Martinez v. Secretary of Health and Human Services ( 2022 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 16-738V
(to be published)
************************* Chief Special Master Corcoran
THEODORE MARTINEZ and *
SARAH MARTINEZ *
as parents and natural guardians of W.M., *
*
Petitioners, * Dated: September 9, 2022
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
*************************
David John Carney, Green & Schafle LLC, Philadelphia, PA, for Petitioners.
Naseem Kourosh, U.S. Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION 1
On June 22, 2016, Theodore and Sarah Martinez, on behalf of their minor daughter, W.M.,
filed a petition for compensation under the National Vaccine Injury Compensation Program (the
“Program”). 2 ECF No. 1. Petitioners allege that diphtheria-tetanus-acellular pertussis (“DTaP”)3
1
This Decision will be posted on the United States Court of Federal Claims’ website in accordance with the E-
Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will be available to anyone with access
to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the published
Ruling’s inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party has
fourteen (14) days within which to request redaction “of any information furnished by that party: (1) that is a trade
secret or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files or
similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b).
Otherwise, the entire Decision will be available to the public in its current form. Id.
2
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
3
DTaP is the acronym for the version of the vaccine administered to infants and children younger than seven years of
age, whereas “Tdap” is the version administered to adults. Diphtheria and Tetanus Toxoids and Acellular Pertussis
Vaccine, Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=116510 (last
visited Sept. 9, 2022).
and rotavirus vaccines administered to W.M. on June 26, 2013, caused their daughter to develop
transverse myelitis (“TM”). A two-day entitlement hearing in the matter was held in Washington,
D.C. on November 16-17, 2021.
Having reviewed the record, all expert reports and associated literature, and listened to the
testimony at hearing, I hereby deny an entitlement award. As discussed in greater detail below,
Petitioners have not preponderantly established that W.M.’s TM occurred within a medically
acceptable timeframe.
I. Fact History
Early Life and Vaccination Event in Question
W.M. was born on December 23, 2012, to Petitioners. Ex. 7 at 31–37, 64; Ex. 10 at 24. She
was born prematurely at 34 weeks as an identical twin. Id.
On December 27, 2012, W.M. received a Hepatitis B vaccine for her first-week wellness
check. Ex. 2 at 4. On March 6, 2013, W.M. was seen by her pediatrician at the Affinity Clinic for
a two-month check-up. Ex. 8 at 28, 31–32. During this visit she received Pediarix (a combination
of DTaP, Hepatitis B, and Polio vaccines), ActHIB (haemophilus influenza type B (“Hib”)),
Prevnar 13 (“pneumococcal”), and the RotaTeq (“rotavirus”) vaccines. Id. Her exam during this
visit was normal. Id. She had a four-month well-child check-up at Affinity Clinic on April 23,
2013, at which time she received the DTaP, Hepatitis B, Polio, Hib, pneumococcal, and rotavirus
vaccines. Ex. 8 at 33–37. A six-month visit followed on June 26, 2013. Ex. 8 at 38, 42. Her exam
was again normal, and she received the DTaP and rotavirus vaccines at issue that afternoon (at
2:46 and 2:48 P.M, respectively). Id.
Onset of Symptoms
W.M. returned to the Affinity Clinic approximately five days later, on July 1, 2013.
Petitioners now reported that after receiving her DTaP vaccine the prior week, W.M. had not been
moving or bearing any weight on her legs, and had a tremor when trying to stand or use her arms.
Ex. 8 at 43. They also informed treaters that she was constipated, hypotonic (meaning low muscle
tone), lethargic, not acting like herself, and had a fever of 100.9 degrees, and that her symptoms
were not worsening but also not improving either. Id. Mrs. Martinez specifically expressed a
concern about the possibility of seizures. Id.
No specific onset date for this constellation of symptoms was provided at this time,
however, beyond the general assertion that they had manifested “since” the time of vaccination.
And there is no record filed in this case of any intervening doctor’s visit prior to the encounter at
Affinity Clinic on July 1. At most, Mrs. Martinez has averred (in a June 23, 2016 affidavit) that
2
after receiving the DTaP and the rotavirus vaccines, both W.M. and her twin sister 4 were tired, a
bit cranky and had sore legs from the injections. Ex. 18 at 2. However, after a few days, Mrs.
Martinez became concerned for W.M. specifically because she continued to be lethargic, and was
not moving her legs while her twin sister had recovered from any initial apparent vaccine reaction.
Ex. 9 at 2; Ex. 18 at 2. Furthermore, Mrs. Martinez has alleged that Mr. Martinez took W.M. to
the Affinity Clinic urgent care on June 29, 2013 (a Saturday), but that there is no record of this
visit because he only briefly spoke with a doctor in the waiting room. Ex. 8 at 43 (noting that this
may be the interaction referred to in the July 1, 2013 record, which stated (under Chief Complaint)
“[s]een by Dr. [Teresa] Stewart in EC on 6/29/13”); Ex. 18 at 3.
At the Affinity Clinic visit on July 1, 2013, W.M. was seen by nurse practitioner Ramona
Cawley. Ex. 8 at 43. Petitioners (who were deemed in the record to be “very familiar” with the
relevant history) reported that W.M. would not move her legs or bear weight on them “since” the
vaccination event (although no specific onset was identified). Id. The record also noted that she
had been constipated. Id. Overall, her symptoms were deemed to be “not worsening but also not
improving over time.” Id. Exam showed that W.M. would not bear weight on her legs, had limited
active movement in her lower extremities, and a tremor in her arms when reaching. Id. at 44. The
assessment was generalized muscle weakness, and W.M. was referred to neurology. Id.
Two days later (July 3, 2013), W.M. was seen by pediatric neurologist Yong Park, M.D.
Ex. 9 at 7. Petitioners informed Dr. Park that W.M. had been doing well until she received the
DTaP vaccine the week prior, after which she was very cranky and stopped using her legs. Id.
They also reported that W.M.’s twin sister had received her vaccinations without any problems,
and there was no family history of neurological disorders. Id. It was also noted that the neurologic
referral occurred because W.M.’s symptoms had “progressed”—and since the referral occurred on
July 1 (two days before Dr. Park saw W.M.), this reasonably means that the progression occurred
up to July 1 rather than after.
Upon physical exam, Dr. Park noted that W.M.’s lower extremities showed spasticity and
clonus, which were more pronounced on the left than right side. Ex. 9 at 7. There was also
hyporeflexia and brisk deep tendon reflexes (“DTRs”) in the lower extremity, minimal reaction to
stimulation on the left leg. and a wink in the anal sphincter tone. Id. at 7–8. Dr. Park’s assessment
was spastic paraparesis “acute in onset since 2nd [DTaP] vaccination.” Id. at 8. He noted that he
was concerned about a vaccination reaction such as TM, but that a spinal cord lesion was in his
opinion unlikely due to W.M.’s clinical presentation. Id. Dr. Park made an urgent transfer to the
hospital for W.M. to undergo further testing, which was to include a spinal tap/lumbar puncture
(“LP”) and MRI. Id.
4
Although it was not evidenced by the medical records at this time, W.M.’s twin sister, R.M., also received the DTaP
and rotavirus vaccines on June 26, 2013. Ex. 18 at 2; Tr. at 135, 187–88.
3
Hospital Admittance
That same day, W.M. was admitted to the Children’s Hospital of Georgia. Ex. 10 at 21.
Upon admission, Mrs. Martinez provided additional specific information about the circumstances
of W.M.’s symptoms manifestation—and again suggested an onset close in time to the vaccination
date. W.M., she reported, had received the DTaP and rotavirus vaccines on June 26, 2013, and
after returning home developed a decreased activity level (including less rolling) that evening, and
had a temperature of 99 degrees. Id. at 24. By the next morning (June 27, 2013), both of W.M.’s
legs were limp, and she continued not to move her lower extremities or stand on her legs. Id. In
addition, W.M. now had a temperature of 100.9 degrees, which continued through that day. Id.
And as of June 28, 2013, both of W.M.’s legs were stiff, and at some point around this time, her
stools became more frequent and of lesser quantity, although her urination pattern was normal. Id.
at 3, 24.
W.M. was also examined by George Lazari, M.D., PGY1,5 and an attending physician. He
reported that the chief complaint was that W.M. was “limp after shots.” Ex. 10 at 24. He also
completed a musculoskeletal exam, which revealed “[d]ecreased range of motion, [s]pasticity and
decreased movements in lower extremities.” Id. at 25. Treating physicians had a differential
diagnosis of Guillain-Barré syndrome (“GBS”) or transverse myelitis. Id. at 27. An MRI done that
same day showed thoracic spinal cord intermedullary enhancement at T3-T4 that was concerning
for early stages of acute TM. Id. at 97–98. The LP performed that day showed slightly elevated
protein of 51 and slightly decreased glucose of 38, RBC 1, WBC 3 with 59 percent lymphocytes
and 41 percent monocytes. Id. at 53–54, 92. CSF Oligoclonal bands were negative, however, and
CSF myelin basic protein was elevated at 6.40 ng/mL. Id. at 93–94.
W.M. was then evaluated by pediatric neurologist Suzanne Strickland, M.D. on that same
day (July 3, 2013). Ex. 10 at 57. Dr. Strickland considered W.M.’s prior history reported by her
mother, as well as the written pediatric transfer note and additional medical documentation. Id. at
57, 62–66. Based on these disclosures plus the testing results, Dr. Strickland diagnosed W.M. with
TM, deeming W.M.’s radiology results and clinical presentation as consistent with this diagnosis.
Id. at 54, 61.
W.M. was subsequently administered a high dose of methylprednisolone over the next five
days. Ex. 10 at 4–6. Her lower extremity movement began to improve on the second day, and her
neurological exam improved slightly each day, but she was still moving significantly less than
normal. Id. She was discharged on July 7, 2013, with a diagnosis of TM and instructions to
continue oral steroids. Id. at 5–6.
5
This indicates that it was the first year of graduate training after completion of medical school.
4
Post-TM Diagnosis Treatment
On July 12, 2013, W.M. presented for outpatient physical therapy (“PT”), with her parents.
Petitioners now reported that within hours of receiving a DTaP vaccine, W.M. developed extreme
weakness, tremulousness, and lethargy. Id. at 1. A few days later, on July 15, 2013, W.M. was
seen in a follow-up appointment at the Affinity Clinic, with Mrs. Martinez informing treaters that
W.M. was doing better with leg movements, and that she was receiving oral steroids in conjunction
with her PT sessions. Id. at 50.
On August 1, 2013, W.M. returned to the Affinity Clinic and was seen by pediatrician
Dixie Griffin, M.D. Ex. 8 at 54. W.M. was now reported to be doing well—moving her lower
extremities, trying to crawl, urinating—but had mild constipation, and was shaking her head. Id.
Dr. Griffin noted that she discussed vaccines with Mrs. Martinez, noting the close temporal
relationship of the onset of W.M.’s symptoms following vaccination but nevertheless stating that
“I do not feel [acute transverse myelitis] is related to DTaP vaccinations because symptoms
occurred 2 days after vaccine(s). Most studies suggest 2–3-week lag between inciting event and
A[cute] TM.” Id. at 54–55.
On August 5, 2013, W.M. was seen by neurologist Sheisa Claudio-Sandoval, M.D. Once
again, Petitioners stated that W.M. had manifested symptoms associated with TM within a few
hours of receiving a DTaP vaccine. Ex. 10 at 448. Dr. Claudio-Sandoval concurred in the TM
diagnosis. Id. at 450. A month later, on September 4, 2013, W.M. was seen at the Affinity Clinic
by NP Cawley. Ex. 8 at 72. NP Cawley noted that Mrs. Martinez was concerned about vaccines
and reported that neurology had told her to wait on further vaccination. Id. at 73. NP Cawley
discussed this issue with Dr. Griffin, who suggested that W.M. be referred to an infectious disease
specialist so that she could discuss her vaccine concerns. Id.
W.M. next went to an outpatient clinic and saw neurologist James Carroll, M.D., on
September 17, 2013. Ex. 10 at 469. W.M. was reported to have demonstrated improvement since
her PT, and an exam confirmed that many symptoms and associated issues had diminished. Id. at
469–70. An MRI performed that day showed that the spinal cord lesion at T3-T4 was resolved and
no new lesions were identified. Id. at 473. The improvements were also reflected in the record
from W.M.’s nine-month check-up at the Affinity Clinic on September 25, 2013. Ex. 8 at 80, 82.
Treatment in 2014 and Thereafter
Months later, on June 5, 2014, W.M. began services with an early intervention program
focusing on PT to improve motor skills. Ex. 12 at 2. Neurology outpatient visits confirmed her
progress—although many deficits remained. Ex. 10 at 505–06. This incomplete improvement
5
remained a constant for the remainder of the year. See, e.g., Ex. 7 at 154 (July 9, 2014 Affinity
Clinic check-up); Ex. 13 at 1, 3 (December 4, 2014 primary care visit).
W.M.’s course since the start of 2015 is consistent, demonstrating improvement without
elimination of prior issues—and no recurrence of new neurologic concerns that might suggest her
TM did not reflect a single monophasic event. One pediatric neurologist—William Taft, M.D.—
who saw W.M. in January 2015 did propose that a real link between her vaccination to neurologic
symptoms was evident, and asked to see other testing results to explore the possibility further. Ex.
14 at 1–2. Mrs. Martinez has stated that W.M. continues to have pain and displays “difficulty
walking long periods of time or long distances; difficulty running; [gait] issues and concerns;
balance issues and concerns; short tendons and tight muscles; hip joint concerns; some bladder
and constipation concerns and frequently asks to wear a pull up; issues dressing and undressing;
and poor balance and flexibility.” Ex. 9 at 4. W.M. uses a walker for distances, AFOs, and orthotic
shoes. Id.
II. Witness Testimony
A. Petitioner’s Fact Witnesses
1. Ms. Sarah Martinez – Mrs. Martinez, W.M.’s mother, was the first witness
to testify at the hearing. See generally Tr. 7–90. She began with an overview of the first sixth
months of W.M.’s life. Id. at 9–13. As she recalled, W.M. (and her twin sister R.M.) were
developing normally and hitting their milestones prior to their sixth-month wellness check. Id. at
10, 12, 48. The twins attended other wellness checks after their birth, where they received vaccines.
Id. at 9. Thus, at the first-week wellness check they both received the Hepatitis B vaccine, at the
two-month wellness check they received the pneumococcal, rotavirus, Hib, and Pediarix vaccines,
and at the fourth-month wellness check they received the second dose in the series for the
pneumococcal, rotavirus, Hib, and Pediarix vaccines. Id. at 9, 11–12. Mrs. Martinez noted that
after the two-month and four-month wellness check vaccinations, the twins appeared fatigued, but
returned to their normal behaviors the following day. Id. at 12.
During their six-month wellness check, on June 26, 2013, the twins received the DTaP and
rotavirus vaccines. Id. at 13–14. Prior to the administration of these vaccines, Mrs. Martinez
recalled, neither twin had recently suffered from any kind of infection or illness. Id. at 12.
However, after the girls returned home and Mrs. Martinez went out to dinner with her husband
that night, she was told by her mother (who was watching the girls) to come back because the
twins were upset. Id. at 15, 51–52, 62; Ex. 18 at 2.
When Mrs. Martinez returned, she found the girls irritable, crying, and lethargic, with
elevated temperatures around 99 degrees. Tr. at 15–16, 53–54, 62. Mrs. Martinez gave them each
a dose of Tylenol before bed, but the next morning (June 27, 2016), the girls were exhibiting
6
similar symptoms of irritability, lethargy, and elevated temperatures around 100.7 degrees. Id. at
17. Mrs. Martinez also noticed that on all other nights the twins would move around, and she would
find them in different positions the following morning, but on this night, she found them in the
exact same positions she placed them in the night before. Id. at 55–57. Although their temperatures
dissipated after another dose of Tylenol, the other symptoms continued, and the twins would not
engage in their normal activities of moving around and playing. Id.
The following day (June 28, 2013), however, the twins started to display different
symptoms, with R.M. improving while W.M.’s symptoms remained consistent with the day before.
Tr. at 19, 59. Mrs. Martinez observed that W.M. did not want to move her upper or lower body
when laying down and required a lot of holding and breastfeeding for comfort. Id. at 70. Mrs.
Martinez maintains she did not at this time notice anything abnormal in W.M.’s legs (even though
statements from the contemporaneous medical record do contain these kinds of observations),
though she admits she did nothing to informally examine W.M. in this regard at this time. Id. at
70, 85. She called the pediatrician’s nurse hotline and was told that this behavior was normal after
receiving a vaccination due to injection site soreness, and was not recommended to go to the
hospital. Id. at 20–21.
On June 29, 2013, R.M. improved significantly and was almost back to her usual self, but
not W.M. Tr. at 22–23, 62. As a result, Mr. Martinez took W.M. to the Affinity Clinic urgent care
center, where they were reassured that W.M. was simply irritable from the injection site. Id. at 23–
24, 62–63. They were advised to take her to a pediatrician on Monday (July 1) if her symptoms
did not improve. Id. at 24, 63. On June 30, Mrs. Martinez noted slight improvement such as
alertness and more active movement with her hands, but W.M. had now also developed severe
constipation that caused bleeding (although the bleeding was not mentioned in the medical record).
Id. at 25–26, 28, 60, 64–66. Up until this point, W.M. was urinating and passing stools normally.
Id. at 17, 20, 22.
On July 1, 2013, Mrs. Martinez called the Affinity Clinic, as W.M. still appeared lethargic.
She was told that W.M.’s symptoms were normal but was given a same-day appointment with NP
Cawley, who had conducted the twins’ well-check visits previously. Tr. at 28–30, 64, 87. Mrs.
Martinez testified that NP Cawley had consulted with another pediatrician, Dr. Griffin, at this time.
Id. at 31–32. Dr. Griffin said that he wanted W.M. evaluated by a pediatric neurologist, but Mrs.
Martinez was not told that it was an urgent issue. Id. at 32–33.
Upon leaving the Affinity Clinic, Mrs. Martinez testified that she noticed for the first time
that W.M. had begun straightening out her legs rigidly and then bending her knees, before relaxing
and then repeating this behavior. Id. at 35–36, 61–62, 83–84. Mrs. Martinez denied specific
concerns with W.M.’s legs before this time, but it was not until after NP Cawley had completed
her physical examination. Tr. at 66, 80; Ex. 9 at 7.
7
W.M. was subsequently evaluated at an outpatient neurological visit by Dr. Park on July
3, 2013, and at that point Mrs. Martinez described what she had witnessed of W.M.’s behavior
after the last Affinity Clinic visit. Id. at 34–35. (She again took issue with contemporaneous
medical record evidence from the time of this visit suggesting that the Petitioners had previously
observed W.M.’s leg issues closer-in-time to vaccination). Tr. at 66, 85; Ex. 10 at 24, 55. Dr. Park
stated that this behavior indicated neurological issues and wanted to confirm with testing as it
suggested acute TM. Id. at 36–37, 84.
There was, Mrs. Martinez recalled, now a new sense of urgency as Dr. Park sent the family
immediately to the Medical College of Georgia, where the family was met with a handful of
doctors conducting diagnostic tests. Tr. at 38–40. Mrs. Martinez described several instances where
she gave a rushed explanation to multiple doctors of W.M.’s medical history, with short follow-
up questions (since the treaters were focused on W.M.’s care). Id. at 40–42, 71. During this time
she noticed that W.M.’s upper body movements had returned to her usual state. Id. at 45. After a
spinal tap and MRI, the doctors diagnosed W.M. with TM. Id. at 44.
W.M. was subsequently admitted to the hospital in early July and discharged on July 7,
2013. Tr. at 45. During that time Mrs. Martinez had conversations with doctors regarding the cause
of W.M.’s injuries. Id. Specifically, Dr. Strickland and Dr. Carroll discussed the role vaccinations
could have played on W.M.’s injury, as there were no prior events of note, although treaters
hesitated to predict future treatment requirements or likely outcomes. Id. at 46, 47. As of the date
of the hearing, W.M. was eight years old, and used assistive devices like ankle foot orthotics and
forearm crutches to get around. Id. at 47.
Besides the foregoing, Mrs. Martinez also attempted to correct medical records that she
deemed inaccurate or incomplete. Tr. at 77–80. For example, she identified W.M.’s appointment
with Dr. Claudio-Sandoval on August 5, 2013, where the history stated that “[W.M.] was admitted
to PICU on July 3, 2013, after develop[ing] low extremity weakness after a few hours of receiving
second DTaP dose.” Tr. at 78; Ex. 10 at 448 (emphasis added). Mrs. Martinez contended, to the
contrary, that W.M. was simply lethargic after receiving this vaccine. Tr. at 79. Additionally, she
questioned the accuracy of the record of W.M.’s appointment with Dr. Taft on January 30, 2015,
which reported under history of present illness that “[p]arents report that [W.M.] was doing well
until the day after she received her DTaP. That night she began to exhibit flaccid weakness of her
legs on both sides. Her arms were moving appropriately, and she was cognitively normal.” Id.; Ex.
14 at 1 (emphasis added). Mrs. Martinez maintained that she had not noticed anything abnormal
in terms of W.M. bearing weight on her legs immediately after vaccination, and that she had simply
appeared lethargic. Tr. at 79–80.
2. Mr. Theodore Martinez – Mr. Martinez (W.M.’s father) was the second
witness to testify at the hearing, and his testimony was generally consistent with Mrs. Martinez’s
testimony. See generally Tr. at 91–118. He characterized W.M. and R.M.’s development as normal
8
prior to vaccination, and noted they were beginning to make noises, crawl, and roll. Id. at 93, 106.
He did not see signs of illness in either twin in the days leading up to their vaccination. Id. at 104.
But two days later, W.M. and R.M. were extremely lethargic, crying more, and their voices were
weaker than usual. Id. at 94–95, 106. He noticed that they did not want to play as they typically
did, but only wanted to be held and fed. Id. at 106.
On June 28, 2013, R.M. improved and became more active, but W.M. remained lethargic.
Tr. at 95–96, 106. That day, Petitioners called the nurse hotline, but wanted to see a doctor in
person, so Mr. Martinez took W.M. to urgent care the next day due to her ongoing lethargy, where
he saw Dr. Stewart. Id. at 96–97. (There remains a factual dispute about this visit that was never
resolved, despite the parties’ efforts and although this visit was discussed in Mrs. Martinez’s
affidavit, there is no formal record of it). Tr. at 96–97; Ex. 18 at 3. 6 W.M. never went into an
examination room but remained in her car seat in the lobby, where Dr. Stewart checked W.M.’s
reflexes, deeming them normal (beyond inflammation at the vaccination site). Tr. at 98, 100, 106,
108-09, 118. She advised Mr. Martinez to continue giving W.M. Tylenol as needed, adding that
W.M. should be taken to Dr. Griffin on Monday if her symptoms persisted. Id. at 98–99, 109–110.
W.M. subsequently saw Dr. Park on July 3, 2013. Tr. at 102, 110. During this visit, Mr.
Martinez recalled that Dr. Park became concerned with W.M.’s leg movements and subsequently
rushed the family to the hospital for treatment. Id. at 102–03, 110, 117. There, Mrs. Martinez was
mostly responsible for providing specifics about W.M.’s more-recent medical history. Id. at 103–
1\04. Mr. Martinez also recalled that during W.M.’s hospitalization, Dr. Taft and other treaters had
discussed W.M.’s TM and its possible links to her vaccinations. Id. at 104.
B. Petitioner’s Experts
1. Justin Willer, M.D. – Dr. Willer, a board-certified neurologist with a
subspeciality in neuromuscular diseases and epilepsy, submitted four written expert reports and
testified for Petitioners. See generally Tr. at 120–227. Report, dated Jan. 12, 2018, filed as Ex. 20
(ECF No. 31-1) (“Willer First Rep.”); Report, dated Mar. 15, 2019, filed as Ex. 28 (ECF No. 41-
1) (“Willer Second Rep.”); Report, dated Nov. 8, 2019, filed as Ex. 31 (ECF No. 52-1) (“Willer
Third Rep.”); Report, dated Mar. 13, 2020, filed as Ex. 34 (ECF No. 59-1) (“Willer Fourth Rep.”).
Dr. Willer did not, however, offer any opinion specific to the “can cause” causation issues in
dispute, leaving that topic to Petitioners’ other expert.7
6
Petitioners subpoenaed the Affinity Clinic, but despite their best efforts were not able to obtain a record of this
specific visit. ECF Nos. 88-89.
7
One of Respondent’s expert, Dr. Lotze, criticized some of Dr. Willer’s publications addressing autoinflammatory
syndrome induced by adjuvants (“ASIA”) syndrome, but Dr. Willer did not allege in this case that aluminum contained
in the vaccine was the cause of W.M.’s TM. Willer Third Rep. at 4; Lotze Second Rep. at 2; R. Ameratunga et al.,
Evidence Refuting the Existence of Autoimmune/Autoinflammatory Syndrome Induced by Adjuvants (ASIA), 5 J.
9Dr. Willer received his undergraduate degree from Columbia College of Columbia
University and his medical degree from the University of Health Sciences/The Chicago Medical
School. See Curriculum Vitae, filed Oct. 27, 2021 (ECF No. 84-1) (“Willer CV”) at 1; Tr. at 121.
Beginning in 1995, he has held hospital appointments at University Hospital, Long Island College
Hospital, Maimonides Hospital Medical Center, and Kings County Medical Center, but he has not
treated pediatric patients since 2000. Willer CV at 1; Tr. 122–23, 176. He has also held academic
appointments as a Neuromuscular Consultant and Assistant Professor of Clinical Neurology at the
State University of New York, HSC at Brooklyn. Willer CV at 1; Tr. at 123. He is licensed to
practice medicine in New York, New Jersey, and Florida, and is board certified by the American
Board of Psychiatry and Neurology, with added qualifications in clinical neurophysiology, and
American Board of Electrodiagnostic Medicine. Willer CV at 2; Tr. at 122–23. None of Dr.
Willer’s publications are related to pediatric neurology, TM, or other autoimmune diseases. Tr. at
176.
Dr. Willer began his testimony with an overview of W.M.’s diagnosis. He opined that she
had experienced TM, 8 with her initial symptoms rapidly progressing to hypertonicity and then
spastic paraparesis. Tr. at 126–27. In so proposing, he defined some of the terms he was using
applicable to W.M.’s muscle and motor-related symptoms. Id. Human limbs generally display
some amount of muscle resistance as they are moving, but where the resistance is more labile,
“hypotonicity” is displayed, as opposed to “hypertonicity,” which occurs in the presence of muscle
rigidity. Id. at 133–34. The outset of TM is typically characterized by hypotonia, which
subsequently progresses to hypertonia unless there is “deafferentation” (meaning where the
sensory supply to the lower limbs becomes completely cut off). Id. at 133. Dr. Willer also defined
spastic paraparesis as weakness of two arms or two legs (as relevant to W.M.) with increased tone.
Id. at 134. In TM, there is an initial phase where tone is decreased (consistent with hypotonia)
before it increases. Id. at 179.
As Dr. Willer explained, TM is a rapidly evolving disease, reaching nadir between 4-21
days from its start and involving spinal cord demyelination. Tr. at 129, 132–33, 178; Willer First
Allergy Clinical Immunology 1551, 1551–54 (2017), filed as Ex. C-1 (ECF No. 49-2). At most, Dr. Willer argued
that vaccines produce antibodies that cause TM, which are similar or identical to the antibodies causing TM by natural
infection, but deferred to Dr. Gershwin on such matters more generally. Willer Third Rep. at 4.
8
Dr. Willer’s written reports had also discussed a possible diagnosis of acute disseminated encephalomyelitis
(“ADEM”), which he felt could not be ruled out given the absence of MRI imaging results that would bear on such a
diagnosis. Tr. at 179; Willer First Rep. at 9; Willer Second Rep. at 4–5; Willer Third Rep. at 5. He contended there
was at least case report support for the proposition that tetanus-containing vaccines can cause ADEM. See, e.g., F.
Cisse et al., [Acute Disseminated Encephalomyelitis After Tetanus Vaccination of a Pregnant Woman in Senegal], 22
Médecine et Santé Tropicales 103, 103–05 (2012), filed as Ex. 26 (ECF No. 32-6). But at trial he made it clear that he
accepted and favored TM as the proper diagnosis. Tr. at 179.
10
Rep. at 4. Although often idiopathic, (meaning no cause can be identified),9 it can be attributable
to infectious/post-infectious causes (or vaccination). Tr. at 129, 170; Willer First Rep. at 4. It can
also be the presenting symptom of a larger disease, like multiple sclerosis (“MS”) or neuromyelitis
optica spectrum disorder (“NMOSD”). Tr. at 170–71, 222. TM can feature sensory symptoms,
weakness, bowel or bladder complaints, urinary retention, constipation, or pain. Id. at 129. The
typical work-up to identify its cause begins first with eliminating an injury from outside the spinal
cord through imaging studies, followed by an LP aimed at identifying signs of inflammation or
other biomarkers associated with known causal diseases (for example, oligoclonal bands, which
are associated with MS), and then an antibody test. Id. at 130. An MRI can assist in diagnosis as
well, since it can reveal a breakdown of the blood-brain barrier and the presence of active lesions
or inflammation. Id. at 130. After diagnosis, treatment consists of steroids during initial symptoms,
although treatment approaches require adjustment depending on its ultimate determined etiology.
Id. at 131; Willer First Rep. at 5.
Next, Dr. Willer addressed the medical record, attempting to demonstrate how it supported
the conclusion that the DTaP vaccine could have caused W.M.’s TM. 10 Tr. at 166, 179–80; Willer
Third Rep. at 6; Willer Fourth Rep. at 3. There was no evidence that W.M. had any type of viral
or bacterial illness prior to vaccination or during her pediatric visits and hospital visit. Tr. at 135,
170–72, 226–27. W.M. was never diagnosed with MS or NMOSD. Id. at 170–72, 215. And even
though Dr. Willer found some of Dr. Park’s information lacking from the July 3, 2013 progress
notes, Dr. Park seemed to embrace the possibility that W.M.’s vaccination had caused her TM. Id.at 158–59; Ex. 9 at 8. Because Dr. Park is a pediatric neurologist likely familiar with neurologic
complications of vaccines in children, his views deserved extra weight in Dr. Willer’s opinion. Tr.
at 159–60.
In addition, other treaters at the hospital also questioned whether W.M.’s injury was caused
by vaccination (although some speculated about a possible infectious cause). Tr. at 172–75, 205–
07; Ex. 10 at 65 (noting an impression that W.M.’s injury was vaccine induced), 68 (contemplating
a vaccine reaction versus an infectious/post-infectious case), and 70 (indicating a potential vaccine
or viral illness caused W.M.’s injury); Ex. 14 at 2 (stating that W.M.’s injury occurred after
vaccination, but too vague to indicate whether the treater thought it was caused by vaccination).
No other physician—either Dr. Park or a treater at the hospital—suggested an idiopathic etiology,
and Dr. Willer felt that the likelihood of idiopathic TM in a six-month-old was low in any event.
Tr. at 171.
9
Though in a few medical records the treaters contemplate whether the injury was caused by vaccination or a viral
illness, and thus seem unable to identify a cause, Dr. Willer was careful to iterate that this was not the same as an
affirmative determination that idiopathic best described TM’s cause in this case. Id. at 207–08.
10
Dr. Willer briefly discussed W.M.’s receipt of the rotavirus vaccine (also received on June 26 along with the DTaP
vaccine) but deemed it less likely causal. Tr. at 180; Willer Second Rep. at 3. Literature Petitioners otherwise relied
upon did not show a TM-rotavirus vaccine association. Willer Second Rep. at 3 (citations omitted).
11
Dr. Willer deemed the temporal relationship between W.M.’s onset and date of vaccination
consistent with causation by the DTaP vaccine. Tr. at 216; Willer First Rep. at 9; Willer Second
Rep. at 3; Willer Third Rep. at 6. He proposed that TM could begin after a vaccine trigger any
time between three to four days to a few weeks post-vaccination, although onset within two days
was also possible. Tr. at 167. In support, Dr. Willer referenced several case reports. Id. at 167–69,
185–87; Willer First Rep. at 4; Willer Fourth Rep. at 1, 5; N. Agmon-Levin et al., Transverse
Myelitis and Vaccines: A Multi-Analysis, 18 Lupus 1198, 1200 (2009), filed as Ex. 25 (ECF No.
32-5) (“Agmon-Levin”) (finding the shortest onset for TM occurred two days after a rabies
injection, and another case of TM with an onset of 4 days following rubella vaccination—but most
other cases occurred after a few weeks); R. Riel-Romero, Acute Transverse Myelitis in a 7-Month-
old Boy After Diphtheria-Tetanus-Pertussis Immunization, 44 Spinal Cord 688, 688–91 (2006),
filed as Ex. 22 (ECF No. 32-2) (noting that an individual with an upper respiratory infection two
weeks prior to onset developed TM 17 days post-vaccination) (“Riel-Romero”); E. Whittle & N.
Robertson, Transverse Myelitis After Diphtheria, Tetanus and Polio Immunisation, Brit. Med. J.
1450, 1450 (1977), filed as Ex. 23 (ECF No. 32-3) (finding onset began 6-17 days post-
vaccination) (“Whittle”); D. Karussis & P. Petrou, The Spectrum of Post-Vaccination
Inflammatory CNS Demyelinating Syndromes, 13 Autoimmunity Revs. 215, 221 (2014), filed as
Ex. 24 (ECF No. 32-4) (stating that the authors inferred vaccine causation of TM based on case
reports of temporal association).
Dr. Willer then turned to W.M.’s own medical history, arguing that the record supported
the conclusion that her symptoms most likely began on June 30, 2013—four days post-vaccination.
Tr. at 166, 175, 189, 217; Willer Second Rep. at 3; Willer Fourth Rep. at 1–2. Although this was
not discussed in detail his expert reports, 11 he relied on trial testimony about W.M.’s symptoms
(in particular, her constipation) for his determination. Tr. at 128, 164–65, 189–90. The Petitioners’
testimony had persuaded Dr. Willer that W.M.’s bleeding from severe constipation (which
purportedly began on June 30) suggested the presence of intra-abdominal pressure, 12 which
typically causes hemorrhoids to bleed. Id. at 128, 137, 139. This kind of constipation would be an
outward manifestation of the neurologic harm attributable to TM. 13 Id.Other parts of the medical record, Dr. Willer maintained, corroborated his proposed onset
date. Tr. at 140–66. He started with the July 1, 2013 pediatric visit, chronologically the next
11
Dr. Willer specifically explained that the description of constipation in the medical records did not invoke the
gravitas that Ms. Martinez explained in her testimony, which changed Dr. Willer’s assessment of the clinical picture
significantly. Tr. at 190–91, 218–19.
12
It could not, Dr. Willer believed, have been evidence of bleeding coming from the GI tract because this would cause
rapid bowel movements as opposed to constipation. Tr. at 128, 137, 139.
13
Dr. Willer did not address this issue in depth in his expert reports as the severity of W.M.’s constipation was not
revealed to him until the hearing. Tr. 127–28.
12
medical record after the June 26 vaccination. Tr. at 141; Ex. 8 at 43. Under history of present
illness, it notes that Mrs. Martinez was “complaining of [W.M.] being lethargic and hypotonic. . .
[w]ill not move legs and does not bear [weight] on legs since getting DTaP.” Tr. at 143; Ex. 8 at
43. The physical exam did not discuss an assessment of stiff legs, clonus, hypertonicity, or spastic
paraparesis—all of which Dr. Willer would expect to have manifested had onset begun closer in
time to vaccination. Id. at 146–49; Ex. 8 at 44. 14 Then there were the notes from the July 3 visit
with Dr. Park. Tr. at 152–55; Ex. 9 at 7; Willer Fourth Rep. at 2. Unlike the July 1 encounter, the
exam from this later visit clearly noted that W.M. had displayed spasticity, and otherwise
evidenced disease progression since the earlier treater event—bulwarking the conclusion that
W.M.’s course was moving toward nadir since that time. Tr. at 156–57; Willer Third Rep. at 3.
Dr. Willer rejected the possibility that W.M.’s TM onset occurred within or just after 24
hours of her receipt of the DTaP vaccine. In his opinion, “her parents would not have sat at home
with an infant who is not moving her legs for 7 days,” since that would have resulted in “Sarah
Martinez sitting at home with a . . . paraplegic infant for days before seeking medical attention . .
. .” Tr. at 208–09; Willer Third Rep. at 6; Willer Fourth Rep. at 2. When confronted (during cross-
examination) with the fact that Petitioners did seek medical attention shortly after vaccination, Dr.
Willer speculated that treaters like Dr. Stewart would not have ignored obviously-neurologic
symptoms. Tr. at 209.
More broadly, Dr. Willer admitted that he could not identify medical record evidence to
corroborate his contention that W.M. had not likely experienced TM-associated symptoms sooner
than July 1. Willer Third Rep. at 3. But he maintained nevertheless that the totality of the record
suggested an earlier onset was unlikely. Tr. at 136–66. W.M.’s behavior shortly after and in the
days following vaccination, for example, was in Dr. Willer’s view simply evidence she was
experiencing a common form of nonspecific reaction to vaccination. Id. at 136–38; DTaP Package
Insert at 1, filed as Ex. 78 on Nov. 12, 2021 (ECF No. 85-6) (stating that “systematic reactions that
occurred in [less than] 50 percent of subjects following any dose included fussiness/irritability,
inconsolable crying, and decreased activity/lethargy”). W.M.’s twin sister also initially
experienced a similar nonspecific, malaise-like reaction, featuring lethargy and fussiness. Tr. at
136–37, 150–51, 198. However, the twins’ symptoms began to diverge not long after. Id. at 137.
14
Dr. Willer also quibbled with the inclusion of “hypotonic” as a symptom the Petitioners purportedly reported to
treaters at this time. He deemed it unlikely that a parent would use such a medical term unless they had previous
experience with some kind of disabled child. Tr. at 143, 192–93. I take Dr. Willer’s point, but also find it likely that
in recording W.M.’s history, the treater who took down this note likely substituted the medical term for a more
generalized description the Petitioners had provided—and thus do not find (as Dr. Willer is seeming to suggest) that
the use of the term is an outright impossibility (even though it is in fact unlikely the Petitioners used it specifically).
13
Dr. Willer further challenged Dr. Lazari’s progress note 15 regarding W.M.’s course (which
if accurate would suggest an onset before July 1, and likely far closer to vaccination). Tr. at 161–
62, 164; Ex. 10 at 24. Dr. Lazari’s notes were, in Dr. Willer’s estimation, illogical, since they
described circumstances in which W.M. had progressed rapidly, experienced no symptoms
development for two to three day, and then underwent a downward course symptomatically
thereafter. Tr. at 163, 200–01, 220; Willer Fourth Rep. at 2. If in fact W.M. had been experiencing
TM’s progression starting on an earlier date, then she should have reached nadir sooner than what
the record actually suggested had occurred. 16 Tr. at 150, 163–64, 197, 200–05, 220; Willer Third
Rep. at 3, 6.
In addressing the above, Dr. Willer acknowledged inconsistencies between the medical
records and the Petitioners’ testimony or witness statements regarding onset and the nature of the
symptoms they observed, and admitted they had provided histories of W.M.’s health that (in some
cases) suggested an earlier onset. Tr. at 195–96; Willer Second Rep. at 3, 6; Willer Fourth Rep. at
2. But he deemed the Petitioners’ descriptions during the hearing more reliable than the medical
records made closer in time to W.M.’s injury. Tr. at 198; Willer Third Rep. at 6; Willer Fourth
Rep. at 2. And Dr. Willer otherwise considered some histories or symptoms descriptions simply
to be unlikely, for the reasons mentioned above. Tr. at 195–98; Willer Fourth Rep. at 2.
Although Dr. Willer deferred to his co-expert, Dr. Gershwin, on the larger issues of
causation, he briefly addressed whether epidemiologic evidence could discount the possibility of
causation. Tr. at 181–84; Willer Third Rep. at 4. Dr. Willer argued that studies with enough
statistical power to prove a causative relationship between vaccines and TM were not possible. Tr.
at 181; Willer First Rep. at 3; Willer Second Rep. at 3–4; Willer Third Rep. at 1. Most
epidemiologic evidence was, therefore, not useful in assessing causation with respect to a rare
disease like TM. Tr. at 181.
In the course of this testimony, Dr. Willer referenced a study that seemed to discount a
Tdap-TM relationship. R. Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-
Centered Analysis, 63 Clinical Infectious Diseases 1456, 1456–61 (2016) filed as Ex. 27 (ECF No.
32-7) (“Baxter”). Baxter found no increased risk for TM in association with any vaccine, including
the DTaP vaccine. Baxter at 1456–61. Out of 64 million vaccinations considered, Baxter’s authors
15
Besides the content of this record, Dr. Willer maintained that Dr. Lazari was merely an intern, increasing the
likelihood that the history he had provided was inaccurate. Tr. at 210–14, 221; Willer Third Rep. at 3, 6; Willer Fourth
Rep. at 2. In addition, he argued that electronic medical record-keeping often resulted in the automatic repeat of older
histories in subsequent records, and thus could maintain error over time. Id. at 212–214. While these contentions are
not without merit, I also do not find that they provide more than a speculative basis for doubting the accuracy of the
record at issue—since the Dr. Lazari notes themselves have not been established to be likely in error (whether because
of his experience or for some other reason).
During cross examination, Dr. Willer did admit that nadir can occur between 4 hours (though he corrected it was
16
more like 4 days) to 21 days following symptom onset. Tr. at 129, 132–33, 178, 203; Willer First Rep. at 4.
14
observed approximately 81 cases of acute-onset TM—but only 67 of those cases reported
vaccination within nine months prior to the onset of symptoms, one of which occurred after DTaP
(out of approximately 1.7 million doses administered for the studied subjects). Id.; Willer First
Rep. at 5; Willer Second Rep. at 4; Baxter at 1459–60. Despite the facially large number of
vaccination events at issue, Dr. Willer maintained Baxter was too underpowered to rely upon. Tr.
at 181–84; Baxter at 1456–61; Willer Second Rep. at 4. And if it were credited, Baxter would
essentially indicate that vaccines could help prevent TM, since the infections they targeted were
more likely causal of TM in most cases. Tr. at 184; Willer First Rep. at 4; Willer Second Rep. at
4. But this did not rule out the possibility of vaccine causation completely. Willer Third Rep. at 4.
Until a study could eliminate the effect of the vaccine decreasing the risk of preventing the
infection, or could reliably focus on such rare diseases, case reports remained, in Dr. Willer’s view,
the best evidence to assess causation. Tr. at 223–25.
2. Eric Gershwin, M.D., MACR, MACP – Dr. Gershwin, a board-certified
immunologist with expertise in internal medicine, rheumatic disease, allergy, and immunology,
submitted an expert report and testified for the Petitioners, offering the opinion that the DTaP
vaccine can cause TM. See generally Tr. at 228–304, 525–36. Report, dated July 27, 2020, filed
as Ex. 35 (ECF No. 64-1) (“Gershwin Rep.”).
Dr. Gershwin received his undergraduate degree from Syracuse University, his medical
degree from Stanford University, and his graduate degree from the Centre for Astrophysics and
Supercomputing. See Curriculum Vitae, filed July 27, 2020 (ECF No. 64-2) (“Gershwin CV”), at
1; Tr. at 228. He completed his internship and residency at Tufts New England Medical Center,
and two fellowships in rheumatology and allergy/immunology at the National Institutes of Health.
Gershwin CV at 2; Tr. at 229. He is currently employed as chief of the Division of Rheumatology
and Clinical Immunology and professor of medicine at University of California at Davis (“UC
Davis”). Gershwin CV at 1; Tr. at 230. Dr. Gershwin is licensed to practice medicine in California
and is board certified in allergy and immunology, rheumatology, and internal medicine. Gershwin
CV at 2; Tr. at 229. Dr. Gershwin also publishes extensively and is well researched in
epidemiological studies. Tr. at 231–33, 265. He has also seen 25 to 50 TM patients. Id. at 239. He
currently serves as the editor of the Journal of Autoimmunity, Clinical Reviews in Allergy,
Autoimmunity Reviews, and Reviews in Autoimmunity. Gershwin CV at 5.
Dr. Gershwin only briefly reviewed TM’s characteristics, stating that Dr. Willer’s
testimony adequately set forth the nature of the injury. Tr. at 238–39. He described TM as a rare
immunological or inflammatory disease, with a prevalence of one to eight per million people (even
rarer if individuals with MS or other diseases, whose presenting symptom was TM, are excluded).
Id. at 239–40; Gershwin Rep. at 2, 6. TM more frequently occurs in adults rather than children.
Tr. at 240. Dr. Gershwin spent a great deal of time deciphering the question of how one explains
an immune response that is localized to a limited area of the spinal cord, versus one that affects
the entire spinal column (longitudinally). Tr. at 239; Gershwin Rep. at 2. In Dr. Gershwin’s view,
15
there had to be something unique at the local microenvironment level for TM to occur focally—
although far more medical and scientific research would be needed to understand what might
explain this process. Tr. at 239–40, 287; Gershwin Rep. at 2–3.
W.M.’s TM, Dr. Gershwin maintained, was most likely caused by the DTaP vaccine. He
discussed several points in the medical record that he believed supported this conclusion. Tr. at
236, 268; Gershwin Rep. at 9. In particular, the record provided no evidence of a genetic
predisposition, environmental trigger, or immunological insult other than vaccination. Tr. at 237;
Gershwin Rep. at 2, 10. And as of the date of the hearing (approximately eight years after the
injury), there was no evidence of another autoimmune neurologic disease either. Tr. at 248. This
left only the vaccine as likely causal. Id.Dr. Gershwin opined that molecular mimicry was the most applicable mechanistic
explanation for how the DTaP vaccine could result in TM. Tr. at 237, 247, 277; Gershwin Rep. at
9. As he explained, a foreign antigen (specifically the amino acid sequences that comprise its
proteins), can sometimes resemble a protein structure found in the person’s body. Tr. at 243;
Gershwin Rep. at 8. Thus, in addition to provoking an immune response, antigens in a vaccine can
cause a cross-reaction in which antibodies produced in reaction to the vaccine attack self tissues
(here, the spinal cord). Tr. at 242–43, 258. This occurs in the context of inflammation (featuring a
variety of infiltrating T cells, B cells, and other monocytic population) that leads to local nerve
damage. Id. at 258, 302. Molecular mimicry ultimately involves homology between presenting
antigen and self-antigen—a process that is extremely difficult to study or observe scientifically,
no matter its reliability as a theory. Id. at 246–47, 278; Gershwin Rep. at 8; Palatnik-de-Sousa et
al., Editorial: Epitope Discovery and Synthetic Vaccine Design, 9 Frontiers in Immunology 1, 1–
2 (2018), filed as Ex. 71 (ECF No. 80-8).
Dr. Gershwin next expanded upon how the innate and adaptive immune responses impact
the mechanism of molecular mimicry, leading to an autoimmune process causal of disease like
TM. Tr. at 280; Gershwin Rep. at 7, 9. Molecular mimicry occurs as part of the adaptive immune
response (since the antibodies critical to the theorized cross-attack do not come into being until
this phase of an immune reaction), and thus is preceded by the more-immediate innate response.
Tr. at 280–81, 301. After vaccination, the innate, largely-nonspecific reaction (which is often
deemed the “humoral” phase) 17 occurs first, mediated by cytokines. Then, as the immune response
continues, shifting toward the memory-oriented adaptive response, IgM antibodies respond,
followed later by a more specific IgG response,18 in which resident immune cells within the spinal
17
Humoral, Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=23202 (last
visited Sept. 9, 2022).
18
IgM and IgG are antibodies produced in response to infection, and their titer levels can help monitor or detect
immune deficiencies. See Immunoglobulins (IgG, IgA, and IgM), Serum, Mayo Clinic Med. Laboratories,
https://www mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/8156 (last accessed August 22,
16
column and the cells that are stimulated by the antigen begin the adaptive focal attack on spinal
cord nerves and tissue. Tr. at 287–89; Gershwin Rep. at 3.
Dr. Gershwin was able to marshal little in the way of direct scientific or medical literature
evidence to support a TM-DTaP association. At most, he referenced a recent article specific to the
COVID-19 vaccine, arguing that it showed how vaccination could theoretically stimulate a
molecular mimicry-driven autoimmune process. Tr. at 255–57; E. Khan et al., Acute Transverse
Myelitis Following SARS-CoV-2 Vaccination: A Case Report and Review of the Literature, J.
Neurology 1, 1–5 (2021), filed as Ex. 65 (ECF No. 80-2) (“Khan”) (reporting a case of TM after
receipt of a COVID-19 vaccination). He otherwise emphasized case reports. Tr. at 271; Gershwin
Rep. at 5–6. Agmon-Levin, for example, gathered 37 case reports of TM following vaccination—
although only five involved diphtheria and tetanus-containing vaccines. Tr. at 271–73; Agmon-
Levin at 1200. And Dr. Gershwin also admitted that existing epidemiological evidence, such as
Baxter, did not establish any association between vaccination and TM, but (echoing Dr. Willer)
maintained that such studies, even when seemingly quite large, lacked the power to reliably detect
such a rare disease (although comparable studies supporting causation have in the Program also
been relied upon). Tr. at 272–73, 303; Gershwin Rep. at 2, 6. 19
Besides attempting to affirmatively support his opinion, Dr. Gershwin took issue with a
number of rebuttal points raised by Respondent’s primary causation expert, Dr. Moy. First, he
denied that damaging autoimmune disease processes could only occur in the context of an ongoing
infectious process (which would include substantial cell damage propagated directly through
infection that would in turn expose more self-antigens to the immune system, promoting
autoimmune cross-reactions as a result). Tr. at 528, 533–34. Dr. Gershwin argued that Dr. Moy’s
literature used to support this argument was not peer reviewed. See M. De Martino et al., Vaccines
and Autoimmunity, 26 Int’l J. of Immunopathology and Pharmacology 283, 283, 288 (2013), filed
as Ex. I-3 (ECF No. 72-4) (“De Martino”) (editorial reporting the existence of strong evidence of
the role of infection in the development of autoimmunity, and it was unlikely that vaccines alone
2022). Although Dr. Gershwin characterized IgM as an element of the body’s innate immune response (Tr. at 259,
281–82), this is somewhat imprecise. IgM is better understood as a nonspecific, fast-developing “natural” antibody
that bridges the immune response between the immediate innate and subsequent adaptive phases, with the latter being
the phase in which antibodies specific to an antigen (or, as Dr. Gershwin proposes, capable of cross-reacting with a
self-structure that mimics the antigen that caused the antibody to generate in the first place) come into being and cross-
react as part of an autoimmune process. IgM’s presence is believed to suggest an existing infection, whereas IgG
reveals a resolved, prior infection (since IgG antibodies are more specific and generate later in the immune process).
19
On cross examination, Dr. Gershwin was asked, in effect, whether this criticism could be equally applied to studies
that support causation, and in the context of equally rare diseases. See, e.g., Tr. at 274-75; L. B. Schonberger et al.,
Guillain-Barre Syndrome Following Vaccination in the National Influenza Immunization Program, United States
1976-1977, 110 Am. J. Epidemiology 105, 105 (1979), filed as Ex. I-7 (ECF No. 72-8) (“Schonberger”) (looking at
the rates of GBS after the 1977 flu season, where they looked at 45 million doses and found a correlation between an
increased incidence of GBS following vaccination). He argued in response that such a study still could not be read as
“100 percent proof” of causation, although he went on to maintain that Schonberger was more reliable than Baxter for
several reasons specific to their distinguishable methodologies. Tr. at 274–75
17
are a significant source of autoimmune diseases, although vaccines could theoretically trigger
autoimmunity). And Dr. Gershwin maintained that if cell damage alone was so critical to sparking
an autoimmune response, then burn victims should be routinely experiencing secondary
autoimmune disease. Tr. at 528.
Another argument advanced by Dr. Moy (that Dr. Gershwin briefly mentioned) was that
the blood-brain barrier would likely prevent antibodies generated in response to the DTaP vaccine
from crossing into the spinal cord. Tr. at 266–67, 528–29; Moy Rep. at 7. Dr. Gershwin argued
that Dr. Moy lacked literature support for this assertion, adding that not enough was yet known
about how the blood-brain barrier functioned to reach any conclusions about such matters, or even
if the blood-brain barrier was involved in this immune response. Tr. at 266, 290–91. Crossover
between the blood and the brain did occur, as proved in the case of fetuses in gestation. Id. at 266–
67, 290–91, 528–29.
Dr. Gershwin did not deem meaningful the fact that W.M.’s twin did not develop post-
vaccination TM. Tr. at 248–50. First, he noted that often twins were mistakenly thought to be
identical genetically, when that contention had not been medically confirmed (and thus it could
not be assumed that both twins in this case had the precisely same immune systems). Id. at 249.
Although it was noted in the medical records that W.M. and R.M. had shared a placenta, it can be
difficult to determine whether twins are identical without tissue typing. Id. at 294–95; Ex. 3 at 100.
Second, the immune responses of twins are known to be distinguishable. Tr. at 250, 267, 526–27,
532–33. Somatic mutation, recombination, and transposons make immune responses unique, so it
was hardly surprising that W.M. developed TM while her twin did not. Id. at 276, 295–97, 526–
27, 532–33.
Regarding onset, Dr. Gershwin deferred to Dr. Willer’s proposed date of July 1—but added
that onsets slower or faster 20 would still be consistent with his causation theory. Tr. at 237–38,
240–41, 259, 268, 300; Gershwin Rep. at 2, 9. A more abrupt onset (between 24-48 hours) would
suggest an innate immune mechanism’s involvement—likely a localized IgM response leading to
the chronic inflammation characteristic of TM. 21 Tr. at 237–38, 259, 281; Gershwin Rep. at 7–9;
D. M. Herrin et al., Comparison of Adaptive and Innate Immune Responses Induced by Licensed
20
Dr. Gershwin stated that it was unlikely onset would begin within 24 hours, but 24-48 hours was appropriate. Tr. at
298; Gershwin Rep. at 9.
21
Serum IgM, Dr. Gershwin maintained, could appear within a few days of symptoms following an infection. Tr. at
251–52, 259, 281–84; Gershwin Rep. at 2–3, 9. Maternal IgG is still present in newborn infants, so if an onset of TM
was found within a shorter timeframe—24 hours—those innate immune mechanisms would likely be involved.
Gershwin Rep. at 9; A. Haider, Serum IgM in Diagnosis of Infection in the Newborn, 47 Archives Disease in Childhood
382, 382–83, 392–93 (1972), filed as Ex. 37 (ECF No. 64-3) (infants start to produce their own immunoglobins as the
maternal immunoglobins start to fade); C. Herve et al., The How's and What's of Vaccine Reactogenicity, 4 Nature
Partner J. Vaccines 38, 38–40 (2019), filed as Ex. 60 (ECF No. 66-6) (noting that within hours of vaccination,
inflammatory molecules are produced in the sera, and it does not stay localized to the injection site). But Dr. Gershwin
maintained that he ultimately relied on, and accepted, the onset timeframe proposed by Dr. Willer. Tr. at 237–38.
18
Vaccines for Human Papillomavirus, 10 Hum. Vaccine Immunotherapy 3446, 3446–52 (2014),
filed as Ex. 59 (ECF No. 66-5). Since the vaccination at issue was W.M.’s third DTaP dose, the
time to mount a significant immune response would inherently be shorter. Tr. at 292; Gershwin
Rep. at 3. 22 Alternatively, onset could reasonably occur days later (up to two to three weeks). Tr.
at 259. If so, it would reveal that the IgM response had evolved to IgG antibodies. Tr. at 238, 259,
292; Gershwin Rep. at 3. He deemed Agmon-Levin (which revealed a variety of case study
instances of onset), plus another article specific to the COVID-19 vaccine, as supportive of his
overall timing opinion. Tr. at 241, 253–54; Gershwin Rep. at 9; Agmon-Levin at 1200, 1202
(standing for the fact that individuals had an onset of TM within days of vaccination); M. Khayat-
Khoel et al., Covid-mRNA Vaccination Leading to CNS Inflammation: A Case Series, J. Neurology
1, 1, 11 (2021), filed as Ex. 64 (ECF No. 80-1) (citing to neurologic symptomatology following
COVID-19 vaccinations between 1-21 days).
B. Respondent’s Experts
1. Timothy Lotze, M.D. – Dr. Lotze, a pediatric neurologist, testified on behalf
of Respondent, and submitted three expert reports. See generally Tr. at 310–445; Report, dated
Apr. 24, 2018, filed as Ex. A (ECF No. 35-1) (“Lotze First Rep.”); Report, dated July 17, 2019,
filed as Ex. C (ECF No. 49-1) (“Lotze Second Rep.”); Report, dated July 29, 2020, filed as Ex. D
(ECF No. 68-1) (“Lotze Third Rep.”). Dr. Lotze largely focused his opinion on what might
constitute W.M.’s TM onset—and whether the vaccine could be implicated in the timeframe he
favored.
Dr. Lotze obtained his bachelor's degree from Texas A&M University in College Station,
Texas, followed by his medical degree at the University of Texas, San Antonio. See Curriculum
Vitae, filed as Ex. B (ECF No. 35-2) (“Lotze CV”) at 1; Tr. at 311. Thereafter, he completed two
residencies and an internship at The Ohio State University finishing his education with a residency
in Child Neurology at Baylor College of Medicine in Waco, Texas. Lotze CV at 1; Tr. at 311. He
was then hired as a faculty member at the Baylor College of Medicine, where he is currently
employed. Lotze CV at 1; Tr. at 311. He also serves as the Director for the pediatric multiple
sclerosis clinic, fellowship program for pediatric multiple sclerosis and neuroimmunology, and
neuromuscular program at Texas Children’s Hospital. Tr. at 312. He is board certified by the
American Board of Pediatrics and the American Board of Psychiatry and Neurology, with a special
qualification in child neurology. Lotze CV at 2; Tr. at 311. He has also published close to 100
articles of peer-reviewed literature. Tr. at 314.
22
On cross examination, however, Dr. Gershwin admitted that W.M. had not experienced any adverse reaction to the
prior doses—thus reducing the reliability of any argument that she had demonstrated “rechallenge” to the dose at
issue. Tr. at 292–93; see generally Nussman v. Sec'y of Health & Hum. Servs., No. 99-500V, 2008 WL 449656, at *9
(Fed. Cl. Spec. Mstr. Jan. 31, 2008), aff'd, 83 Fed. Cl. 111 (2008) (defining challenge-rechallenge as “when a person
(1) is exposed to one antigen, (2) reacts to that antigen in a particular way, (3) is given the same antigen again, and (4)
reacts to that antigen similarly”).
19
Dr. Lotze agreed with Petitioners’ experts that W.M. was accurately diagnosed with TM.23
Tr. at 318, 387; Lotze First Rep. at 3. TM, an autoimmune disease, typically manifests with
weakness in the lower extremities plus evidence of bowel issues, and can be confirmed with MRI
studies. Id. at 318, 325, 445. Dr. Lotze also noted that TM can be classified as partial or complete,24
depending upon the degree of symptoms and severity of impairment. Id. at 319–20, 326, 378. In
infants, TM can appear as a regression in motor skills and development, change in bowel or bladder
habits, and irritability—all of which W.M.’s medical records support occurred in this case. Id. at
376, 378. W.M.’s TM initially presented with decreased tone, weakness, and movement, followed
by increased tone and movement in the affected limbs as underlying inflammation resolved.25 Id.
at 324–27, 378; Lotze Third Rep. at 2; V. L. Wolf et al., Pediatric Acute Transverse Myelitis
Overview and Differential Diagnosis, 27 J. Child Neurology 1426, 1428 (2012), filed as Ex. F
(ECF 68-3) (“Wolf”).
Dr. Lotze also noted that TM can either reflect the existence of a greater neurologic
condition or be a monophasic singular occurrence. Tr. at 445. In the context of disease-related TM
(for example, TM as a presenting symptom of some greater neurologic inflammatory injury), the
primary pathogenic driver is a specific antibody that causes the initial symptoms, whereas TM in
other contexts is attributable simply to immune system factors. Id.; Lotze First Rep. at 3. Disease-
associated TM less commonly occurs in infants, whose TM is more often deemed idiopathic. Tr.
at 319–22, 420; Lotze First Rep. at 3; Absoud et al., Pediatric Transverse Myelitis, 87 Neurology
S46, S47 (2016), filed as Ex. A-1 (ECF No. 82-1) (“Absoud”) (noting that the majority of children
with TM have an unknown cause to the disease); Wolf at 1428 (highlighting that idiopathic acute
TM can account for up to 89 percent of cases in pediatric studies). Dr. Lotze agreed that TM was
a rare disease generally, but deemed idiopathic TM relatively common in a pediatric population.
Tr. at 322–23.
23
Dr. Lotze specifically characterized W.M.’s condition as idiopathic, partial TM, of an unknown origin and unrelated
to her DTaP vaccine receipt. Tr. at 331, 420-25; D. M. Wingerchuk & B. G. Weinshenker, Acute Disseminated
Encephalomyelitis, Transverse Myelitis, and Neuromyelitis Optica, 19 Continuum 944, 953 (2013), filed as Ex. 21
(ECF No. 32-1).
24
The key difference between partial and complete TM is the degree of cord injury as well as symmetry of symptoms.
Tr. at 328–29. In partial TM, tonic spasms—which Dr. Lotze defined as episodic events involving the extension,
stiffening, and subsequent relaxing of the legs—are more common. Id. at 325, 330
25
On cross examination Dr. Lotze explained the differences between hypotonicity, hypertonicity, and spastic
paraparesis in the evolution of TM symptoms. Tr. at 378–86. He defined hypotonicity as a complete absence or
decrease from the normal amount of muscle tone, which is often described by patients as limpness or floppiness. Id.
at 378–79, 439–440. Hypertonicity is the opposite end of the spectrum, generally described as stiffness or resistance
to passive movements. Id. at 379, 382. The normal progression in TM is an evolution from hypotonicity to
hypertonicity. Id. at 379, 385. Spastic paraparesis refers to upper motor neuron findings of stiffness in the legs, often
discussed as spasticity. Id. at 383. Spastic paraparesis typically occurs in the context of hypertonicity. Id. at 383–84.
20
Although he did not act as Respondent’s primary causation expert, Dr. Lotze denied that
TM could reasonably be associated with vaccination, noting an absence of medical or scientific
literature connecting the two. Tr. at 331–33, 366–67, 370–73 (deferring to Dr. Moy on questions
involving immunology); Lotze First Rep. at 4; Lotze Second Rep. at 3; Lotze Third Rep. at 3; K.
Stratton et al., Adverse Effects of Vaccines: Evidence and Causality 542, 547–48 (Committee to
Review Adverse Effects of Vaccines et al. 2012), filed as Ex. A-2 (ECF No. 82-2) (“IOM Rep.”)
(finding insufficient evidence to assess any connection between vaccines and TM); T. Rasmussen
et al., Use of Population Based Background Rates of Disease to Assess Vaccine Safety in
Childhood and Mass Immunisation in Denmark: Nationwide Population Based Cohort Study,
British Med. J. 1, 1, 3 (2012), filed as Ex. A-3 (ECF No. 82-3) (“Rasmussen”) (looking at 2.3
million infants and 37 million persons and observing only two cases of TM for every 100,000
people occurring within 7-42 days, thus calling into question the relationship between vaccinations
and TM); Baxter at 1459–61.
Although Dr. Lotze admitted that TM’s rarity made it harder for studies to determine its
vaccine-associated risk with any degree of certainty, he maintained that studies like Rasmussen
and Baxter were scientifically reliable. Tr. at 367–70. By contrast, he criticized the probative value
of case reports as causation evidence. Tr. at 335–39. Agmon-Levin, for example, was little more
than the results of an internet search for publications addressing TM after vaccination—and its
authors did not establish that they had thoroughly reviewed each article to confirm that the alleged
instances of TM met any common or accepted diagnostic criteria, or ensured that the TM cases
were good comparables. 26 Id. at 334–35, 337; Lotze Second Rep. at 2.
Two of the specific case studies out of the 37 relevant instances identified in Agmon-Levin
were illustrative of the article’s unreliability. For example, one involved a case of TM where
Agmon-Levin reported that onset occurred within two days after rabies vaccination, but according
to Dr. Lotze the underlying case at issue revealed that onset was actually seven days 27 later. Tr. at
335–36; Lotze Third Rep. at 3; L. Label & D. Batts, Transverse Myelitis Caused by Duck Embryo
Rabies Vaccine, 39 Archives Neurology 426, 426 (1982), filed as Ex. G (ECF No. 68-4) (“Label”).
In addition, the Label patient had an infected wound—an alternative cause for TM given no weight
by Label’s authors (or Agmon-Levin’s for that matter). Tr. at 30; Label at 426. In another, the case
report’s authors expressly disclaimed confidence in whether the relevant vaccine (rubella) had
been causal, noting that the patient’s presenting TM symptoms may have been impacted by his
Dr. Lotze contrasted Agmon-Levin with Baxter, noting that Baxter’s authors used reasonable diagnostic criteria for
26
TM and rigidly applied them to the cases they considered. Tr. at 334.
27
Label actually noted that TM occurred even later (within eleven days of the rabies vaccination). Label at 426 (noting
that in 1979, “transverse myelitis developed in a 50-year-old man 11 days after passive and actives rabies
immunization.”).
21
dysplasia. 28 Tr. at 336–37; Lotze Third Rep. at 3; S. Holt et al., Diffuse Myelitis Associated with
Rubella Vaccination, 2 British Med. J. 1037, 1037–38 (1976), filed as Ex. H (ECF No. 68-5). 29
The record in this case, Dr. Lotze maintained, did not support the conclusion that the DTaP
vaccine had caused W.M.’s TM. 30 Tr. at 361. In so opining, he deemed the contemporaneous
medical records for W.M.’s treatment more accurate than subsequent witness statements. Id. at
355, 399. This was especially so since W.M. had been hospitalized at a teaching hospital, where
multiple interviewers are likely to interact with patients or their guardians. 31 Id. at 339–40. Dr.
Lotze also highlighted record evidence that he felt underscored the possibility of post-infectious
TM. In particular, W.M. had been reported to be experiencing a low-grade fever, and displayed
enlarged lymph nodes, shortly after vaccination. Id. at 341–43, 424; Lotze First Rep. at 4. Some
antecedent infections were known triggers of TM. Tr. at 357–58. At the same time, however, the
fever had occurred in the wake of vaccination, and W.M.’s parents did not recall any prior illness,
so the absence of lab testing for a potential viral cause made it difficult to corroborate this
possibility. Id. at 342–43, 424. And Dr. Lotze admitted that some of W.M.’s treaters had discussed
the possibility of a vaccine reaction, although he was ultimately unpersuaded by their reasoning.
Id. at 426–27; Ex. 10 at 24.32
Dr. Lotze next offered several comments on W.M.’s purported onset—and specifically
whether it had occurred when Dr. Willer maintained, or far closer in time to vaccination. As a
general matter, he proposed that TM’s symptoms would have evolved over the course of a two-to-
four-day timeframe. Tr. at 323–24, 386; Lotze Third Rep. at 2; Absoud at S47 (listing an onset
date between two to four days). Thus, although the range of a few hours to 28 days for reaching
28
Dysplasia is an abnormality of development. Dysplasia, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=15275&searchterm=dysplasia (last visited Sept. 9, 2022).
29
Dr. Lotze also mentioned Khan (a case report already deemed not all that probative, since it involved the COVID-
19 vaccine), finding it unlikely that TM symptoms would begin within 24 hours of vaccination. Tr. at 337–38; Khan
at 2.
30
Dr. Lotze did not, however, give much weight to the fact that the Martinez twins had not both experienced TM. It
is not uncommon for one child to present with an illness while a sibling does not. Although siblings—especially
twins—go through similar experiences, there are differences in their environmental exposures, and therefore it cannot
be assumed that they will in all cases suffer the same injuries. Tr. at 344–45.
31
Dr. Willer’s supposition that unskilled or inexperienced treaters would more likely make errors in their notes was
rejected by Dr. Lotze. In his experience, the faculty in a teaching hospital context would take steps to ensure the
accuracy of recorded facts about medical histories or treatments. Tr. at 340–41.
32
The issue of whether the blood-brain barrier might prevent an aberrant immune response (by preventing immune
cells from attacking the spinal cord) was briefly considered by Dr. Lotze. He described the blood-brain barrier as a
unique biological structure known to make it hard for certain pathogens (and even drugs) get through to the central
nervous system. Tr. at 338–39. Evidence that would establish whether the blood-brain barrier had been breached
would include neurologic problems, such as weakness in the legs, sensory disturbances, and bowel impairments if the
breach occurred in the spinal cord. Id. at 442–44.
22
nadir, as described by Drs. Willer and Gershwin, had some utility in differentiating a case of TM
from other kinds of disease processes, TM most typically would occur (in Dr. Lotze’s experience)
over a tighter timeframe of around five to six days after onset. 33 Tr. at 327–28, 356, 429, 437;
Lotze Third Rep. at 2.
The relevant medical record revealed that in W.M.’s case, TM onset had most likely
occurred within 24 hours (between June 26-27) of her vaccination, with nadir arriving four days
later—a timeframe Dr. Lotze deemed not medically reasonable for causation under the
circumstances. Tr. at 345, 353, 438; Lotze First Rep. at 3; Lotze Second Rep. at 1. To support this
aspect of his opinion, Dr. Lotze provided a detailed review of W.M.’s medical history.
First, Dr. Lotze noted the concerns expressed on the evening of June 26 (the same day as
vaccination) when W.M. was not rolling around, which raised the possibility of the manifestation
of initial symptoms. By the following morning, she showed more certain indicators of TM, such
as an inability to move her legs, then periodic stiffening on June 28, implying the beginning of
abnormal movements and tonic spasms. 34 Tr. at 345–47, 353, 359–60, 388–92, 405; Lotze First
Rep. at 3; Lotze Second Rep. at 1; Lotze Third Rep. at 1–2. Other notes from treaters corroborated
that her symptoms had likely begun the same day as vaccination. Tr. at 346–48, 350, 435–37; Ex.
8 at 43–44 (reporting on July 1 from Dr. Griffin and NP Cawley that W.M. would not bear weight
or move her legs, and that she was lethargic and hypotonic since vaccination); Ex. 8 at 54–55
(during a visit on August 1, 2013, Dr. Griffin disputed that W.M.’s symptoms were related to her
vaccination, since they occurred no more than two days after the fact); Ex. 9 at 7 (indicating under
history of present illness that after W.M. received her vaccination, her parents noticed irritability
and lack of leg movement); Ex. 10 at 24 (reporting from Dr. Lazari that W.M. was “limp after
shots,”); Ex. 10 at 62 (indicating in W.M.’s medical history taken by Dr. Strickland on July 3,
2013, that the night of W.M.’s vaccination, there was observed decreased tone in her legs, which
thereafter were not moving over the following 48 hours); Ex. 10 at 149 (finding from a neurology
visit on August 5, 2013, with Drs. Claudio-Sandoval and Carrol that W.M. developed lower
extremity weakness within a few hours of her vaccination).
On cross examination, Dr. Lotze was asked about the absence of medical record evidence
specifically from the 24-hour post-vaccination period, as well as the fact that none of the records
used the word “weakness” to describe W.M.’s symptoms. Tr. at 388–91, 394. Dr. Lotze argued in
33
Dr. Lotze specified that the timeframe to symptoms nadir is not differentiated between children and adults. Tr. at
328.
34
Dr. Lotze contended that the description of periodic stiffening on June 28, 2013, did not necessarily imply there was
hypertonicity, but actually tonic spasms, which can occur in the midst of the acute inflammatory process. Tr. at 405–
06, 418, 430; Lotze First Rep. at 2. Although the word used in the record was “stiffening” and not “spasm,” he did not
find this necessarily signified hypertonicity. Tr. at 406–11; Ex. 10 at 24. As the stiffening was described as periodic,
Dr. Lotze found it normal it was not mentioned in future visits, adding that this symptom could resolve with the
progression of TM. Tr. at 412–13, 438–40; Ex. 8 at 44.
23
response that other descriptions (i.e., limp, decreased activity levels, “will not bear weight on
legs”) were suggestive of weakness even if that precise term had not been employed. Tr. at 388–
90, 394, 397. Dr. Lotze also agreed that the DTaP package insert reports that infants may
experience post-vaccination fatigue,35 irritability, fever, and become inconsolable, and W.M.’s
sister appeared to experience some of these symptoms shortly after vaccination, but he deemed
these confounding variables. Tr. at 395–97, 431; DTaP Package Insert at 1. At bottom, the record
in his reading revealed that W.M. was unable to move her legs on June 27, 2013—a distinguishable
symptom from the post-vaccine reaction symptoms listed in the package insert. Tr. at 435; Lotze
Second Rep. at 1.
Dr. Lotze was unable to offer comment on the findings from W.M.’s urgent care visit on
June 29, 2013, since there were no medical records memorializing the event. In addition, it had
been represented that W.M. was not taken out of her car seat during this treater visit, so a
neurologic exam in such a position would make it impossible to identify features of TM. Tr. at
352–53. He also did not deem significant W.M.’s episode of constipation on June 30, 2013. While
bowel issues are seen in the context of TM, they would not present immediately, but would instead
be secondary to other symptoms and problems, like the weakness of abdominal muscles and an
inability to bear down. Id. at 351–52, 416–18.
Dr. Lotze also felt that W.M.’s subsequent history was consistent with the onset he
proposed. He highlighted Petitioners’ testimony that W.M. began straightening and stiffening her
leg following the July 1, 2013 visit, deeming this evidence that W.M. was by this point evolving
into the next stage of TM, where weakness and low tone is replaced by spasticity, increased tone,
and increased reflexes. Tr. at 348–49, 354–55. The subsequent July 3, 2013 visit to Dr. Park
resulted in additional evidence of spasticity—and then W.M.’s hospital stay ultimately confirmed
TM in a true neurologic exam. Ex. At 349–51; Ex. 9 at 7; Ex. 10 at 24. Thus, W.M.’s overall
course was consistent with TM’s usual evolution—but her onset close-in-time to vaccination did
not permit the conclusion that the vaccine had caused it. 36 Tr. at 350, 543.
2. James Moy, M.D. – Dr. Moy, an attending physician specializing in allergy
and immunology, testified on Respondent’s behalf and prepared a written report, as well. See
generally Tr. at 446–524; Report, dated October 16, 2020, filed as Ex. I (ECF No. 72-1) (“Moy
Rep.”). He sought to rebut Petitioner’s argument that the DTaP vaccine can cause TM.
35
There was much discussion at hearing regarding W.M.’s fatigue, and whether the medical records established that
W.M. was fatigued or if it was something greater. Tr. at 431–32. Relying on the medical records, Dr. Lotze pointed
out that W.M. was unable to move her legs on June 27, which is an indicator for TM rather than symptoms indicated
on the package insert, whereas the Petitioners testified that W.M. was lethargic throughout her whole body, which fits
more easily under the description of symptoms following vaccination. Id. Dr. Lotze relied on the medical records as
better evidence of the contemporaneous facts. Id. at 432.
Thus, Dr. Lotze found that Dr. Lazari’s description of timing and sequence of events was likely correct, despite Dr.
36
Willer’s objections. Tr. at 359.
24
Dr. Moy received his undergraduate degree from Northwestern University and his medical
degree from the University of Illinois College of Medicine. See Curriculum Vitae, filed as Ex. J
on October 19, 2020 (ECF No. 72-9) (“Moy CV”) at 1; Tr. at 446. Thereafter he completed his
residency in pediatrics at the University of Minnesota and a fellowship in allergy/immunology at
Rush University Medical Center. Moy CV at 1; Tr. at 446. Dr. Moy is currently an associate
professor in the Departments of Immunology/Microbiology, Pediatrics and Internal Medicine, as
well as the associate training program director for the allergy/immunology fellowship program, at
Rush University Medical Center. Moy CV at 1; Moy Rep. at 1; Tr. at 447. He is board certified by
the American Board of Pediatrics and the American Board of Allergy and Immunology. Moy CV
at 2; Tr. at 447. Dr. Moy has also authored 60 publications in peer-reviewed journals in the areas
of asthma, allergic reactions, medication side-effects and immunodeficiency diseases. Moy Rep.
at 1; Tr. at 448. Since 1990, he has evaluated and managed over 300 pediatric, adolescent, and
young adult patients with autoimmune diseases and disorders. Moy Rep. at 1.
Dr. Moy accepted W.M.’s TM diagnosis as substantiated by the medical record. Tr. at 452,
488. He also described TM’s characteristics and etiology, explaining that TM is considered an
immunological inflammatory disease, and is most often thought to be propagated by antibodies
against nerve tissues on the spinal cord. Id. at 453; Moy Rep. at 5. TM is likely triggered by an
inciting factor getting into the central nervous system. Tr. 489, 516. It most commonly occurs in a
post-infectious context, but it can also be idiopathic—as in W.M.’s case, he proposed. Id. at 453.
Dr. Moy did not accept that TM could be vaccine-caused. First, he attacked the independent
scientific evidence offered by Petitioner—primarily case reports, which he deemed poor evidence
for causality. Tr. at 455, 507; Moy Rep. at 8; T. Nissen & R. Wynn, The Clinical Case Report: A
Review of its Merits and Limitations, 7 BioMed Central Research Notes 1, 1, 4–5 (2014), filed as
Ex. I-2 (ECF No. 72-3) (mentioning the occurrences in a case report cannot be generalized from
one patient to the broader population, causality cannot be inferred from an uncontrolled
observation, and temporal association does not imply a cause-and-effect relationship). Although
Petitioners’ experts had objected that the rarity of relevant evidence on the topic required giving
case reports some consideration, Dr. Moy deemed epidemiologic evidence more probative. In
support of this argument, he pointed to GBS (also a rare disease), noting that epidemiological
studies were available to reliably establish an increased incidence of GBS following flu
vaccination. Tr. at 456–57, 493–94; Moy Rep. at 8; L. B. Schonberger et al., Guillain-Barre
Syndrome Following Vaccination in the National Influenza Immunization Program, United States
1976-1977, 110 Am. J. Epidemiology 105, 105 (1979), filed as Ex. I-7 (ECF No. 72-8)
(“Schonberger”). Here, comparable on-point studies were not supportive of the relationship, and
they merited greater weight than case reports. Tr. at 456, 509–11, 521; Moy Rep. at 8; Baxter at
1456, 1461.
25
Second, Dr. Moy questioned molecular mimicry’s value as a putative pathologic
mechanism. Molecular mimicry is thought to occur when amino acid sequences constituting virus
or bacteria antigenic proteins have homology 37 with amino acid sequences in the human body,
resulting in a putative, immune cell-driven cross-reaction when antibodies to the antigen also
attack homologous self-structures by mistake. But Dr. Moy maintained that whether molecular
mimicry will actually result in an autoimmune disease process depends on whether the homology
occurs in the context of an infection or vaccination.38 Tr. at 461, 466–67, 495; Moy Rep. at 6. In
Dr. Moy’s view, an infectious process would tend to be more all-encompassing, not only
stimulating an immune response (which vaccination seeks to “copy” to some extent) but also
causing cell damage (as the replicating infection leads to cell death), which in turn would instigate
the release of numerous self-antigens which could spark additional bases for autoimmune cross-
reaction. Tr. at 497; Moy Rep. at 6. 39 He also noted that ample evidence establishes the role of
infections in the development of autoimmune diseases—and even there, molecular mimicry is not
always understood to be the relevant biologic mechanism driving the pathologic process. Tr. at
467–68; Moy Rep. at 6.
Dr. Moy also rejected Dr. Gershwin’s contention that TM could arise as the product of an
immediate, innate immune response (rather than the secondary, more immune memory-oriented
adaptive response). Tr. at 475; Moy Rep. at 7. The innate response occurs first in reaction to a
foreign antigen, and attempts to control an infection, leading to common symptoms of malaise
(fever and muscle ache), whereas the adaptive immune system takes longer to ramp up, with B
cells making antibodies and T cells killing viruses. Tr. at 461–62, 466. The process of molecular
mimicry occurs during the adaptive response. Id. at 465, 483. The harm to the spinal cord caused
by TM would more likely be the product of an auto-immune cross-reaction occurring during the
latter, adaptive response, Dr. Moy argued.
37
Homology was defined as an identity between a portion of a protein from one organism and another. Tr. at 468;
Moy Rep. at 6. But Dr. Moy maintained that homology alone is not enough to trigger molecular mimicry, because
linear amino acid sequences are actually very common. Tr. at 468–69, 471. Otherwise, autoimmune diseases would
be far more prevalent. Id. at 470.
38
Of the potential reasons for these differences, vaccines—unlike infections—do not cause cell damage, which would
release many more antigens from the human cells, increasing the likelihood of autoimmune reactions. Tr. at 497; Moy
Rep. at 6.
39
In support of this contention, Dr. Moy referenced De Martino—an editorial from a scientific publication arguing
that although vaccines could theoretically trigger autoimmunity, there is no evidence that they tend to do so, given
how different vaccination is from a wild infectious process. Tr. at 467–68, 514; Moy Rep. at 6; De Martino at 288.
When cross-examined about the strength of the editorial’s contentions, Dr. Moy proposed (somewhat unpersuasively)
that editorials should carry more weight than case reports, since the former are not based solely on a single observed
temporal instance of post-vaccination disease. Tr. at 522. While I deem Dr. Moy’s argument on this topic to have
some persuasive value—vaccination is inherently and contextually distinguishable from an infectious milieu—I also
agree with Petitioners that an editorial item lacks the same probative value as an actual study, and therefore overall, I
do not give these contentions the weight Respondent urges.
26
Another factor that limited the likelihood of vaccine-induced TM in Dr. Moy’s view was
the blood-brain barrier, which Dr. Moy noted can impede the crossing-over of immune cells into
the central nervous system (the “CNS”). Tr. at 472, 518. The blood-brain barrier is semi-
permeable, permitting only some substances to easily cross. Id. at 471; Moy Rep. at 7. Dr.
Gershwin’s theory was that the vaccine’s antigen-presenting cells were carried into the CNS, and
hence crossed the blood-brain barrier—yet, Dr. Moy maintained, there was no literature offered in
this case establishing how immune cells can get into the CNS in the absence of an actual “break”
in the blood-brain barrier. Tr. at 473, 475-76, 518. Thus, this fact also weighed against the
likelihood of vaccination causing TM. Id.
Dr. Moy then raised three issues relevant to the medical record that he deemed strengthened
his conclusion that vaccination did not likely cause W.M.’s TM. Moy Rep. at 8–9. First, Dr. Moy
found significant that W.M.’s sister had not also developed TM post-vaccination. Tr. at 478. Since
the twins likely shared the same genetics, their immune responses to the vaccine should have been
identical, but were not, undermining the possibility that the vaccine itself was the causal factor. Id.
He accepted the possibility that external environmental factors, or outright genetic mutation, could
result in distinguishable immune systems between the two, but deemed the chance of mutation in
this case low, given the twins’ young ages. Id. at 476–78, 501, 523–24; Moy Rep. at 8. Indeed, Dr.
Gershwin had assumed that the twins’ initial vaccine-reactive malaise, which they both
experienced, was common, underscoring why both should have also been harmed by the vaccine
in the same way if it had the capacity to trigger TM. Tr. at 178–79.
Second, Dr. Moy took note of W.M.’s vaccination history. W.M. had received prior DTaP
doses with no reaction, making it unlikely that the dose at issue had triggered autoimmunity where
prior doses had not. Id. at 481, 499–500; Moy Rep. at 8. Finally, Dr. Moy noted a lack of evidence
that W.M. had an infection or illness prior to vaccination. Although this fact could rebut the
argument that an infection better explained W.M.’s TM (and indeed, Petitioners argue that no
identified alternative cause exists), Dr. Moy found significant something else about a preexisting
infection: that it might have had the secondary impact of causing the kind of blood-brain barrier
weakening or breach that would be necessary to allow the antigen of antibodies to get across the
CNS. 40 Tr. at 481–83, 490–92; Moy Rep. at 9. Since no infection that could have acted in this way
had been identified, a blood-brain barrier breach was rendered more unlikely.
Dr. Moy concluded with some discussion of onset, largely relying on Dr. Lotze’s opinion
but providing some testimony relevant to the timeframes implicated in the two immune response
arms. Tr. at 492. The innate response, he explained, occurs immediately and could last hours to a
few days, whereas the adaptive response (measured by IgM at first) occurs within a few days and
can last for 7-10 days, with IgG levels rising around 5-7 days later, and peaking around 3-4 weeks.
40
Dr. Moy also noted, however, that it was possible to have an immune response to a pathogen that did not manifest
in symptoms, similar to those unknowingly infected with COVID. Tr. at 518–19.
27
Id. at 462–63, 483, 486–87. A second exposure to an antigen would result in a somewhat faster
adaptive immune response due to memory B cells, with the fastest response one day for IgM and
4-5 days for IgG. Id. at 484, 488.
Because of the foregoing (and regardless of literal onset date), it was implausible to Dr.
Moy that the DTaP vaccine had caused W.M.’s TM given the facts in this case. Tr. at 503; Moy
Rep. at 9. Even if the Tdap vaccine could be causal, the shorter onset favored by Dr. Lotze would
require TM to spring up a day or two post-vaccination, despite an absence of independent evidence
demonstrating that the innate response drives the inflammation characteristic of TM. Moy Rep. at
7. The onset favored by Petitioners (several days after vaccination) was no better, since the
adaptive response that more likely is associated with TM would only then be starting to occur, and
would also require certain secondary steps—crossing the blood-brain barrier, local production of
IgG in the spinal cord, etc. Id. In effect, onset should have occurred later than what Petitioners
alleged, given what was known about TM and the timeframes for the adaptive immune process.
III. Procedural History
Petitioners initiated this case in 2016, and the matter was at first assigned to another special
master. ECF No. 1. Until late 2016, Petitioners continued to file medical records, and the case was
in this period reassigned to another special master. Respondent then filed a Rule 4(c) Report on
December 19, 2016, contesting Petitioners’ right to compensation. ECF No. 18. The case was
subsequently transferred to me before being reassigned (again) to another special master. ECF
Nos. 26, 29. The parties began filing of expert reports, completing the process by the spring of
2020. The matter was finally transferred back to me on January 26, 2021, and I held a status
conference with the parties, setting a two-day hearing to be held on November 16-17, 2021. ECF
No. 77. The trial occurred as scheduled, and the parties submitted post hearing briefs on March
16, 2022. Petitioners’ Post Trial Brief, dated March 16, 2022 (ECF No. 97) (“Post-Trial Br.”);
Respondent’s Post Trial Brief, dated March 16, 2022 (ECF No. 98). The claim is now ripe for
resolution.
IV. Applicable Legal Standards
A. Petitioners’ Overall Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.
28
Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).41
In this case, Petitioners do not assert a Table claim.
For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344,
1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen, 418 F.3d at 1278: “(1) a medical theory causally connecting the vaccination and
the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason
for the injury; and (3) a showing of proximate temporal relationship between vaccination and
injury.”
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must
only be “legally probable, not medically or scientifically certain.” Id. at 549.
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not empowered by
41
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,
2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
29
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras, 121 Fed.
Cl. at 245.
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. 42 See Boatmon v. Sec’y of Health &
Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum.
Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that
simply identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her
burden of proof” (citing Moberly, 592 F.3d at 1322)). And petitioners always have the ultimate
burden of establishing their overall Vaccine Act claim with preponderant evidence. W.C. v. Sec’y
of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted); Tarsell v.
United States, 133 Fed. Cl. 782, 793 (2017) (noting that Moberly “addresses the petitioner’s overall
burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
Medical records and statements of a treating physician, however, do not per se bind the
special master to adopt the conclusions of such an individual, even if they must be considered and
carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment,
test result, report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y
of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing . . . that mandates
that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and
cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the
42
Because Petitioners have advanced the argument (primarily in their post-trial brief) that the actual prong one
standard is in fact plausibility, I briefly discuss the merits of that contention in my prong one analysis below.
30
opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their
suppositions or bases. The views of treating physicians should be weighed against other, contrary
evidence also present in the record—including conflicting opinions among such individuals.
Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious
for special master to weigh competing treating physicians’ conclusions against each other), aff’d,
698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must align with the theory of how the relevant vaccine can
cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.
Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,
2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. denied (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Legal Standards Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [ ] relevant medical and scientific evidence contained in the record,” including
“any diagnosis, conclusion, medical judgment, or autopsy or coroner's report which is contained
in the record regarding the nature, causation, and aggravation of the petitioner's illness, disability,
injury, condition, or death,” as well as the “results of any diagnostic or evaluative test which are
contained in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special
master is then required to weigh the evidence presented, including contemporaneous medical
records and testimony. See Burns v. Sec'y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir.
1993) (determining that it is within the special master's discretion to determine whether to afford
greater weight to contemporaneous medical records than to other evidence, such as oral testimony
surrounding the events in question that was given at a later date, provided that such determination
is evidenced by a rational determination).
As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as
trustworthy evidence.” Cucuras, 993 F.2d at 1528; Doe/70 v. Sec'y of Health & Hum. Servs., 95
31
Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner's testimony and his
contemporaneous medical records, the special master's decision to rely on petitioner's medical
records was rational and consistent with applicable law”), aff'd, Rickett v. Sec'y of Health & Hum.
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked
propositions explains why such records deserve some weight: (i) sick people visit medical
professionals; (ii) sick people attempt to honestly report their health problems to those
professionals; and (iii) medical professionals record what they are told or observe when examining
their patients in as accurate a manner as possible, so that they are aware of enough relevant facts
to make appropriate treatment decisions. Sanchez v. Sec'y of Health & Hum. Servs., No. 11–685V,
2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Hum.
Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993 F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to
conclude that petitioners would fail to accurately report the onset of their daughter's symptoms”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are often found to be deserving of greater evidentiary weight than oral testimony—especially
where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also
Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d
1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States
v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral
testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).
However, the Federal Circuit has also noted that there is no formal “presumption” that
records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which
compelling oral or written testimony (provided in the form of an affidavit or declaration) may be
more persuasive than written records, such as where records are deemed to be incomplete or
inaccurate. Campbell v. Sec'y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any
norm based upon common sense and experience, this rule should not be treated as an absolute and
must yield where the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL
6117475, at *19 (“[w]ritten records which are, themselves, inconsistent, should be accorded less
deference than those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)).
Ultimately, a determination regarding a witness's credibility is needed when determining the
weight that such testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec'y of
Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
32
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec'y of Health & Hum. Servs.,
No. 90–2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In determining the
accuracy and completeness of medical records, the Court of Federal Claims has listed four possible
explanations for inconsistencies between contemporaneously created medical records and later
testimony: (1) a person's failure to recount to the medical professional everything that happened
during the relevant time period; (2) the medical professional's failure to document everything
reported to her or him; (3) a person's faulty recollection of the events when presenting testimony;
or (4) a person's purposeful recounting of symptoms that did not exist. La Londe v. Sec'y of Health
& Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334 (Fed. Cir. 2014). In making
a determination regarding whether to afford greater weight to contemporaneous medical records
or other evidence, such as testimony at hearing, there must be evidence that this decision was the
result of a rational determination. Burns, 3 F.3d at 417.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,
1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the
factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.
Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).
Under Daubert, the factors for analyzing the reliability of testimony are:
(1) whether a theory or technique can be (and has been) tested; (2) whether the
theory or technique has been subjected to peer review and publication; (3) whether
there is a known or potential rate of error and whether there are standards for
controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.
Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).
In the Vaccine Program the Daubert factors play a slightly different role than they do when
applied in other federal judicial settings, like the district courts. Typically, Daubert factors are
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are
used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &
Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
33
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts in order to rebut a petitioner’s case.
Where both sides offer expert testimony, a special master's decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert's conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec'y of Health & Hum.
Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert's credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court
has unambiguously explained that special masters are expected to consider the credibility of expert
witnesses in evaluating petitions for compensation under the Vaccine Act”).
D. Consideration of Medical Literature
Both parties filed numerous items of medical and scientific literature in this case, but not
all such items factor into the outcome of this decision. While I have reviewed all the medical
literature submitted in this case, I discuss only those articles that are most relevant to my
determination and/or are central to Petitioner’s case—just as I have not exhaustively discussed
every individual medical record filed. Moriarty v. Sec’y of Health & Hum. Servs., No. 2015–5072,
2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally presume that a special master
considered the relevant record evidence even though he does not explicitly reference such evidence
in his decision”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F.
App’x 875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does not lead to—
and likely undermines—the conclusion that it was not considered”).
34
ANALYSIS
I. TM as Vaccine Injury in Prior Program Decisions
The experts on both sides agreed that W.M. was properly diagnosed with TM, and this
diagnosis finds ample record substantiation. Thus, resolution of this claim does not require
determining the injury at issue.
Claims alleging TM following vaccination are common in the Vaccine Program. Many
involve TM after receipt of the Hepatitis B vaccine. See, e.g., Pearson v. Sec’y of Health & Hum.
Servs., No. 03-2751V, 2008 WL 5093378, at *3 (Fed. Cl. Spec. Mstr. Nov. 6, 2008); Stevens v.
Sec’y of Health & Hum. Servs., No. 99-594V, 2006 WL 659525, at *1, 8 (Fed. Cl. Spec. Mstr.
Feb. 24, 2006). In Pearson, the special master found in the petitioner’s favor, but did not identify
the proposed causal theory at all, relying on the prior ruling from Stevens. Pearson, 2008 WL
5093378, at *3. And in Stevens, the petitioner successfully established causation on a theory of
challenge/rechallenge after she had an adverse reaction to two doses of the Hepatitis B vaccine
and subsequently developed TM. Stevens, 2006 WL 659525, at *1. As already noted, however, no
such challenge/rechallenge evidence has been offered in this matter.
I also have granted entitlement in a case where an infant developed TM after receipt of the
Hepatitis B vaccine. McGrail v. Sec'y of Health & Hum. Servs., No. 17-926V, 2021 WL 1728706,
at *25 (Fed. Cl. Spec. Mstr. Apr. 23, 2021). The petitioners in that case, as here, argued that
molecular mimicry was the applicable mechanism. McGrail, 2021 WL 1728706, at *9, 11.
However, I noted in McGrail that the petitioners’ causation showing was not particularly robust,
and thus an alternative outcome was possible in other cases, depending on the mix of evidence. Id.
at *26. I also found that symptoms onset of 77 hours, or a little more than three days post-
vaccination, was a medically appropriate timeframe. Id. at *27. While McGrail has some parallels
to the present matter, it involved both a different vaccine and distinguishable onset—factors highly
relevant to the outcome herein.
I have identified fewer cases involving TM after receipt of a Tdap/DTaP vaccine. 43 And
their success or failure can turn on the timing of onset, as opposed to the causal capacity of the
vaccine generally. 44
43
Claims alleging TM following a rotavirus vaccine alone are quite uncommon. Rather, this vaccine is usually one of
several received at the same time (and such cases when successful have typically been the result of settlement rather
than reasoned decision). See, e.g., Davis v. Sec'y of Health & Hum. Servs., No. 19-410V, 2022 WL 1469328 (Fed. Cl.
Spec. Mstr. Apr. 19, 2022); Martin v. Sec'y of Health & Hum. Servs., No. 16-318V, 2017 WL 6522406 (Fed. Cl. Spec.
Mstr. Oct. 23, 2017); Nichols v. Sec'y of Health & Hum. Servs., No. 11-417V, 2013 WL 599104, at *1 (Fed. Cl. Spec.
Mstr. Jan. 22, 2013). However, because Petitioners’ experts did not focus on rotavirus as the most likely causal
vaccine, I do not evaluate it extensively herein.
44
Petitioners’ filings in this case highlight the fact that I recently issued (on remand, and after denying entitlement
due to a failure to meet the first Althen prong) a favorable entitlement ruling for an adult petitioner alleging TM due
35
For example (and contrary to McGrail), I denied compensation in another case involving
pediatric TM. Palattao v. Sec’y of Health & Hum. Servs., No. 13-591V, 2019 WL 989380 (Fed.
Cl. Spec. Mstr. Feb. 4, 2019). There, petitioners alleged that several vaccines—including DTaP—
caused an infant’s TM after an onset between 30-36 hours post-vaccination. I found, however, that
the onset date was inconsistent with the proposed causation theory, occurring too close in time to
vaccination for an adaptive immune response (which most likely characterized TM’s pathogenesis)
to have occurred. Palattao, 2019 WL 989380, at *34. I also determined that the Palattao
petitioners had failed to establish that TM could be mediated by a cytokine-driven process
occurring a part of the initial, innate immune response. Id. at *36. Petitioners’ experts in Palattao
had expressly rejected the theory of molecular mimicry (which was relied upon in this claim),
proposing instead that the child’s TM reflected an aberrant innate response driven by cytokines.
Id. at *8. Although Palattao is clearly distinguishable in important respects, its findings about what
is a reasonable onset timeframe for TM has relevance to this case, as well.
By contrast, timeframes for post-vaccination TM onset have often been deemed acceptable
when the period of time between onset and vaccination exceeded a week. See, e.g., I.J. v. Sec'y of
Health & Hum. Servs., No. 16-864V, 2021 WL 1232733, at *34 (Fed. Cl. Spec. Mstr. Jan. 4, 2021),
mot. for review granted on other grounds, 155 Fed. Cl. 20 (2021) (TM beginning approximately
two weeks after receipt of the Tdap vaccine); Schmidt v. Sec'y of Health & Hum. Servs., No. 07-
020V, 2009 WL 5196169, at *14 (Fed. Cl. Spec. Mstr. Dec. 17, 2009) (onset of TM one month
after receiving the flu vaccine fell within a medically acceptable timeframe). These determinations
are thus consistent with the view that a pathologic process driven by the adaptive response will not
occur too close-in-time to vaccination.
to the Tdap vaccine. I.J. v. Sec'y of Health & Hum. Servs., No. 16-864V, 2022 WL 277555, at *5–6 (Fed. Cl. Spec.
Mstr. Jan. 4, 2022). But that petitioner prevailed mainly because I deemed the first Althen prong satisfied under the
evidentiary standard of mere plausibility that had been embraced in that case by the Court’s remand order. I.J. is
otherwise not controlling of the outcome in this case, since it does not reflect a Federal Circuit determination (although,
as discussed below, I do not find that the evidentiary standard it embraced was an accurate reflection of controlling
precedent on the first prong).
36
II. Petitioners Have Not Carried Their Burden of Proof 45
A. Althen Prong Three
The experts disagreed on the precise onset date, with Drs. Willer and Gershwin favoring a
four-day post-vaccination onset (beginning on June 30, 2013), while Drs. Lotze and Moy proposed
an onset occurring within 24 hours (beginning on the June 26 vaccination date). The record best
supports Respondent’s position, which is too close in time to have been caused by the vaccination
(assuming the DTaP vaccine could cause TM) under the “medically acceptable” standard applied
to timeframe issues in the Vaccine Program.
Numerous medical records from different visits substantiate that onset began within 24
hours of vaccination, or not appreciably long thereafter. Evidence of onset the morning after
vaccination, or sometime that day, is found in records prepared by many treaters, including NP
Cawley and Drs. Griffin, Lazari, Strickland, Claudio-Sandoval and Carrol. Ex. 8 at 43–44, 54–55;
Ex. 9 at 7; Ex. 10 at 24, 62, 149. These records preponderantly establish clear concern for W.M.’s
lack of leg movement as soon as the day of vaccination. In particular, the July 1, 2013, and July 3,
2013 records (the earliest treatment evidence in this case after the vaccination date) refer to leg
issues “since” vaccination, or having “progressed” up to July 1—all of which reasonably suggests
an onset before July 1. Ex. 8 at 43; Ex 9 at 7.
Then, subsequent records from W.M.’s hospitalization memorialize statements by the
Petitioners (in recounting W.M.’s history) that they had observed leg-related symptoms by the
morning of June 27—and these were the symptoms that later impelled them to seek treatment for
W.M. (as opposed to her twin, whose initial vaccine malaise improved). See Ex. 10 at 24, 448. The
record by itself is thus consistent in reporting neurologic-like symptoms prior to June 30—and
closer to the morning of June 27. While these presenting issues cannot be neatly separated from
the post-vaccination malaise that both twins appear to have experienced, it can be determined on
this record that by June 27, 2013, W.M.’s leg issues had more likely than not manifested, and were
notably distinguishable—enough to prompt Petitioners to seek care for W.M., and to express
concerns that went beyond the fact that she was taking longer to recover from malaise than her
twin.
Petitioners contest the accuracy of these records, or (via Dr. Willer) maintain that they are
in some cases untrustworthy because a less-experienced treater prepared them (an argument I deem
largely speculative). But they ultimately have not provided a persuasive reason to discount the
45
I address the Althen prongs herein in order of their significance to my Decision, rather than in the order they are
typically presented. I also include no detailed discussion of the second, “did cause” prong. My determination that
W.M.’s onset was not medically acceptable for causation makes it impossible to find the vaccine was causal, even if
there is some record evidence Petitioners might point to in support of the second prong, like treater speculation about
vaccine causality.
37
overall contemporaneous record, which consistently points to an onset prior to June 30. Petitioners
simply cannot simply gainsay these contemporaneous records, given the consistent picture they
paint, and have provided no compelling reason to find their subsequent testimony or statements
more credible. Petitioners also refer to the urgent care car seat “exam” with Dr. Stewart on June
29, arguing that it was more routine than reflective of concern about leg issues/spasticity. But not
only was no record ever filed to document it (despite due effort by the parties), but this appeared
to be a quick exam that cannot be deemed as substantively comparable to the full medical exams
performed thereafter by W.M.’s other treaters. Indeed, the fact itself of this incident is somewhat
supportive of the conclusion that by this time W.M.’s symptoms were alarming enough to seek
additional treatment, thus bulwarking the inference that her neurologic symptoms had begun
before early July.
I also do not give great weight to the argument that W.M.’s constipation was the presenting
symptom of her TM on June 30. It simply cannot be concluded from the record that this was what
drove Petitioners to bring W.M. to see treaters on July 1 or 3 (let alone why she was later
hospitalized). Moreover, although constipation (which was more thoroughly discussed during the
hearing than in the medical records or expert reports) was noted on a few medical records, none of
the treaters attributed constipation to the beginning of her TM symptoms. Dr. Willer’s arguments
to the contrary are unpersuasive, while Dr. Lotze credibly explained how constipation would more
likely reflect the existence of other neurologic issues, and thus have a somewhat (although not
completely) secondary character.
Finally, I did not find compelling Petitioners’ arguments attempting to pinpoint when W.M.
displayed hypertonicity versus hypotonicity, and/or what stage she had reached in her disease
process as of July 1. Again, the medical histories that the contemporaneous records contain are
reliable, and they consistently point to an onset earlier than July 1. Dr. Willer’s contention that a
timeframe of onset on June 27 was incompatible with W.M.’s progression was unpersuasive—
rather, the record is overall consistent with an onset a few days before Petitioners took W.M. to
Affinity Clinic on July 1, 2013 (three days post-onset), with hospitalization by July 3. Dr. Lotze
reasonably and credibly explained how this course would fit TM’s progression to nadir.
Given my finding that onset likely occurred within a day of vaccination, I cannot find that
Petitioners have successfully established that W.M.’s TM began in a medically acceptable
timeframe, given their causation theory. 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 exposure (here, from the Tdap vaccine), a
relatively short onset timeframe is simply not medically acceptable. See, e.g., Palattao, 2019 WL
989380 at *34 (finding that a 30-36-hour period is too soon to be medically acceptable); Mosley
v. Sec’y of Health & Human Servs., No. 08-724V, 2015 WL 2354316, at *19 (Fed. Cl. Spec. Mstr.
Apr. 27, 2015) (“onset of TM one day after tetanus vaccine is too soon to support vaccine
38
causation”); Jagoe v. Sec’y of Health & Human Servs., No. 08-678V, 2012 WL 13036265, at *28
(Fed. Cl. Spec. Mstr. Aug. 3, 2012) (determining that TM symptoms occurring within 24 hours of
vaccination were not a medically appropriate timeframe for vaccine causation); Crosby v. Sec’y of
Health & Human Servs., No. 08-799V, 2012 WL 13036266, at *38–39 (Fed. Cl. Spec. Mstr. June
20, 2012) (finding similar to Jagoe that 24 hours is too soon to infer vaccine causation for an injury
of TM). In fact, an onset occurring within a day of vaccination points to an adaptive process that
likely began before vaccination, since it would take several days from an inciting event (if that
were the cause of TM—not something that can be reasonably assumed) for the antibodies that
would drive TM to generate.
Dr. Willer did not successfully rebut the above. Rather, he unpersuasively cited to case
reports involving pediatric cases of TM—but with onset timeframes consistently longer than what
W.M. experienced. See, e.g., Label at 426 (observing that onset began 11 days after rabies
vaccination); Riel-Romero at 688–91 (mentioning that onset developed 17 days post-vaccination);
Whittle at 1450 (noting that onset began 6-17 days post-vaccination). Dr. Gershwin mostly
deferred to Dr. Willer’s proposed onset and timeframe, and did not otherwise persuasively
establish that an earlier timeframe was also medically acceptable, even if he proposed some
scientifically plausible arguments for an innate-driven disease process. Dr. Moy, by contrast,
accurately observed in providing his expert opinion that even if the mechanism at issue could be
shown to be innate in nature (and hence cytokine-driven—contrary to Petitioners’ causation
theory), the process leading to clinical symptoms manifestation would still take more than 24 hours
to “get up to speed” before symptoms would manifest. Moy Rep. at 7, 9.
Ultimately, Petitioners’ arguments regarding the onset of W.M.’s TM symptoms are at
odds with the evidence in this case, including their own consistent reporting to medical providers,
as documented in the contemporaneous medical records. Their proposed timeline is not
substantiated by the record. See, e.g., Ex. 8 at 43–44, 54–55; Ex. 9 at 7; Ex. 10 at 24, 62, 149.
Because a short timeframe for onset is not possible under Petitioner’s causation theory, the onset
that the record establishes cannot be deemed to have occurred in a medically acceptable timeframe
after vaccination.
B. Althen Prong One
Although Petitioners assert that they have provided preponderant proof that meets each of
the Althen prongs, they also maintain that a plausibility standard I applied in a different case is
applicable to the first prong. See Post-Trial Br. at 59–62, 80, 105–06; I.J. v. Sec'y of Health &
Hum. Servs., No. 16-864V, 2022 WL 277555, at *5–6 (Fed. Cl. Spec. Mstr. Jan. 4, 2022). I utilized
that lower standard in I.J. because that petitioner had successfully appealed my initial decision,
and I was obliged on remand to follow the legal determinations made by the Court of Federal
39
Claims. 46 Remand did not, however, come from the Federal Circuit, 47 and thus it does not control
how I apply the legal standard herein.
More significantly, there is good reason not to adopt a plausibility standard of proof to the
first Althen prong in any case, since controlling Federal Circuit decisions do not stand for that
supposition. Boatmon, 941 F.3d at 1359; LaLonde, 746 F.3d at 1339; see also Moberly, 592 F.3d
at 1322. As the Circuit pointedly noted in Moberly, “proof of causation by . . . something closer to
proof of a “plausible” or “possible” causal link between the vaccine and the injury . . . is not the
statutory standard” (emphasis added). Nothing the Circuit has decided in the intervening ten to
fifteen years suggests that this preponderant requirement has been abandoned. Boatmon, 941 F.3d
at 1360 (“[w]e have 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”).48 Thus,
I shall not apply a standard of mere plausibility in evaluating if Petitioners have successfully met
the first prong’s burden of proof.
Dr. Gershwin proposed a theory of molecular mimicry, arguing that the DTaP vaccine’s
antigens could mimic homologous sequences on the spinal cord resulting in cross-reactivity. But
although he reliably described how this mechanism might apply to other autoimmune diseases or
vaccines, he did not offer sufficient comparable evidence for the relevant context. As Dr. Moy
noted, despite the prevalence of linear sequence homologies, autoimmunity does not occur in most
cases—and if homology alone was enough, then autoimmunity would be much more common. Tr.
at 468–69, 471. Thus (and as I have noted in many prior cases) the general reliability of molecular
mimicry as a theoretic explanation for how some kinds of autoimmune conditions occur
pathologically does not mean it applies in every single vaccine injury case. See, e.g., McKown v.
Sec'y of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr.
July 15, 2019) (citing Devonshire v. Sec'y of Health & Hum. Servs., No. 99-031V, 2006 WL
2970418, at *15 (Fed. Cl. Spec. Mstr. Sept. 2006) (“[b]ut merely chanting the magic words
‘molecular mimicry’ in a Vaccine Act case does not render a causation theory scientifically
reliable, absent additional evidence specifically tying the mechanism to the injury and/or vaccine
in question”) (emphasis in original), mot. for review den’d, 76 Fed. Cl. 452 (2007)).
46
In I.J., I originally denied compensation after finding that the petitioner had offered insufficient preponderant
evidence to establish that the Tdap vaccine can cause TM. I.J., 2021 WL 1232733, at *30–34. However, the Court of
Federal Claims granted review and subsequently vacated my prior determination, finding, among other things, that
the plausibility standard should be applied. I.J., 155 Fed. Cl. at 43. On remand, I applied the law to the claim as
directed. I.J., 2022 WL 277555, at *4 n. 5.
47
Petitioners erroneously assert the contrary in their Post-Trial Brief. See Post-Trial Br. at 59 (“[t]he Federal Circuit
stated in [I.J.] that it did not reject outright the “plausibility” standard for a medical theory”).
48
The Court in I.J., by contrast, reasoned that a recent Circuit court decision had rejected Boatmon on the question of
the standard applicable to the first prong. I explained in my remand decision that this was an unpersuasive and likely
incorrect reading of the relevant decisions, although I applied the law as directed by the Court on remand. I.J., 2022
WL 277555, at *4 n. 5.
40
Accordingly, the fact that this mechanism has been successfully invoked in other cases
involving pediatric TM after receipt of different vaccines does not mean the same is true herein,
no matter how reliable the theory is in a general sense. 49 McGrail, 2021 WL 1728706, at *25.
Indeed, even cases involving TM and Tdap/DTaP referenced by Petitioners do not provide much
in the way of persuasive guidance. Post-Trial Brief at 59; see also Raymo v. Sec'y of Health &
Hum. Servs., No. 11-654V, 2014 WL 1092274, at *21 (Fed. Cl. Spec. Mstr. Apr. 23, 2021). Raymo
does not explain at all how components of the DTaP vaccine can cause TM, and was also decided
before the advent of some relevant epidemiologic proof. Compare Post-Trial Br. at 59, citing
Raymo, 2014 WL 1092274, at 20-21 (“[t]here are no epidemiologic studies of the causes of ATM,
and thus no studies linking or refuting a link between the condition and vaccinations”) with Baxter
(published in 2016—two years after Raymo).
Otherwise, Dr. Gershwin marshalled limited reliable scientific or medical proof to make
the kind of necessary connections between the DTaP vaccine and TM. He instead relied on case
reports. But this kind of evidence as a general rule does not receive great weight when assessing
causation. See, e.g., Campbell v. Sec'y of Health & Hum. Servs., 97 Fed. Cl. 650, 668 (2011)
(“[c]ase reports do not purport to establish causation definitively, and this deficiency does indeed
reduce their evidentiary value ... [but] the fact that case reports can by their nature only present
indicia of causation does not deprive them of all evidentiary weight.”). And some of the items he
offered have been specifically deemed unpersuasive before. Agmon-Levin, for example, has
received criticism in the past for only identifying a small number of instances linking TM to
vaccination—despite having reviewed years of published data in the search for such evidence. See
Pearson v. Sec'y of Health & Hum. Servs., No. 16-9V, 2019 WL 3852633, at *14 (Fed. Cl Spec.
Mstr. July 31, 2019) (giving limited weight to Agmon-Levin in a case alleging that flu vaccine
caused TM, since Agmon-Levin referenced only two post-flu vaccine TM cases—based on a
review of 39 years of published case reports) (emphasis in original). Others involved the COVID
vaccine, which functions in a completely different manner,50 and thus provided a poor comparison.
Khan at 1–5; Khayat at 11.
49
Indeed, Program findings specific to the Hepatitis B vaccine strengthen the conclusion that it can cause
demyelinating conditions like TM. On October 13-14, 2004, former Special Master (and later Chief Judge of the Court
of Federal Claims) Margaret Sweeney held a hearing—which became known as the “Hepatitis B – Neurological
Demyelinating Omnibus Proceeding”—to determine whether a causal association exists between the Hepatitis B
vaccine and several demyelinating illnesses (multiple sclerosis, TM, chronic inflammatory demyelinating
polyneuropathy, and GBS) alleged in four paradigm cases. Stevens, 2006 WL 659525; Werderitsh v. Sec'y of Dept. of
Health & Hum. Servs., No. 99-638V, 2006 WL 1672884 (Fed. Cl. Spec. Mstr. May 26, 2006); Peugh v. Sec'y of Dept.
of Health & Hum. Servs., No. 99-319V, 2007 WL 1531666 (Fed. Cl. Spec. Mstr. May 8, 2007); Gilbert v. Sec'y of
Dept. of Health & Hum. Servs., No. 04-455V, 2006 WL 1006612 (Fed. Cl. Spec. Mstr. Mar. 30, 2006). These cases
were then reassigned to former Special Master Laura Millman, who found that in all four cases, the Hepatitis B vaccine
was causal. Peugh, 2007 WL 1006612, at *1, 17–18. No similar kind of determination has been made for DTaP or
Tdap.
50
The main type of COVID-19 vaccine in use relies on genetically engineered messenger RNA (mRNA), which gives
cells instructions on how to make S protein found on the surface of the COVID-19 virus. Different Types of COVID-
41
There was also the epidemiologic evidence filed by Respondent. To be clear: this kind of
proof is not dispositive of causation, and Petitioners are never affirmatively required to offer it.
But (and contrary to Petitioners’ arguments), it is relevant to the causation inquiry, nonetheless.
King v. Sec'y of Health & Hum. Servs., No. 03-584V, 2010 WL 892296, at *74 (Fed. Cl. Spec.
Mstr. Mar. 12, 2010) (“[c]onsistent with the teachings of Daubert, Terran, and Grant, special
masters have routinely found that epidemiologic evidence, and/or other medical journal articles,
while not dispositive, should be considered in evaluating scientific theories.”). Indeed, as Dr. Moy
observed, applicable epidemiologic studies have been employed as strong proof in favor of
causation in other contexts. See Schonberger at 105 (connecting greater incidence of post-flu
vaccine GBS). While the absence of such evidence cannot be held against a petitioner, it warrants
evaluation when it exists.
Articles like Baxter suggested that there was no statistically significant association between
TM and any vaccine. Baxter at 1456–61. It is reasonable to contend, as Petitioners do, that Baxter
contains some methodologic weaknesses that limit how much probative weight its findings should
receive. I.J., 155 Fed. Cl. at 46–47. But it still undermines Petitioner’s theory—especially given
the degree to which Petitioners relied on case reports in the alternative. If Baxter only amounts to
the aggregation of hundreds of thousands of individual case report instances in which the vaccine
did not cause TM, to be disregarded as unpersuasive evidence rebutting causation, then why should
the comparatively lesser sum of 37 instances (only 5 of which involved diphtheria and tetanus-
containing vaccines) of post-vaccination causation noted in Agmon-Levin be given more weight?
This is not a case in which the Respondent’s experts convincingly and completely rebutted
Petitioners’ causation arguments. To the contrary, many of Dr. Moy’s contentions specific to
causation were unpersuasive.51 Dr. Gershwin for his part was a competent expert with
demonstrated understanding of the topics relevant to the case, and his general assertions about
autoimmune processes were reasonable. But ultimately it is the claimant’s burden to prove
causation.
In the end, I cannot conclude that the “can cause” prong was preponderantly met, although
resolving this part of the claim proved more difficult than deciding the third prong. Certainly (and
19 Vaccines: How They Work, Mayo Clinic, https://www.mayoclinic.org/diseases-conditions/coronavirus/in-
depth/different-types-of-covid-19-vaccines/art-20506465 (last accessed Sept. 6, 2022). This is facially distinguishable
from vaccines containing viral or bacterial particles, where the vaccine functions by provoking a direct adaptive
response to its antigenic components.
51
His arguments about the relevance of W.M.’s twin and her immune response did not appreciably undermine the
possibility of vaccine causality, for example. And although I do not find that it was preponderantly shown in this case
how weakening of the blood-brain barrier could have occurred in the relevant timeframe, sufficient for immune cells
driving disease to reach the central nervous system, I also do not accept Dr. Moy’s contentions about the singular
importance of this factor under the circumstances.
42
given the number of cases finding a TM-vaccine association) causality remains an open issue in
the Program, even if in this case Petitioners could not quite meet their burden. At bottom,
Petitioners have clearly placed excessive weight on the temporal relationship between the date of
vaccination and Petitioner’s subsequent onset and diagnosis. Temporal association alone cannot
establish causality—a concept well-understood in the Program. Moberly, 592 F.3d at 1323.
CONCLUSION
The Martinez family has my utmost sympathy for the suffering they have experienced, and
I credit their demonstrated efforts to ameliorate W.M.’s condition and provide her with loving
care. It is clear from this record that, based on the temporal coincidence of vaccination with
evidence that she was ill, Petitioners reasonably believed the DTaP vaccine might have triggered
her TM. But the record evidence does not support the claim.
A Program entitlement award is only appropriate for claims supported by preponderant
evidence. Here, Petitioners have not made such as showing. Petitioners are therefore not entitled
to compensation.
In the absence of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the
Court SHALL ENTER JUDGMENT in accordance with the terms of this decision. 52
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
52
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices
renouncing their right to seek review.
43