VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_18-vv-00410
Package ID: USCOURTS-cofc-1_18-vv-00410
Petitioner: Shelle Johnson
Filed: 2018-03-19
Decided: 2025-06-17
Vaccine: influenza
Vaccination date: 2016-09-28
Condition: transverse myelitis
Outcome: denied
Award amount USD: 

AI-assisted case summary:
On March 19, 2018, Shelle Johnson filed a petition for compensation under the National Vaccine Injury Compensation Program, alleging that the influenza vaccine she received on September 28, 2016, caused her to develop transverse myelitis (TM) and subsequent medical issues, including leg weakness, numbness, and tingling. Petitioner's initial symptoms of fatigue in her legs began approximately two days after vaccination. She was hospitalized and underwent extensive medical evaluation, with differential diagnoses including spinal cord injury (SCI) and TM. Despite her treating physicians' inability to reach a definitive diagnosis and some recommending she avoid future flu vaccines, the medical records at crucial points noted probable SCI. Petitioner's counsel was Courtney Christine Jorgenson of Siri & Glimstad, LLP. Respondent's counsel was Nina Ren of the United States Department of Justice. Special Master Herbrina D.S. Young reviewed the case. Petitioner's expert, Dr. Peter-Brian Andersson, opined that the flu vaccine caused TM through molecular mimicry. Respondent's experts, Dr. Dara Jamieson and Dr. Thomas Forsthuber, argued that Petitioner's condition was more consistent with SCI and that the evidence did not support a causal link between the flu vaccine and TM. The Special Master found that Petitioner failed to establish by a preponderance of the evidence that she suffered from TM, nor that the vaccine caused her condition. Specifically, the Special Master found the temporal relationship between vaccination and symptom onset was too short to be medically acceptable for vaccine-induced TM via molecular mimicry. Therefore, Petitioner's claim was denied.

Theory of causation field:
Influenza vaccine on September 28, 2016, age 52, followed roughly two days later by leg fatigue, weakness, numbness, tingling, and dispute over transverse myelitis versus spinal cord injury. DENIED. Petitioner Shelle Johnson relied on Dr. Peter-Brian Andersson and molecular mimicry/steroid-response reasoning. Respondent's Dr. Dara Jamieson and Dr. Thomas Forsthuber argued the record favored spinal cord injury or non-inflammatory pathology and that 1.5-2 days was too short for vaccine-induced autoimmune TM. Special Master Herbrina Sanders Young denied entitlement June 17, 2025.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_18-vv-00410-1
Date issued/filed: 2025-07-14
Pages: 32
Docket text: PUBLIC DECISION (Originally filed: 6/17/25) regarding 72 DECISION of Special Master. Signed by Special Master Herbrina D S Young. (kis) Service on parties made.
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Case 1:18-vv-00410-UNJ Document 73 Filed 07/14/25 Page 1 of 32
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: June 17, 2025
* * * * * * * * * * * * * * * *
SHELLE JOHNSON, *
*
Petitioner, * No. 18-410V
*
v. * Special Master Young
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
* * * * * * * * * * * * * * * *
Courtney Christine Jorgenson, Siri & Glimstad, LLP, Phoenix, AZ, for Petitioner.
Nina Ren, United States Department of Justice, Washington, DC, for Respondent.
DECISION ON ENTITLEMENT1
On March 19, 2018, Shelle Johnson (“Petitioner”) filed a petition for compensation in the
National Vaccine Injury Compensation Program (“the Program”)2 alleging that the influenza
(“flu”) vaccine Petitioner received on September 28, 2016, caused her to suffer from transverse
myelitis (“TM”) and subsequent “medical issues as a result of her [TM], including lack of mobility,
tingling in her feet bilaterally, and weakness of her lower extremity.” Pet. at 1, ECF No. 1. After
carefully analyzing and weighing all the evidence and testimony presented in this case in
accordance with the applicable legal standards,3 I find that Petitioner has failed to provide
1 Because this Decision contains a reasoned explanation for the action taken in this case, it must be made
publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or at
https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act
of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government
Services). This means the Decision will be available to anyone with access to the internet. In
accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or
other information, the disclosure of which would constitute an unwarranted invasion of privacy. If, upon
review, I agree that the identified material fits within this definition, I will redact such material from
public access.
2 National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755 (“the Vaccine Act”
or “Act”). Hereinafter, for ease of citation, all “§” references to the Vaccine Act will be to the pertinent
subparagraph of 42 U.S.C. § 300aa (2018).
3 While I have reviewed all of the information filed in this case, only those filings and records that are
most relevant to the decision will be discussed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d
1322, 1328 (Fed. Cir. 2016) (“We 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. App’x 875, 884 (Fed. Cir. 2013) (“Finding

Case 1:18-vv-00410-UNJ Document 73 Filed 07/14/25 Page 2 of 32
preponderant evidence that the flu vaccine Petitioner received on September 28, 2016, caused her
to develop transverse myelitis or any other medical issues. Accordingly, Petitioner is not entitled
to compensation.
I. Procedural History
Petitioner filed her petition on March 19, 2018. Pet. On April 5, 2018, Petitioner filed
medical records and a statement of completion. Pet’r’s Exs. 1–7, ECF No. 8; ECF No. 9
Respondent filed his Rule 4(c) Report, recommending that compensation be denied on
January 28, 2019. Resp’t’s Report, ECF No. 17. Petitioner filed an expert report from Peter-Brian
Andersson, M.D., PhD as well as his curriculum vitae (“CV”) on November 2, 2020. Pet’r’s Exs.
10–11, ECF No. 40. On November 6, 2020, and November 17, 2020, Petitioner filed vaccine
exemption documents. Pet’r’s Exs. 12–13, ECF Nos. 41–42. Supporting medical literature was
submitted by Petitioner on December 3, 2020. Pet’r’s Exs. 14–30, ECF Nos. 43–44.
Respondent filed expert reports from Dara Jamieson, M.D., and Thomas Forsthuber, M.D.,
along with their CVs and accompanying medical literature on March 3, 2021. Resp’t’s Ex. A, Tabs
1–21, ECF No. 46; Resp’t’s Ex. B, ECF No. 47; Resp’t’s Ex. C, Tabs 1–15, ECF No. 48; Resp’t’s
Ex. D, ECF No. 49
On July 19, 2021, Petitioner filed a supplemental expert report from Dr. Andersson. Pet’r’s
Ex. 31, ECF No. 52. Respondent filed responsive supplemental expert reports from Drs. Jamieson
and Forsthuber on September 19, 2021. Resp’t’s Exs. E, Tabs 1–10, F, Tab 1, ECF No. 54.
Petitioner submitted additional medical records on April 5, 2022, June 7, 2022, and May 18, 2023.
Pet’r’s Exs. 32–35, ECF Nos. 55–56, 59.
On May 26, 2023, I issued an order for an entitlement hearing scheduled for February 6–
7, 2024. ECF No. 60. After informal communications with the parties, a status conference was
held on July 19, 2023. Min. Entry, docketed July 19, 2023. Respondent stated that his expert had
a work conflict during the scheduled hearing dates. Id.; ECF No. 61. The parties determined that
in lieu of rescheduling the hearing, they would agree to a ruling on the record. ECF No. 61. An
order cancelling the entitlement hearing issued on August 10, 2023. Id. On August 21, 2023,
Petitioner filed supplemental medical records. Pet’r’s Ex. 36, ECF No. 62.
On November 14, 2024, Petitioner filed a motion for ruling on the record. Pet’r’s Mot.,
ECF No. 64. Respondent filed his response on December 27, 2024; Petitioner replied on January
2, 2025. Resp’t’s Response, ECF No. 65; Pet’r’s Reply, ECF No. 66. Petitioner filed letters from
Nurse Practitioner Anne Beighley and Dr. Brian Crum on March 14, 2025. Pet’r’s Exs. 37–38,
ECF No. 71.
This matter is now ripe for consideration.
certain information not relevant does not lead to—and likely undermines—the conclusion that it was not
considered.”).
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II. Factual Background
A. Medical Records
Petitioner was 52 years old when she received her flu vaccine on September 28, 2016.
Pet’r’s. Ex. 3 at 1. Her medical history included a vertebrobasilar vascular insufficiency in 2015.
Pet’r’s Ex. 5 at 27. Two days post vaccination, on September 30, 2016, Petitioner presented to the
emergency department (“ED”) with complaints of “some ‘fatigue’ feeling in back of her legs” that
occurred the previous night at about 9:00 pm. Pet’r’s Ex. 4 at 1. She was unable to stand in the
morning and had since developed a numb feeling in the back of her left leg. Id. Petitioner also
reported a little pain in her right mid-back. Id. Preliminary differential diagnoses included back
pain, sciatica, spinal stenosis, cauda equine syndrome, and anxiety. Id. at 3.
On September 30, 2016, Petitioner was seen at the Mayo Clinic with a chief complaint of
leg weakness. Pet’r’s Ex. 5 at 1. She stated that she did not believe she had the “strength to stand
and walk.” Id. at 5. She also reported “a sense of numbness that radiates down the posterior aspect
of both legs.” Id. Petitioner denied trauma and recent infectious symptoms. Id. On examination,
she had tenderness at the T11 area and weakness on standing in both legs. Id. Her patellar reflexes
were brisk. Id. Differential diagnoses included TM, epidural hematoma, abscess, mass, or early
Guillain-Barré syndrome (“GBS”).4 Id. A neurologic examination revealed “an upper motor
neuron pattern of weakness in the bilateral lower extremities, more pronounced in the right lower
extremity than the left, with distal greater than proximal flexor weakness.” Id. at 11. Petitioner had
back allodynia below the T5-7 level and “decreased sensation in the left lower extremity compared
to the right lower extremity with pinprick.” Id. Her examination was concerning for thoracic
myelopathy5 and magnetic resonance imaging (“MRI”) of the thoracic spine was ordered. Id. at
12. The MRI did not reveal an obvious lesion, and the weakness was still present on the right lower
side, although less convincing on reexamination. Id. Petitioner was able to squat on both legs, but
could not squat on the right leg alone, and she had an antalgic gait. Id. The diagnosis was uncertain,
and Petitioner was admitted for further evaluation. Id. Differentials included query spinal cord
infarction6 (“SCI”) versus thoracic myelopathy and paraparesis,7 right greater than left. Id. at 15.
A repeat MRI done on October 3, 2016, showed a single change in the thoracic cord,
4 GBS is a “rapidly progressive ascending motor neuron paralysis of unknown etiology, frequently seen
after an enteric or respiratory infection.” Guillain-Barré Syndrome, DORLAND’S MED. DICTIONARY
ONLINE, https://www.dorlandsonline.com/dorland/definition?id=110689 (last visited June 11, 2025). “It
begins with paresthesias of the feet, followed by flaccid paralysis of the entire lower limbs, ascending to
the trunk, upper limbs, and face; other characteristics include slight fever, bulbar palsy, absent or lessened
tendon reflexes, and increased protein in the cerebrospinal fluid without a corresponding increase in
cells.” Id.
5 Myelopathy refers to “any of various functional disturbances or pathologic changes in the spinal cord,
often referring to nonspecific lesions in contrast to the inflammatory lesions of myelitis.” Myelopathy,
DORLAND’S MED. DICTIONARY ONLINE.
6 Infarction is “an area of coagulation necrosis in a tissue due to local ischemia resulting from obstruction
of circulation to the area, most commonly by a thrombus or embolus.” Infarct, DORLAND’S MED.
DICTIONARY ONLINE.
7 Paraparesis is “partial paralysis of the lower limbs.” Paraparesis, DORLAND’S MED. DICTIONARY
ONLINE.
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consistent with either an inflammatory/immune-mediated response or possible ischemia.8 Pet’r’s
Ex. 5 at 39. No structural cause for Petitioner’s symptoms was found and there was “no abnormal
cord signal or compression.” Id. at 36. The next day, Dr. Lyell K. Jones, a neurologist, “personally
met with and examined [Petitioner] after a detailed review of the record with the Inpatient
Neurology Team.” Id. at 42. Dr. Jones concluded Petitioner “likely ha[d] a thoracic [SCI] to
account for her asymmetric paraparesis.” Id. He noted that “a workup looking for
autoinflammatory or coagulopathic mechanisms for her infarction” would be completed. Id. Dr.
Jones further ordered that Petitioner “complete three days of IV methylprednisolone and pursue
continued aggressive rehabilitative therapy.” Id.
A transesophageal echocardiogram conducted on October 4, 2016, was normal. Pet’r’s Ex.
5 at 48. Her neurology hospital service records at discharge listed probable thoracic SCI and noted
“[r]egarding her thoracic myelopathy, likely reflecting a [SCI].” Id. at 51. Additionally, a “repeated
thoracic MRI . . . show[ed] T2 hyperintensity at the T8 level. This likely represent[ed] a thoracic
cord infarction.” Id. at 56. Petitioner was discharged for rehabilitation on October 5, 2016. Id. at
48–49. Her final primary diagnosis was “acute paraparesis, right greater than left – suspect [SCI].”
Id. at 62. Rehabilitation facility admission records listed Petitioner’s assessment as acute thoracic
myelopathy. Id. at 72. Petitioner’s course of treatment included physical and occupational therapy
to allow her to “ascend and descend three stairs to enter her home as well as manage in-home
mobility independently.” Id. Her treaters agreed that inpatient treatment was needed but added that
she would “only need a relatively brief inpatient rehabilitation stay.” Id.
Dr. Jeffrey A. Strommen, a physiatrist with the Mayo Clinic, examined Petitioner on
October 6, 2016. Pet’r’s Ex. 5 at 88. He noted her history included a “comprehensive neurologic
evaluation, including spinal imaging. It was felt that she likely had a spinal cord infarct versus
myelitis.” Id. Dr. Strommen agreed that the etiology was uncertain, but saw Petitioner’s
“substantial improvement with steroids,” as evidence that her condition was “more of a [TM]-type
picture.” Id. On October 7, 2016, Petitioner started on a low dose of gabapentin at night to ease
burning and aching in her right lower limb. Id. at 97. She was discharged on October 12, 2016. Id.
at 109–14. The discharge summary noted that her antinuclear antibodies (“ANA”) were mildly
elevated at 3.1 and that her cerebrospinal fluid (“CSF”) was normal. Id. at 64. A thrombophilia
workup was pending at the time of discharge. Id. The final primary diagnosis was listed as “spinal
cord injury, non-traumatic, paraplegia, incomplete.” Id. at 109. Additional diagnoses included
thoracis myelopathy; paraparesis, right greater than left, lower extremity only; probable thoracic
SCI versus inflammation; urinary retention; transient diplopia9 (approximately one year ago); and
anxiety. Id.
On October 27, 2016, Petitioner saw her primary care physician (“PCP”), Dr. Melanie
McKendrick Johnson, for a checkup “after being hospitalized for myelitis of the spinal cord.”
Pet’r’s Ex. 4 at 4. She complained of right leg spasticity at night, which caused her difficulty
sleeping. Id. Petitioner requested an increase in her gabapentin dosage to alleviate her continued
symptoms. Id. She noted that she was doing well in physical therapy and planned to return to work
8 Ischemia is a “deficiency of blood in a part, usually due to functional constriction or actual obstruction
of a blood vessel.” Ischemia, DORLAND’S MED. DICTIONARY ONLINE.
9 Diplopia is “the perception of two images of a single object.” Diplopia, DORLAND’S MED. DICTIONARY
ONLINE.
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the following day. Id. Petitioner reported that she still had decreased sensation to temperature in
her left leg and foot and weakness in the quadriceps. Id. An examination revealed hyperactive
reflexes in her right leg, and normal reflexes on the left. Id. Her strength was normal and symmetric
in both legs. Id. The impression was myelitis with the note that “there [was] some thought that this
may be secondary to the flu shot and we . . . added that to allergies.” Id. at 6. Dr. McKendrick
Johnson also noted positive ANA test results. Id. Petitioner’s gabapentin was increased to 600 mg
at bedtime. Id.
Petitioner had a follow up visit with the Mayo Clinic Physical Medicine and Rehabilitation
Department on November 14, 2016. Pet’r’s Ex. 5 at 125. She reported that she was continuing to
improve and had returned to work. Id. Petitioner felt about 95% better but still had some deficits.
Id. She “continue[d] on a daily aspirin for potential infarction,” and tramadol and gabapentin for
neuropathic pain. Id.
On December 12, 2016, Petitioner saw her PCP for a general examination. Pet’r’s Ex. 4 at
7. She reported that she had restless leg syndrome and that she thought she may have shingles. Id.
Her neurologic and musculoskeletal examinations were normal. Id. at 9.
On Wednesday, December 21, 2016, Petitioner called the Mayo Clinic Neurology
Department and reported left lower extremity numbness and difficulty walking since Monday.
Pet’r’s Ex. 5 at 127. When the call was returned, she reported that she had improved somewhat.
Id. Dr. M.W. Ruff expressed concern because “the etiology of her prior paraparesis was felt to be
a probable [SCI], but this was indeterminate.” Id. She was advised to schedule an appointment for
follow-up or come to the ED as soon as possible. Id. Petitioner was seen in the ED the next day
for left leg numbness. Id. at 128. The ED record noted flu virus vaccines under allergies/adverse
reactions with a note that “[a]llergies above current as of Thursday, 22-Dec-2016 at 18:01.” Id. It
was noted that Petitioner was told to come in for a repeat thoracic spine MRI due to a recent
increase in left lower extremity weakness. Id. at 129. During her neurology consultation, Petitioner
reported that roughly ten days earlier (December 11, 2016), she had an outbreak of shingles on her
right leg. Id. at 136. Three days before that, she developed sudden onset left lower extremity
numbness, which she described as a loss of feeling with an occasional pins and needles sensation.
Id. Petitioner did not report weakness but did describe difficulty walking because of the feeling of
heaviness. Id. She noted improvement over the last two days. Id.
On examination, Petitioner had near normal strength, brisk reflexes, and upgoing toes
bilaterally. Pet’r’s Ex. 5 at 138. She had decreased sensation to temperature, and pinprick on the
left, and some impairment of proprioception and vibratory sense (distal greater than proximal). Id.
There was a minimal level change to pinprick at around T9-10. Id. The MRI showed a T2
hyperintense lesion without mass effect or enhancement involving the right lateral aspect of the
thoracic cord at the T8 level. Id. “A demyelinating or inflammatory focus remain[ed] the primary
considerations.” Id. at 122. Dr. K.N. Kreck noted the “finding remain[ed] nonspecific, but
suspicious for focal cord infarction.” Id. at 123.
On March 17, 2017, Petitioner called the Mayo Neurology Department to report slight
weakness of her legs, numbness in her left leg, lack of sensation to temperature, walking with a
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hitch, restless legs at night, and difficulty urinating. Pet’r’s Ex. 5 at 142. During a follow-up call
on March 23, 2017, she was advised to schedule an appointment. Id. at 144.
On April 17, 2017, Petitioner saw neurologist Dr. Brian Crum and reported that her
symptoms had been stable since late December, with no worsening but not much improvement
either. Pet’r’s Ex. 5 at 146. She reported some trouble initiating urination and some trouble with
constipation, numbness in her left leg, and an inability to run. Id. Examination revealed a very mild
upper motor neuron pattern of weakness of the right leg and no weakness of the left leg. Id. at 147.
She had decreased sensation to pinprick up to about T10 on the left. Id. Her gait showed some
right lower extremity spasticity. Id. New imaging showed “improvement in the hyperintense area
in the mid-thoracic spine when you look at her previous studies compared to the one in December.”
Id. Petitioner was advised to follow up with rehabilitation to see if additional therapies might help
her. Id. She was also assured that she had improved and that nothing she did “would significantly
harm her or set her back or cause any increasing neurological attacks to occur of her central
nervous system.” Id. Dr. Crum told Petitioner that “[w]e may not have a good explanation for what
happened to her in September but at this point six months out, she is definitely improved and has
imaging studies which are improved as well, which is all reassuring.” Id. His listed diagnoses were
modified slightly from previous records and listed thoracic myelopathy, myelitis versus cord
infarction, and lower extremity spasticity. Id at 147.
An MRI scan completed on September 14, 2017, revealed “no change compared to the
MRI scans done in the past with a small area of T2 hyperintensity in the right spinal cord at T8.
There are no other abnormalities seen in the thoracic spine.” Pet’r’s Ex. 34 at 35. Petitioner’s
neurological examinations remained unchanged through August of 2018. Id. at 29.
Petitioner was seen at Olmsted Medical Center on November 9, 2020, with a chief
complaint of TM and spasticity. Pet’r’s Ex. 33 at 222. She reported a four-year history of
myelopathy of presumed autoimmune cause following her flu shot. Id. Dr. Keith Gonzalez noted
that Petitioner had “a history of acute onset of myelopathy most consistent with TM. The etiology
of which is unclear.” Id. at 225. Petitioner’s diagnosis “suggest[ed] the possibility of demyelinating
disease either as clinically isolated syndrome or with risk of developing multiple sclerosis.” Id. Dr.
Gonzalez ordered “an MRI of the brain [and] cervical and thoracic spine with and without
contrast.” Id. He also noted that “it [did] not appear that there [was] a clear medical solution.” Id.
Results from a December 10, 2020 MRI revealed “[n]o abnormal enhancement.” Id. at 231. Dr.
Gonzalez did note “areas of [non-enhancing] high T2 signal in the cord [were] concerning for
demyelination.” Id. A medical record dated December 21, 2020, documented Dr. Gonzalez’s
comparison of Petitioner’s brain CT dated July 29, 2015, and her MRI from December 10, 2020.
Id. at 241. His impression was that “[n]onspecific foci of T2/FLAIR signal hyperintensity within
the subcortical white matter regions bilaterally[, but t]hese may be related to chronic small vessel
ischemic changes.” Id. at 242. Dr. Gonzalez also noted that a demyelinating process cannot be
entirely excluded.” Id.
No other relevant medical records were filed.
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B. Vaccine Exemption Letters
Nurse Practitioner Anne Beighley submitted a letter dated October 28, 2020, that detailed
how Petitioner was advised “not to get a seasonal [flu] vaccination” because of her “chronic
medical condition.” Pet’r’s Ex. 12. Dr. Crum submitted a letter dated November 5, 2020, that noted
Petitioner had been his patient “since 2016 when she developed a myelitis (spinal cord
inflammation) following a flu shot.” Pet’r’s Ex. 13. Dr. Crum continued that Petitioner’s condition,
“which has been noted to happen after flu shots,” led him to recommend “that she not receive a flu
vaccination again due to risk of another, or worse, reaction to it.” Id.
C. Petitioner’s Affidavit
Petitioner submitted an affidavit that briefly noted her receipt of the flu vaccine on
September 28, 2016, her symptom onset of bilateral leg numbness “shortly after receiving the . . .
vaccination,” and her subsequent hospitalization. Pet’r’s Ex. 2 at 1. She added that she “was
eventually diagnosed with [TM] and was told this was more than likely from the flu vaccination.”
Id. Petitioner stated that she “believe[s her] diagnosis of [TM] occurred as a result of the flu
vaccination.” Id. at 2.
III. Experts
A. Expert Backgrounds and Qualifications
1. Petitioner’s Expert, Peter-Brian Andersson, M.D., Ph.D
Dr. Andersson is a board-certified clinical neurologist and professor and at the University
of California, Los Angeles. Pet’r’s Ex. 10 at 1. Dr. Andersson received his medical degree from
the University of Cape Town in South Africa. Pet’r’s Ex. 11 at 1. He completed his internship,
residency, and chief residency at the University of California, San Francisco. Pet’r’s Ex. 10 at 1.
Dr. Andersson then completed two fellowships at Stanford University in Neuroimmunology &
Multiple Sclerosis and Neuromuscular Disease & Electrodiagnostic Medicine. Id. He also has a
Ph.D in neuroimmunology. Id. at 2. Dr. Andersson has done research on the central nervous system
(“CNS”) immune response and published original research in clinical neurology. Id. Over the
course of his 24-year clinical practice, including managed care neurology, Dr. Andersson has
“performed thousands of inpatient and outpatient consultations for weakness, numbness and gait
difficulty, and have examined and/or treated at least 100-200 cases of [TM].” Id.
2. Respondent’s Expert, Dara G. Jamieson, M.D.
Dr. Jamieson was a board-certified practicing neurologist for 32 years before transitioning
to a teaching appointment. Resp’t’s Ex. A at 1. She received her medical degree from the
University of Pennsylvania School of Medicine, followed by a neurology residency and a
cerebrovascular fellowship at the Hospital of the University of Pennsylvania. Id.; Resp’t’s Ex. B
at 1. She is currently a Clinical Associate Professor of Neurology at Weill Cornell Medicine where
she teaches neurology courses and clinical inpatient clerkships. Resp’t’s Ex. A at 1. Dr. Jamieson
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has authored or co-authored several publications on multiple neurological topics. Id. at 2; see
Resp’t’s Ex. B at 11–17.
3. Respondent’s Expert, Thomas Forsthuber, M.D.
Dr. Forsthuber is board certified in anatomical and clinical pathology. Resp’t’s Ex. C at 1.
He received his medical degree from the University of Tübingen in Germany and completed a
residency in pathology at the University Hospitals in Cleveland. Resp’t’s Ex. D at 2. He is currently
a Professor of Immunology at the University of Texas at San Antonio and Adjunct Professor of
Pathology and Microbiology & Immunology at the University of Texas Health Sciences Center,
San Antonio. Resp’t’s Ex. C at 1. He has “over 25 years of experience in immunology, in particular
in autoimmune disease research and T cell immunology.” Id. Dr. Forsthuber has numerous
publications in the fields of T cell immunology and autoimmune diseases including multiple
sclerosis (“MS”), autoimmune diabetes, autoimmune heart disease, and their respective animal
models. Id.; see Resp’t’s Ex. D at 21–30.
B. Expert Opinions
1. Dr. Andersson’s First Report
In his first expert report, Dr. Andersson defined TM as a “a heterogenous, acquired,
immune-mediated disorder causing injury to spinal cord neurons and oligodendrocytes which
results in weakness, numbness and autonomic dysfunction.” Pet’r’s Ex. 10 at 9. He explained that
TM has been associated with CNS and systemic autoimmune disorders; viral, bacterial, and fungal
infections; and parasites. Id.at 10. TM is also associated with small cell lung carcinoma or can be
idiopathic in many cases. Id. Dr. Andersson noted that TM was described as a complication of
smallpox and rabies vaccines in 1922 and 1923, but “[a] direct causal relationship by vaccination
to TM has still not been definitively established.” Id. He cited to the National Institute of Health’s,
National Institute of Neurological Disorders and Stroke (“NINDS”) Transverse Myelitis Fact
Sheet, which stated that the condition can be caused by “post-infectious or post-vaccine
autoimmune phenomenon, in which the body’s immune system mistakenly attacks the body’s own
tissue while responding to the infection or, less commonly, a vaccine.” Id. (citing Pet’r’s Ex. 14 at
2).10
In identifying molecular mimicry as the biological mechanism for vaccine-caused TM, Dr.
Andersson asserted that “[t]he current understanding of the etiology of vaccination-induced TM is
the same as for vaccination induced [GBS].” Pet’r’s Ex. 10 at 10. He described the immune
system’s response to the flu vaccine as a “misdirected humeral and/or cell-mediated attack on the
host’s spinal cord because of antigens possessed both by the triggering agent and the host’s spinal
cord tissues, causing a ‘friendly fire’ injury.” Id. at 11. As evidence to support a molecular mimicry
process, Dr. Andersson noted that in TM cases, there can be “histopathological evidence of a
cellular and humoral immune attack on the nerves and oligodendrocytes associated with microgial
10 Transverse Myelitis Fact Sheet, NINDS, http://www.ninds.nih.gov/Disorders/Patient-Caregiver-
Education/Fact-Sheets/Transverse-Myelitis-FactSheet (last reviewed Oct. 25, 2020).
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and astrocyte activation.” Id. Dr. Andersson also named neuromyelitis optica11 and MOG-
Antibody disorder as comparable myelin-related conditions with “identified pathogenetic
antibodies” susceptible to molecular mimicry. Id. He identified immune complex depositions as
a “mechanism proposed to explain recurrent attacks in a patient with high circulating anti-hepatitis
B surface antigen in whom these antibodies were also found in the CSF,” and described plasma
exchange as “a beneficial therapy” for TM consistent with the presence of these autoantibodies.
Id. He also referred to animal models where encephalomyelitis was induced by injecting T-cells
from vaccinated subjects and mentioned an increased distribution of TM cases within six weeks
of vaccination according to Vaccine Adverse Event Reporting System (“VAERS”) data. Id.
Following his discussion of molecular mimicry, Dr. Andersson referenced a notation from
Petitioner’s PCP that the flu vaccine was a potential cause of her myelitis. Pet’r’s Ex. 10 at 12
(citing Pet’r’s 4 at 6). Based on multiple medical records, Dr. Andersson placed the initial onset
of Petitioner’s relevant symptoms—leg fatigue—at 9:00 pm the day following her vaccination. Id.
Dr. Andersson then opined that the proper diagnosis for Petitioner is TM, and the cause was her
flu vaccine. Id. at 13.
Dr. Andersson acknowledged that “[r]esolving between [TM] and [SCI] is frequently
difficult because of their similar clinical and radiologic features.” Pet’r’s Ex. 10 at 13. He provided
the definition of TM from the National Institute of Neurological Disorders and Stroke—“an
inflammation of the spinal cord;” and the definition of SCI from the American Heart Association—
“cell death attributable to ischemia, based on . . . evidence of spinal cord focal ischemic injury in
a defined vascular distribution.” Id. Dr. Andersson noted that severe back pain is a symptom of
infarction, but asserted that “Petitioner’s pain was not severe” and not limited in location. Id. He
argued that her symptoms do, however, satisfy three of the six most critical inclusion criteria
articulated by the Transverse Myelitis Consortium Working Group (“TMCWG”). Id. at 14 (citing
Pet’r’s Ex. 25).12 These three criteria are “[s]ensory, motor or autonomic dysfunction attributable
to the spinal cord, T2 hyperintense signal change on MRI and no evidence of compressive cord
lesion.” Id. Dr. Andersson argued that TMCWG’s full list of six inclusion and six exclusion criteria
were for research purposes and relied on one medical reference source, UpToDate, that reported
“not all [criteria] are necessarily required to make the diagnosis in clinical practice.” Id. (citing
Pet’r’s Ex. 26).13 Dr. Andersson asserted that Petitioner “satisfie[d] these critical three criteria
easily.” Id. Specifically, Dr. Andersson noted the following:
To wit, she had asymmetric numbness and weakness in both legs and urinary
retention satisfying the first criterion, a T2 spinal cord hyperintense lesion on MRI
thoracic spine imaging satisfying the second and no cord compression on the
October 2, October 3 and December 22 scans satisfying the third critical criterion.
11 Neuromyelitis optica is the “combined, but not usually clinically simultaneous, demyelination of the
optic nerve and the spinal cord; it is marked by diminution of vision and possibly blindness, flaccid
paralysis of the extremities, and sensory and genitourinary disturbances.” Neuromyelitis Optica,
DORLAND’S MED. DICTIONARY ONLINE.
12 Transverse Myelitis Consortium Working Group, Proposed Diagnostic Criteria and Nosology of Acute
Transverse Myelitis, 59 NEUROLOGY 499 (2002).
13 Chitra Krishnan & Benjamin Greenberg, Transverse Myelitis, UPTODATE (May 28, 2020),
http://www.uptodate.com/contents/transverse-myelitis/print.
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Id. Dr. Andersson further asserted that Petitioner “satisfie[d] [five] of the [six] inclusion criteria
and all [six] of the exclusion criteria.” Id. The only criterion that Petitioner did not meet was
“[i]nflammation defined by [CSF] pleocytosis, elevated immunoglobin G index or gadolinium
enhancement on MRI.” Id. This is inconsequential according to Dr. Andersson “because an
absence of gadolinium enhancement, an absence of CSF pleocytosis[,] and an absence of CSF
oligoclonal bands is commonly found in idiopathic [TM], specifically in 32%- 62%, 43-80% and
55-83% of cases.” Id. Additionally, he relied on submitted medical literature to opine that “the
absence of inflammatory markers does not rule out TM,” in individuals “with a clinical pattern
that otherwise resembles TM.” Id. at 15 (citing Pet’r’s Ex. 26).
Petitioner filed the TMCWG proposed diagnostic criteria of acute TM (“ATM”). Pet’r’s
Ex. 25. The authors expressed a need for uniform diagnostic criteria to “ensure a common language
of classification, reduce diagnostic confusion, and lay the groundwork necessary for multicenter
clinical trials.” Id. at 1. They noted that “[a]cute transverse myelopathy (which includes
noninflammatory causes) and ATM have often been used interchangeably throughout published
literature.” Id. at 1–2. After several diagnostic iterations, “cases of ATM were classified as
parainfectious, related to MS, spinal cord ischemia, or idiopathic.” Id. at 2. Furthermore, “acute
noncompressive myelopathies were classified according to an etiologic scheme: [to include] 5)
spinal cord infarct, and 6) idiopathic myelopathy.” Id.
The TMCWG paper stated that “[a] diagnosis of idiopathic ATM should require that all of
the inclusion criteria and none of the exclusion criteria are fulfilled.” Pet’r’s Ex. 25 at 2. The
criteria table app ears below:
Inclusion criteria Exclusion criteria
Development of sensory, motor, or autonomic dysfunction History of previous radiation to the spine within the last
attributable to the spinal cord 10 y
Bilateral signs and/or symptoms (though not necessarily symmetric) Clear arterial distribution clinical deficit consistent with
Clearly defined sensory level thrombosis of the anterior spinal artery
Exclusion of extra-axial compressive etiology by neuroimaging (MRI Abnormal flow voids on the surface of the spinal cord
or myelography; CT of spine not adequate) c/w AVM
Inflammation within the spinal cord demonstrated by CSF Serologic or clinical evidence of connective tissue disease
pleocytosis or elevated IgG index or gadolinium enhancement. If (sarcoidosis, Behc¸et’s disease, Sjo¨gren’s syndrome,
none of the inflammatory criteria is met at symptom onset, repeat SLE, mixed connective tissue disorder, etc.)*
MRI and lumbar puncture evaluation between 2 and 7 d following CNS manifestations of syphilis, Lyme disease, HIV,
symptom onset meet criteria HTLV-1, Mycoplasma, other viral infection (e.g. HSV-
Progression to nadir between 4 h and 21 d following the onset of 1, HSV-2, VZV, EBV, CMV, HHV-6, enteroviruses)*
symptoms (if patient awakens with symptoms, symptoms must Brain MRI abnormalities suggestive of MS*
become more pronounced from point of awakening) History of clinically apparent optic neuritis*
*Do not exclude disease-associated acute transverse myelitis.
Id. at 2 tbl. 1. Further, they noted “ATM represents a subset of acute myelopathies,” and that “[a]
diagnosis of ATM requires evidence of inflammation within the spinal cord.” Id. at 2. Therefore,
“[e]nhanced spinal MRI and a lumbar puncture are mandatory in the evaluation of suspected
ATM.” Id. In cases where a “spinal MRI shows an appropriately located high signal intensity
lesion on T2-weighted sequences but no clear-cut enhancement,” and CSF testing is normal, “then
a diagnosis of ATM would not be possible.” Id. at 3. Indeed, “cases that fulfill all of the proposed
criteria with the exception of objective documentation of inflammation within the spinal cord”
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may be best labeled as “possible ATM.” Id. The “interval between symptom onset and maximal
deficit” is also a noteworthy criterion that can be used to distinguish “ATM from a rapidly evolving
vascular myelopathy [from] a slowly progressive or stuttering hereditary myelopathy.” Id.
The authors caution that “[i]f these diagnostic criteria are going to be used to identify
patients for prospective therapeutic trials, it will be critical to exclude patients with ischemic
myelopathies for whom anti-inflammatory strategies may not be indicated.” Pet’r’s Ex. 25 at 3.
For patient workup and evaluation, “a lumbar puncture should be performed to distinguish an
inflammatory from a noninflammatory myelopathy.” Id. at 4. Spinal cord ischemia “should be
considered” in cases where “no gadolinium enhancement is seen on spinal cord MRI and the CSF
does not show pleocytosis or increased IgG index.” Id. “Alternatively, individuals who have mono-
focal demyelination in the spinal cord (evoked potential and brain MRI do not show
demyelination) and meet the criteria set forth above are defined as having ATM.” Id.
The Krishnan & Greenberg article is a TM primer pulled directly from the UpToDate website.
Pet’r’s Ex. 26. The authors defined the condition and identified the following categories of causes:
CNS inflammatory demyelinating disorders, systemic inflammatory disorders, infectious causes,
paraneoplastic syndromes, and deficiency syndromes. Id. at 9–11. They also noted case reports
that have associated TM with vaccination; however, they found that in “[c]omparing each TM case
with all matched subjects in the exposure interval who received the same vaccination, there was
no association of TM with prior vaccination.” Id. at 2. Molecular mimicry was discussed “as [a]
potential mechanism of autoimmunity” causing TM, following a pinworm infection. Id. The
authors also stated that “some autoantibodies initiate a direct and selective injury of neurons or
glia that express antigens that cross-react with antibodies directed against infectious pathogens.”
Id. at 3. In addition to focusing on the most critical inclusionary features Dr. Andersson mentioned,
the authors noted that a TM diagnosis “requires exclusion of a compressive cord lesion, usually by
MRI.” Id. at 7, They also recommended a gadolinium-enhanced MRI or lumbar puncture. Id. at 8.
Anterior spinal artery infarction is identified as a noninflammatory condition that may mimic TM.
Id. at 12.
The medical literature filed with Dr. Andersson’s report also included an article by de Seze
et al.14 Pet’r’s Ex. 27. This article identified the “main etiologies of [ATM as] systemic diseases,
spinal cord infarct, parainfectious events, and, more rarely, multiple sclerosis.” Id. at 1. The authors
conducted a retrospective study of ATM patients in the context of the TMCWG’s criteria. Id. The
authors described the criteria for idiopathic TM as stringent, but without the support of patient
studies. Id. Study results showed that the criteria “lead to a relatively homogenous group in terms
of clinical and MRI data but that . . . the outcome remain[ed] unpredictable.” Id. at 3. The authors
noted one third of the study’s patients were designated with possible idiopathic ATM because “of
the lack of inflammatory signs in CSF or on MRI,” and consequent inability to meet all of the
criteria. Id. Ultimately, the study did not reveal any “difference between the definite and possible
idiopathic ATM groups, especially regarding the outcome.” Id.
Dr. Andersson rejected Petitioner’s differential diagnosis of SCI because of the length of
her temporal course. Pet’r’s Ex. 10 at 15. He explained that “[a] subacute presentation suggests an
14 J. de Seze et al., Idiopathic Acute Transverse Myelitis: Application of the Recent Diagnostic Criteria,
65 NEUROLOGY 1950 (2005).
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inflammatory etiology . . . while a hyperacute presentation suggests a spinal cord ischemic stroke.”
Id. The “largest cohort study in the literature” distinguishing TM and infarction cases showed that
90% of [infarction] patients had a nadir to maximum deficits within 24 hours. Id. (citing Pet’r’s
Ex. 28 at 5).15 Additionally, in the remaining 10% of cases, “all had a stuttering and stepwise
decline and all severe deficits had occurred by 12 hours.” Id. Petitioner’s onset to nadir lasted at a
minimum of 39 hours and 47 minutes, excluding an infarction diagnosis. Id. Dr. Andersson also
opined that the success of Petitioner’s intravenous methylprednisolone is indicative of TM. Id. at
16. This treatment is not “not indicated for [SCI] but [does] reduce[] the severity and duration of
attacks of demyelinating disease and [TM].” Id. Petitioner’s “symptoms improved 50 percent after
the first dose.” Id.
The Zalewski et al. article, which proposed diagnostic criteria for spontaneous SCI, was
heavily relied on by Petitioner. Pet’r’s Ex. 28 at 5. The authors noted that SCI patients “are often
misdiagnosed as having [TM],” and they aim “[t]o describe the characteristics of spontaneous SCI
and propose diagnostic criteria.” Id. at 1. The following table was proposed for definite, probable,
and possible SCI:
Id. at 5.
15 Nicholas L. Zalewski et al., Characteristics of Spontaneous Spinal Cord Infarction and Proposed
Diagnostic Criteria, 76 JAMA NEUROLOGY 56 (2019).
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The authors stressed that because infarction “is underrecognized and misdiagnosed,” there
is “a need for diagnostic criteria that can be broadly applied to patients with spontaneous and
periprocedural SCI.” Pet’r’s Ex. 28 at 6. They went on to identify “[t]he most critical component
[as] the rapid accumulation of severe deficits within 12 hours because more gradual worsening
favors alternative etiologies.” Id. Common features that are “often considered to be atypical
[include] >4 hours to nadir, MRI and clinical evidence outside the anterior spinal artery territory,
and gadolinium enhancement.” Id. The authors cautioned against physicians ruling out SCI if one
or more of these is present. Id. They also studied the use of different therapies and found that
“[e]mpirical intravenous methylprednisolone treatment is reasonable when concern remains for a
possible inflammatory myelopathy.” Id. at 7.
Finally, Dr. Andersson noted that Petitioner has no history to explain her symptoms, nor
has there been any evidence of trauma, rash, systemic illness, infectious or rheumatologic cause.
Pet’r’s Ex. 10 at 16. Petitioner’s symptoms developed two days following her vaccination, and Dr.
Andersson could identify “no competing precipitating causes.” Id. He reasoned that although this
time frame for TM “is shorter than any case [series], it is within hours and consistent with their
short interval to onset and the activation of a memory response.” Id. at 17. Dr. Andersson cited the
Van Ussel et al.16 paper to provide examples of “acute, even dramatic demyelination of the central
nervous system and encephalitis [that] can occur after viral i.e. [flu] A/H1N1 vaccination or
infection.” Pet’r’s Ex. 20 at 1. The authors reviewed 22 patients and found the time lapse from
vaccination/infection to symptom onset ranged from one day in the case of a 77-year-old patient
who was also suffering from rectal cancer and developed TM post vaccination, to one month in a
case involving a 44-year-old that developed TM post vaccination with no comorbidities. Id. at 4.
Two other patients included in the study, a five-year-old and six-year-old, both with no
comorbidities, each had two-day onsets from vaccination/infection respectively, to development
of acute disseminated encephalomyelitis (“ADEM”). Id. There was one patient listed in the study
that developed TM four days post vaccination without any relevant comorbidities, but no age was
provided. Id. The article noted that “ADEM following the administration of an inactivated
component or live vaccine may be temporally associated with, but is not necessarily the result of,
the administration of a vaccine.” Id. at 6. Likewise, the authors noted an association seen in some
patients between vaccination and acute transverse myelitis, but they do not conclude the
relationships to be causal. Id. Their “case report and the review of the literature indicate that both
infection with or vaccination for [flu] A/H1N1 virus may be linked rarely to central nervous system
demyelination,” including TM and ADEM. Id. at 7. Dr. Andersson argued that Petitioner’s 17-
year vaccination history is evidence of a “a primary immune response and this rapid onset of
[TM].” Id.
2. Dr. Jamieson’s First Report
Dr. Jamieson provided a very detailed recount of Petitioner’s medical records beginning
with her vaccination on September 28, 2016. Resp’t’s Ex. A at 2. She noted Petitioner’s first
neurological symptom was lower extremity fatigue that occurred “within a very short period of
time” following vaccination, inconsistent with an immunological cause. Id. at 11. Dr. Jamieson
also noted Petitioner’s laboratory tests did not reveal any inflammatory cause for her weakness as
16 Isabelle Van Ussel et al., Encephalitis Related to a H1N1 Vaccination: Case Report and Review of the
Literature, 124 CLINICAL NEUROLOGY & NEUROSURGERY 8 (2014).
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her CSF was bland and the very subtle spinal cord lesion was non-enhancing. Id. “Thoracic spine
imaging was [also] originally unrevealing.” Id. Identifying SCI as the appropriate diagnosis for
Petitioner, Dr. Jamieson noted that 20%-40% of cases “remain cryptogenic despite extensive
diagnostic investigation.” Id. at 12. Dr. Jamieson also discussed the Zalewski et al. article’s SCI
criteria in the context of Petitioner’s symptoms. Id. at 13. She noted that symptom onset is variable
and may be abrupt or may result in “a decline over a few to several hours.” Id. She also noted one
case series wherein “the time from symptom onset to nadir deficit was more than four hours in 44
percent of patients, and greater than 12 hours in 23 percent.” Id. (citing Pet’r’s Ex. 28). Petitioner’s
“symptoms of right sided leg weakness with left sided decrease in pain and temperature are
consistent with an anatomic pattern of a spinal cord infarct.” Id. at 13. Dr. Jamieson noted that “[a]
hemi-spinal cord (Brown-Séquard) infarct of the thoracic spinal cord produces ipsilateral unilateral
leg weakness hemiparesis; contralateral loss of pain/temperature beginning two dermatomes below
the lesion; and ipsilateral loss of light touch, proprioception, and vibration below the lesion.” Id.
In comparison, Dr. Jamieson explained that “[p]atients initially suspected as having
idiopathic [TM] often are given another diagnosis after completion of an appropriate diagnostic
evaluation.” Resp’t’s Ex. A at 14. TM is defined by
acute or subacute spinal cord dysfunction resulting in weakness and sensory loss
below the level of the lesion and impairment in autonomic functioning, with the
symptoms due to disruption of descending (motor) and ascending (sensory) neural
pathways causing a disconnection between the spinal cord below the level of the
lesion and the brain.
Id. at 13. After presenting with a “loss of sensation to sensory modalities such as pain,” an MRI of
the spinal cord will localize the offending lesion and spinal cord final analysis will reveal
inflammation or elevated protein levels. Id. at 14. One study of Mayo Clinic patients revealed that
out of 226 patients initially suspected of having TM, ultimately 18.1% of them met the diagnostic
criteria. Id. (citing Resp’t’s Ex. A, Tab 5).17 The preferred treatment initially is generally high dose
intravenous corticosteroids, that “[vary] with extent of return of function dependent on etiology of
the [TM] and the extent of the spinal cord damage.” Id. at 14–15.
TM is a syndrome, Dr. Jamieson further explained, and “rather than a specific disease
entity, there may be variable and non-specific supposed linkages to environmental triggers,
including to vaccinations.” Resp’t’s Ex. A at 15. However, she added that the “[t]he linkage to the
injected inactivated [flu] vaccination however is particularly weak, with a case-centered analysis
showing no association between [TM] and prior immunization.” Id. The specific vaccines used are
often unknown, and she also questioned whether these cases relied on to make this argument
“would be classified as [TM] today using the 2002 [TMCWG] diagnostic criteria.” Id. Dr.
Jamieson discussed several case studies, arguing that in two articles “the authors mischaracterized
these [four] cases as isolated myelitis occurring after [flu] vaccination, when in fact they were not
isolated and did not occur de novo.” Id. at 16 (viting Resp’t’s Ex. A, Tab 18;18 Resp’t’s Ex. A, Tab
17 Nicholas L. Zalewski et al., Evaluation of Idiopathic Transverse Myelitis Revealing Specific
Myelopathy Diagnoses, 90 NEUROLOGY e96 (2018).
18 Naoko Nakamura et al., Neurologic Complications Associated with Influenza Vaccination: Two Adult
Cases, 42 INTERNAL MED. 191 (2003).
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19).19 According to Dr. Jamieson, these cases were then “incorrectly classified as isolated myelitis
related to [flu] vaccination by Karussis and Petrou; and they do not advance the hypothesis that
injected [flu] vaccination causes transverse myelitis.” Id. at 16 (citing Resp’t’s Ex. A, Tab 17).20
Dr. Jamieson argued that these cases have been repeatedly used by subsequent researchers,
“giv[ing] the false impression that there are more instances of [TM] following [flu] vaccinations
than actually exist in the medical literature.” Id. She then identified a case of TM following a flu
vaccination where, unlike Petitioner, “this young woman showed an extensive lesion extending
from C3 to the upper thoracic level spinal cord and the CSF was abnormal with an elevated white
blood cell count and protein level.” Id. at 17 (citing Resp’t’s Ex. A, Tab 21).21
In summary, Dr. Jamieson argued that Petitioner did not have TM because: 1) her MRI did
not reveal a lesion “extending for more than two spinal column segments and involving more than
two thirds of the transverse extent of the spinal cord;” 2) there was no evidence of inflammation;
and 3) her “hemi spinal cord symptoms with unilateral crossed motor and sensory deficits [were]
not consistent with a transverse lesion . . . of the spinal cord.” Resp’t’s Ex. A at 18.
3. Dr. Forsthuber’s First Report
Dr. Forsthuber’s expert report included a summary of relevant medical history and
background information on TM and molecular mimicry before his assessment of Petitioner’s case.
See Resp’t’s Ex. C at 3–5. He defined TM as “a monofocal inflammatory myelopathy of the spinal
cord in which an immune-mediated process causes rapid onset of varying degrees of weakness
(paralysis), sensory alterations, and autonomic dysfunction.” Id. at 3. Dr. Forsthuber continued
that TM’s pathogenesis is not fully understood, but that “a wide range of infectious pathogens have
been implicated in post-infectious TM.” Id. Pathological evidence collected during autopsies and
biopsies reveals “that TM patients show focal monocytic and lymphocytic infiltrates in spinal cord
tissue and perivascular spaces, astroglial and microglial activation, and demyelination and axonal
injury.” Id. Dr. Forsthuber also noted the “[CSF] pleocytosis and blood-brain-barrier breakdown
within a focal area of the spinal cord, consistent with an (auto)immune-mediated mechanism,” in
TM patients. Id. He identified a number of potential mechanisms, “such as autoimmune disease
pathology induced by molecular mimicry, microbial superantigen-mediated inflammation, or
humoral (antibody)-mediated derangements.” Id. at 4.
Dr. Forsthuber explained molecular mimicry generally as “the induction of T cells, B cells,
and/or antibodies that cross-react between antigens on microorganisms and host self-antigens, and
this cross-reactivity may lead to autoimmune disease pathology.” Resp’t’s Ex. C at 4.
“Specifically, T cells recognize epitopes of generally [eight to] 15 amino acid length presented by
MHC1 class I or II molecules on antigen presenting cells.” Id. They “are highly specific for a
particular antigen,” compared to antibodies and B cells that “can bind to linear and/or
conformational epitopes and to a wide variety of molecules including proteins, lipids,
19 Sabrina Ravaglia et al., Post-Infectious and Post-Vaccinal Acute Disseminated Encephalomyelitis
Occurring in the Same Patients, 251 J. NEUROLOGY 1147 (2004).
20 Dimitrios Karussis & Panayiota Petrou, The Spectrum of Post-Vaccination Inflammatory CNS
Demyelinating Syndromes, 13 AUTOIMMUNITY REVS. 215 (2014).
21 Rohit Bakshi & John C. Mazziotta, Acute Transverse Myelitis After Influenza Vaccination: Magnetic
Resonance Imaging Findings, 6 J. NEUROIMAGING 248 (1996).
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polysaccharides, and chemicals.” Id. Dr. Forsthuber noted studies that “have focused on the
analysis of sequence similarities between linear epitopes on microorganisms and self-antigens,”
but given the “enormous number” of sequence matches, he doubted that molecular mimicry is a
principal cause of autoimmune disease as once postulated. Id.
Conversely, Dr. Forsthuber argued that “remarkable contradictions can be found in most
situations where molecular mimicry was alleged as the cause of human autoimmune diseases.”
Resp’t’s Ex. C at 5. He referenced the initial hypothesis that molecular mimicry occurred between
“a hepatitis B peptide and myelin basic protein, but injection of the hepatitis peptide failed to
induce clinical [experimental autoimmune encephalomyelitis (“EAE”)] even when injected in
complete Freund’s adjuvant.” Id. In most cases, “failure to induce autoimmune diseases in animal
models with molecular mimic antigens is the rule, not the exception,” as in that case. Id. at 5. This
inability to uncover “solid” evidence of molecular mimicry’s role in autoimmune disease
pathology “despite massive research efforts” dating back to the 1980s has led Dr. Forsthuber and
others to believe that “molecular mimicry may be necessary, but not sufficient to induce human
autoimmune pathology.” Id. Other factors may include bystander activation, dual T cell receptors,
regulatory T cell failure, individual genetic susceptibility, “as well as external and internal
environmental factors.” Id. He concluded for these reasons that “molecular mimicry is not
generally accepted as the mechanism for the induction of autoimmune diseases, let alone for
autoimmune diseases allegedly induced by vaccines.” Id.
Dr. Forsthuber analyzed Petitioner’s case by responding directly to contentions made by
her expert, Dr. Andersson. Resp’t’s Ex. C at 6–19. He highlighted Dr. Crum’s diagnoses of
thoracic myelopathy, myelitis versus cord infarct, and lower elastic spasticity at the time of her
October 2016 hospitalization, and how that did not change through to her last medical visit with
Dr. Crum documented in the record on April 17, 2017. Id. at 6 (citing Pet’r’s Ex. 5 at 146–47).
He also noted that Dr. Crum “did not raise concerns about her [flu] vaccination.” Id. Dr. Forsthuber
acknowledged that Dr. Crum did write the November 5, 2020 letter recommending that Petitioner
not receive the flu vaccine again. Id. However, Dr. Forsthuber focused on Dr. Crum’s notes during
the time of Petitioner treatment in 2016 and 2017, which did not identify Petitioner’s vaccine as
the casual factor for her condition. Id.
Dr. Andersson’s reliance on “neurological complications after smallpox and rabies
vaccines in the 1920s,” was another point of contention for Dr. Forsthuber. Resp’t’s Ex. C at 7.
Dr. Forsthuber explained that these vaccines “are different vaccines that have nothing in common
with the [flu] vaccine used in the present case, including that the smallpox vaccine is a live virus
vaccine, . . . [with] completely different virus proteins and are manufactured in completely
different ways.” Id. Similarly, Dr. Forsthuber objected to Dr. Andersson’s use of vaccine-induced
GBS as an analogy for TM via molecular mimicry. Id. at 8. Dr. Forsthuber asserted that GBS “is
probably one of the most robust examples of molecular mimicry as the cause of human
autoimmune diseases and reliable evidence from both animal models and human studies supports
that immunological cross-reactivity.” Id. By comparison, TM is an unrelated neurological
condition, whose cause remains unknown. Id. Dr. Forsthuber argued that “Dr. Andersson has
merely invoked a generic concept of molecular mimicry without providing any further arguments
for molecular mimicry in general in TM, or with the [flu] vaccine and TM in the present case.” Id.
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The arguments that Dr. Andersson made to support his conclusion that vaccination can
trigger TM are individually addressed by Dr. Forsthuber. Resp’t’s Ex. C at 8–13. Dr. Forsthuber
asserted that evidence of inflammatory events resulting from an immune-mediated attack is not de
facto evidence of a vaccine causation without a link. Id. at 8. He also argued that the presence of
specific antibodies in TM patients has not revealed “an inciting infectious agent [], and certainly
not a particular vaccine.” Id. Dr. Forsthuber opined that “there is no reliable link between [flu]
vaccination and autoantibodies in TM,” and therefore, Dr. Andersson’s “claims are speculative
and not applicable to TM or the neurological condition in the present case.” Id. at 9. Dr. Forsthuber
also disagreed with Dr. Andersson’s interpretation of the Matsui et al.22 article to support his focus
on pathogenic circulating antibodies and the premise that immune complex depositions could
explain recurrent TM attacks. Id. at 9. The article noted that “[t]here were neither autoantibodies
nor evidence of vasculitis” in the case study. Pet’r’s Ex. 17 at 1. However, the authors opined that
“circulating immune complexes composed of [hepatitis B surface] antigen disappeared after
treatment, indicating that [virus immunity] played a role in the demyelinating lesion formation in
the central nervous system.” Id.
Dr. Forsthuber cautioned against Dr. Andersson’s citation of publications that discussed
the development of TM following rabies, hepatitis B, and oral polio vaccines. Resp’t’s Ex. C at
10. He argued that they are not analogous to the flu vaccine at issue here. Id. He further cautioned
that many of the case studies Petitioner filed contained other potential issues, including the
presence of comorbidities or imprecise diagnosis of TM, inappropriate temporal relationships
between vaccination and disease onset, and clearly identified alternative causes besides
vaccination. Id. at 10–11. Dr. Forsthuber included the Institute of Medicine’s (“IOM”)23
assessment that “the mechanistic evidence of an association between [flu] vaccine and TM [is]
weak,” and based on “temporal association.” Id. at 12. He also discussed “two large studies
conducted since the publication of the 2012 IOM report.” Id. The first study was retrospective
observational cohort study using Vaccine Safety Datalink data of 75,906 pregnant women
vaccinated with the trivalent inactivated flu vaccine and 147,992 unvaccinated women. Resp’t’s
Ex, C, Tab 10.24 Nordin et al. “found no cases of TM in the first 42 days after vaccination.” Resp’t’s
Ex. C at 12. A second VSD study conducted by Baxter et al.,25 found no statistically significant
increased risk of TM following vaccination in nearly 64 million inoculations. Id. (citing Resp’t’s
Ex. C, Tab 11).
Following his discussion of Petitioner’s general proposed mechanism, Dr. Forsthuber
turned to the specifics of Petitioner’s case. See Resp’t’s Ex. C at 13. He questioned “whether it is
probable that within 1.5 days after vaccination of [Petitioner] meaningful autoimmune T cell, B
cell, and autoantibody responses would be generated that could have resulted in her neurological
condition.” Id. Dr. Forsthuber answered this question in the negative by breaking down the process
of autoimmune disease following a primary immune response and a secondary immune response.
22 Makoto Matsui et al., Recurrent Demyelinating Transverse Myelitis in a High Titer HBs-Antigen
Carrier, 139 J. NEUROLOGICAL SCIS. 235 (1996).
23 The IOM is now called the National Academy of Medicine.
24 James D. Nordin et al., Maternal Safety of Trivalent Inactivated Influenza Vaccine in Pregnant Women,
121 OBSTETRICS & GYNECOLOGY 519 (2013).
25 Roger Baxter et al., Acute Demyelinating Events Following Vaccines: A Case Centered Analysis, 63
CLINICAL INFECTIOUS DISEASES 1456 (2016).
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Id. at 13–17. He noted that “it takes at least two to three days for the initial T and B cell responses
to become detectable in regional lymph nodes at the site of the infection or vaccine injection,” in
the case of an initial exposure. Id. at 13–14. This delay includes the time for the body to recognize
the presence of an antigen and mount an acute, innate immune response, typically during the first
48 hours following introduction. Id. at 14.
During this time and in order to properly activate cells of the adaptive immune
system, specialized cells called dendritic cells need to migrate to the site of the
infection/vaccination, find and capture the antigens/microbes, break them down
into small fragments (peptides), and then transport these fragments to regional
lymph nodes where they “present” these fragments to T and B cells in order to
activate them.
Id. Following activation, these cells enter the next “phase of lymphocyte activation, proliferation,
and acquisition of effector functions.” Id. at 15. Eventually, IgM antibodies are produced, a process
that “generally takes [two to three] days” to reach detectable levels. Id. at 16. This is followed by
“[p]roduction of the much more powerful class of IgG antibodies [that] takes significantly longer.”
Id. Dr. Forsthuber explained that “IgG responses begin to peak approximately [two] weeks after
infection/antigen encounter.” Id. The period during a secondary immune response is shortened
because once the body has encountered an antigen (via a primary response), memory T cells that
were created initially, can “facilitate[] and accelerate[] initiation of immune responses after re-
infection and curtail[] the severity of this infection.” Id. “Nevertheless,” Dr. Forsthuber argued, “it
will still take longer than 1.5 days for a notable immune response to develop, because even memory
T and B cells still have to become activated and expanded before they can generate an effective
immune response.” Id. Furthermore, “additional time is required after an autoimmune response
has already formed on a cellular-only level,” until symptoms develop and “disease can be detected
by clinical tests.” Id. Dr. Forsthuber explained that this process includes the proliferation of T cells
to the CNS and spinal cord where damage is sustained, and the autoimmune disease manifests. Id.
He noted that models show it can be nine to 11 days post immunization “until the animals develop
the first neurological symptoms.” Id. Dr. Forsthuber agreed with Dr. Andersson’s concession that
Petitioner’s case “is shorter than any case” referenced. Id. at 17. Dr. Forsthuber noted that “the
development of TM is typically observed [three to four] weeks after exposure.” Id. at 18.
In response to Dr. Andersson’s reliance on a memory response to explain the short onset
time, Dr. Forsthuber argued that Petitioner received the flu vaccine for 15 years following her
initial exposure with no incident. Resp’t’s Ex. C at 18. He found it improbable that this most recent
vaccination would cause a memory response sufficient to cause her neurological condition. Id. Dr.
Forsthuber argued that Dr. Andersson “has merely invoked the generic concept of memory
responses without providing any reasoning of how the [flu] vaccination would cause TM in the
present case via a memory response.” Id. He concluded that 1.5 days was not an appropriate
temporal relationship for vaccine-caused TM via a primary or secondary response. Id.
4. Dr. Andersson’s Supplemental Report
Dr. Andersson filed a supplemental report to respond to Respondent’s experts. Pet’r’s Ex.
31. His responses to Dr. Jamieson are reiterations of his previously asserted points. See id.
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Specifically, Dr. Andersson characterized Dr. Jamieson’s opinions as false and contrived. Id. at 1.
He asserted that she “merely erected her own more stringent criteria than are used in clinical
practice then applied them to find Petitioner fail[ed] to make the requirements for a TM diagnosis.”
Id. at 1. Despite Dr. Jamieson’s concern that Petitioner did not have a clearly defined sensory level,
Dr. Andersson argued that clear definition ensures that “it localizes to the spinal cord,” and
“Petitioner’s doctors never doubt a myelopathy localization” to meet that criterion. Id. He
reiterated that inflammation is not necessary for a diagnosis, that her doctors did not arrive at a
definitive diagnosis, and that thoracic myelopathy/myelitis remained a differential. Id. at 3. Dr.
Andersson did not dispute Dr. Jamieson’s opinion on the strength of published literature linking
flu vaccination to TM, however he described the evidence as “rare rather than weak” and argued
that it “does not disprove linkage.” Id. at 4.
Responding to Dr. Forsthuber, Dr. Andersson offered conclusions that can be drawn “to a
reasonable medical probability,” due to Drs. Crum and McKendrick Johnson instructing Petitioner
to refrain from future flu vaccines. Pet’r’s Ex. 31 at 5. He articulated:
1) both Dr Crum and Dr McKendrick Johnson diagnose[d] Petitioner with [TM],
not spinal cord stroke. Their instruction [was] meaningless otherwise, and
potentially harmful too.
2) both Dr Crum and Dr McKendrick Johnson believe[d] Petitioner’s flu
vaccination may have been responsible for her [TM]. There is no reason to deprive
health benefits of a flu vaccine otherwise.
3) both Dr Crum and Dr McKendrick [Johnson] [made] their recommendation to a
likelihood that is at least greater than the cumulated lost health benefits of an annual
flu vaccination, for the rest of her life.
Id.
Dr Andersson then turned to Dr. Forsthuber’s objection to discussion of rabies and
smallpox vaccines causing TM. Pet’r’s Ex. 31 at 5. He clarified that it is “self-evident” that
these two vaccines differ from each other and flu vaccines. Id. However, he argued that
“[t]he evidence of their association is offered as one of the lines of evidence for a sound
reliable theory of how flu vaccination could cause [TM].” Id. Dr. Andersson noted that Dr.
Forsthuber’s discussion “does nothing to refute the published cases of flu vaccination
associated [TM] in principle or in the specific.” Id. at 6. Further, Dr. Andersson noted that
the evidence presented is “limited by existing knowledge . . . . In the same way, the lack of
an explicit step-by-step explanation by which vaccination can trigger this same disease
fails as a reason for skepticism.” Id. He asserted that he “offer[ed] a theory how flu
vaccination could reasonably [cause TM], logically and plausibly and probably.” Id. Dr.
Andersson cited the NINDS TM Fact Sheet, UpToDate, Victor and Adams’s Neurology
and Harrison’s Textbook of Medicine,26 and the package insert for Fluvarix to make the
point that “the association of [TM] with vaccination” is in line with “mainstream thinking.”
Id.
In a corrective note, Dr. Andersson acknowledged that immune complex deposition
in the CNS was not shown in the Matsui et al. article. Pet’r’s Ex. 31 at 7. However, he
26 Petitioner did not file this literature.
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argued “[w]hat was shown was evidence to support [TM] having an immune-mediated
pathogenesis effected by molecular mimicry,” consistent with his theory. Id. Due to the
peptide homology between hepatitis B and rabbit myelin basic protein, “immunization of
rabbits with a relevant peptide of [hepatitis B virus] polymerase actually induced [an
autoimmune] response” via molecular mimicry. Id.
Dr. Andersson continued and addressed the significance of Petitioner’s adverse
reaction occurring after her 16th flu vaccination. Pet’r’s Ex. 31 at 9–10. He submitted that
it is probable “there were antigens in the 16th [flu] vaccination which activated a memory
response against host antigens through molecular mimicry causing [TM].” Id. at 9. Lastly,
Dr. Andersson objected to Dr. Forsthuber’s criticism of his memory cell analysis. Dr.
Anderson responded:
Again, the specific antigens and step-by-step pathway of the pathogenesis
is not known for [TM] as a disease, but its existence as a disease and its
association with vaccination stands undiminished by this ignorance, and so
too the theory [he] offered to explain all that is known, with what is
currently known.
Id.
5. Dr. Jamieson’s Supplemental Report
Dr. Jamieson also sought to clarify arguments previously made in her initial report.
Resp’t’s Ex. F. She noted that TMCWG criteria, like all diagnostic criteria, “are used all the time
by physicians to determine as accurate and specific a diagnosis as possible for patients’ treatment
and counseling.” Id. at 1. Dr. Jamieson acknowledged that diagnostic certainty is not always
possible, and indeed, here Petitioner was treated both for SCI and TM. Id. However, she argued
that “discordance between the TMCWG criteria and her clinical presentation was the reason why
[Petitioner] was evaluated and treated for [SCI], as well as for [TM].” Id.
Both Drs. Jamieson and Andersson agreed that Petitioner “had a myelopathy.” Resp’t’s
Ex. F at 1. Dr. Jamieson argued that “because [TM] is, by definition, an ‘itis’ or an inflammatory
condition,” the absence of inflammation in the spinal cord is not insignificant. Id. Further, Dr.
Jamieson opined that Petitioner had one of the exclusion criteria: an arterial distribution clinical
deficit consistent with thrombosis of the anterior spinal artery. Id. (citing Pet’r’s Ex. 25 at 2).
According to Dr. Jamieson, Petitioner’s “sensory examinations varied from being normal
to showing unilateral subjective sensory findings on one leg or the other, without a level of sensory
loss referable to a localized spinal cord lesion” Resp’t’s Ex. F at 2. She concluded that “there was
no clearly defined sensory level to indicate a specific transverse demyelinating lesion, as opposed
to a more diffuse ischemic lesion.” Id. Alternatively, her variable sensation loss was “characteristic
of an anterior spinal artery infarct with leg weakness with lateral spinothalamic tract involvement
and preservation of posterior column function.” Id. at 3.
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Dr. Jamieson cited to the Goh et al.27 article to support her premise that classic TM lesions
extend over more than two spinal cord segments and involves more than two-thirds cross section
of the cord. Resp’t’s Ex. F at 3 (citing Resp’t’s Ex. F, Tab 1 at 3). The article discussed clinical
symptoms, diagnostic criteria and related features of TM. Resp’t’s Ex. F, Tab 1 at 1. The article
also included diagnostic criteria noting “that evolution of symptoms to the maximal clinical
severity must be between [four] hours and 21 days . . . to prevent cases of cord infarction, typically
of abrupt onset, from being erroneously diagnosed as [TM].” Id. The authors noted “the
heterogeneous pathogenesis and prognosis of [TM, and stated] it is vitally important that there be
uniformly applied criteria for diagnosis and classification.” Id. They identified confirmation of an
active inflammatory process by presence of a cellular infiltrate and/or elevated protein” as a
requirement for diagnosis. Id. The authors noted a study of transverse myelopathy patients and
found they “could be grouped as 15.6% idiopathic, 20.5% systemic disease, 17.3% infectious or
parainfectious, . . . with a further 18.8% found to have [SCI] instead of [TM].” Id. at 2. The article
noted that “[p]ostvaccination [TM] seems to be a rare complication of vaccination.” Id. at 12. The
“vaccines implicated” included flu, and it was noted that “[t]he pathogenesis is likely similar to
the proposed mechanisms of immune-mediated neural damage described in parainfectious [TM].”
Id.
The timing of Petitioner’s symptom onset was readdressed by Dr. Jamieson in response to
Dr. Andersson. Rep’t’s Ex. F at 3. She maintained that Petitioner experienced “the onset of severe
deficits within 12 hours of symptom [manifestation].” Id. Adding that “[t]he time over which
symptoms of spinal cord infarcts evolve is variable,” Dr. Jamieson opined that Petitioner’s
“clinical course [was] consistent with both the medical literature and [her] experience in making
the diagnosis of spinal cord ischemia.” Id. She also reasoned that Petitioner’s inconsistent
“neurological examinations may have been related to her varying participation in her
examinations; [or] reflect the ‘stuttering course’ that Dr. Andersson believe[d] [was] necessary”
for SCI diagnosis. Id.
Again noting that TM and SCI were incorporated into the treatment plan, Dr. Jamieson
asserted that “[w]ith the benefit of reviewing the record retrospectively, the diagnosis is more
likely than not SCI.” Resp’t’s Ex. F at 3. The advice “offered in an abundance of caution, to avoid
future [flu] vaccination [was not] persuasive in establishing the diagnosis of [TM] or as endorsing
a causative linkage between the [flu] vaccine and [TM].” Id. at 4.
6. Dr. Forsthuber’s Supplemental Report
Noting again that Dr. Crum did not diagnose Petitioner with TM, Dr. Forsthuber discounted
the opinion of Dr. McKendrick Johnson, “a family medicine specialist.” Resp’t’s Ex. E at 2. Dr.
Forsthuber opined that as a neurologist, Dr. Crum’s “impressions of [Petitioner’s] medical
condition seem[d] more reliable than that of Dr. McKendrick Johnson’s.” Id. As of April 2017,
Dr. Crum had still not resolved Petitioner’s diagnosis. Id. Dr. Forsthuber thought “it is unclear
how Dr. Crum arrived at his diagnosis of ‘myelitis’ in 2020, given the fact that he previously did
not have a definitive explanation for her medical condition.” Id.
27 Christine Goh et al., Neuroimaging in Acute Transverse Myelitis, 21 NEUROIMAGING CLINICS N. AM.
951 (2011).
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Drs. Andersson and Forsthuber disagreed about the viability of the comparison between
rabies vaccine-induced neuroinflammation and flu vaccine-induced TM. Resp’t’s Ex. E at 3. Dr.
Forsthuber argued that unlike the rabies vaccine, the flu vaccine “is not contaminated with
autoantigens, . . . does not contain an adjuvant,” and “[i]mmunization of animals with the [flu]
vaccine does not induce neuroinflammation.” Id. According to Dr. Forsthuber, these differences
are critical in illustrating why the former process cannot be used to explain the latter. Id.
The experts also disagreed on whether there is a medical community consensus on flu
vaccine-induced TM. Resp’t’s Ex. E at 3–4. Dr. Forsthuber noted the NINDS TM Fact Sheet lists
as potential causes of TM: parasites; viral, bacterial, and fungal infections; and immune system,
vascular, and other inflammatory disorders. Id. at 4 (citing Pet’r’s Ex. 14). Likewise, UpToDate
and Victor and Adams’s Neurology and Harrison’s Textbook “do not specifically refer to [flu]
vaccines.” Id. The Fluarix vaccine insert package lists myelitis and encephalomyelitis, but not TM.
Id. Dr. Forsthuber argued that this is not a medical document. Id. He noted that the package lists
“all events observed in all studies of the vaccine including post-marketing studies, irrespective of
whether or not these events are statistically significantly increased.” Id. He continued “myelitis or
TM have not been listed in the ‘Warnings and Precautions’ section of the 2016-2017 Fluarix
vaccine insert, which lists adverse events based on scientific evidence.” Id. Likewise, “[t]he
VAERS database is useful as an early warning system to identify rare adverse events, but VAERS
cannot be used to establish causality.” Id. at 5.
Lastly, Dr. Forsthuber responded to Dr. Andersson’s assertion that a memory response is
responsible for Petitioner’s molecular mimicry reaction to the flu vaccine after 15 previous
exposures. Resp’t’s Ex. E at 5–9. He explained that a memory response only occurs when the
adaptive immune system’s T and B cells are “exposed to the same recall antigen for a second
time.” Id. at 6. Dr. Forsthuber noted that the flu vaccines that Petitioner received from 2014 to
2016 all “contained hemagglutinin derived from the identical vaccine strains A/California/7/2009
(H1N1)-like virus, B/Brisbane/60/2008-like (Victoria lineage), and B/Phuket/3073/2013-like
(Yamagata lineage).” Id. Despite this, she did not develop TM following any of these vaccinations.
Id. Further, antigen presentation and cell activation “reasonably takes an estimated one to two
days, even for memory T cells, to be become activated by secondary immunization with their recall
antigens.” Id. Dr. Forsthuber argued that once that process is complete, additional time is needed
for tissue damage to occur and “become detectable in [the] form of neurological deficits.” Id. In
the case of B cells, memory cells “do not produce antibodies,” and need four to five days to
“develop into antibody secreting cells.” Id. at 6–7. Dr. Forsthuber asserted that in the Krammer et
al. study,28 individuals without previous exposure to SARS-CoV-2 mounted an antibody response
“within [nine to] 12 days after vaccination,” while “individuals with preexisting SARS-CoV-2
immunity showed an increase in IgG antibodies by [five to eight] days after vaccination, but not
before that.” Id. at 8 (citing Resp’t’s Ex. E, Tab 9). He concluded that “[e]ven after adoptive
transfer of large numbers of pre-activated, autoimmune T cells, it takes approximately four to six
days before the onset of clinical disease becomes notable.” Id. This explanation, according to Dr.
Forsthuber, is based on “reliable and scientific facts,” and “soundly disprove what Dr. Andersson
claim[ed] as a theory.” Id. at 9.
28 F. Krammer et al., Antibody Responses in Seropositive Persons After a Single Dose of SARS-CoV-2
mRNA Vaccine, 384 NEW ENG. J. MED. 1372 (2021).
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IV. Applicable Legal Standards
To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth
at 42 U.S.C. § 300aa-14, as modified by 42 C.F.R. § 100.3; or (2) that petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See §
11(c)(1)(C); 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, 1319–20 (Fed. Cir. 2006). In this
case, Petitioner does not allege a Table injury and must prove that her injury was caused-in-fact
by a Table vaccine.
To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the
evidence that the vaccine was the cause of the injury. § 13(a)(1)(A). A petitioner is required to
prove that the vaccine was “not only a but-for cause of the injury but also a substantial factor in
bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of Health &
Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).
In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs, the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). In
Broekelschen v. Sec’y of Health and Hum. Servs., the Federal Circuit recognized that in some
circumstances, the special master may “first determine which injury was best supported by the
evidence in the record before applying the Althen test.” 618 F.3d 1339, 1346 (Fed. Cir. 2010). This
principle also means that a petitioner must establish that the vaccinee suffers the injury allegedly
linked to the vaccination. Lombardi v. Sec’y of Health & Hum. Servs., 656 F.3d 1343, 1353–54
(Fed. Cir. 2011).
The Althen test requires petitioners to set forth: “(1) a medical theory causally connecting
the vaccination and the injury; (2) a logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship
between vaccination and injury.” 418 F.3d at 1278. To establish entitlement to compensation under
the Program, a petitioner is required to establish each of the three prongs of Althen by a
preponderance of the evidence. Id. “[C]lose calls regarding causation are resolved in favor of
injured claimants.” Id. at 1280. Further, evidence used to satisfy one prong of the test may overlap
to satisfy another prong. Capizzano, 440 F.3d at 1326.
Under the first prong of Althen, a petitioner must offer a scientific or medical theory that
answers in the affirmative the question: “can the vaccine . . . at issue cause the type of injury
alleged?” Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4 (Fed.
Cl. Spec. Mstr. July 16, 2004), mot. for rev. denied, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d 1352
(Fed. Cir. 2006). 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 548–49. Petitioners are not required to identify “specific biological mechanisms”
to establish causation, nor are they required to present “epidemiologic studies, rechallenge . . . the
presence of pathological markers or genetic disposition, or general acceptance in the scientific or
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medical communities.” Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). Scientific
and “objective confirmation” of the medical theory with additional medical documentation is
unnecessary. Althen, 418 F.3d at 1278–81; see also Moberly, 592 F.3d at 1322. However, as the
Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of causation is insufficient
for a petitioner to meet her burden of proof.” LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d
1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592 F.3d at 1322). Indeed, the Federal Circuit has
“consistently rejected theories that the vaccine only ‘likely caused’ the injury and reiterated that a
‘plausible’ or ‘possible’ causal theory does not satisfy the standard.” Boatmon v. Sec’y of Health
& Hum. Servs., 941 F.3d 1351, (Fed. Cir. 2019) (citing Moberly, 592 F.3d at 1322 and LaLonde,
746 F.3d at 1339). Rather, “[a] petitioner must provide a reputable medical or scientific
explanation that pertains specifically to the petitioner’s case.” Moberly, 592 F.3d at 1322. In
general, “the statutory standard of preponderance of the evidence requires a petitioner to
demonstrate that the vaccine more likely than not caused the condition alleged.” LaLonde, 746
F.3d at 1339.
Furthermore, establishing a sound and reliable medical theory connecting the vaccine to
the injury often requires a petitioner to present expert testimony in support of her claim. Lampe v.
Sec’y of Health & Hum. Servs., 219 F.3d 1357,1361 (Fed. Cir. 2000). The Supreme Court’s
opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc.requires that courts determine the
reliability of an expert opinion before it may be considered as evidence. 509 U.S. 579 (1993).
However, in the Vaccine Program, the Daubert 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) (“[U]niquely 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.”);
see also 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).
The Daubert factors are “meant to be helpful, not definitive.” Kumho Tire Co. v.
Carmichael, 526 U.S. 137, 151 (1999). The factors do not “constitute ‘a definitive checklist or
test’” and may be applied differently depending on the facts of a particular case. Id. at 150 (quoting
Daubert, 509 U.S. at 593).
“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’
establishes a standard of evidentiary reliability.” Daubert, 509 U.S. at 590 (citation omitted). Thus,
for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support
the assertion of the expert witness.” Moberly, 592 F.3d at 1324. Nothing requires the acceptance
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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 v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen.
Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also D’Tiole v. Sec’y of Health & Hum. Servs.,
No. 15-085V, 2016 WL 7664475, at *24 (Fed. Cl. Spec. Mstr. Nov. 28, 2016) (stating that the
Vaccine Act “require[s] a chain of reliable propositions supporting [a] petitioner’s theory”).
Under the second prong of Althen, a petitioner must prove that the vaccine actually caused
the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418 F.3d at
1279. 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;
Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.
Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association
between the vaccination and the injury; instead, the petitioner “must explain how and why the
injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in
Pafford noted petitioners “must prove . . . both that her vaccinations were a substantial factor in
causing the illness . . . and that the harm would not have occurred in the absence of the
vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or
scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of
Health & Hum. Servs., 9 F.3d 958, 961 (Fed Cir. 1993) (citation omitted). Nevertheless,
“[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical
communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the
system created by Congress.” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding causation
are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.
In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed,
when reviewing the record, a special master must consider the opinions of treating physicians.
Capizzano, 440 F.3d at 1326. This is because “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.’” Id. In addition, “[m]edical records, in general, warrant
consideration as trustworthy evidence. The records contain information supplied to or by health
professionals to facilitate diagnosis and treatment of medical conditions. With proper treatment
hanging in the balance, accuracy has an extra premium. These records are also generally
contemporaneous to the medical events.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d
1525, 1528 (Fed. Cir. 1993). While a special master must consider these opinions and records,
they are not “binding on the special master or court.” § 13(b)(1). Rather, when “evaluating the
weight to be afforded to any such . . . [evidence], the special master . . . shall consider the entire
record.” Id.
To satisfy the third Althen prong, a petitioner must establish a “proximate temporal
relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This
“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,
given the medical understanding of the disorder’s etiology, it is medically acceptable to infer
causation-in-fact.” de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir.
2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due
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to the fact that onset was too late after the administration of a vaccine for the vaccine to be the
cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the
temporal relationship is not such that it is medically acceptable to conclude that the vaccination
and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Hum. Servs., 685
F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered,
logically, the vaccine could not have caused the illness.”).
Although a temporal association alone is insufficient to establish causation, under the third
prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory.
See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity
alone. See Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Fed. Cl. 400, 403–04 (1991); see also
Grant, 956 F.2d at 1148 (“[T]he inoculation is not the cause of every event that occurs within the
ten[-]day period . . . [w]ithout more, this proximate temporal relationship will not support a finding
of causation.” (quoting Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983))).
A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A
petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused
by vaccination is entitled to compensation unless the respondent can demonstrate by a
preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.
See Althen, 418 F.3d at 1278; Knudsen, 35 F.3d at 547. In such a case, the government must not
merely prove the existence of an alternative cause, but that such an alternative actually caused the
injury. Knudsen, 35 F.3d at 549. Consequently, when and if the petitioner establishes a prima facie
case, the burden then shifts to the government to prove that an alternative cause, unrelated to the
administration of the vaccine, was the “sole substantial factor” in causing the alleged injury. See
de Bazan, 539 F.3d at 1354; see also Hammitt, 98 Fed. Cl. at 726 (explaining that the respondent’s
burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury).
Additionally, a factor unrelated “may not include ‘any idiopathic, unexplained, unknown,
hypothetical, or undocumentable cause, factor, injury, illness or condition.’” § 13(a)(2); see also
Doe v. Sec’y of Health & Hum. Servs., 601 F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic
diagnosis cannot be a “factor unrelated,” as it is idiopathic).
V. Discussion
A. Diagnosis
Petitioner alleged that she developed TM as a result of her flu vaccine. Respondent
countered that Petitioner suffered from SCI unrelated to her vaccination. As Federal Circuit
precedent establishes, in certain cases it is appropriate to determine the nature of an injury before
engaging in the Althen analysis. Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339,
1346 (Fed. Cir. 2010). Since “each prong of the Althen test is decided relative to the injury,”
determining facts relating to the claimed injury can be significant. Id. In this case, the medical
records provide some evidence for both perspectives, but ultimately Petitioner’s burden is to
provide preponderant evidence that she suffered from TM. Petitioner failed to do so.
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There is strong disagreement between the parties’ experts, Drs. Andersson and Jamieson,
on Petitioner’s diagnosis, and they both discuss the significance of the presence or absence of
certain criteria used to distinguish TM from SCI. These criteria are key supporting factors for each
expert’s respective opinion.
Dr. Andersson asserted that the proper diagnosis for Petitioner is TM based on the
TMCWG’s criteria. Dr. Andersson noted that Petitioner developed sensory, motor, or autonomic
dysfunction attributable to her spinal cord that was bilateral with a clearly defined sensory level.
Petitioner’s neurological examination on September 30, 2016, revealed “an upper motor neuron
pattern of weakness in the bilateral lower extremities.” Pet’r’s Ex. 5 at 11. She also exhibited
allodynia starting at T5-T7. These symptoms are consistent with TM; however, Dr. Jamieson more
strictly applied the inclusionary criteria of TM to Petitioner’s case. She noted that the TMCWG’s
diagnostic criteria, according to the group’s guidance, requires evidence of inflammation within
the spinal cord. Without evidence of inflammation via gandolinium enhancement and abnormal
CSF results, the TMCWG advised that “noninflammatory myelopathy should be considered.”
Pet’r’s Ex. 25 at 4. Furthermore, Dr. Jamieson made the rudimentary point that myelitis by
definition, indicates inflammation of the spinal cord. Conversely, Dorland’s Medical Dictionary
includes in the definition the disclaimer that “[i]n practice, the term is also used to denote
noninflammatory lesions of the spinal cord.” Myelitis, DORLAND’S MED. DICTIONARY ONLINE.
Throughout her treatment, Petitioner’s medical records maintained a diagnosis of thoracic
myelopathy, but TM is not always listed. Her treaters also noted “[t]he abrupt onset of symptoms
was initially concerning for ischemia to the cord.” Pet’r’s Ex. 5 at 12.
Dr. Andersson further argued that Petitioner suffered from TM because “Petitioner’s pain
was not severe and so not discriminatory, and at times not even midline in location.” Pet’r’s Ex.
10 at 13. He reasoned, supported by filed literature, that SCI patients more often have severe limb
or back pain at onset. Petitioner’s medical records from the September 30, 2016 Mayo Clinic ED
record a complaint of “discomfort in her lower thoracic midline spine” that “worsened with
movement,” and could not be alleviated with over-the-counter pain medication. Pet’r’s Ex. 5 at 5.
Based on this account, combined with reported leg weakness and numbness, treaters initially
considered TM and GBS. This is consistent with Dr. Andersson’s opinion.
Dr. Jamieson argued that many patients who are initially suspected of suffering from TM
are diagnosed with another type of myelopathy following further evaluation. In Petitioner’s case,
an MRI completed on September 30, 2016, revealed no obvious lesion or evidence of compression.
Her treater also noted “right lower extremity weakness predominantly in an upper motor neuron
pattern with generally brisk reflexes.” Pet’r’s Ex. 5 at 15. Petitioner’s diagnosis was changed to
SCI versus thoracic myelopathy due to a lack of inflammation or demyelination. Dr. Jamieson
argued that Petitioner’s ipsilateral unilateral leg weakness hemiparesis, contralateral loss of
pain/temperature beginning two dermatomes below the lesion, and ipsilateral loss of light touch,
proprioception, and vibration below the lesion are characteristic of SCI. See Resp’t’s Ex. A at 13.
Dr. Andersson argued that SCI is excluded as a possible diagnosis because Petitioner’s
temporal profile “at a minimum 39 hours and 47 minutes from onset to nadir,” is too long. Pet’r’s
Ex. 10 at 15. He cited the Zalewski et al. article’s findings to support his claim, which recorded
maximum deficits in 90% of the study’s patients by 24 hours, and that “the 10% with a nadir longer
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than 24 hours all had a stuttering and stepwise decline and all had ‘severe’ deficits already by 12
hours.” Id. Dr. Jamieson responded to Dr. Andersson’s argument on this point over the course of
two pages in her initial report. However, her explanation merely consisted of a general statement
that Petitioner’s symptoms started on September 29, 2016, and worsened the next day. See Respt’s’
A at 13. She noted that in 23% of patients, it can take over 12 hours from symptom onset to nadir
but provided no additional information on longer periods more consistent with the time frame in
Petitioner’s case. Dr. Jamieson argued that Petitioner’s variable presentations upon examination
were consistent with a stuttering course seen within 12 hours in patients with a longer period from
onset to nadir. Petitioner’s treaters do not note this factor in Petitioner’s records and do not base
her diagnosis on the timing of her symptom onset or nadir of symptoms.
Dr. Jamieson also discussed exclusionary criteria for TM and argued that Petitioner had a
“clear arterial distribution clinical deficit consistent with thrombosis of the anterior spinal artery”
that rules out TM. Resp’t’s Ex. F at 1. Petitioner’s pinprick sensory deficit was inconsistent, and
Dr. Andersson disagreed with this assertion outright.
Particularly in a case like this where the experts don’t agree, the opinions of Petitioner’s
treating physicians, even in their equivocations, are instructive, because they are “in the best
position” to determine Petitioner’s injury. See Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at
1326; Cucuras, 993 F.2d at 1528 (noting contemporaneous medical records, “in general, warrant
consideration as trustworthy evidence”). Petitioner’s treaters remained unable to make a definitive
diagnosis during the course of her hospitalization. They maintained the differential diagnoses of
paraparesis, SCI versus thoracis myelopathy/myelitis. A medical record dated October 3, 2016,
recorded neurologist Dr. Jones’ opinion that Petitioner likely had SCI. See Pet’r’s Ex. 5 at 42.
Petitioner’s neurology hospital service records at the time of discharge provide the most definitive
assertation by a treater, namely that she had probable SCI. See id. at 51. There is no mention of
TM in this record, but myelitis does reappear later in the record as a differential.
Petitioner has the burden of establishing each of the elements of her claim by a
preponderance of the evidence. There is evidence in the record that TM was considered by
Petitioner’s treaters as a possible diagnosis. This is seen in the multiprong treatment approach from
her doctors, the continued testing and follow-ups, the precautionary vaccination prohibition, and
the equivocation in the medical record. However, the neurology records from Petitioner’s
treatment at the most crucial points during her hospitalization and throughout the trajectory of her
condition noted probable SCI. I am not a physician, and it is not possible nor required that I
accurately diagnose Petitioner when her treaters could not, and the medical experts disagree. I must
determine if, based on the evidence presented, Petitioner’s has established it more likely than not
that she suffers from TM. The evidence does not identify a definitive diagnosis, and the “probable
SCI” note is the most decisive opinion from a treater. Therefore, Petitioner has failed to establish
TM as the more likely than not condition she suffers from.
B. Althen Prong One – Medical Theory
Dr. Andersson asserted that the “etiology of vaccination-induced TM is the same as” in
GBS cases. Pet’t’s Ex. 10 at 10. He argued further that this theory is applicable to many other
myelin-related disorders, including MOG-Antibody disorder and neuromyelitis optica. Dr.
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Andersson acknowledged that the published literature to support his theory is rare as applied to
TM, but he explained that molecular mimicry is commonly accepted as a mechanism for vaccine-
caused neurological disease and TM specifically. In support of this contention, Dr. Andersson
relied on general references from sources that suggest a link without further analysis. For example,
Dr. Andersson referred to the NINDS TM Fact Sheet for evidence of a causal link between flu
vaccination and TM. The authors did note that TM can result from “a post-vaccine autoimmune
phenomenon, in which the body’s immune system mistakenly attacks the body’s own tissue while
responding to the infection or, less commonly, a vaccine.” Pet’r’s Ex. 14 at 2. However, this
nonspecific reference to molecular mimicry does not articulate a sound and reliable theory that
connects the flu vaccine to TM. Dr. Andersson admitted that he is limited by existing knowledge
and without specifics of shared homology for cross-reactivity or pathological antibodies for
evidence specific to flu and TM. He further admitted that a direct causal relationship “has still not
been definitively established.” Pet’r’s Ex. 10 at 10. In fact, none of Petitioner’s submissions
endeavor to explain how the flu vaccine causes TM via the mechanism of molecular mimicry. The
papers that do deliberate a causal process for vaccine-induced disease focus on the polio, rabies,
and hepatitis B vaccines. Dr. Forsthuber argued that these vaccines are not similar to the flu
vaccine, and Dr. Anderson did not explain why papers discussing these vaccines are instructive or
identify relevant comparable qualities to the flu vaccine. I must stress that conclusive medical
literature is not a requirement in order to establish causation in the Program. However, to the extent
it is filed and relied upon, the authors’ opinions, suggestions, and omissions may be considered.
See Knudsen, 35 F.3d at 549; Andreu, 569 F.3d at 1378–79 (citing Capizzano, 440 F.3d at 1325–
26).
Dr. Forsthuber’s report conceded that, although not perfect, molecular mimicry could be a
viable mechanism for neurological disease under very rare and specific circumstances. He defined
molecular mimicry generally as a pathogenic cross-reaction between microorganism antigens and
host antigens that induce immune cells and antibodies and cause autoimmune disease. However,
he asserted that other processes, such as bystander activation, may also be necessary for the type
of sustained immune response that could dysfunction and ultimately lead to autoimmune disease.
I find this reasoning persuasive. Furthermore, as my colleagues and I have said in previous
decisions, to the extent that molecular mimicry is offered as a theory, it must be supported by a
sound and reliable medical or scientific explanation.” Knudsen, 35 F.3d at 548.
There must also be some degree of selectivity. See W.C. v. Sec’y of Health & Hum. Servs.,
704 F.3d 1352, 1360 (2013) (finding that a petitioner cannot prevail by simply invoking a
biological term, or by showing that the mechanism is a valid theory to explain how other triggers
may have induced other diseases and determining that a petitioner must produce additional
evidence that the mechanism can cause that vaccine to cause a specific disease); Caves v. Sec’y of
Health & Hum. Servs., 100 Fed. Cl. 119, 135 (2011), aff’d, 463 F. App’x. 932 (2012); McKown v.
Sec’y of Health & Hum. Servs., No. 15-1451, 2019 WL 4072113, *50 (Fed. Cl. Spec. Mstr. July
15, 2019). Petitioner does not have to provide a specific mechanism, but it must be detailed enough
to apply to the administered vaccine and alleged injury in this case. Otherwise, any vaccination,
by nature of its purpose to illicit an immune response, could be asserted as the cause of any
autoimmune disease that later developed in an individual, and Althen prong one “would be
rendered meaningless.” See Caves, 100 Fed. Cl. at 135; see also McKown, 2019 WL 4072113, *50
(“[M]erely chanting the words ‘molecular mimicry’ in a Vaccine Act case does not render a
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causation theory scientifically reliable, absent additional evidence specifically tying the
mechanism to the injury and/or the vaccine in question.”). Petitioner is not limited to any one type
of evidence in support of a molecular mimicry mechanism. A non-exhaustive list of potential
evidence includes homology evidence, epidemiology studies, pathogenic antibodies, relevant
animal models, or disease etiology specific to the vaccine’s live virus counterpart. See
Broekelschen, 618 F.3d 1339; Dougherty v. Sec’y of Health & Hum. Servs., 141 Fed. Cl. 223
(2018); Brayboy v. Sec’y of Health & Hum. Servs., No. 15-183, 2021 WL 4453146, (Fed. Cl. Spec.
Mstr. August 30, 2021). I reiterate, Petitioner is under no obligation to provide any one or more of
those types of evidence. This list serves only to illustrate that even in cases of rare and understudied
phenomena, Petitioner’s must provide preponderant evidence of causation in support of any
identified mechanism. Petitioner did not provide such evidence here, and therefore, does not meet
her burden pursuant to Althen prong one.
C. Althen Prong Two – Actual Causation
It is difficult to evaluate whether a Petitioner has provided preponderant evidence of a
causal relationship between her vaccination and injury when preponderant evidence of the injury
has not been provided. That difficulty is magnified when Petitioner has not provided preponderant
evidence that the injury alleged can be caused by the vaccine, because the mechanism itself is
unclear. Dr. Andersson noted the absence of any other known cause for Petitioner’s condition and
her symptom onset within two days of vaccination as evidence of causation. He declared “to a
reasonable medical probability” that Petitioner received a flu vaccine on September 28, 2016, and
became symptomatic at approximately 9:00 pm the next day. Pet’r’s Ex. 10 at 12. He then declared
that TM was the cause of Petitioner’s symptoms. At no point during the section in Dr. Andersson’s
report that purported to discuss actual causation is the molecular mimicry theory applied to
Petitioner. Dr. Andersson correctly titled the section: “A Logical Sequence of Cause and Effect,”
but he neglected the directive that the sequence must show the vaccination was the reason for the
injury. See id.
In this case, Petitioner presented an association between her vaccine and her condition,
specifically that the former directly preceded the latter. However, a chronological relationship and
lack of alternative cause, without more, are insufficient to meet the preponderant standard.
Furthermore, as discussed below, the temporal relationship between Petitioner’s vaccination and
symptom onset is not consistent with the general understanding of molecular mimicry as asserted.
Recall challenge notwithstanding, Dr. Andersson did not analyze Petitioner’s clinical presentation
in the context of his theory to distinguish an idiopathic TM or SCI from what happened in
Petitioner’s case. He argued that the specifics of the immune pathogenesis of TM are unknown,
including “how exactly and by what antigen exactly.” Pet’r’s Ex. 31 at 8. However, “its existence
as a disease and its association with vaccination stands undiminished by this ignorance, and so too
the theory [he] offered to explain all that is known, with what is currently known.” Id. at 9. This
acknowledgment that there is no mechanism or subsequent application to Petitioner’s presentation
best illustrates the lack of preponderant evidence here to satisfy Althen prong two.
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D. Althen Prong Three – Temporal Relationship
There is also strong disagreement between the parties’ experts, Drs. Andersson and
Jamieson, regarding both the onset and progression of Petitioner’s symptoms. The temporal
relationship between vaccination and symptom onset is a key supporting factor for the viability of
a molecular mimicry mechanism in this case. Dr. Andersson argued that Petitioner’s symptoms
began two days post vaccination, while Dr. Jamieson more precisely placed Petitioner’s initial
feeling of fatigue “in the back of her legs,” at 1.5 days post vaccination. Pet’r’s Ex. 4 at 1; see
Resp’t’s Ex. F at 3. The medical records do not specify what time of day Petitioner received her
flu shot; and Petitioner’s expert ultimately incorporated 1.5 days into his supplemental report,
asserting that this shortened time is of no consequence.
However, Dr. Andersson argued that “the etiology of vaccination-induced TM is the same
as for vaccination-induced [GBS].” Pet’r’s Ex. 10 at 10. The appropriate timeframe for symptom
onset of flu vaccine-caused GBS, as articulated on the Vaccine Injury Table, is between three and
42 days. 42 C.F.R. § 100.3(a)(XIV)(D). Indeed, the initial immune system processes that occur as
a prerequisite to molecular mimicry and are described by Dr. Forsthuber, including T and B cell
activation and the production of IgG antibodies, occur during this time. Dr. Andersson addressed
this discrepancy by conceding that a 1.5-day time frame is shorter than the case studies he
presented. However, he relied on case studies with two-day (ADEM) and four-day (TM) onset
periods and reiterated that the difference of a few days is inconsequential. It is unclear whether he
is contending that Petitioner’s case is an example of “the activation of a memory response,” or “a
primary immune response and this rapid onset of [TM].” Pet’r’s Ex. 10 at 17. The latter argument
is inconsistent with his supplemental report. Dr. Andersson stated that “[a] probable and logical
theory was offered in my report by invoking a memory response for the rapid time course and
molecular mimicry as mechanism for the host attack.” Pet’r’s Ex. 31 at 8. He never provided a
mechanism based on a primary immune response that is consistent with such a short onset. In fact,
Dr. Andersson asserted that the short onset of Petitioner’s symptoms “demand . . . a memory
response mechanism.” Id. In the case of the former, Dr. Forsthuber noted the peculiarity of
Petitioner experiencing a pathological memory response that caused a neurological disorder after
15 prior exposures to the flu vaccine without incident. Dr. Andersson’s response to this concern
was that “[t]he demand for a probable theory [is] unreasonable.” Id. He argued that this “is a
skepticism that could be applied to every case of vaccination associated [TM] with a prior similar
vaccination, and every case of vaccination associated [GBS] with a similar prior vaccination too.”
Id. Petitioner did not provide any information on the number of GBS-flu claims involving a
Petitioner previously vaccinated over a decade without incident. Petitioner did not acknowledge
that Table cases, which require a three-day onset, do not rely on a biological mechanism including
a memory response. Petitioners are not required to provide conclusive evidence to establish any
element of their claim. The temporal relationship need only be a medically acceptable inference,
“given the medical understanding of the disorder’s etiology.” de Bazan, 539 F.3d at 1352. Dr.
Andersson’s reliance on memory response to account for the shortened time frame is ill-reasoned
and not persuasive.
Decisions from other special masters where petitions alleging vaccine-induced TM in the
Program have been dismissed for similar onset being found too close in time to vaccination to be
medically reasonable. True v Sec’y of Health & Hum. Servs., No. 21-1100V, 2025 WL 1343027
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at *30 (Fed. Cl. Spec. Mstr. April 1, 2025); See, e.g., Martinez ex rel. W.M. v. Sec’y of Health &
Hum. Servs., No. 16-738V, 2022 WL 4884923, at *27 (Fed Cl. Spec. Mstr. Sept. 9, 2022)
(“Because TM is reasonably understood to be mediated by an autoimmune reaction involving
antibodies or other immune cells associated with the adaptive, lagging immune response in
reaction to antigenic exposures . . . , a relatively short onset timeframe is simply not medically
acceptable.” (emphasis omitted)); Palattao v. Sec’y of Health & Hum. Servs., No. 13-591V, 2019
WL 989380, *35 (Fed. Cl. Spec. Mstr. Feb. 4, 2019) (citing dismissals of cases with 24-hour onset
for vaccine-related TM and finding a 30- to 36-hour onset to not be medically acceptable);
Brancheau v. Sec’y of Health & Hum. Servs., No. 21-1209V 2024 WL 1619606, at *23-26 (Fed.
Cl. Spec. Mstr. Mar. 21, 2024) (finding a one-day onset of TM following flu vaccination not
appropriate given the theory of molecular mimicry).
Specifically, in Helen Forrest v. Sec’y of Health & Hum. Servs., the petitioner’s expert
proposed that the flu vaccine can cause TM via molecular mimicry. No. 14-1046V, 2019 WL
925495, at *3 (Fed. Cl. Spec. Mstr. Jan. 28, 2019). To explain the 36-hour onset, the expert
proposed that the petitioner had a recall response due to previous flu vaccinations. Id. at *4. The
special master found that “[e]ven if molecular mimicry could be accepted to explain how the flu
vaccine can cause [TM] abstractly, . . . a preponderance of the evidence shows that molecular
mimicry is not likely to happen within 36 hours, even for a recall response.” Id. at *6; see also
Mosley v. Sec’y of Health & Hum. Servs., No. 08-724V, 2015 WL 2354316, at *19 (Fed. Cl. Spec.
Mstr. Apr. 27, 2015) (denying compensation where “onset of TM one day after tetanus vaccination
[was] too soon to support vaccine causation”); Jagoe v. Sec’y of Health & Hum. Servs., No. 08-
678V, 2012 WL13036265, at *28 (Fed. Cl. Spec. Mstr. Aug. 3, 2012) (finding a 24-hour onset not
medically appropriate for a vaccine-induced TM injury); Crosby v. Sec’y of Health & Hum, Servs.,
No. 08-799V, 2012 WL 13036266, at *38–39 (Fed. Cl. Spec. Mstr. June 20, 2012) (same).
Petitioner has not provided preponderant evidence of an appropriate temporal relationship
for the onset of TM symptoms following flu vaccination generally, or in Petitioner’s specific case.
Accordingly, Petitioner has failed to satisfy Althen prong three.
VI. Conclusion
After a careful review of the record, Petitioner has failed to prove by preponderant evidence
that she suffered from TM as a result of her September 28, 2016 flu vaccination. Further, Petitioner
has failed to provide preponderant evidence that her condition was caused by vaccination.
Accordingly, I DENY Petitioner’s claim and DISMISS her petition.29
IT IS SO ORDERED.
s/Herbrina D.S Young
Herbrina D.S. Young
Special Master
29 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
32