of an inflammatory process as causal. Ex.

1 at 3783. Upon examination, the neurologist did not observe any voluntary movement in

petitioner’s upper or lower extremities. Id. at 3787.

5

On February 10, 2020, Ms. Henningsen underwent another MRI of her cervical spine, and

it revealed extensive diffuse multifocal areas of hyperintensity in the cervical and upper thoracic

cord. See Ex. 13 at 1218. The radiologist noted that many of these lesions were “associated with

cord volume loss suggest[ing] chronicity.” Id. Further, many “appear[ed] to predominantly involve

the peripheral white matter regions within the cord, which would favor chronic demyelinating

disease. Other considerations include[d] neuromyelitis optica although no abnormality [was] seen

in the optic nerves.” Id. at 1219. The following month, another cervical and thoracic MRI was

performed, and it did not identify any new or enlarging areas of cord signal abnormality. See Ex.

13 at 854. There was ongoing slight volume loss at C2-T3, but also substantial resolution of prior

abnormal enhancement of central gray matter from C3-T3, which may have reflected “evolution

of encephalomalacia.” Id. at 855. This radiologist proposed a cord ischemia insult, given the rapid

disease progression revealed from prior MRIs, plus the lack of imaging evidence of brain

involvement. Id.

On March 27, 2020, petitioner was discharged from Craig Hospital, with a diagnosis of

tetraplegia likely due to seronegative NMOSD. See Ex. 1 at 3330. NMOSD was favored “given

morphology of long segment transverse myelitis extending up to dorsal medulla and presenting

with acute onset tetraplegia and nausea suspected to be due to involvement of area postrema,”

although other indicia for NMOSD (a funduscopic exam and an MRI of optic nerve) were negative,

and thus not supportive of this diagnosis. Id. A vascular event was also not ruled out, although

repeat spinal angiograms had produced negative results. Id. In addition, testing for AQP4-IGG

(aquaporin-4 antibodies) was also negative (meaning the possible NMOSD was classified as

seronegative). Id. Further evaluation for other causes of transverse myelitis were negative,

following testing for lipoprotein insulin resistance done by Swedish Medical Center, and CSF

cultures and cell counts came within normal limits. Id.

Subsequent Treatment and Neurology Consults

After discharge, Petitioner made significant improvement in power-wheelchair mobility

and medical stability, but nevertheless spent time in a long-term post-acute care medical facility

(beginning in late March) for continued rehabilitation. Ex.1 at 3331; Ex. 3 at 31. Petitioner’s

diagnosis upon admission was tetraplegia secondary to “neuromyelitis optica spectrum disorder

versus spinal infarct versus TM,” with it being emphasized that her etiology remained unknown.

Ex. 3 at 31. She remained in the acute care facility until April 17, 2020, when she was discharged

home due to improvement, with the same differential she was provided at her admission. Id. at 36;

Ex. 4 at 22. Upon discharge, she was in a wheelchair and her tracheostomy tube was capped. Id.

She was to begin receiving home health nursing and physical therapy. Id. at 212.

On May 12, 2020, Ms. Henningsen returned to Craig Hospital for a post-discharge

assessment. She was described as a 26-year-old “previously healthy female with C2 ASIA B spinal

6

cord injury due to likely Seronegative NMOSD.” See Ex. 1 at 938. Petitioner reported that her

right upper extremity was weaker, and over all she felt she had lost some sensation, but other than

blurry vision reported no eye concerns. Id. at 939. There was no plan in place for neurology follow-

up, but it was recommended. Id.

Two months later (July 2020—approximately seven months from onset and initial

emergency treatment), Ms. Henningsen saw neuro-ophthalmologist Jeffery Bennett, M.D., for an

in-person evaluation of “acute onset transverse myelitis.” See Ex. 7 at 2. 6 Dr. Bennett noted that

the lesions revealed from Petitioner’s most recent MRI (performed in March 2020—three months

post-onset) appeared more discrete than in prior imaging, and also stated that a cell binding assay

for AQB4 antibodies had not been performed, nor was testing performed to assess the presence of

oligoclonal bands (which can be a biomarker for multiple sclerosis (“MS”)). Id. Dr. Bennett’s

working diagnosis was “post-vaccination TM,” and to support this view he referred to “case reports

in the literature that describe [post-vaccination TM],” before positing that it was unclear if

petitioner had a propensity for autoimmune response. Id. But more generally, Dr. Bennett

described Petitioner’s differential diagnosis as follows:

[w]hile this could be a seronegative NMO [neuromyelitis optica], her lack

of other consistent features outside of LETM [longitudinally extensive TM]

makes this less likely. Less likely to be MOG [myelin oligodendrocyte

glycoprotein] given severity of insult. Other diagnoses to consider include

spinal cord infarction vs spinal cord fistula vs alternative inflammatory

etiology such as sarcoidosis.

Id. (emphasis added).

Dr. Bennett ordered further serum testing for antibodies related to NMOSD (which yielded

negative results) and a repeat MRI. Ex. 7 at 2, 11–12. This MRI was performed on August 15,

2020. See Ex. 13 at 728–29. It revealed resolved cord expansion and abnormal enhancement, but

also severe cord atrophy below C4 and extending to T2 with myelomalacia, plus possible abnormal

signal in a few lower levels. Id. at 729. At a follow-up telehealth visit on August 31, 2020, Dr.

Bennett discussed the aforementioned findings with Petitioner. He explained that she was

clinically stable, and that the MRI demonstrated resolution of the cord edema and secondary cord

atrophy. Ex. 7 at 8. He contended that there was “no evidence of an alternative non-inflammatory

cause of spinal cord injury.” Id. Dr. Bennett assessed Petitioner with TM. Id.

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Dr. Bennett’s treatment of Petitioner appears to have been limited to “an outpatient history and examination on July

27,2020, [and] a telehealth conference on August 31, 2020,” along with some records review. See Report, dated

February 24, 2022, filed as Ex. 16 (ECF No. 17-1).

7

Petitioner has since continued to be treated for her debilitating condition. See, e.g., Ex. 151.

Despite the catastrophic impact of her illness on her life, Petitioner has endeavored to find ways

to lead as productive an existence as possible. In March 2024, for example, she had completed a

master’s program, and was preparing for a social work exam. Id. at 7.

II. Hearing Witnesses

Both sides offered the testimony of three kinds of experts: a clinical neurologist; a

radiologist and/or expert in the reading and interpretation of MRI results; and finally an

immunologist to comment on the underlying causation issues in this case. I address herein only

the expert opinions and testimony bearing on the outcome. 7

A. Fact Witness – Alice Henningsen

Petitioner was the only fact witness to testify at hearing. See generally Transcript, filed

June 20, 2025 (ECF No. 91) (“Tr.”) at 7–31. Prior to October 2019, Petitioner worked for Comcare,

a community mental health organization, in the Youth Services branch, and volunteered at the

Wichita Area Sexual Assault Center (“WASAC”). Id. at 8. At Comcare, Petitioner would meet

with children “to develop and work towards their treatment goals”, and for WASAC, she worked

the 24-hour crisis response line, as well as provided advocacy to survivors of sexual assault in a

hospital setting. Id. In addition, Petitioner was attending school to obtain a master’s degree in

social work. Id. at 9. She described her typical week—noting how incredibly busy it was with

being a student, working/volunteering, all while maintaining an active lifestyle and partaking in

hobbies such as attending live music and spending time with friends. Id. And she emphasized the

lack of any restrictions preventing her from doing her activities of daily living. Id. at 10.

She briefly recounted the day she received her flu vaccine on October 31, 2019, explaining

that it was her first time receiving the flu shot. Tr. at 10. She then spent some time discussing the

state of her mental health while hospitalized and noting how severely impacted it was. 8

Specifically, Petitioner suffered from “ongoing panic attacks” that would last all day, and

oftentimes she would “count the minutes until [she] would receive medication that would help

with [her] anxiety.” Id. Moreover, the physical pain was so bad that at times it would take her

breath away. Id. Petitioner further stated that she would completely disassociate for “weeks on

7

I thus do not summarize the testimony of either side’s immunologic experts—Drs. Steven Bradfute and William

Hawes—whose testimony primarily pertains to the “can cause” prong for causation. My decision turns on the issue of

diagnosis, as well as whether the flu vaccine likely did cause Petitioner’s injury (assuming it was TM, and that TM

could be vaccine-caused).

8

Throughout her testimony, Petitioner emphasized how much she struggled mentally and the overall mental strain the

panic attacks and her paralysis had on her. See, e.g., Tr. at 11, 14, 16, 18.

8

end” as a result of being caught in such a traumatic experience without the ability to fight or flee.

Id. at 11.

Petitioner remained in the hospital ICU for approximately one month before being

transferred to an inpatient rehab facility at Craig Hospital for an additional three months. Tr. at 13,

14. While in rehab, Petitioner had to relearn many basic skills of living, such as eating, swallowing,

breathing without assistance, as well as positioning herself properly in bed or in her chair. Id. at

13. She then was discharged and transferred to a skilled nursing facility for approximately two

weeks. Id. at 14. Following her stay at the skilled nursing facility, Petitioner was eventually

discharged to her mother’s home where she required in-home healthcare assistance in addition to

the support her mother provided.

Petitioner attempted to return to school in the spring of 2021 to complete her last semester

but lacked the technological support to successfully do so at that time. Tr. at 17. She later returned

to school in the summer of 2023, and graduated that December with a degree in psychology

followed by a master’s in social work. Id. at 20. Petitioner currently works part-time as a therapist,

seeing clients regularly and assisting them with their treatment plans and goals. Id. In addition,

Petitioner provides “safety plans for clients that have high acuity, meaning they have a long history

of suicidal ideation or attempts or high incidence of self-harm.” Id. During her testimony,

Petitioner further noted that her overall career path changed due to her injury as it was not feasible

for her to pursue case management like she originally hoped.

Petitioner concluded her direct testimony describing her current living situation and

explaining the various challenges she faces with living alone, navigating her apartment complex,

and adjusting her schedule when aides call in sick, etc. She continues to rely heavily on home

health aides twice a day for approximately two to three and a half hours at a time. Tr. at 22.

Petitioner stated that she has gotten more comfortable with leaving her house to visit family and

friends, but that she rarely is able to travel since her injury. Id. at 27. Overall, Petitioner emphasized

the impact her injury has had on her quality of life—noting that she has been stripped of “some of

the most meaningful parts of [her] life” such as her independence and ability to be self-sufficient;

however, she tries her hardest to focus on what she can do. Tr. at 29.

B. Petitioner’s Experts

1. Dr. Andrew Pachner – Dr. Pachner is a neurologist, and he testified at

hearing and prepared three expert reports on Petitioner’s behalf. Report, dated Jan. 23, 2023, filed

as Ex. 62 (ECF No. 31-1) (“First Pachner Rep.”); Report, dated Feb. 19, 2024, filed as Ex. 108

(ECF No. 55-1); Report, filed Oct. 7, 2024, filed as Ex. 158 (ECF No. 64-9).

9

Dr. Pachner attended Yale College for his undergraduate degree, and Yale University

School of Medicine for his medical degree. Curriculum Vitae, filed as Ex. 63 (ECF No. 31-2)

(“Pachner CV”); Tr. at 33. He then completed an internship and residency in Internal Medicine at

Johns Hopkins Hospital, followed by fellowship and chief residency position in Neurology at

Yale-New Haven Hospital. Id. He has held several academic appointments and currently serves as

the Murray B. Bornstein Professor of Neurology in the Department of Neurology, as well as the

Director of the Multiple Sclerosis Center, at Darthmouth-Hitchcock Medical Center and Geisel

School of Medicine. Pachner CV at 2; Tr. at 34. Dr. Pachner is board certified by the American

Board of Psychiatry and Neurology in Neurology with added qualification in Neuromuscular

Medicine. First Pachner Rep. at 1; Tr. at 34. He has published extensively in the areas of

Neuroimmunology and Neuroinfectious disease. Tr. at 37; Pachner CV at 22–35. Dr. Pachner

admitted his expertise ran more to neurologic matters than with respect to strokes, although he

noted he had in his professional career been involved in treatment of some spinal cord infarcts. Tr.

at 98–99, 460–61; First Pachner Rep. at 1.

Dr. Pachner began his testimony explaining some of the medical concepts relevant to the

parties’ diagnostic dispute. He slightly differentiated between a “myelopathy” (which he defined

to mean “any damage to the spinal cord causing clinical symptoms,” such as would result from the

mechanical harm due to a vertebral disc herniation), and “myelitis” (meaning “damage to the spinal

cord caused by inflammation”). Tr. at 38, 39. It was the later kind of harm that Petitioner had likely

experienced, he proposed (with myelitis essentially a subset of myelopathy). Id. at 39. TM was a

form of myelitis involving inflammatory harm “across the whole width” of the spinal cord (and

hence distinguishable from a more limited, localized harm). Id. The location of such

neuroinflammatory harm was “critical for trying to understand the clinical sequelae of the

damage.” Id.

TM, in Dr. Pachner’s view, was the proper diagnosis for Petitioner’s illness. Tr. at 45. And

he reached this conclusion even while allowing that infarct had been appropriately included in

Petitioner’s overall differential diagnosis. Id. at 46–47. To substantiate the diagnosis, Dr. Pachner

referenced current criteria applied to TM, endeavoring to show that the required elements were all

satisfied. Id. at 48–49; G. Barnes, et al. (on behalf of “Transverse Myelitis Consortium Working

Group”), Proposed Diagnostic Criteria and Nosology of Acute Transverse Myelitis, 59 Neurol.

499 (2002), filed as Ex. 18 (ECF No. 17-3) (“Working Group Criteria”). As Dr. Pachner noted,

Ms. Henningsen had “bilateral signs or symptoms,” (Tr. at 49), and a “clearly defined sensory

level” (meaning her clinical sensory issues corresponded to the location of inflammation on the

cord (Tr. at 49–50)). He also noted (as reviewed in more detail below) the evidence from CSF

testing for inflammation (here an elevated white blood cell count), along with MRI enhancement

(which confirmed compromise of the blood-brain barrier). Id. at 51–52. Dr. Pachner highlighted

as well the fact that the TM diagnosis had been embraced by treating physician Dr. Bennett, whom

he characterized as “one of the preeminent neuroimmunologists in the world.” Tr. at 47.

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At the same time, certain exclusionary factors that would disfavor a TM diagnosis were

absent. Tr. at 56. For example, there was no evidence of a compressive etiology (due to a vertebral

disc). Id. at 50. Petitioner had been exposed to no spinal radiation. Id. at 53. There was no evidence

of arteriovenous malformations. Id. at 55. There was an absence of evidence of an infectious

explanation for the inflammation, no proof Petitioner had experienced a systemic autoimmune

disease, and no way to attribute the spinal cord issues to a different kind of CNS neuropathic

disease, like MS. Id. at 55–56.

Dr. Pachner also maintained that the evidence of inflammation (as seen in the MRI images)

did not appear to be “confined” to the anterior spinal artery section of the cord. Tr. at 53–54, 74,

77–78. This kind of territorial “grouping” of inflammation was, Dr. Pachner maintained, “the most

common, by far, cause of . . . spinal cord stroke.” Tr. at 53. That aspect of the spinal cord was

oriented to motor nerves, rather than sensory—and transverse myelitis would usually involve “the

posterior part [of the cord], which predominantly carries sensory modalities.” Id. at 54. Thus, the

“vast majority [of infarct patients]” experience sparing of sensitivity to “vibration and position

sense,” while TM patients have all “sensory modalities” impacted (since the TM-associated

inflammation is not confined). Id. at 74. Yet Petitioner appeared in neurologic exams to have lost

vibration sense—inconsistent with an infarct. Id. at 75. In reaching this opinion, however, Dr.

Pachner relied somewhat on Dr. Bajakian’s interpretation of the imaging, although he noted that

this exclusionary criteria involved clinical evidence of “deficits.” Id. at 54–55, 76.

Imaging results further supported TM as the proper diagnosis. Tr. at 72–78. For example,

there was evidence of signal enhancement in some images—something more usually characteristic

of TM (although it was “not obviously impossible” for an infarct). Id. at 72, 73. Dr. Pachner also

highlighted the fact that imaging of infarcts usually reveals “shorter involvement” of the cord,

longitudinally—but in this case, imaging revealed “extensive involvement of the spinal cord all

the way down to the thoracic cord,” more consistent with TM (although Dr. Pachner admitted that

length could occur in the context of an infarct as well). Id. at 76, 77. And the mere location of the

lesion, as revealed in imaging, was characteristic of TM. Id. at 77. Infarcts were usually seen “in

the mid to lower thoracic cord,” while TM lesions occurred “in the cervical and upper thoracic

cord.” Id. at 77, 108 (stating that “vast majority” of infarcts are below cervical region).

Dr. Pachner provided greater detail as to why he believed Petitioner’s initial, clinical course

was consistent with acutely-presenting TM. As he noted, the diagnostic criteria required evidence

of “progressive worsening to nadir” (meaning “lowest level of damage that occurs) occurring

within 4 hours to 21 days. Tr. at 52; Working Group Criteria at 500 Table 1. This had happened in

Petitioner’s case. Tr. at 53. Petitioner had reported first experiencing back pain and shoulder

tightness the evening of December 7, 2019. Tr. at 57–58. By the next day (December 8th at 11:15

am), the pain returned along with bilateral arm and back numbness/tingling, and it worsened in

11

two hours, progressing to an inability to move and ultimately evidencing quadriplegia. Id. (Dr.

Pachner later admitted that early treaters were unsure as to the precise nature of Petitioner’s injury,

and reasonably not only included infarct in the differential but even included some possible initial

treatment for it. Tr. at 465–66).

In Dr. Pachner’s view, Petitioner’s progression continued downward through the next day

(December 9th). Overnight, she experienced breathing difficulties that required attention on the

10th, which Dr. Pachner considered evidence that “the process that was affecting her spinal cord

had moved up to the breathing centers in her spinal cord” and requiring intubation. Tr. at 60. Dr

Pachner viewed this as a significant negative change in Petitioner’s progression. Id. at 61. Thus,

by this time, a few days had passed—long enough to fit the timeframe for TM, but less acute than

what would be expected for an infarct. Id. at 63.

In so opining, Dr. Pachner rejected the conclusion of Respondent’s experts that progression

to nadir had unfolded more rapidly, over the space of no more than four or five hours. Tr. at 60–

63. A shorter progression would, he admitted, be more associated with infarcts. Id. at 66 (“within

minutes to a few hours”). But Dr. Pachner favored an onset of somewhere between five hours and

two days, based on his belief that nadir was actually reached after December 8, 2019. Tr. at 106–

08, 468–70. As he stated, “it wasn’t until later that her work of breathing was felt to be so impaired

that she needed to be intubated. But that was not true earlier in her course.” Id. at 470. He also

noted literature offered as evidence of the diagnostic criteria for a spinal cord infarct. N. Zalewski

et al., Characteristics of Spontaneous Spinal Cord Infarction and Proposed Diagnostic Criteria,

76 JAMA Neurol. 1:56 (2018), filed as Ex. E-1 (ECF No. 41-2) (“Zalewski”). Zalewski included

a temporal criterion of “onset to nadir deficits 12 h or less,” but the timeframe here was plainly

longer, in Dr. Pachner’s opinion. Tr. at 63; Zalewski at 60 (Box). Nevertheless, Dr. Pachner

contended, a rapid symptoms progression could still occur in a very short time and be consistent

with TM. Id. at 467–68; Working Group Criteria at 500 Table 1.

By contrast, Dr. Pachner denied that a number of criteria relevant to a spinal cord infarct

had been established. For example, Petitioner was not in the cohort of individuals old enough to

be at risk for stroke. Tr. at 65. She also lacked many of the other associated health risk factors for

a vascular event, such as “diabetes, hypertension, [or] hyperlipidemia . . .” Id. In addition, TM

usually impacted the cervical section of the spinal cord (in the neck, from the base of the skull to

the start of the upper back), 9 affecting the arms and legs (and thus presenting sometimes with

quadriplegia), whereas an infarct would occur in a lower spinal cord segment. Id. at 66–67.

The CSF testing results also supported TM, in Dr. Pacher’s view. Tr. at 67–72. Dr. Pachner

proposed that “the medical literature is pretty much unanimous that anything over five white

9

See Park at 7 (stating that “TM on the other hand, is mainly distributed across the cervical and upper thoracic levels.”).

12

[blood] cells per microliter is abnormal and indicative of an inflammatory or infectious process

within the spinal fluid.” Id. at 68; R. Fishman, “Composition of Cerebrospinal Fluid,” in

Cerebrospinal Fluid in Diseases of the Nervous System (1980), filed as Ex. 161 (ECF No. 75-2)

(“Fishman”), at 175 (“a [WBC] count greater than 10 cells per mm3 is pathognomic of disease in

the central nervous system”). 10 And there was a high correlation between white blood cell count

in CSF testing and TM. Tr. at 69; S. Al Deeb et al., Acute Transverse Myelitis: A Localized Form

of Postinfectious Encephalomyelitis, 120 Brain 1115 (1997), filed as Ex. 70 (ECF No. 31-9) (“Al

Deeb”), at 1120 (finding CSF results were abnormal in 94 percent of 31 patient sample, although

WBC count levels correlated less to outcome than protein levels). Here, Petitioner’s testing

revealed 11 white blood cells—a number that was “clearly abnormal” in Dr. Pachner’s view, even

if it was not notably “massive” either. Tr. at 70, 71. Dr. Pachner also proposed that the testing

hospital applied an overly-expansive testing range (zero to ten as normal) that undervalued the

significance of Petitioner’s result. Id. at 71–72, 110 (deeming range applied by testing hospital in

this case too improper).

Dr. Pachner denied that the level of pleocytosis should be much higher for TM (due to the

neuroinflammation in the cord that it would reflect), contending that “there’s essentially no

correlation between the extent of inflammation in the parenchyma of the brain and what you see

in CSF,” and noting that MS patients often have “incredible inflammation” in their brains but

reveal low-elevated white blood cell levels (although this case does not involve brain lesions, or

MS for that matter). Tr. at 470, 471. An active spinal cord infectious process, such as the kind of

bacterial infection resulting in meningitis, might reveal high levels of white blood cells in CSF

testing, but “when the inflammation is limited to the parenchyma, . . . there’s frequently no

correlation.” Id. at 471. 11

On cross-examination, Respondent questioned Dr. Pachner about some of his contentions

regarding clinical or testing factors in this case favoring TM over an infarct. See generally Tr. at

98–123. Dr. Pachner admitted that according to the Working Group Criteria, evidence of

inflammation (whether from CSF testing or enhancement seen in imaging) needed to be present at

time of onset or within seven days thereafter. Id. at 101; S. Beh et al., Transverse Myelitis, 31

Neurol. Clin. 79 (2013), filed as Ex. A-1 (ECF No. 22-2) (“Beh”), at 98 Table 8. Here, however,

10

Fishman, as filed in this case, appears to be a single page from a larger text. Not only is it not a particularly recent

publication, however, but the cited page also states as follows: “[a] pleocytosis of 5 to 50, 50 to 200, or more than 200

white cells is graded as mild, moderate, or marked, respectively.” Fishman at 175. Thus, even if Dr. Pachner was

correct in his contention that a cell count of 11, as here, was evidence of CNS inflammation, that total count constitutes

only a low-range “mild” degree of inflammation, at least as defined by Fishman.

11

Dr. Pachner’s direct testimony also included explanations for how the flu vaccine could cause TM. Tr. at 80–82,

84–95. But the resolution of this claim does not turn on a “can cause” analysis, and I do not therefore include an in-

depth review of this aspect of his opinion. Dr. Pachner did admit that a “substantial proportion” of TM cases are

idiopathic in origin (Id. at 100), and that he lacked specific immunologic expertise. Id. at 110–12.

13

Petitioner’s initial WBC testing revealed normal results, and a re-test of the CSF did not later show

even mild levels of inflammation until about ten days post-onset. Id. at 102. But Dr. Pachner denied

this elapse of time in excess of the testing interval set forth in Beh was relevant, deeming the seven-

day timeframe artificially short, in order to exclude longer periods (and he also opined it was likely

that if Petitioner had been tested in the period between December 8th and 18th, her WBC levels

would likely have been high since her nadir occurred in that timeframe). Id. at 102–03, 104.

Dr. Pachner was later called back to the stand for Petitioner’s rebuttal case, and he

addressed several of Respondent’s arguments. He contended that Respondent over-relied on

Zalewski for the proposition that infarcts were very commonly misdiagnosed as TM, maintaining

that the article fell victim to referral bias. Tr. at 461–62. The patients evaluated in Zalewski were

unique cases seen at the Mayo Clinic due to their diagnostic complexity, and therefore were not

representative of the “vast majority” of TM patients seen is less specialized medical environments

(whose diagnoses were likely easier to ascertain). Id. at 462. At most, Zalewski reflected the fact

that diagnosing TM could be difficult (although Dr. Pachner added that he would not himself have

found it necessary to refer Petitioner to a place like the Mayo Clinic for more diagnostic specificity

under the circumstances). Id. at 463–64. 12 (Of course, this overall argument somewhat flies in the

face of the fact that this case itself is illustrative of the very degree of diagnostic complexity that

Zalewski’s authors were addressing).

Dr. Pachner also endeavored to highlight a purported factual dispute between the radiologic

experts as to the nature of Petitioner’s neurologic deficits, and what that said about the proper

diagnosis. He contended that while “the deficit and the imaging all was consistent with a lot more

than just the anterior spinal artery distribution,” Respondent’s own experts 13 disagreed as to

whether evidence of spinal cord harm in this case was territorially limited to one portion of the

cord or had impacted the cord more indiscriminately. Tr. at 465. In Dr. Pachner’s view, infarct was

more likely to impact only the anterior portion of the cord – as assumed by treaters close-in-time

to Petitioner’s initial presentation, who noted no sparing of vibration sensation – so a more

expansive injury was less compatible with infarct. Id.

12

Dr. Pachner also noted that Petitioner had received a “good second look” at her diagnosis—both when treaters

endeavored to rule out the possibility of neuromyelitis optica, and then later, when she saw Dr. Bennett in 2020. Tr.

at 464.

13

The question posited to Dr. Pachner that elicited this testimony assumed that while Respondent’s diagnostic expert,

Dr. Price, had testified that he believed cord damage in this case was not limited to the anterior territory, Dr. Zucconi

(Respondent’s radiologic expert) had proposed a more limited cord territorial impact. Tr. at 465. In fact, although Dr.

Zucconi emphasized that (as evidenced by earlier imaging) he considered the central gray matter in the cord (which

he deemed the “most sensitive area to ischemia” (Tr. at 238)) impacted primarily, this is not the same as concluding

that only one territorial portion of the cord was affected. It also is not inconsistent with the fact that infarcts often are

limited to the anterior part of the cord (something that can be corroborated by the presence of vibration sensitivity

“sparing,” since that neurologic function comes from a different part of the cord). Id. at 346–47. But it has not been

shown in this case that infarcts only occur in the anterior of the cord (any more than it would be true that TM can

never occur in the same rapid timeframe as what Petitioner experienced).

14

2. Dr. Richard L. Bajakian – Dr. Bajakian is a neuroradiologist, and he offered

an opinion (both via written reports and testimony) arising from his interpretation of the various

MRI findings obtained during Petitioner’s treatment course. Report, dated Jan. 30, 2023, filed as

Ex. 44 (ECF No. 30-1) (“First Bajakian Rep.”); Report, dated July 20, 2023, filed as Ex. 96 (ECF

No. 45-1) (“Second Bajakian Rep.”). Dr. Bajakian overall opined that Petitioner’s imaging results

were most consistent with some form of TM-like inflammatory myelopathy. Tr. at 132.

Dr. Bajakian attended Syracuse University for his undergraduate degree, and New Jersey

Medical School for his medical degree. Curriculum Vitae, filed as Ex. 45 (ECF No. 30-2)

(“Bajakian CV”) at 1; Tr. at 129. Thereafter, he completed an internship at Monmouth Medical

Center and his residency in Diagnostic Radiology at Morriston Memorial Hospital. Bajakian CV

at 1; Tr. at 130. Dr. Bajakian also completed a fellowship in Neuroradiology at Brigham and

Women’s Hospital. Id. He held several academic appointments, as well as opened an outpatient

MRI center in 2001 with another physician. Tr. at 131. Dr. Bajakian eventually sold his practice

in 2021 and no longer practices clinical medicine since October 2022. Id. He further estimated that

over the course of his career, he has reviewed approximately 100,000 to 200,000 MRIs of the

cervical, thoracic, and lumber spine. Id. at 131–32. Dr. Bajakian was board certified by the

American Board of Radiology with a subspeciality in Neuroradiology. First Bajakian Rep. at 1.

Dr. Bajakian framed his imaging opinions with an explanation of the distinction between

TM and a spinal cord infarct. Tr. at 133–40. He characterized infarcts as “fixed” lesions reflecting

specific areas of cord death—in contrast to a myelitis, which is “a much more dynamic process”

due to its inflammatory origin. Id. at 133. He noted that three blood vessels “feed” the spinal cord—

an anterior artery (on the front of the body) and two posterior arteries. Id. at 134–35. Most spinal

cord infarctions would involve a “sing[ular] vascular territory,” would not be visible from initial

imaging, are usually not “longitudinally extensive,” and would not enhance (or if so only faintly).

Id. at 137–38. TM, by contrast, will involve “signal abnormality on presentation,” with enhancing

lesions that are extensive (“spanning more than three [spinal] segments”), and that are not as

confined, involving “gray and white matter indiscriminately.” Id. at 138.

In addition, Dr. Bajakian maintained that infarcts were more commonly limited to the

thoracic region of the spine, whereas TM is mostly cervical or cervical/thoracic. Tr. at 191. And

cord swelling and edema generally were not common to infarct (noting that even in articles like

Zalewski specific to diagnosing infarcts, only a fifth of the patients studied experienced swelling

and edema). Id. at 280–81; Zalewski at 59 Table 2. By contrast, Dr. Bajakian contended,

“vasogenic edema” would more commonly be seen with TM, another product of the

neuroinflammation driving it. Id. at 281.

15

Another overarching factor that Dr. Bajakian deemed significant in interpreting MRI

studies to support infarct versus TM was the presence of enhancement. Although he allowed that

infarct imaging could feature enhancement, this was not their “typical pattern.” Tr. at 189. In

addition, any enhancement present should not cross “multiple vascular territories,” and should

more often than not be faint. Id; Zalewski at 62. Where (as here, in Dr. Bajakian’s opinion) the

imaging revealed greater spinal cord involvement, and TM became a more likely diagnosis. Tr. at

189–90. (Later on, however, Dr. Bajakian contended that “pencil-like hyperintensities” seen on

some of the images in question in this matter—especially some of the initial imaging—were not

necessarily specific to infarcts, and he seemed to give more weight to evidence of multiple vascular

territory enhancement as proof of TM). Id. at 191–92).

Dr. Bajakian subsequently provided commentary on the critical sequence of imaging in

this case. (For ease of analysis and review, I address this portion of his testimony according to the

image sets in question):

(a) First December 8, 2019 Images – Dr. Bajakian noted that imaging of the

cervical cord from the afternoon of December 8th demonstrated “increased signal centrally within

the spinal cord,” noting what he saw as indicia of cord swelling at this time. Tr. at 141, 276. He

considered this result to be abnormal, and to evidence diffuse inflammation, impacting the anterior

and posterior spinal cord and with proof of the kind of longitudinally-extensive signal (from the

C3 to T2 level—seven segments) common to inflammatory myelopathies. Id. at 142. (These initial

images did not involve the use of contrast, so no enhancement of signal abnormalities could be

detected in them).

TM, Dr. Bajakian contended, was more likely to present with this kind of proof of signal

abnormality than an infarct. Tr. at 145–46; C. Alblas et al., Acute Spinal-Cord Ischemia: Evolution

of MRI Findings, 8 J. Clin. Neurol. 218 (2012), filed as Ex. 46 (ECF No. 30-3) (“Alblas”), at 222

(imaging usually normal in acute phase of ischemia compared to myelitis). He later referenced

other literature specific to infarct supporting the view that no abnormal signal might be evident

even within 12 hours of an infarct’s onset. Tr. at 201–02; D. Park et al., Spinal Cord Infarction: A

Single Center Experience and the Usefulness of Evoked Potential as An Early Diagnostic Tool, 11

Front. Neurol. 1 (October 2020), filed as Ex. 59 (ECF No. 30-16) (“Park”), at 3, 5 Table 3 (noting

that of 14 cases of patients with spinal cord infarct, nine had no evidence of T2 signal intensity in

initial imaging performed within 12 hours of onset). Park also noted, however (since all of its

sample patients later showed DWI results consistent with infarct), that the lack of initial imaging

evidence supportive of infarct likely meant that “it is not easy to diagnose [infarct] based on an

initial T2 image”—not that the lack of such evidence in initial imaging counseled against an infarct

diagnosis entirely. Park at 8.

16

Early swelling of the cord was also consistent with TM more than infarct. Tr. at 188, 276.

And Dr. Bajakian directly contested the view of Respondent’s neuroimmunologist, Dr. Zucconi,

that swelling was not yet present (but showed up later). Although he allowed that there was

evidence of a “fuller” cord at the C3-C4 level, he denied it could be attributable to a “partial

voluming effect,” because if so, the fullness should have been more broadly evident. Id. at 276–

77.

Dr. Bajakian disagreed with the contemporaneous radiologic treater who deemed these

initial results normal—an opinion that he correctly noted he shared with Respondent’s imaging

expert (Dr. Zucconi). Tr. at 143–45. Dr. Bajakian allowed for the reasonableness of Dr. Zucconi’s

observation that the initial image revealed a “pencil-like hyperintensity” (an indicia of infarct), but

disputed its pertinence, maintaining that both clinically and radiologically, there was evidence of

“posterior spinal cord involvement,” rather than the territorial limitation to the anterior cord that

would be expected for an infarct. Tr. at 147.

(b) Second December 8, 2019 Images – For the next round of imaging,

performed later in the evening of December 8th, treaters had employed DWI, which Dr. Bajakian

explained can help reveal the presence of “areas of dead or dying cells.” Tr. at 149. (Dr. Bajakian

did not expressly acknowledge, however, that DWI is most commonly used to evaluate the

presence of an infarct. Id.; see also K. O’Connor et al., “Dazed and Diffused”: Making Sense of

Diffusion Abnormalities in Neurologic Pathologies, 86 Br. J. Radiol. 1 (2013), filed as Ex. 52

(ECF No. 30-9) (“O’Connor”), at 1 (stating that “the best known use of [DWI] in MRI of the brain

is detection of acute vaso-occlusive infarct”); Y. Kim et al., The Role of Diffusion-Weighted MRI

in Differentiation of Idiopathic Acute Transverse Myelitis and Acute Spinal Cord Infarction, 65 J.

Korean Soc. Radiol. 2:101 (2011), filed as Ex. 97 (ECF No. 46-1) (“Kim”), at 105 (noting “[t]he

usefulness of DWI in spinal cord infarction has been demonstrated in several papers,” and

differentiating infarct from TM is important for treatment purposes)). Dr. Bajakian nevertheless

questioned whether the DWI technique results favored infarct (as proposed by Dr. Zucconi), saying

he did not detect in the relevant image evidence of sufficient white-dark contrast needed to suggest

the presence of dead tissue areas, and that he felt the evidence of increased signal favored the

posterior portion of the cord—meaning “not in a single vascular distribution.” Id. at 151, 154.

In support of this argument, Dr. Bajakian cited O’Connor, which observed that acute MS

plaques in the brain commonly demonstrate DWI signal, thus underscoring the fact that “[o]ther

things can have restricted diffusion.” Tr. at 152; O’Connor at 7. O’Connor does not, however,

expressly state this, and only discusses MS lesions in the specific context of brain MRI results. Tr.

at 196; see generally O’Connor. Since this case involves spinal cord and not brain lesions,

comparisons to the utility and function of brain-oriented MRIs employing the DWI technique shed

little light on what DWI reveals with respect to the spine.

17

Dr. Bajakian also cited Kim as supporting his argument that DWI was not necessarily only

relevant to establishing the presence of infarct. Kim’s authors concluded that TM “usually does

not demonstrate restricted diffusion, which can be a clue to differentiate it from [infarct], … [but]

idiopathic ATM with larger segment involvement can show focal diffusion restriction.” Kim at

101; Tr. at 153. (Kim also notes, however, that “[i]n most cases of [acute transverse myelitis],

diffusion restriction was not identified,” whereas it is “noted in most [infarct] cases”) (Kim at

106)). TM featuring diffusion restriction was nevertheless consistent with what Petitioner likely

experienced, Dr. Bajakian opined. Other literature also filed in the case was, he contended,

consistent in concluding that positive DWI findings could be seen in connection with

demyelination due to inflammation. Tr. at 153–54 (citations omitted). Later in his testimony, Dr.

Bajakian took the more maximalist view that the kind of restrictive diffusion disclosed in DWI

imagining “can be seen in many diseases,” and therefore has less specific diagnostic value. Tr. at

192–93. 14

Besides downplaying the significance of the DWI findings, Dr. Bajakian emphasized the

situs of diffusion observed on this MRI. He deemed it inconsistent with an anterior cord infarct,

since there was evidence of some increased signal “all the way to the back of the cord.” Tr. at 154.

He also addressed the extent to which (as Dr. Zucconi contended) this imaging revealed

“preferential disease in the distribution” (favoring the gray matter, which is understood to be more

impacted by infarct). Id. at 155, 282. Dr. Bajakian accepted that “the central gray is more sensitive

to ischemia,” but added that too much of the “vascular territories” were impacted to deem an infarct

had occurred (which would more commonly be “confined to a solitary vascular territory”). Id. at

155, 156. And TM could involve evidence of lesions in both white and gray matter. Id. at 156

(citation omitted), 282.

The number of affected spinal segments evident from this imaging event was additional

proof favoring TM over infarct, in Dr. Bajakian’s view. Tr. at 157–58. Seven cord segments were

involved at this early stage in Petitioner’s presentation, consistent with TM (since the cord “has a

lot of collateral flow that helps to protect longitudinally extensive infarcts,” but which cannot stop

the progression of inflammation as easily). Id. at 158. Longer lesions, Dr. Bajakian maintained,

were more generally associated with TM than infarcts. Id. at 190–91; Park at 7 Figure 3 (depicting

comparison of 14 infarct patients versus 15 TM patients and revealed the latter had longer lesion

lengths). And enhancement (which Dr. Bajakian opined appeared to be impacting the whole of the

cord) could also be seen in this imaging, which would be a “very atypical first spinal cord infarct.”

Id. at 159.

14

This tendency to rule out any kinds of diagnostic findings as supportive in this case of infarct (while over-valuing

findings that are non-specific, or not wholly inconsistent with TM) undercut the probative strength of Dr. Bajakian’s

testimony as a general matter, as discussed below.

18

Dr. Bajakian also referenced the brain MRI performed on December 8th, the results of

which he deemed inconsistent with an infarct. He noted that vascular aspects of the upper spinal

cord would feed a number of brain components, and therefore emboli—“the most common cause

for spinal cord infarct, especially in young people” like Ms. Henningsen—should be potentially

evident in the brain (where they could cause infarcts as well). Tr. at 162. But such a finding was

absent from the brain MRI, undermining infarct (at least indirectly). Id.

Other features of this set of MRI images were, in Dr. Bajakian’s view, inconsistent with

Dr. Zucconi’s opinion. Dr. Bajakian denied, for example, that there was any evidence in this set

of images suggesting an explanation for infarct (i.e., disc protrusion). Tr. at 277. Rather, in Dr.

Bajakian’s view the image at most revealed “mild bulging” (as confirmed by the treater who

performed the MRI), and was not the kind of herniation that would be capable of causing an infarct.

Id. at 277–79. Nor did Dr. Bajakian agree that the cause of the infarct could have been a

fibrocartilaginous embolism, since the imaging again did not establish the kind of foundational

circumstances for such an occurrence. Id. at 279–80. Overall, Dr. Bajakian argued, by this time on

December 8th imaging was most consistent with TM. “Differential Diagnosis of SCI and TM”

Chart (litigation demonstrative aid), filed as Ex. 171 (ECF No. 87-3).

(c) December 10, 2019 Imaging Results – Dr. Bajakian deemed these results to

reveal that “the entire spinal cord from front to back is abnormal,” with no evidence at all of sparing

(which he assumed would occur with an infarct). Tr. at 163, 164 (deeming the cord involvement

to be close to 90 percent). He also observed hyperintense abnormal signaling higher up the cord,

in places, plus evidence of a central “hypointense nodule” that he proposed was consistent with

TM. Id. at 165. And even if there was some higher cord evidence of abnormality specific to gray

matter, the shaping and posterior locality was not in Dr. Bajakian’s view consistent with the

distribution characteristic of an anterior spinal cord infarct. Id. at 166.

In addition, Dr. Bajakian stressed that these images did not reveal evidence of secondary,

vertebral artery infarcts (which could often be seen in follow-up imaging) that would confirm an

initial spinal cord infarct (although their absence does not negate the possibility of a spinal cord

infarction). Tr. at 166–68, 187–88, 204; J. Faig et al., Vertebral Body Infarction as a Confirmatory

Sign of Spinal Cord Ischemic Stroke: Report of Three Cases and Review of the Literature, 29

Stroke (AHA J.) 239 (1998), filed as Ex. 55 (ECF No. 30-12), at 243 (“it is a strong argument for

spinal ischemia if there is an evolution of signal abnormalities in a vertebral body associated with

spinal cord syndromes at an appropriate level”).

(d) December 18, 2019 Imaging – Dr. Bajakian opined that the repeat cervical

MRI performed at this time did not reflect the kind of “enhancement pattern” characteristic of an

infarction, but was instead atypical for infarction. Tr. at 168–69. Enhancement of infarction

imaging usually produced evidence of a “faint thin line in the anterior artery vascular territory.”

19

Id. at 169. Here, however, there was “diffuse enhancement of the entire spinal cord along its

margins,” “with just a small area of peripheral preservation”—thus establishing total cord

inflammation. Id. at 169, 170–71. An anterior spinal cord infarct would not only be more limited

in enhancement, but would reveal sparing in the non-anterior areas—thus imaging revealed harm

that was “not respecting a vascular territory.” Id. at 171. And at higher cervical levels, the anterior

territory was not even involved. Id. at 171–72.

The treater who performed/interpreted this set of images had opined that the gray matter

involvement in the upper thoracic-imaged regions of the spine was likely supportive of an infarct,

but Dr. Bajakian disagreed. Tr. at 172, 190. He emphasized in reaction the fact that (a) imaging

suggested whole cord involvement (and not simply gray matter), including the posterior cord, and

(b) the area highlighted by the interpreting treater revealed (in Dr. Bajakian’s opinion) no

enhancement or diffusion abnormality, let alone in the anterior cord. Id. at 173. In effect, Dr.

Bajakian contended, this reading of this set of images relied on only a partial view of the whole

set. Id. And otherwise it was incorrect to assume that the “indiscriminate” nature of myelitis

neuroinflammation could not impact the gray matter, even if infarcts more usually were limited in

this respect. Id. at 173, 190.

DWI imaging performed at this time in December was also, Dr. Bajakian maintained, less

supportive of infarct over TM. Diffuse signal could now be seen throughout the cord, in both

“anterior and posterior spinal artery vascular territories”—not the more restricted/limited kind of

abnormality Dr. Bajakian seemed to believe was characteristic of an infarct. Tr. at 174–75. Dr.

Bajakian deemed this set of imaging to be more valuable from a diagnostic standpoint than DWI

imaging previously performed on December 8th. Id. at 176. And he highlighted a suggestion in

the imaging interpretation report that DWI-associated findings were new, not a persistently-

observed phenomenon. Id. at 281. In fact, they were not even discussed in the December 8th

imaging studies. Id. at 281–82.

Dr. Bajakian took issue with Dr. Zucconi’s interpretation of this imaging, with how Dr.

Zucconi downplayed signal abnormalities as connected to evidence of diffusion restriction, and

otherwise maintained that general cord swelling could explain the results. Tr. at 176–77. Dr.

Bajakian argued that the kind of edema associated with TM was more likely the explanation for

swelling than infarct, and that the images in question did not support the latter. Id. at 177–79. He

also on rebuttal contended that Dr. Zucconi’s emphasis of evidence of upper/cervical cord

inflammation, with an infarct below, made no sense, complicating a medical picture that was more

easily and correctly viewed as a single inflammatory process. Id. at 280.

(e) Subsequent Imaging – Dr. Bajakian offered commentary on several of the

other imaging studies that occurred in 2020, and he largely deemed them consistent with TM over

infarct. A cervical MRI performed in February 2020, for example, revealed more increased signal

20

in the posterior cord, not the anterior section (as again Dr. Bajakian seemed to believe would be

evidenced in an infarction). Tr. at 179–81. In addition, the interpreting treater had noted that lesions

were likely chronic and attributable to cord volume loss, while also mostly impacting peripheral

white matter sections, and hence demyelinating in character—conclusions Dr. Bajakian deemed

well founded. Id. at 181–82; Ex. 13 at 1218.

MRIs of Petitioner’s cervical and thoracic spine performed in March 2020 noted no new

or expanded cord signal abnormalities, along with resolution of prior enhancement. Ex. 13 at 855–

56, Tr. at 182–83. Dr. Bajakian felt this was consistent with an inflammation-driven process, which

could be partially arrested over time—as opposed to an infarct, which if enhancing would be more

limited on MRI and not likely to regress. Tr. at 183, 184 (“[s]o a spinal cord infarct is a fixed

lesion, right? Once it dies, there’s no coming back from that”). The imaging from this point in

Petitioner’s medical history (now three months post-onset) suggested to Dr. Bajakian that

treatments Petitioner was receiving had helped a bit (if not clinically). Id. at 184. (Dr. Bajakian

admitted on cross, however, that an infarct would also not likely result in enhancement three

months after onset. Tr. at 198–99). Dr. Bajakian reached similar conclusions with respect to

August 2020 imaging. Id. at 184–87.

C. Respondent’s Experts

1. William Zucconi, D.O. – Dr. Zucconi is a neuroradiologic expert, like Dr.

Bajakian, and he offered a written report and testimony for Respondent. Report, dated June 27,

2023, filed as Ex. E (ECF No. 41-1) (“Zucconi Rep.”), Dr. Zucconi opined that Petitioner had

likely experienced “a catastrophic spinal cord injury” more consistent with infarct than TM. Tr. at

220.

Dr. Zucconi attended State University of New York (“SUNY”) at Geneseo for his

undergraduate and graduate degrees. Curriculum Vitae, filed as Ex. F (ECF No. 41-8) (“Zucconi

CV”) at 1; Tr. at 215. He then attended the New York College of Osteopathic Medicine, where he

also completed a one-year integrated anatomy fellowship. Zucconi CV at 2; Tr. at 215. Thereafter,

Dr. Zucconi completed an internship at New York Hospital in Queens, followed by residency in

Neuroradiology at Stony Brook University Medical Center, Long Island, and a fellowship in

Neuroradiology at The Mount Sinai Hospital. Id. Currently, Dr. Zucconi is an Associate Professor

of Radiology at the Geisel School of Medicine, Dartmouth, as well as a staff neuroradiologist at

the Dartmouth Hitchcock Group. Tr. at 216, 217; Zucconi Rep. at 1. Dr. Zucconi is board-certified

by the American Board of Radiology with a Certificate of Added Qualification in Neuroradiology.

Over the course of his career, Dr. Zucconi has reviewed and consulted on a significant number of

cases involving compressive and traumatic myelopathy, spinal cord tumors, spinal cord infarcts,

and a diverse array of spinal pathologies. Zucconi Rep. at 1.

21

Setting the stage for his evaluation of the same images discussed by Dr. Bajakian, Dr.

Zucconi commented on the practice of imaging in general. Tr. at 224–34. He explained the

mechanical process by which an MRI functions, and how it “allows us to create really highly

sensitive tissue information imaging.” Id. at 224. MRIs can obtain different imaging “cuts” of the

body, depending upon the plane utilized (axial vs. sagittal). Id. at 224–26. For spinal imaging, the

focus is on the cord and canal within the bone vertebrae. Id. at 226. Gray matter tissue is found in

the center of the cord, with white matter surrounding it. Id. at 226–27.

MRI processes can yield different kinds of images depending on the specific technique

used. TS-weighted images, Dr. Zucconi noted, are “sensitive to the presence of water.” Tr. at 229.

They thus reveal the presence of “swelling or abnormal tissue content.” Id. T2-weighted images

would cause cerebrospinal fluid in the cord to appear bright—and “many, many pathologies show

abnormal tissue water content” that can reflect the presence of an infarct, tumor, edema/swelling

(sometimes attributable to vertebral compression), or infectious/inflammatory process. Tr. at 229,

230. The kind of imaging “slice” obtained could also establish the location in the cord of the

damage. Id.at 231.

In addition, contrast (a gadolinium agent) can be injected into the body when an MRI is to

be performed, and it can be seen on imaging “in the vessels or in the tissue,” helping with

diagnoses. Tr. at 231–32. The contrasting agent can pass the blood-brain barrier (the breach of

which demonstrates the presence of cord harm/inflammation) and “seep out into the tissue,”

subsequently showing up in imaging and revealing the presence of an active inflammatory process.

Id. at 231. Dr. Zucconi also mentioned another imaging technique—“short tau inversion recovery,”

or “STIR.” Id. at 234. STIR involves a “T2-weighted sequence” that increases the light-dark

contrast, in order to create a highly-sensitive image that helps identify “subtle cord pathology.” Id.

at 235.

Dr. Zucconi preliminarily discussed the competing diagnoses and how they would usually

be confirmed via imaging. Tr. at 220–21, 232–34. TM, he contended, is “an inflammatory

condition of the spinal cord,” and its most “common presentation” on imaging is “enhancement in

T2 signal.” Id. at 221. Dr. Zucconi noted in particular that usually the radiologic evidence of

inflammation will be evident “when patients present,” and thus at the time they are experiencing

acute clinical symptoms. Id. Infarcts can have different causes, but an ischemic spinal cord infarct

specifically involves “deprivation of blood flow,” thus depriving the CNS of oxygen and resulting

in tissue death. Id. Infarcts can affect a portion of the cord (often the anterior, or front) but can also

have “holocord” impact—although even then, some sparing of the CNS tissue can still occur. Id.

at 227.

Imaging can corroborate the existence of an infarct, albeit in a way somewhat differently

from what establishes TM. This confirmation cannot often be obtained during an infarct’s acute

22

stage, however, “because the onset [of symptoms] is so dramatic from a clinical standpoint”—and

thus there will be “very little, if any, findings within the first several hours,” with a subsequent

“relatively predictable course of events,” characterized by evidence of “signal abnormalities,

subsequent cord swelling, and then enhancement.” Tr. at 220, 221. Often, the enhancement of an

infarct will reveal somewhat more localized signal in specific parts of the cord, however. Id. at

232. In particular, the gray matter sections of the cord are more likely to be impacted. Id. at 233

(imaging will reveal patterns that establish “various degrees of selective insult to that sensitive

tissue within the cord”). Enhancement is not usually evident early on with an infarct, “because the

injury has not evolved” to the point where blood-brain barrier breakdown occurs (necessary for

the contrast agent to flow into the cord and then be observed). Id. at 245.

Dr. Zucconi then went on to provide commentary on the same imaging progression

discussed by Dr. Bajakian, as follows:

(a) First December 8, 2019 Images – Dr. Zucconi noted that Petitioner had

arrived at the hospital emergency department in the early afternoon of December 8th. Tr. at 222.

She had initially complained of back pain while at home, beginning around lunch time, which later

progressed so rapidly to “flaccid quadriplegia” that she became unable to “move her extremities

at all” (although she had been able to walk into the hospital two or so hours earlier). Id. at 222,

223. Thus, Petitioner was already in the midst of an obviously severe and progressive disease

process when this initial imaging was performed.

The first images were obtained mid-afternoon (around 3 pm), and after Petitioner had

appeared at the ED. See generally Ex. 5 at 15–17. In Dr. Zucconi’s reading, the cervical spine

imaging revealed evidence of subtle (meaning difficult to see) hyperintensity/abnormal signal on

the cord front/anterior (and thus he agreed with Dr. Bajakian that initial findings were not normal—

contrary to what the contemporaneous treaters who performed these MRIs had indicated). Tr. at

235, 237–38. 15 Dr. Zucconi denied that this imaging showed any cord swelling, however, and he

referenced top to bottom aspects of the imaging that in his view established expected/natural

variance in cord width. Tr. at 235–37. The initial imaging results were, he opined, supportive of

infarct in an important regard: the “largest area of gray matter, that [is] most sensitive to ischemia”

was the locus of the abnormality (although he admitted that the evidence for this was quite subtle).

Id. at 238, 241. Imaging could nevertheless reveal these kind of findings around the time of an

especially-acute infarct, as was experienced here. Id. at 241–42.

15

Dr. Zucconi speculated that this set of images may have been erroneously deemed normal because they were

obtained on a Sunday afternoon, when he proposed a radiology department might be “short-staffed”—although this is

an uncorroborated contention (and in any event both radiologic experts agreed these images did reveal abnormalities).

Tr. at 239.

23

(b) Second December 8, 2019 Images – Some images from this next set

(obtained in the evening of December 8th) reflected application of the “flair sequence”

technique—an MRI sequence that suppresses signal from free water in the CSF, while keeping

white matter pathology (lesions) bright) 16 to provide a means of increasing “conspicuity” of

lesions. Tr. at 243. Treaters also at this time employed the DWI technique, which in Dr. Zucconi’s

view had “the greatest degree of utility” to identify a suspected infarction; DWI would help yield

images reflecting that “water molecules are trapped in dying and dead cells,” consistent with CNS

tissue deprived of blood, which an infarct would cause. Id. at 244, 246.

The results from this MRI round, Dr. Zucconi maintained, further supported infarct over

TM. Tr. at 244–50. The relevant images again revealed subtle abnormalities in the gray matter/cord

central section, with some “pencil like hyperintensity” evident in the anterior portion of the cord.

Id. at 245; Zucconi Rep. at 4. In addition, the DWI imaging did not reveal the kind of “diffusion

restriction” that a demyelinating cord lesion attributable to inflammation would feature, but instead

yielded a selective pattern (primarily impacting the gray matter) more consistent with infarct. Tr.

at 246. Enhancement was otherwise missing (although contrast had been used in this second round

of imaging). Id.

Dr. Zucconi disputed Dr. Bajakian’s contention that there was a problem with the reliability

of this set of DWI images. Tr. at 246. He agreed that the image in question was “noisy” and difficult

to interpret, but deemed it a positive (favoring infarction) scan “based on what we know about the

T2 information and the pattern of signal in this.” Id. at 247.

(c) December 10, 2019 Images – These images (obtained two days after

Petitioner’s emergency hospitalization) revealed, in Dr. Zucconi’s reading, “bright T2 signal

within the central aspect of the spinal cord,” and thus (again) within the gray matter. Tr. at 248.

He observed no enhancement, however (consistent with the fact that it would take time for an

infarct to begin to damage cord tissue sufficiently for contrast to leak into the spine and “show up”

in imaging), and thus contested Dr. Bajakian’s argument that there was by this point evidence of

scattered enhancement. Id. at 248, 249, 273–74; Zucconi Rep. at 5. Only when the damage due to

the initial infarct was extensive enough to result in secondary inflammation, he contended, would

enhancement be observable on imaging (as the ongoing inflammation would result in subsequent

blood-brain barrier weakening). Id. at 249 (“[a]s part of that infarct, you have dying tissue and

what happens is the blood vessels open up and they allow contrast to leak. Their tight, porous,

nonporous boundaries allow the contrast into the tissue”).

16

“Fluid-attenuated inversion recovery (FLAIR)” is “a magnetic resonance imaging (MRI) sequence that produces

strong T2 weighting, suppresses the CSF signal, and minimizes contrast between gray matter and white matter” which

“produces images with significantly increased lesion-to-background CSF contrast and enhances the visibility of

lesions as well as their detectability, particularly in the peripheral subcortical and periventricular regions.” National

Library of Medicine, https://pubmed.ncbi.nlm.nih.gov/9402679/ (last visited May 8, 2026).

24

Dr. Zucconi disputed other aspects of Dr. Bajakian’s interpretation of these images. Dr.

Zucconi did observe evidence of cord “sparing” (parts of the cord not impacted by tissue harm),

even if the damage from the infarct was now progressing throughout the cord. Tr. at 249. This was

consistent with the nature of infarct, but less so with TM, which he maintained would result in

imaging evidence of a “process more advanced at [clinical] presentation.” Id. at 250.

(d) December 18, 2019 Images – Dr. Zucconi further commented on the

cervical and thoracic images obtained ten days after Petitioner’s initial acute symptoms and

hospitalization (now well into the “subacute” phase of the infarct’s development). He noted a T2-

weighted sequence had been run at this time, due likely to the sensitivity of this imaging technique,

and thus its capacity to reveal “the presence of hemorrhage.” Tr. at 250. These images in his

opinion showed the dramatic degree of cord injury progression and confirmed (as evidenced by a

dark spot) an area of hemorrhage common to an ischemic infarction in its later stages. Id. at 251;

M. Lee et al., Diagnostic Approach to Intrinsic Abnormality of Spinal Cord Infarct, 39

Radiographics J. 6:1824 (2019), filed as Ex. 50 (ECF No. 30-7) (“Lee”), at 1830 (noting that

“hemorrhagic conversion” could be seen on MRI as infarct progressed). Dr. Zucconi did not agree

with Dr. Bajakian’s reading of these images that a possible hemorrhage was simply a “flow-related

artifact.” Tr. at 251. He also assessed the images from this time as revealing excessive cord

swelling (“it’s occupying essentially the entire area of the spinal canal”); “in the absence of an

underling hypervascular lesion,” flow was not likely. Id. at 251, 252.

Dr. Zucconi also opined that certain of the images from this MRI sequence did not reveal

enhancement or restricted diffusion correlating to the initial areas of signal abnormality from the

earlier imaging obtained on December 8th and 10th. Zucconi Rep. at 5, 7. Instead, they established

the progression of cord swelling and edema, all the way up the cord into the brainstem. Id. at 252.

Severe infarcts, he stated, could progress in this manner. Id. at 252–53. Dr. Zucconi acknowledged

that enhancement could now also be detected somewhat in later images, but deemed it the product

of an earlier “underlying insult” significant enough to cause tissue injury across the cord over the

course of ten days. Id. at 253; Zucconi Rep. at 5. In TM, by contrast, such results would not be

seen so long after initial clinical presentation. Tr. at 253–54.

In addition, the thoracic cord MRI imaging from December 18th revealed “clear

confinement of signal abnormality to the central gray area.” Zucconi Rep. at 7 (Figure 5); Tr. at

254. This kind of selective process was more consistent with infarct than TM, since the gray matter

was particularly “sensitive to ischemia.” Tr. at 255. And in fact, treaters who performed, and then

assessed the results of, this MRI agreed that it favored infarct as the proper diagnosis. Id. at 256

(referencing Ex. 5 at 1503). (At the same time, however, Dr. Zucconi conceded that this imaging

25

suggested an alternative explanation—“[a] vascular or inflammatory myelopathy that did not

ultimately cause myelomalacia” 17—inconsistent with infarct. Zucconi Rep. at 7; Tr. at 274).

(e) Other Imaging – Dr. Zucconi’s testimony also included discussion of later

imaging evidence bearing on the parties’ diagnostic disputes. A spinal angiogram (employed to

look for potential vascular malformations/occlusions) 18 was performed on December 19, 2019,

and it yielded negative results that could have offered an explanation for the possible infarct

Petitioner experienced. Tr. at 256–57. Dr. Zucconi maintained, however, that this angiogram

procedure is not used for treatment of existing ischemia, but instead is aimed at resolving potential

future harms. Id. at 257. The angiogram would not be able to identify the cause of a prior ischemia

(such as an embolism). Id. In his view, the results of this testing only established “that her

infarction was not secondary to an acute venous congestive phenomenon due to an underlying

vascular abnormality.” Id. at 258.

The final imaging Dr. Zucconi commented on was from an MRI performed months later,

in August 2020. Zucconi Rep. at 8 (Figure 6). This set of images certainly, he admitted, would be

seen in “any form of severe spinal cord insult” months after onset. Tr. at 259. But Dr. Zucconi also

maintained these later images revealed overall cord atrophy, with volume loss that “reinforces the

severity of the tissue damage,” but with some other evidence of “residual signal abnormality” in

the central part of the cord. Tr. at 259. Dr. Zucconi particularly highlighted the latter, deeming it

consistent with “cases of chronic spinal cord infarction,” and known as “[c]entral cystic

myelomalacia.” Id. Thus, this final set of images corroborated the infarct diagnosis overall.

To give some substantiation for his reading of the previously-discussed imaging, Dr.

Zucconi referenced several items of literature. Zalewski, for example, considered a sample of 126

individuals with spinal cord infarctions, and noted a number of sub-findings from MRIs performed

on those studied patients that were consistent with what he saw from the imaging in Petitioner’s

medical record. Zalewski at 59 (Table 2). Here, Dr. Zucconi maintained, there was evidence of

diffusion restriction as early as December 8th, along with gray matter involvement, and thin/linear

enhancement on “arterial territory,” plus subtle but present early abnormal signal. Tr. at 260. And

(as Zalewski noted) the presence of “atypical” features on imaging (such as evidence of issues

outside the anterior territory of the cord) did not rule out an infarct, since it was common to

misdiagnose infarct as TM. Id. at 265–66; Zalewski at 61.

17

“Myelomalacia” is defined as the “morbid softening of the spinal cord.” Myelomalacia, Dorland’s Medical

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

visited May 8, 2026).

18

“Vascular Malformation” is defined as “an abnormal vascular formation resulting from a developmental anomaly

rather than from neoplastic growth; common types include arteriovenous fistulas, some types of hemangiomas and

lymphangiomas, nevus anemicus, and nevus flammeus.” Vascular Malformation, Dorland’s Medical Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=87817&searchterm=vascular+malformation (last

visited May 8, 2026).

26

An item of literature also offered imaging comparable to what Petitioner’s MRIs

revealed—“selective” harm to the gray matter/cord anterior, with abnormal signal in that section

and correlated enhancement. See generally M. Vargas et al., Spinal Cord Ischemia: Practical

Imaging Tips, Pearls, and Pitfalls, 36 Am. J. Neuroradiol. 825 (2015), filed as Ex. 54 (ECF No.

30-10) (“Vargas”), at 829 Fig. 6 (image of ischemia during subacute/later phase). Another article

confirmed that imaging of a progressing infarct, relying on techniques with specific utility in the

context of infarct, like DWI, could reveal signal abnormalities very early on (“within hours of

onset”)—as evidenced here by the December 8th imaging—even though initial imaging could be

often inconclusive. Tr. at 262; N. Yadav et al., Spinal Cord Infarction: Clinical and Radiological

Features, 27 J. Stroke & Cerebrovasc. Dis. 10:2810 (2018), filed as Ex. E-3 (ECF No. 41-4)

(“Yadav”), at 2810, 2817 (although “conventional MRI may be normal in some patients especially

in the acute stage” of clinical symptoms, use of DWI technique could corroborate infarct within

minutes to hours of onset).

Dr. Zucconi did briefly propose some potential explanations for Petitioner’s infarct

(although as discussed below, the medical record ultimately does not permit a conclusion as to a

likely cause). One article—a case series involving two patients—discussed how a

fibrocartilaginous embolism 19 could look initially like TM, but that this kind of infarct trigger was

a common cause of infarcts in younger patients not otherwise possessing the risk factors commonly

associated with infarct. Tr. at 265; M. AbdelRazek et al., Case Series of Two Patients with

Fibrocartilaginous Embolism Mimicking Transverse Myelitis of the Spinal Cord, 40 J. Clin.

Neurosci. 66 (2017), filed as Ex. E-6 (ECF No. 41-7). He noted, however, that spinal cord infarcts

could be properly diagnosed even in the absence of evidence of such possible explanations. Tr. at

271. On cross-examination, Dr. Zucconi admitted that fibrocartilaginous infarcts were rare, and

that none of Petitioner’s treaters proposed one had occurred in Petitioner’s own case. Id. at 272–

73.

Overall, Dr. Zucconi maintained that the diagnostic criteria for infarct were met in this

case, based on both imaging and Petitioner’s clinical history, and he followed Zalewski’s

diagnostic criteria to explain why. Tr. at 266–69; Zalewski at 60 (“Box. Proposed Spinal Cord

Infarction (SCI) Diagnostic Criteria”); see also Tr. at 270. First, her nadir occurred within twelve

hours of onset, and with no evidence close in time to some immediate traumatic incident. Tr. at

267. The tempo of Petitioner’s injury progression was especially important, as underscored in

items of literature like Vargas. Id. at 268–69; Vargas at 825 (“[a]s with cerebral infarction, the

onset of spinal cord infarction is typically abrupt. Most patients develop symptoms quickly, with

a maximal symptomatology reached within 12 hours for 50% of patients and within 72 hours for

most patients”).

19

A fibrocartilaginous embolism, Dr. Zucconi maintained, would occur “when a small amount of the internal disc

material herniates out of the disc and gains access to the adjacent arterial system of the cord and it ends up blocking

one of the arteries that goes directly to the spinal cord.” Tr. at 264.

27

Second, the MRIs revealed no evidence of a likely disc compression explanation for

Petitioner’s cord injury, T2-hyperintense signal, and DWI positive findings (although they were

stronger by December 18th). Tr. at 267. The progression that imaging revealed over the first ten

days of Petitioner’s illness, coupled with the hyperacute clinical onset, was especially consistent

with infarct in Dr. Zucconi’s view. Id. at 270 And (in Dr. Zucconi’s opinion—thus despite the

competing TM diagnosis) no other explanation existed as more likely. Id. at 268. (Dr. Zucconi

deferred to Dr. Price, Respondent’s neurologic treatment/diagnosis expert, as to whether CSF lab

testing results supported infarct).

2. Dr. Raymond Price – Dr. Price is a neurologist, and he opined in

Respondent’s favor on the issue of diagnosis. Report, dated July 11, 2022, filed as Ex. A (ECF No.

22-1) (“First Price Rep.”); Report, dated July 24, 2023, filed as Ex. G (ECF No. 43-1).

Dr. Price attended the University of North Caroline-Chapel Hill for his undergraduate

degree, and the University of Pennsylvania for his medical degree. Curriculum Vitae, filed as Ex.

B (ECF No. 22-4) (“Price CV”) at 1; Tr. at 317–18. He then completed his internship in Internal

Medicine and residency in Neurology at the Hospital of the University of Pennsylvania. Price CV

at 1; Tr. at 318. Thereafter, he pursued a fellowship in Clinical Neurophysiology with a

Neuromuscular focus at the same institution. Id. Currently, Dr. Price is an Associate Professor of

Clinical Neurology, as well as the Neurology Residency Director and Neurohospitalist Division

Co-Director in the Department of Neurology at the University of Pennsylvania. Price CV at 1; Tr.

at 318–19. He is board certified by the American Board of Psychiatry and Neurology in Neurology

with added qualification in Neuromuscular medicine. Price CV at 2; Tr. at 318. He estimates that

he has personally cared for hundreds of patients with myelopathies, including spinal cord

infarction, longitudinally extensive transverse myelitis, multiple sclerosis, and other inflammatory

diseases affecting the spinal cord. First Price Rep. at 1. Dr. Price did, however, acknowledge that

he does not have any specific training in neuroimmunology or that he specializes in neuroimmune

disorders. Tr. at 392.

Dr. Price offered his views on the general indicia for the competing diagnoses in this

matter. Infarcts, he contended, reflect circumstances where “tissue does not get enough blood

supply, and as a result, the tissue will die.” Tr. at 322. Spinal cord infarcts can be the result of

ischemia, direct trauma to the cord (an accident, or sometimes in the context of a surgery), an

aneurysm, or some other unidentified spontaneous factor. Id. at 322–23. Cord infarcts often present

very acutely—hours to a day or two—with clinical evidence of unilateral or bilateral dysfunction,

including sensory issues below the spinal level of the infarct, while sparing function above it. Id.

at 323-24.

To diagnose an infarct, treaters take into account (a) the sudden nature of onset of

symptoms, (b) clinical evidence of myelopathy (meaning the nature of the symptoms), and (c)

28

corroborative evidence, like MRI results. Tr. at 325. Proof of vertebral body etiology is helpful,

but such explanatory factors are not seen in more than a third of infarcts. Id. And proof of

inflammation (as would be indirectly provided by CSF testing) can help qualify whether in fact an

infarct is likely occurring. Id.

Dr. Price also reviewed the features and diagnostic criteria for TM. He defined TM

generally to be spinal cord injury attributable to inflammation, adding that the term “TM”

constituted a “grab bag” for many possible disease processes or causes (in some cases, for example,

MS or other CNS-impacting injuries can initially present with what looks like a single occurrence

of TM), or can be due to a prior infection. Tr. at 325–26. TM’s cause often cannot be identified,

leading treaters to deem it idiopathic in origin. Id. at 326. TM features symptoms comparable to

an infarct—“the symptoms are typically going to be a sensory level, a motor deficit, a sensory

deficit.” Id. at 327.

The speed of onset of clinical symptoms, Dr. Price maintained, was highly significant in

differentiating TM from an infarct. Tr. at 394. He noted that, from a clinical standpoint, onset to

nadir within four hours was generally agreed to be evidence favoring infarct, whereas a progression

to nadir that took two or three weeks would very likely not be consistent with infarct. Tr. at 327.

Dr. Price allowed that a timeframe of more than four hours to up to 24 or 48 hours placed diagnosis

into a “gray zone,” but emphasized that in such a case the totality of evidence was critical in

evaluating what diagnosis better fit the circumstances. Id. at 328.

Dr. Price next reviewed the Petitioner’s medical history—both contemporaneous treatment

evidence as well as later histories provided in subsequent treatment obtained in 2020. Although he

conceded overall that the record contained “a lot of diagnostic uncertainty” as to the nature of

Petitioner’s injury, he ultimately favored infarct. Tr. at 374, 375.

Particularly important to Dr. Price was the overall short timeframe from onset to nadir. An

initial treatment note from around 1:00 pm on December 8, 2019, noted that Petitioner’s onset of

back pain and arm weakness began earlier that day, after she had left the gym. Tr. at 331–33; Ex.

5 at 19. Tightness in her back from the prior day was reported but deemed by Petitioner to be

something she often experienced, and distinguishable from what occurred on the 8th. Tr. at 333.

And there was otherwise no evidence from the days or weeks prior of Petitioner having

experienced any neurological deficits. Id. at 334.

Later records from December 8th confirmed this fast timeline. Tr. at 335–39. In January

2020, it was noted that Petitioner had previously experienced general “tightness” in her shoulders,

but that she did not view this as pain. Tr. at 328 (referencing Ex. 1 at 63). But Petitioner recalled

that the morning of December 8, 2019, she had worked out, and then at home while showering

began to experience sudden intense pain in her back, followed by right-arm numbness and

29

weakness within ten minutes. Id. at 329. A friend transported her to the emergency department,

and although she had been able to walk in unassisted, she could no longer move her legs within 30

to 60 minutes. Id. And her clinical symptoms encouraged treaters to perform an MRI (although it

had been interpreted as normal—something both radiologic experts disputed). Id. at 339.

Dr. Price deemed this to be evidence of how rapid Petitioner’s progression to nadir had

been. Tr. at 330 (“she is basically at her nadir from a motor and sensory function, or at least from

a motor function, . . . within 40 to 60 minutes of symptoms onset, which would put us in the . . .

the more clearly defined spinal cord infarction category”). By 5:30 pm, Petitioner’s “motor deficits

are maximal and as severe as you could possibly imagine.” Id. at 340. The same extremely rapid

disease progression was evidenced by other documents from treatment events in 2020. See

generally Id. at 330–31. Dr. Price thus concluded the temporal period from onset to nadir was four

to five hours total. Id. at 343-44. By the afternoon of December 8th, Petitioner’s symptoms overall

reflected an infarct impacting the total cord, anterior and posterior. Id. at 401–02.

This rapid temporal progression was, Dr. Price reasoned, consistent with literature

addressing features of infarcts. Tr. at 334. Zalewski proposed that a timeframe from onset to nadir

of less than 12 hours was consistent with infarct. Zalewski at 58 Table 1. And evidence of “severe

motor loss,” as here, plus objective sensory loss, was strong proof of nadir. Tr. at 334, 336. Other

literature similarly differentiated from a progression to nadir in less than six hours (supporting

infarct) versus more than 72 hours in TM, if not longer. Id. at 375–76; Park at 3 (study contrasted

timeframe to nadir in sample of 14 infarct patients (with 9 experiencing nadir in less than six hours)

versus TM group of 15 patients (13 of whose timeframes to nadir took more than 72 hours)).

Dr. Price disputed that Petitioner’s nadir occurred on December 10th, as contended by Dr.

Pachner. At the time of Petitioner’s arrival at the ED on the afternoon of December 8, 2019, her

breathing rate was notably elevated. Tr. at 335; Ex. 5 at 21. By later that same day, Petitioner’s

voice was weak, and “that would be expected if she’s having trouble moving air through her vocal

cords” due to neurologic injury. Tr. at 339. Other evidence of shortness of breath or difficulty

swallowing, however, was more equivocal. Id. at 340–41. But Dr. Price nevertheless opined that

as of the 8th, Petitioner’s “respiratory status is incredibly tenuous . . . and very concerning,” and at

this stage “she’s in clear respiratory distress heading towards intubation and likely should be

intubated very soon.” Id. at 341. The record did not suggest this particular symptom worsened

thereafter, moreover. Id. at 342. And treaters took note of the matter (suggesting it was evident to

them as an existing problem, as opposed to something that worsened later). Id. at 350.

Dr. Price admitted that treaters did not act to test Petitioner’s respiratory function on

December 8th, but he speculated this was because imaging was given priority. Tr. at 350.

Respiratory monitoring and maintenance occurred later—and Dr. Price allowed that it evidenced

“severe respiratory compromise.” Id. at 351, 352 (Petitioner displayed “less than 10 percent of

30

normal on the vital capacity”). But Dr. Price felt intubation could have been performed earlier than

December 10th, given Petitioner’s condition, and that it was possible the initial MRI imaging

(interpreted as normal) gave treaters a false complacency. Id. at 352–53, 355, 357. Dr. Price

acknowledged that the level of cervical involvement was consistent with respiratory issues. Id. at

354. Ultimately, however, Dr. Price viewed the treatment decision to intubate on December 10th

to be a function of prior treatment decisions and assessments about what was necessary. Id. at 356–

57, 358 (“I think her respiratory status is poor and she just kind of tires out [later]”). He therefore

did not consider more intrusive treatment of respiratory issues by December 10th to undermine his

conclusion that nadir was reached “at a maximum of five-ish hours, maybe even four hours,” with

the respiratory dysfunction already having occurred in that same timeframe as her other, more

clinically-immediate symptoms of quadriplegia. Id. at 360.

Other treatment decisions suggested to Dr. Price that an infarct was more likely the “best”

diagnosis. For example, a repeat MRI was performed the evening of December 8th—this time with

DWI “to rule out cervical cord ischemia.” Tr. at 345. One initial treater had considered the issue

of Petitioner’s “mean arterial pressure—another consideration relevant to infarct. Id. at 350, 355

(evidence treater ordered others to “keep her mean arterial pressure up”); Ex. 5 at 2737 (states “CV

[cardiovascular]: MAP goal > 80 for spinal cord perfusion.”).

Dr. Price acknowledged that a factor often thought to disfavor infarction—evidence that

sensation to vibration had been “lost on examination”—was also present, since there was none of

the sparing of regions of the cord often thought to be characteristic of an infarct. But he maintained

that this finding still allowed for an infarct—and that it was a diagnostic oversimplification to

assume infarcts always involve sparing. Tr. at 345–46. The “classical teaching” about which

arteries service the anterior portion of the cord (often associated with infarcts, though not

exclusively) simplifies the distinction between posterior and anterior cord impacts—such that

clinical evidence of vibration sensitivity sparing is viewed to support the diagnosis of infarct

(which will often impact only the anterior portion of the cord—and hence involve anterior arteries,

with unaffected arteries still supplying blood to other parts of the cord). Id. at 346. But literature

like Zalewski gave more weight, diagnostically, to evidence of selective sparing of pain or

temperature loss sensation (with loss of vibration sensation actually common in the sample

considered in that study). Zalewski at 58 Table 1 (95 percent of 133 patient sample revealed

sensory loss of some kind, and Zalewski only included a subcategory for “selective

pain/temperature loss” as opposed to vibration sensitivity). Thus, infarcts did not unerringly

“follow an anterior posterior gradient,” and the presence or absence of vibration sensitivity was

not necessarily determinative of an infarct. 20 Tr. at 349.

20

At trial, Petitioner’s counsel objected to this line of testimony, on the grounds that it constituted an “undisclosed”

opinion not formally memorialized in Dr. Price’s expert report. Tr. at 347–48. However, Dr. Pachner unquestionably

had already addressed in his direct testimony the evidence pertaining to sparing of vibration sense, and the significance

of that to the argument that the anterior cord impact was so limited and/or revealed any neurologic function “sparing.”

See generally Tr. at 74–76. This topic was also glancingly referenced in Dr. Pachner’s first report. First Pachner Rep.

31

Another factor bearing on the proper diagnosis was the CSF testing Petitioner underwent.

Dr. Price noted that the first such testing (performed December 8th) revealed a completely normal

white blood cell count (one out of a normal range of zero to ten). Tr. at 360. Although Dr. Price

allowed evidence of pleocytosis was not always seen in TM (and therefore its absence was not

exclusionary for the diagnosis), these results pointed against an inflammatory process underway

(and meant Petitioner’s very rapid progression to nadir deserved even more diagnostic weight). Id.

at 361. The next CSF testing was performed ten days later (December 18th), and now eleven white

blood cells were revealed—exceeding (if slightly) the same normal range used by the treating

hospital. Dr. Price admitted that the normal range defined by the hospital that tested Petitioner’s

CSF—zero to ten white blood cells—was broader than the range he used in his practice (thus

implying the presence of the eleven white blood cells was in fact elevated). Tr. at 402. But even

the level Petitioner demonstrated was not, in his view, particularly alarming; “given her

quadriplegia,” Dr. Price might have expected to see “30, 50, . . . 100, any of those,” had the clinical

symptoms been the product of an ongoing inflammatory process. Id. at 403. Bacterial meningitis

would, for example, potentially result in white blood cells counts in the thousands, and even a viral

form would range up to 40 to 80 white blood cells.

Accordingly, Dr. Price did not deem this second CSF testing result to reflect “a prominent

pleocytosis,” and he added that it could be nonspecific in any event. Tr. at 362, 363–64, 403–04

(“given her degree of [clinical] severity, this is very minimally elevated”). He noted that a study

looking at an “impairment scale” used in medicine to evaluate cases of acute TM showed that

patients with motor involvement far less debilitating than what Petitioner had experienced

displayed moderate levels of pleocytosis comparable to what Petitioner experienced. Id. at 380-

81; J. Sellner et al., Diagnostic Workup of Patients with Acute Transverse Myelitis: Spectrum of

Clinical Presentation, Neuroimaging, and Laboratory Findings, 47 Spinal Cord J. 312 (2009),

filed as Ex. 164 (ECF No. 75-5) (“Sellner”), at 314 (of 59 patients suffering from the mildest level

of impairment due to acute TM, 49 percent had pleocytosis, but with a mean white blood cell count

of nine cells). Thus, the level of pleocytosis revealed by Petitioner’s second round of CSF testing

was not at all equivalent to the degree of clinical harm she had actually experienced, undermining

the conclusion that it was evidence of an inflammatory-driven process.

In addition (and independent of the white blood cell count), CSF testing also revealed a

negative IgG index—inconsistent with the positive index “seen in 70 to 90 percent of patients with

[TM],” and hence corroborating the lack overall of evidence of inflammation in the spinal cord.

Tr. at 374, 376–78, 381; Sellner at 314 (82 percent of a sample of 621 patients displayed abnormal

IgG indices). Dr. Price deemed proof of inflammation within the spinal cord corroborating to onset

of clinical symptoms to be highly important in confirming a TM diagnosis (and he thus disagreed

at 8. It was accordingly a reasonable subject for Dr. Price to discuss (as a witness for Respondent, called to rebut

Petitioner’s case), even if not literally set down in his own report—and I note as well that Dr. Pachner returned to this

same topic during the Petitioner’s closing rebuttal case. See Tr. at 465. I thus do not deem Dr. Price’s mention of this

issue to have been prejudicial to Petitioner, who was provided ample opportunity at trial to respond.

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with Dr. Pachner’s suggestion that it was irrelevant or “too strict” to link the two early on in the

clinical course of injury). Tr. at 385.

Consistent with Dr. Zucconi, Dr. Price read the sequential MRI results to better support

infarct than TM. He accepted the initial MRI revealed no degenerative explanations for Petitioner’s

alarming symptoms. Tr. at 364. But he emphasized the view of both radiologic experts that

(contrary to what contemporaneous treaters proposed) there were “a lot of subtle abnormalities”

in these first images. Id. at 365. Given Petitioner’s progressive and declining clinical presentation

so soon after onset, there was a “gigantic clinical radiologic dissociation” that “argue[d] heavily”

for infarct. Id. at 366. And, Dr. Price opined, contemporaneous treaters seemed eventually to lean

in that direction, since they proposed DWI imaging at this early stage of Petitioner’s treatment. Id.

at 366 (“you request DWI imaging when you are worried about spinal cord infarction”), 367. That

imaging also revealed gray matter focus for signal. Id. at 367–68.

The next imaging from December 10th only underscored why infarct was the more proper

diagnosis, Dr. Price maintained (although he was careful to note that the imaging “nuances”

testified to by the radiologic experts were matters beyond his personal expertise). In the two days

from the time of Petitioner’s emergency department visit, there was already evidence of edema,

which was reported in infarct (although Dr. Price admitted it was not typical). Tr. at 369. Dr. Price

accepted Dr. Zucconi’s contention that this imaging did not reveal enhancement 21—but regardless,

the “big picture” for Petitioner, clinically speaking, was her sudden quadriplegia. Id. at 370. Then,

DWI was utilized again on the 18th of December (further confirming the suspicion of infarct), and

in Dr. Price’s (non-specialist) view the results more reflected infarct. Id. at 371. Dr. Price did not

give the spinal angiogram weight as a diagnostic tool that in this case could help determine

diagnosis. Id. at 372.

Dr. Bennett (who treated Petitioner months after her initial presentation) had opined that

Petitioner’s TM was vaccine-caused, but Dr. Price questioned the evidentiary support for this

opinion. For example, Dr. Price observed that one article specific to TM and vaccines identified

only two case report instances of a flu vaccine-TM association, and even then manifesting only

within two weeks of vaccination—not a month as here. Tr. at 382–83; N. Agmon-Levin et al.,

Transverse Myelitis and Vaccines: A Multi-Analysis, 18 Lupus J. 1198 (2009), filed as Ex. 23

(ECF No. 17-8), at 1200 Table 1. Another epidemiologic study found no TM-vaccine association

(albeit in the context of evaluating the relationship between vaccination and TM plus ADEM). R.

Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-Centered Analysis, 63 Clin.

Infect. Dis. 1456 (2016), filed as Ex. A-2 (ECF No. 22-3), at 1460–61.

On cross examination, however, Dr. Price allowed that evidence of enhancement on imaging within a week of onset

21

would be a factor in support of a TM diagnosis. Tr. at 395–96.

33

Dr. Price also denied the importance of the length of a spinal cord lesion, measured as

vertebral segments, as having diagnostic significance in differentiating between an infarct and TM.

Tr. at 386–87. In support, he noted Zalewski had identified infarcts with significant lesion lengths.

Id. at 387; Zalewski at 59 Table 2, 62. He also stressed how common it was for an infarct to be

misdiagnosed as TM. Tr. at 387–88; N. Zalewski et al., Evaluation of Idiopathic Transverse

Myelitis Revealing Specific Myelopathy Diagnoses, 90 Neurol. E96 (2018), filed as Ex. E-4 (ECF

No. 41-5) (“Zalewski II”), at e97 (“”[i]n our clinical experience, ITM is often proposed as a

specific diagnosis for patients who do not meet the diagnostic criteria”), e100 (emphasizing the

need to better distinguish true TM from “noninflammatory myelopathies” like infarct, in order to

avoid unnecessary therapies).

On cross examination, Dr. Price noted that it was not his conclusion that Petitioner’s injury

could only be diagnosed as an “anterior” spinal artery (“ASA”) infarct. Tr. at 397–98. He did not

see evidence of a “classic anatomic, vascular, . . . organization that falls nicely into those

categories,” suggesting that dividing up infarcts into ASA and non-ASA amounted to an “artificial

dichotomy.” Id. at 398. It was in fact a “gross oversimplification” to view infarcts this way, as

clinical results considered in articles like Zalewski established. Tr. at 399. In this case, Dr. Price

proposed that the damage from Petitioner’s infarct was more global, implicating both the anterior

and posterior portions of the cord. Id. He emphasized that his opinion on diagnosis relied on a

review of the totality of evidence in this case, comparing that to articles discussing different infarct

features. Id. at 400.

D. Treater Opinion

Dr. Jeffrey L. Bennett offered two written letter opinions in this case as to Petitioner’s

proper diagnosis. See Report, dated Feb. 24, 2022, as Ex. 16 (ECF No. 17-1) (“First Bennett

Rep.”); Report, dated Mar. 15, 2022, filed as Ex.39 (ECF No. 21-1) (“Second Bennett Rep.”).

Dr. Bennett attended Case Western Reserve University for his undergraduate degree, and

Stanford University for his medical and post-doctoral degrees. Curriculum Vitae, filed as Ex. 17

(ECF No. 17-2) (“Bennett CV”) at 1. He then completed his internship and a residency in

Neurology at the University of Colorado School of Medicine. Id. Thereafter he pursued a post-

doctoral fellowship at the University of Colorado, Boulder, as well as a Neuro-ophthalmology

fellowship in the Department of Neurology at the University of Pennsylvania. Id. Currently, Dr.

Bennett serves as the Gertrude Gilden Professor for Neurodegenerative Disease Research, is a

member of the Graduate Faculty of the Neurosciences Programs, and is involved in the

Immunology Graduate Program at the University of Colorado School of Medicine. Id. He is board-

certified in Neurology by the American Board of Psychiatry and Neurology. Id.

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In his first report, Dr. Bennett summarized Petitioner’s relevant medical history,

emphasizing the fact that her December 10, 2019 MRI “demonstrated cervical myelitis with

extensive cord edema. Her clinical course worsened to tetraplegia, and MRI imaging on December

19, 2019, revealed abnormal signal, gadolinium enhancement, and edema extending from the

medulla to T5-6 with predominant central cord involvement.” First Bennett Rep. at 1. Dr. Bennett

also noted that other possible “autoimmune and infectious causes” had been ruled out; that support

existed for a vaccine-caused TM; and that Petitioner’s presentation was consistent both with TM

diagnostically, and that her actual experiences “fit” with a vaccine causation. Id. at 1–2. This report

does not, however, mention infarct at all as a possible counter-diagnosis, and almost all of the 21

items of literature filed in association with it deal with infectious causes of TM or the possible

causal association between TM and vaccination. Id. at 2–3 (citations omitted).

Dr. Bennett’s supplemental report is a single-page item summarizing the records filed in

this case (discussed in the medical record fact section above) relating to his actual treatment of

Petitioner. Second Bennett Rep. at 1. He again notes his opinion that TM is the appropriate

diagnosis, although he contrasts it not with infarct but with NMOSD (“Neuromyelitis Optica

Spectrum Disorder”). Id. He also summarizes the various negative test results for other etiologies

for Petitioner’s condition, although he includes no discussion of imaging results, or any of the

evidence referenced herein by Respondent for a counter-diagnosis. Id.

III. Procedural History

The matter was initiated approximately five years ago. After the case’s activation,

Respondent filed his Rule 4(c) Report in January 2022 opposing entitlement. Respondent’s Report,

filed Jan. 14, 2022 (ECF No. 16). The parties thereafter began the process of filing expert reports,

with some delay occurring when current counsel appeared in the matter for Petitioner in late 2022.

Expert report filing was completed in the fall of 2024, and the matter set for hearing in 2025. The

trial occurred as scheduled in May 2025, and post-trial briefing was concluded in August of that

same year. See Petitioner’s Post-Hearing Brief, dated Aug. 11, 2025 (ECF No. 95) (“Br.”);

Respondent’s Post-Hearing Brief, dated Aug. 11, 2025 (ECF No. 96) (“Opp.”). The matter is now

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; §

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11(c)(1)(C)(ii)(I); see also Moberly ex rel. 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). 22 There is no Table claim for TM resulting from any covered vaccine (although

claims alleging TM as a vaccine injury are quite common in the Vaccine Program).

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 and Hum. Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005): “(1) a

medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause

and effect showing that the vaccination was the reason for the injury; and (3) a showing of

proximate temporal relationship between vaccination and injury.”

Each Althen prong 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

22

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. App’x. 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).

36

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. Contreras, 121 Fed.

Cl. at 245 (“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis

in original)).

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 Cerrone v. Sec’y of Health & Hum.

Servs., 146 F.4th 1113, 1121 (Fed. Cir. 2025) (the argument that prong one requires only a showing

of plausibility “understates the burden [a petitioner] bears under the first factor in the Althen

formulation”); Kalajdzic v. Sec’y of Health & Hum. Servs., No. 2023-1321, 2024 WL 3064398, at

*2 (Fed. Cir. June 20, 2024) (arguments “for a less than preponderance standard” deemed “plainly

inconsistent with our precedent” (citing Moberly, 592 F.3d at 1322)); Boatmon v. Sec’y of Health

& Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also Howard v. Sec'y of Health & Hum.

Servs., 2023 WL 4117370, at *4 (Fed. Cl. May 18, 2023) (“[t]he standard has been preponderance

for nearly four decades”), aff’d, 2024 WL 2873301 (Fed. Cir. June 7, 2024) (unpublished). And

petitioners always have the ultimate burden of establishing their overall Vaccine Act claim with

preponderant evidence. 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

‘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).

37

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 den’d, 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. den’d 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. den’d (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, 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.

38

1993) (determining that 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).

As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as

trustworthy evidence.” 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, Rickett v. Sec'y of Health & Hum.

Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked

propositions explains why such records deserve some weight: (i) sick people visit medical

professionals; (ii) sick people attempt to 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 often found to be deserving of greater evidentiary weight than oral testimony—especially

where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also

Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d

1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States

v. 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.”)).

However, the Federal Circuit has also noted that there is no formal “presumption” that

records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health

& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which

compelling oral or written testimony (provided in the form of an affidavit or declaration) 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 records which are, themselves, inconsistent, should be accorded less

39

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. La Londe 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 Pharm., 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).

Under Daubert, the 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).

In the Vaccine Program the Daubert factors play a slightly different role than they do when

applied in other federal judicial settings, like the district courts. Typically, Daubert factors are

40

employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence

that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are

used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &

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. 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

review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 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”).

D. Consideration of Medical Literature

Both parties filed a large number of items of medical and scientific literature in this case,

but not all such items factor into the outcome of this decision. While I have reviewed all the

medical literature submitted, I discuss only those articles that are most relevant to my

determination and/or are 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., No. 2015–5072,

2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 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.

41

App’x 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”).

ANALYSIS

I. Transverse Myelitis vs. Spinal Cord Infarct

Although the parties dispute Petitioner’s proper diagnosis (as well as how the relevant

diagnostic criteria should be interpreted), collectively they have offered reliable evidence

illuminating how the competing diagnoses are understood by medical science. TM is a rare kind

of myelitis 23 (neuroinflammatory condition) attacking the spine, and is “characterized clinically

by acutely or sub-acutely developing symptoms and signs of neurologic dysfunction in motor,

sensory, and autonomic nerves and nerve tracts of the spinal cord. Beh at 1–2. Its symptoms can

vary, but generally TM can present with a number of different clinical symptoms—weakness,

sensory alterations, and often bowel or bladder dysfunction. First Pachner Rep. at 12. TM’s

etiology is varied, and while it has been associated with various infectious or systemic autoimmune

diseases, it can have an idiopathic origin. Beh at 2; A. Borchers & M. Eric Gershwin, Transverse

Myelitis, 11 Autoimm. Rev. 231 (2012), filed as Ex. 67 (ECF No. 31-6), at 232. “There is often a

clearly defined rostral border of sensory dysfunction, and spinal MRI and lumbar puncture often

show evidence of acute inflammation.” Working Group Criteria at 499.

There is growing support for the view that TM may be overinclusive as a diagnostic

classification. C. Goh et al., MRI in Transverse Myelitis, 40 J. Magn. Res. Im. 1267 (2014), filed

as Ex. E-5 (ECF No. 41-6) (“Goh”), 1268 (deeming TM to constitute a “diagnosis of exclusion,”

and adding that it is unclear “that there exists a distinct pathogenetic entity of idiopathic transverse

myelitis,” with the diagnosis incorporating “several underlying entities”). Many neuropathic

conditions feature evidence of spinal cord-associated symptoms, and yet TM may not be the

ultimately-proper diagnostic descriptor for the actual disease at hand. For example, spinal cord

inflammation consistent with TM can often prove to be the precursor for some other chronic

disease process, like MS or NMSOD—meaning it would not thereafter be proper to say the affected

individual had “experienced” an isolated case of TM that evolved into something else. Goh at 1268

Table 1 (noting that evidence supportive of MS, optic neuritis, or other infectious diseases are

exclusionary criteria for a TM diagnosis). In addition, the orientation of a lesion—lateral (up and

down) versus transverse (across)—is not a factor that excludes TM as a diagnosis, even though the

effect of the lesion’s positioning can be relevant to both diagnosis and treatment (and the very term

23

“Myelitis” is defined as “1. Inflammation of the spinal cord, often part of a more specifically defined disease process.

One group of diseases is named according to whether primarily white matter or gray matter is affected (leukomyelitis

and poliomyelitis); another group is defined by whether there is coexistent disease of the meninges (meningomyelitis)

or the brain (encephalomyelitis). In practice, the term is also used to denote noninflammatory lesions of the spinal

cord. 2. Inflammation of the bone marrow.” Myelitis, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=32680&searchterm=myelitis (last visited May 8, 2026).

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“transverse myelitis” incorrectly implies only lesions horizontal to the spinal cord as included).

And finally, spinal cord injuries that present with symptoms that look like they are due to myelitis

can be the product of literal, physical trauma—where neuroinflammation is a secondary result of

that trauma.

Thus—and as numerous items of literature filed in this case suggest—it can be quite easy

to overapply TM as a diagnosis to explain neurologic symptoms. Park at 2 (stating that “Transverse

myelitis (TM) in particular should be excluded, as previous studies have reported that about 15%

of patients diagnosed with TM were actually SCI patients”); Zalewski at 57, 61; Zalewski II at

e97, e99. But nothing filed in this case stands for the opposite conclusion: that TM is likely to be

mistakenly identified as an infarct.

MRI findings usually help treaters confirm the existence of TM (although as this case

demonstrates, it can be very difficult to interpret what imaging actually “shows,” with reasonable

and qualified medical experts disagreeing on what the findings reveal). But imaging generally

reveals what is the source of TM’s clinical symptoms: inflammation in the spinal cord, often

appearing as lesions. Zucconi Rep. at 10, 11. While initial imaging results may not strongly

establish the presence of TM, they should be somewhat supportive of it (and may often reveal

enhancement if contrast is used – evidence of an active inflammatory process sufficient to cause a

breach of the blood-brain barrier). Evidence derived from sequential acts of imaging may later

reveal progression as clinical, outward symptoms occur in real time. See, e.g., Greenslade v. Sec’y

of Health & Hum. Servs., No. 14-1140V, 2024 WL 3527665, at *6–7, 26–28 (Fed. Cl. Spec. Mstr.

June 28, 2024) (claimant’s TM began pre-vaccination, given evidence of prior symptoms; first

post-vaccination MRI (performed several weeks after earlier symptoms) revealed mild T2 signal

intensity but no enhancement, and then claimant’s symptoms continued to present and evolve over

the following several days).

A spinal cord infarct can also involve symptoms comparable to what is seen in TM, but is

distinguishable in nature and cause. Infarcts, or ischemia, reflect dead tissue attributable to a lack

of blood supply to the cord’s nerve tissue. As noted in Zalewski, spinal cord infarct can often be

the product of a variety of risk factors, including hypertension, smoking, hyperlipidemia, and

diabetes mellitus. See Zalewski at 58. Zalewski adds that “[o]nset is more protracted and radiologic

distinction from competing diagnoses is more difficult than with cerebral infarction. Thus, patients

with a spontaneous (i.e., nonprocedural, nontraumatic) [spinal cord infarct] often receive

misdiagnoses.” Id. at 57. Imaging does not always clearly establish TM over infarct or vice versa.

In fact, imaging is not likely to identify infarct when performed fairly close in time to an

individual’s acute presentation. Park at 2; Kouchak v. Sec’y of Health & Hum. Servs., No. 18-

1279V, 2023 WL 6973017, at *5 (Fed. Cl. Spec. Mstr. Sept. 26, 2023) (citing Alblas at 222

(patients examined by MRI within 24 hours after symptom onset showed normal results in four of

the five studied patients)).

43

One very important feature of infarct, however, is its acute nature, evidenced by a rapid

progression to nadir in terms of clinical presentation and symptoms. Numerous items of literature

filed in this case emphasize the fact that infarcts will clinically present with sudden, often-alarming

symptoms, and a fast downward progression to nadir will occur within hours to a few days. Beh at

2 (“[a]n apoplectic event with deficits reaching the nadir in less than 4 hours indicates a vascular

event,” whereas TM is characterized by “neurologic deficits reaching a nadir within a few weeks”).

Case law involving the TM-infarct diagnostic dispute are consistent in recognizing this timeframe

to nadir distinction. I.J. v. Sec'y of Health & Hum. Servs., No. 16-864V, 2021 WL 1232733 (Fed.

Cl. Spec. Mstr. Jan. 4, 2021), at *8, 18, mot. for review granted on other grounds, 155 Fed. Cl. 20

(2021).

TM can also present acutely, but is understood often to feature a longer course progression

timeframe (as reflected in diagnostic criteria that envision progression to nadir in as long as 21

days). Working Group Criteria at 500 Table 1; Pearson v. Sec’y of Health & Hum. Servs., No. 16-

9V, 2019 WL 3852633, at *15 (Fed. Cl. Spec. Mstr. July 31, 2019) (onset to nadir can occur within

a timeframe as long as two to three weeks, although within hours is possible). Thus, although there

is some overlap in the specific timeframes for progression to nadir applicable to TM and infarct;

and although TM can also present rapidly; the medical literature filed in this case stands for the

conclusion that infarcts generally progress much faster to nadir than TM.

Another significant feature of TM that impacts my analysis is how it can be independently

corroborated. In addition to imaging, CSF testing is important, since it can reveal indicia of

inflammation in the cord, such as pleocytosis or other findings. First Price Rep. at 7 (referencing

Beh at 97). Indeed, as Petitioner’s experts acknowledged, some kinds of infections resulting in

myelitis (bacterial meningitis, for example) would likely yield dramatically-high levels of CSF

pleocytosis, consistent with the body’s efforts to fight a wild and uncontrolled infection. Tr. at 71.

Prior Program claimants have received compensation for TM deemed to have been vaccine-

caused (including by the flu vaccine). See, e.g., Schmidt v. Sec'y of Health & Human Servs., No.

07-20V, 2009 WL 5196169 (Fed. Cl. Spec. Mstr. Dec. 17, 2009) (granted entitlement on a claim

that an influenza vaccine caused Petitioner’s TM via molecular mimicry). However, the specific

factors of an individual vaccinee’s medical history can impact success, even when the causal theory

is found to have been preponderantly established. See, e.g., Palattao v. Sec'y of Health & Hum.

Servs., No. 13-591V, 2019 WL 989380 (Fed. Cl. Spec. Mstr. Feb. 4, 2019) (denying entitlement

in TM case where petitioners failed to establish that timing of onset of symptoms was medically

appropriate under their proposed causation theory).

As with this case, fact disputes have arisen in other matters as to whether a spinal cord

injury was likely due to myelitis-related inflammation or more properly attributed to an infarct.

I.J., 2021 WL 1232733 (petitioner found to have more likely experienced TM over infarct). Special

44

master determinations have recognized that what “looks” like TM may often actually reflect an

infarct. See, e.g., DeWit v. Sec’y of Health & Hum. Servs., No. 18-1353V, 2026 WL 822767, at

*33–36 (Fed. Cl. Spec. Mstr. Feb. 25, 2026) (infarct more likely diagnosis than TM; evidence of

enhancement and lesions only began to show up on imaging within a week or so of initially-acute

onset, and predominance of signal in gray matter along with evidence of cord pathology and initial,

if subtle, hyperintensity consistent with infarct); Johnson v. Sec’y of Health & Hum. Servs., No.

18-410V, 2025 WL 1942989, at *21–22 (Fed. Cl. Spec. Mstr. June 17, 2025) (claimant more likely

suffered infarct than TM; initial MRI imaging did not reveal enhancement, CSF results were not

abnormal, and treaters consistently included infarct in differential); see also Broekelschen, 618

F.3d at 1347-49 (special master reasonably weighed evidence in determining that injury was more

likely an anterior spinal cord infarction than TM).

I recently resolved a claim in which the parties were locked in a similar “TM vs. infarct”

diagnosis dispute. See Ross v. Sec’y of Health & Hum. Servs., No. 22-136V, 2025 WL 3531575

(Fed. Cl. Spec. Mstr. Nov. 14, 2025) (Tdap vaccine not shown to have caused petitioner to

experience TM). Some of the same kinds of considerations at issue herein were explored in Ross.

There, after considering the opinions of competing neurologists, I found the TM diagnosis lacked

preponderant support – even though I was unable to also determine that the infarct proposed by

Respondent’s expert was the more likely injury. Ross, 2025 WL 3531575, at *18. In particular, the

evidence in that case established inconclusive MRI results despite an acute presentation. Id. And

there was a temporal gap between the Petitioner’s vaccination and subsequent onset, but with no

intervening medical concerns, undermining the conclusion that the petitioner had been

experiencing some kind of subclinical, antibody-driven inflammatory process before onset. Id. In

addition, DWI techniques that could have confirmed an infarct were never performed (whereas

here they were utilized – and deemed by treaters supportive of infarct). Id. at 19. Thus, although

the diagnostic question was difficult, and evidence existed to support TM, balancing the evidence

in its totality weighed against TM. Id. 24

All of the above establishes that TM is not automatically the correct diagnosis by default,

simply because the spinal cord is involved—and even where the clinical/testing evidence is

somewhat inconclusive. The very existence of ambiguity in interpretation of imaging results

underscores the possibility that clinical symptoms attributable to a spinal cord injury are not

automatically likely to reflect TM. And as is true in any Program case, in instances where diagnosis

is disputed, the evidence in its totality must be considered carefully.

24

I also note, however, that the Ross petitioner possessed a number of infarct risk factors totally absent from this case.

Ross, 2025 WL 3531575, at *18. This is one of several reasons why I do not find that the evidence tips in favor of

infarct, and I certainly do not on this record presume to propose what most likely caused Petitioner’s cord injury. But

it remains the case, as discussed below, that the totality of evidence does not weigh in favor of TM—even if it is

completely true that Petitioner lacked the kinds of classic risk factors associated with infarct (smoking, age, obesity,

etc.).

45

II. Petitioner Did Not Likely Experience TM

Petitioner places all of her causation emphasis on the contention that she likely experienced

TM. She expressly does not endeavor to prove the flu vaccine can cause spinal cord infarcts. Tr.

at 4, 5. And Petitioner bears the burden of proving her proposed diagnosis by a preponderance of

the evidence. Broekelschen, 618 F.3d at 1346. Thus, a determination that she did not experience

TM is fatal to the claim. Id. at 1349 (appropriate for special master to evaluate diagnostic dispute

before reaching Althen analysis).

I do not purport to diagnose Petitioner, nor am I qualified to do so. And I cannot say it is

certain, or even likely, that she experienced an infarct. But after balancing the competing evidence

on the diagnosis question and weighing it in totality, I conclude the evidence does not preponderate

in favor of a TM diagnosis—and the ample proof that supports an infarct diagnosis is integral to

that determination.

My determination relies on several different categories of evidence, and I address them by

grouping each according to topic.

Acute and Rapid Progression of Petitioner’s Initial Clinical Symptoms

One of the most compelling factors leading me to disfavor TM as preponderantly

established was Petitioner’s extremely short, early clinical course. The record preponderates in

favor of the conclusion that Petitioner’s progression from onset to nadir took no more than five

hours, and likely a bit less. Petitioner arrived at the ED by 1:15 – 1:20 pm reporting tightness and

pain in her back, numbness and tingling in her bilateral lower extremities, and altered sensation in

her lower and upper extremities. Ex. 5 at 12, 19–20. Later that same afternoon, she reported the

onset of the acute pain and sensations that lead her to seek emergency care as beginning two hours

prior, or around 12:30 pm. Ex. 5 at 12. In addition, at the time of her arrival at the hospital,

Petitioner was still able to walk, but not long after she could no longer lift her left leg, and had

decreased ability to move her right leg. Id. By the time of admission to the ICU (close to 5:30 pm),

she could not move her extremities at all. Id. at 32, 37.

Petitioner’s experts correctly observed that the temporal criteria for TM and infarct overlap

somewhat, and both allow for onset to nadir timeframes to occur within a four to five-hour period.

There certainly is no bright-line rule for deciding when something suddenly stops being infarct and

becomes TM, based solely on the timing of downward symptoms progression. But it can be

gleaned from the independent evidence filed in this matter that a rapid onset to nadir timeframe is

more likely supportive of an infarct, which occurs abruptly, than TM (where an inflammatory

process causing harm will take time to evince downstream clinical symptoms—and can unfold

over many days). Beh at 2; see also T. West et al., Acute Transverse Myelitis: Demyelinating,

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Inflammatory, and Infectious Myelopathies, 32 Semin. Neurol. 97 (2012), filed as Ex. C-6 (ECF

No. 24-7), at 100 (“[i]n acute transverse myelitis, symptoms typically develop over hours to days

and then worsen over days to weeks”) (emphasis added). And timeframes slightly longer than four

or five hours are still consistent with infarct if they remain compressed. See, e.g., Zalewski at 60,

Box (proposing a timeframe of less than 12 hours to nadir as suggestive of infarct); Yadav at 2811

(setting forth a timeframe of 72 hours from onset to “peak” severity as consistent with infarct).

Thus, the clinical evidence alone from Petitioner’s first day at the hospital strongly supports infarct

over TM.

To get around such a rapid and obviously-catastrophic symptoms progression, Petitioner’s

experts have attempted to identify later occurrences in her treatment as her “true” nadir. In

particular, Dr. Pachner referenced the need for intubation on the morning of December 10th,

suggesting this should be viewed as her nadir. However, the totality of the medical record evidence

suggests that this treatment step alone was not reflective of nadir, but instead illustrates the overall

severe nature of her condition. Petitioner was clearly experiencing respiratory issues prior to this

point. Ex. 5 at 37. In addition, the record supports the conclusion that the decision to intubate

reflected some thinking about the breathing devices and processes being utilized, as opposed to a

clinical symptom as concerning as Petitioner’s immediate progression to quadriplegia the same

day she sought emergency care—and within hours of initial pain. TM, of course, could unfold in

a slower, more stuttering manner, and thus a two-day progression is consistent with it—but the

medical record weighs against the determination in this case that progression to nadir took that

long.

CSF Findings

Also significant in evaluating diagnosis is the lack of corroborative testing evidence that

Petitioner was experiencing a neuroinflammatory-caused condition impacting her spinal cord. TM

involves inflammation-driven harm, but the record does not preponderate in favor of the conclusion

that Petitioner was experiencing CNS inflammation of the sort associated with TM in early-

December 2019. 25

Petitioner’s initial CSF testing was at best faint evidence of active spinal cord

inflammation. The first CSF testing (performed December 8th) unquestionably produced normal

results. Ex. 5 at 1401. Thus, as of the day of Petitioner’s catastrophic onset and rapidly-downward

clinical progression, lab work did not confirm the presence of an inflammatory process that could

25

There is evidence that as Petitioner’s disease process progressed, she later likely experienced neuroinflammation—

as confirmed by MRI results and treatments aimed at curbing such inflammation. But this could occur secondarily to

another ongoing, or completed, disease process. For TM to best explain Petitioner’s condition diagnostically, that

inflammation would have to come first, before clinical symptoms manifested of the sort she experienced on December

8, 2019.

47

secondarily be leading to those very same symptoms that were at that time present. It is not clear,

nor has Petitioner shown otherwise, how such rapid progression of clinical symptoms to nadir

would be accompanied by a lack of evidence of existing inflammation (and Dr. Pachner’s analogy

to MS brain inflammation as not showing up in the cord were unpersuasive for a disease process

alleged to have mostly if not solely impacted the spinal cord). This is so even if CSF testing does

not always immediately display strong evidence of inflammation in the cord in cases of TM.

The next round of CSF testing occurred December 18th, 10 days after onset. By this point,

there was evidence of a slightly elevated WBC count—but not particularly high (even if the

hospital’s somewhat uncommonly-used range of 1-10 is disregarded, in favor of a lower, 1-5

range). As Dr. Price persuasively explained, evidence of the degree of inflammation is what

matters, as opposed to simply evidence of a WBC count exceeding the normal range. Tr. at 402–

03. And here, the degree of abnormality in WBC levels was not indicative of an uncontrolled

inflammatory process at work.

I deem these results to be inconsistent with the proposed TM diagnosis (even if they do not

fully rule it out). 26 As Dr. Price persuasively established, testing should have revealed a more

fulminant level of inflammation earlier on, especially given the severe nature of Petitioner’s

presentation. Dr. Price also offered literature demonstrating (at least for the relevant sample in the

study) that mild outcomes were consistent with lower levels of pleocytosis and thus the levels

Petitioner’s CSF testing revealed should not have been paired with the kind of severe symptoms

that she had experienced more than a week before the second round of testing. See, e.g., Sellner at

314.

Imaging Evidence – Progression in December 2019

I give weight to the imaging results, as interpreted and explained by the parties’ radiologic

experts. Those most relevant to my determination are from Petitioner’s December 2019

presentation, for they are the most contemporaneous findings shedding light on the nature of the

disease process at issue, as seen at the time she presented with sudden and alarming deficiencies.

As noted above, TM can be corroborated with proof of inflammation seen on MRI—perhaps (in a

case involving an acute clinical presentation, as here) evident from the very first imaging obtained.

26

The inconsistency of Petitioner’s CSF te

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