# Greenslade v. Secretary of Health and Human Services

> United States Court of Federal Claims · July 24, 2024

URL: https://www.frixlaw.com/law-library/cases/10734690

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** July 24, 2024
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Daniel T. Horner
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10734690

## How later opinions describe it (automated extraction)

- concluding that a petitioner must have received a covered vaccine to survive a motion to dismiss and that the zoster vaccine is not so covered
- explaining of special masters that “as fact-finders, they may find that truth lies somewhere in between the opposing, uncompromising views of the partisan experts.”
- holding that the special master did not err in refusing to afford significant weight to the opinions of treating physicians that “simply indicat[ed] awareness of a temporal, not causal, relationship” between the vaccination and the condition (emphasis omitted)
- noting that, despite carrying some evidentiary weight, “case reports ‘do not purport to establish causation definitively, and this deficiency does indeed reduce their evidentiary value’” (quoting Campbell v. Sec’y of Health & Human Servs., 97 Fed. Cl. 650, 668 (2011))

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 14-1140V
Filed: June 28, 2024

Special Master Horner
RICHARD GREENSLADE,

Petitioner,
v.

SECRETARY OF HEALTH AND
HUMAN SERVICES,

Respondent.

Leah V. Durant, Law Offices of Leah V. Durant, PLLC, Washington, DC, for petitioner.
Debra A. Filteau Begley, U.S. Department of Justice, Washington, DC, for respondent.

DECISION 1

On November 24, 2014, petitioner filed a petition under the National Childhood
Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012), 2 alleging that the influenza
(“flu”) vaccine he received on November 23, 2011, caused him to develop transverse
myelitis (“TM”). (ECF No. 1.) As of a status conference on October 14, 2015,
petitioner’s counsel clarified that petitioner was also pursuing a claim that his flu
vaccination significantly aggravated the TM he developed following his earlier Zostavax 3

1
Because this decision contains a reasoned explanation for the special master’s action in this case, it will
be posted on the United States Court of Federal Claims’ website in accordance with the E-Government
Act of 2002. See 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic
Government Services). This means the decision will be available to anyone with access to the
Internet. In accordance with Vaccine Rule 18(b), petitioner has 14 days to identify and move to redact
medical or other information the disclosure of which would constitute an unwarranted invasion of privacy.
If the special master, upon review, agrees that the identified material fits within this definition, it will be
redacted from public access.
2
Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.
§ 300aa-10-34.
3
Zostavax is the “trademark for a preparation of zoster vaccine live,” a subcutaneously administered live
attenuated virus vaccine that is used to renew immunity against herpes zoster in older individuals.
Zostavax, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=54152 (last visited Jan. 24, 2023); Zoster Vaccine
Live, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=116591 (last visited Jan. 24, 2024). Throughout
this decision, “Zostavax” or “zoster” vaccine will be used to refer to this vaccine. The Zostavax vaccine is
not covered by this program. 42 C.F.R. § 100.3. Accordingly, petitioner does not have any claim with
and Prevnar vaccinations on September 21, 2011. (ECF No. 42.) Thus, petitioner now
alleges that his condition was caused, or alternatively significantly aggravated, by his flu
vaccination. (ECF No. 144, p. 1, 2 n.2.) For the reasons set forth below, I conclude that
petitioner is not entitled to compensation.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make several factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury.

In some cases, the petitioner may simply demonstrate the occurrence of what
has been called a “Table Injury.” That is, it may be shown that the vaccine recipient
suffered an injury of the type enumerated in the “Vaccine Injury Table,” corresponding to
the vaccination in question, within an applicable time period following the vaccination
also specified in the Table. If so, the Table Injury is presumed to have been caused by
the vaccination, and the petitioner is automatically entitled to compensation, unless it is
affirmatively shown that the injury was caused by some factor other than the
vaccination. §§ 300aa-13(a)(1)(A)-(B); § 300aa-11(c)(1)(C)(i); § 300aa-14(a).

In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(A); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,
the presumptions available under the Vaccine Injury Table are inoperative. The burden
is on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines ex rel. Sevier v. Sec’y of Health & Human Servs.,
940 F.2d 1518, 1525 (Fed. Cir. 1991). Because TM is not a Table Injury, 42 C.F.R. §
100.3, petitioner must satisfy this burden of proof.

The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the

respect to his allegation that the Zostavax vaccine initially caused his TM. See § 300aa-11(c)(A); see
also Scanlon v. Sec’y of Health & Human Servs., 114 Fed. Cl. 135 (2013) (concluding that a petitioner
must have received a covered vaccine to survive a motion to dismiss and that the zoster vaccine is not so
covered).

2
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause of the injury or condition, but must
demonstrate that the vaccination was at least a “substantial factor” in causing the
condition, and was a “but for” cause. Shyface ex rel. Shyface v. Sec’y of Health &
Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply
“proof of a logical sequence of cause and effect showing that the vaccination was the
reason for the injury;” the logical sequence must be supported by “reputable medical or
scientific explanation, i.e., evidence in the form of scientific studies or expert medical
testimony.” Althen, 418 F.3d at 1278; Grant ex rel. Grant v. Sec’y of Health & Human
Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine
Program award based solely on his or her assertions; rather, the petition must be
supported by either medical records or by the opinion of a competent physician. §
300aa-13(a)(1).

In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:

Concisely stated, Althen’s burden is to show by preponderant evidence that
the vaccination brought about her injury by providing: (1) a medical theory
causally connecting the vaccination and the injury; (2) a logical sequence
of cause and effect showing that the vaccination was the reason for the
injury; and (3) a showing of proximate temporal relationship between
vaccination and injury. If Althen satisfies this burden, she is “entitled to
recover unless the [government] shows, also by a preponderance of the
evidence, that the injury was in fact caused by factors unrelated to the
vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The court also indicated that, in finding
causation, a Program fact finder may rely upon “circumstantial evidence,” which the
court found to be consistent with the “system created by Congress, in which close calls
regarding causation are resolved in favor of injured claimants.” Id. at 1280.

Generally, respondent bears the burden of demonstrating the presence of any
alternative cause by preponderant evidence only if petitioner satisfies his prima facie
burden. § 300aa-13(a)(1)(B); Walther v. Sec’y of Health & Human Servs., 485 F.3d
1146, 1150 (Fed. Cir. 2007). Respondent may also present evidence relating to an
alternative cause to demonstrate the inadequacy of petitioner’s evidence supporting his
case in chief, but petitioner does not bear the burden of eliminating alternative causes
where the other evidence on causation is sufficient to establish a prima facie case under
Althen. de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir.
2008); Walther, 485 F.3d at 1149-50.

Petitioner further alleges that his flu vaccination significantly aggravated the
indolent TM he developed following his earlier pneumococcal and zoster vaccinations
on September 21, 2011. (ECF Nos. 42, 144.) The Vaccine Act defines a significant
aggravation as “any change for the worse in a preexisting condition which results in

3
markedly greater disability, pain, or illness accompanied by substantial deterioration of
health.” § 300aa-33(4). Where a petitioner in an off-Table case is seeking to prove that
a vaccination aggravated a preexisting injury, petitioners must establish the three Althen
prongs along with three additional factors described in the prior Loving case. See
Loving ex rel. Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (2009)
(combining the first three Whitecotton factors for claims regarding aggravation of a
Table injury with the three Althen factors for off table injury claims to create a six-part
test for off-Table aggravation claims); see also W.C. v. Sec’y of Health & Human Servs.,
704 F.3d 1352, 1357 (Fed. Cir. 2013) (applying the six-part Loving test). The additional
Loving factors require petitioners to demonstrate aggravation by showing: (1) the
vaccinee’s condition prior to the administration of the vaccine, (2) the vaccinee’s current
condition, and (3) whether the vaccinee’s current condition constitutes a “significant
aggravation” of the condition prior to the vaccination. Loving, 86 Fed. Cl. at 144.

II. Procedural History

On November 24, 2014, petitioner filed his petition, alleging that approximately
two days after he received the flu vaccination, he started experiencing weakness and
numbness, and ultimately suffered TM that was caused-in-fact by the flu vaccination he
received on November 23, 2011. 4 (See ECF No. 1, p. 2.) Along with the petition,
petitioner filed medical records, marked Exhibits 1-2, and an affidavit of petitioner,
marked Exhibit 3. (See ECF No.137, p. 1.) Petitioner subsequently filed additional
medical records via compact disc. (ECF Nos. 7-8, 10; Exs. 4-5.) This case was first
assigned to Special Master Millman. (ECF No. 4.)

During a status conference on August 18, 2022, Special Master Millman advised
that the primary issue in the case was whether petitioner’s November 23, 2011 flu
vaccination significantly aggravated the TM he developed after receiving the Zostavax
and Prevnar vaccinations on September 21, 2011. (ECF No. 41.) In a subsequent
status conference on October 14, 2015, petitioner’s counsel confirmed that petitioner
was pursuing a claim that his flu vaccination significantly aggravated the TM he
developed following his earlier Zostavax and Prevnar vaccinations. (ECF No. 42.)

Petitioner filed additional medical records via compact disc in November and
December 2015, followed by a Statement of Completion on December 28, 2015. (ECF
Nos. 43, 45, 46; Exs. 6-7.) On January 29, 2016, petitioner filed a status report
confirming that he communicated a settlement demand to respondent. (ECF No. 47.)
During a status conference on February 8, 2016, respondent’s counsel indicated that
respondent is not interested in settlement “because the onset of petitioner’s transverse
myelitis came too quickly after receiving [the] influenza vaccine to show causation.”
(ECF No. 48.)

4
Petitioner was initially represented by Scott Rooney. On May 1, 2015, Mr. Rooney filed a motion to
withdraw as attorney, which was granted. (ECF Nos. 18, 28.) On August 10, 2015, petitioner moved to
substitute Leah V. Durant as attorney of record. (ECF No. 37.)

4
On March 24, 2016, respondent filed his Rule 4(c) report, recommending against
compensation. (ECF No. 49.) Respondent stated that it was not clear that petitioner
suffers from TM and noted that some of petitioner’s treating physicians did not believe
his testing was consistent with TM. (Id. at 6-7.) Respondent further asserted that
petitioner exhibited similar symptoms of his alleged condition prior to his flu vaccination.
(Id. at 7 (citing Ex. 1, pp. 565, 581).) Respondent also pointed out that petitioner was
experiencing symptoms of his condition on the day of his flu vaccine and the day after
his flu vaccine, raising a question regarding appropriate temporal association. (Id.
(citing Ex. 1, pp. 569, 572).)

Petitioner then filed an expert opinion by neurologist Lawrence Steinman, M.D.
(ECF Nos. 57, 61; Exs. 12, 55.) After petitioner filed additional medicals records (ECF
Nos. 65, 66, 69; Exs. 56-62), respondent filed responsive expert reports from
neurologist Jeffrey Gelfand, M.D., M.A.S., and immunologist Thomas Forsthuber, M.D.,
Ph.D. (ECF Nos. 70, 71; Ex. A; Ex. B.) The parties then exchanged further reports by
their experts. (ECF Nos. 76, 82, 86, 88; Exs. 64, 75, C, D.)

This case was reassigned to my docket on June 5, 2019, but shortly thereafter
was assigned to Special Master Corcoran for alternative dispute resolution (“ADR”).
(ECF Nos. 89-90, 92-93.) However, on January 23, 2020, the case was removed from
the ADR process without any informal resolution and again reassigned to my docket for
further proceedings. (ECF Nos. 99, 100.)

A two-day entitlement hearing was set to commence on November 12, 2020.
(ECF No. 104.) However, on October 1, 2020, petitioner filed a report from a new
expert, Carlo Tornatore, M.D. (Ex. 81), and additional medical records. (ECF No. 108;
Exs. 78-80, 82-97.) A status conference was held on October 2, 2020, during which
petitioner explained that he was initially unable to confirm Dr. Tornatore’s participation in
the case and received an expert report from him only recently. (ECF No. 112, p.1.)
Respondent requested an opportunity to respond to Dr. Tornatore’s expert report. (Id.
at 2.) Based on my review of the filings and after discussing the issue with the parties, I
concluded that the filing of Dr. Tornatore’s report rendered the case unripe for hearing.
(Id. at 1-2.) Thus, the hearing scheduled for November 2020 was cancelled. (Id. at 2.)

Respondent filed supplemental reports from Dr. Gelfand and Dr. Forsthuber on
December 15, 2020. (ECF Nos. 115, 116; Exs. E; G.) Petitioner then filed
supplemental reports from Drs. Tornatore and Steinman. (ECF Nos. 118, 119; Exs. 98,
103.) The expert report stage concluded with respondent’s subsequent filing of
supplement reports from Drs. Gelfand and Forsthuber on October 22, 2021. (ECF No.
123; Exs. H, I.)

A two-day entitlement hearing was ultimately scheduled to commence on
September 29, 2022. (ECF Nos. 131, 132.) In the interim, petitioner filed updated
medical records, as well as a supplemental affidavit signed by petitioner and two
additional affidavits signed by Jessica Cushard and Elmer S. Kittle. (ECF No. 136; Exs.
108-09, 123-25.) Both parties filed additional medical literature. (ECF Nos. 136, 138;

5
Exs. 110-122, H.) The parties filed simultaneous prehearing briefs on September 6,
2022. (ECF Nos. 143, 144.) A two-day hearing was held on September 29 and 30,
2022, by video conference. (See Transcript of Proceedings (“Tr.”), at ECF Nos. 150-
51.) Drs. Tornatore and Steinman testified on behalf of petitioner, and Drs. Gelfand and
Forsthuber testified on behalf of respondent. (Id.)

At the hearing, there were objections to certain testimony. (See e.g., Tr. 441-47.)
At the close of the hearing, respondent’s counsel requested an opportunity to address
those objections in post-hearing briefs. (Id. at 456.) In a post-hearing order, I directed
both parties to file updated curricula vitae for Drs. Steinman, Tornatore, and Forsthuber
and ordered petitioner to file the medical literature by Talaat et al. that was discussed
during Dr. Tornatore’s rebuttal testimony, as well as the handwritten demonstrative that
was used by petitioner’s counsel during opening statement. (ECF No. 147.) I further
ordered the respondent to file status report upon review of the Talaat article, proposing
a filing deadline for a responsive supplemental report by Dr. Forsthuber. (Id.)
Respondent filed a status report on October 31, 2022, proposing a deadline for filing his
responsive expert report. (ECF No. 152.) Respondent subsequently filed Dr.
Forsthuber’s supplemental report in response to the Talaat article on January 23, 2023.
(ECF No. 153; Ex. J.)

On March 31, 2023, petitioner filed a supplemental report by Dr. Tornatore in
response to Dr. Forthuber’s most recent report. (ECF No. 155; Ex. 130.) Thereafter,
petitioner filed a joint status report on behalf of the parties, confirming that the
evidentiary record is complete. (ECF No. 156.) However, the parties could not agree
with respect to post-hearing briefs. (Id.)

In a Scheduling Order, filed April 7, 2023, I acknowledged the parties’ differing
proposals with respect to any appropriate briefing schedule; however, I concluded that
the parties should have an opportunity to file simultaneous post-hearing briefs. (ECF
No. 157.) Petitioner subsequently filed a joint status report on behalf of the parties
indicating their agreement that post-hearing briefing should be limited to any new issues
raised at the hearing and in the post-hearing filings. (ECF No. 158.) This was later
amended to a sequential briefing schedule. (Non-PDF Scheduling Order, filed June 6,
2023.)

On June 5, 2023, petitioner filed his post-hearing brief. (ECF No. 159.) On June
26, 2023, respondent filed his responsive post-hearing brief. (ECF No. 161.) Petitioner
thereafter filed his reply brief on August 9, 2023. (ECF No. 164.)

Accordingly, this case is now ripe for resolution.

6
III. Factual History

a. As Reflected in the Medical Records

Petitioner was a 66-year-old retiree at the time of his alleged injury. (E.g., Ex. 1,
p. 587.) His medical history prior to vaccination was significant for a vitamin B12
deficiency and chronic abdominal pain secondary to an abdominal surgery he
underwent in the 1960s. (See, e.g., id. at 582-83.) On September 21, 2011, petitioner
visited his primary care physician, Catherine Foster, M.D., with concerns about stomach
pain, his teeth “falling out,” and intermittent right leg pain. (Id. at 587-88.) During this
visit, petitioner received the pneumococcal and zoster (“Zostavax”) vaccines. (Id. at
586-87, 590.) On September 22, 2011, September 23, 2011, September 27, 2011, and
October 12, 2011, petitioner called Dr. Foster’s office to discuss concerns related to
treatment for his vitamin B12 deficiency. (Id. at 584-86.) Petitioner did not report any
neurologic symptoms during these telephone encounters.

Petitioner returned to Dr. Foster on November 23, 2011, with complaints of
continued stomach pain and a “lack of ability to sense [the] need to defecate.” (Ex. 1, p.
581.) He also reported persistent right leg pain for the last three to four years and “pain
in the posterior neck and upper back and shoulders” for the last four weeks. (Id.) He
denied having any recent injuries that would cause his neck, back, and shoulder pain.
(Id.) Dr. Foster assessed the shoulder pain as seemingly muscular and improving. (Id.
at 582.) Petitioner received the flu vaccination at issue during this encounter. (Id. at
580, 583.)

On November 28, 2011, five days following his flu vaccination, petitioner called
Dr. Foster to discuss concerns about “severe myalgias and associated generalized
weakness to the point that he cannot walk.” (Ex. 1, p. 580.) He described weakness in
his bilateral extremities, neck, and upper back. (Id.) He stated that he could barely lift a
coffee cup to his mouth. (Id. at 579.) Dr. Foster noted that these symptoms were new
since his last visit. (Id. at 580.) He reported that his muscle pain began about one
month earlier but went away until it returned the previous Friday, three days prior to the
telephone encounter and two days post flu vaccination. 5 (Id. at 579.) However, he
further indicated that “this is the worst it has been.” (Id.) Dr. Foster recommended
petitioner go to the emergency room (“ER”). (Id. at 580.)

Upon arrival to the Veterans Affairs (“VA”) Ann Arbor ER on November 28, 2011,
petitioner reported that he had been experiencing weakness, numbness, and pain in his
bilateral extremities “for the last [four] days,” which would place onset on the day after
his flu vaccination. 6 (Ex. 1, p. 572.) He also reported leg spasms, and although he
5
The nurse documenting the telephone encounter also noted that petitioner received the flu vaccine on
Friday. (Ex. 1, p. 579.) Petitioner received the flu vaccine on Wednesday, November 23, 2011. (Id. at
580.)
6
The same medical record also documents that petitioner’s symptoms began three days prior. (Ex. 1, p.
574.) Petitioner also previously reported that his extremity weakness began three days prior, on Friday,
November 25, 2011. (Id. at 579-80.) However, it appears from the medical records that petitioner’s

7
reported “problems with his right leg” for the past year, he could not specifically describe
his “problems.” (Id.) Petitioner further explained that he had noticed that he could feel
hot water on his head and shoulders while in the shower, but the water felt cold below
his head and shoulders. (Id.) A physical examination revealed that petitioner had
weakness of his shoulder girdle and was unable to raise his arms against resistance.
(Id. at 573-74.) The ER doctor also found that petitioner had weakness in his hips, but
not in his distal extremities. (Id. at 574.) Petitioner was admitted to the hospital with a
diagnosis of TM. (Id.)

While at the hospital, petitioner reported that his shoulder and neck soreness
started on the previous Thursday, which would be the day after his flu vaccination. (Ex.
1, p. 565.) Petitioner explained that the soreness subsequently spread down his arms
and legs, and he began feeling numbness and coldness in his extremities. (Id.) He
described tightness in his shoulders and stated that it felt like there was “sand in them.”
(Id.) Petitioner also reported feeling a pins and needles sensation in all four extremities.
(Id. at 565-66.) He stated that he experienced “an identical episode” two months prior
and noted that “[t]he onset was identical and the entire symptomatology lasted 3-4 days
and then gradually resolved on its own.” (Id. at 566.) Additionally, he noted that he had
been suffering from painful cramping in his bilateral calves for the last several months,
but the cramping occurred more often in his right calf and seemed to be “more frequent
during [this] constellation of symptoms.” (Id.) Upon physical examination by neurologist
Joseph Corey, M.D., Ph.D., petitioner showed reduced reflexes in his legs, inability to
stand or walk, and decreased sensation in his upper and lower extremities. (Id. at 567.)
Given that all four of petitioner’s extremities were impacted and the pain began in his
neck and shoulders, Dr. Corey noted that petitioner’s symptoms were likely localized in
his cervical spine. (Id.) Dr. Corey assessed petitioner with possible myelopathy,
polyradiculopathy, or TM and recommended cervical spine imaging. (Id.)

Shortly after petitioner was admitted to the hospital, he developed urinary
retention and needed a catheter. (Ex. 1, pp. 550-51.) Petitioner underwent a cervical
spine MRI on November 29, 2011. (Id. at 803-06.) The MRI revealed “moderately
advanced degenerated disc disease with the disc osteophyte complexes causing mild
central spinal stenosis at C3-C4 and C6-C7.” (Id. at 806.) It also showed a “mild” or
“faint T2 signal prolongation,” but there was “no contrast enhancement associated with
it.” (Id. at 805.) The impression included “[m]oderately advanced” and “equivocal
findings [for] small area of focal T2 signal prolongation in the ventral aspect of the right
hemi cord at C3 vertebral level, suggesting either demyelination or gliosis.” (Id. at 806.)
Dr. Corey reviewed the MRI findings and opined that the results showed “T2 signal
change ~C3-C4 and some hazy enhancement at this level, as well as C6-C7 level.” (Id.
at 549.) His impression was that the MRI findings were concerning for an intrinsic cord
process as the cause of the TM. (Id.)

symptoms of shoulder and neck soreness manifested first and symptoms progressed to include
weakness and numbness by the following day. (See id. at 565-66.)

8
Additionally, a cerebrospinal fluid (“CSF”) study showed slightly elevated protein
at 61 mg/dL (reference range of 12 to 60 mg/dL) and an elevated myelin basic protein at
4.0 ng/mL (reference range of 0.0 to 1.0 ng/mL) but was otherwise normal. (Ex. 1, pp.
763, 82.) It was noted that petitioner had an elevated antinuclear antibody (“ANA”),
prompting consideration of a series of autoimmune disorders. (See id. at 709.) Except
for a positive MRSA culture, testing for infectious etiologies was negative. (Id. at 776-
79, 784-85.) Petitioner’s serum was negative for zoster. (Id. at 777.) Testing for
several central nervous system (“CNS”) antibodies was also negative. (Id. at 770-82.)
Also on November 29, 2011, a nurse noted that petitioner complained of his bilateral
shoulders and knees being “locked up” and that petitioner’s range of motion was more
limited than it had been upon arrival. (Id. at 550.)

On December 1, 2011, petitioner attended a physical therapy session while at
the hospital. (Ex. 1, pp. 527-28.) During the session, petitioner was unable to move his
legs, he had significant weakness in his arms, and he had decreased sensation in his
arms and legs. (Id.) On the same date, petitioner saw Dr. Corey for a neurology
evaluation. (Id. at 524-26.) Dr. Corey noted decreased strength and sensation on
physical examination and a differential diagnosis of TM, MS, or potential brain disease.
(Id. at 526.) Dr. Corey again noted that petitioner’s MRI was “concerning for an intrinsic
cord process” as the cause of the TM; however, the cause was still unknown. (Id.)
Petitioner began a three-day course of Solu-Medrol 7 and a seven-day course vitamin
B12 therapy to address the TM and was given Flexeril for his muscle spasms. (Id.) He
was also placed on oxygen due to hyperventilation and prescribed Ativan for anxiety.
(Id.)

The next day, on December 2, 2011, petitioner began showing slight
improvement and regained some use of his right arm. (Ex. 1, pp. 519-20.) He
remained non-ambulatory due to extensive weakness in his legs. (Id. at 520.)
Petitioner’s treating neurologist, Dr. Corey, suggested that TM was unlikely as there
were no inflammatory changes in CSF and petitioner had a non-enhancing lesion. (Id.
at 517.) During a neurology consultation on December 3, 2011, Dr. Corey again noted,
“Transverse Myelitis and Multiple Sclerosis are on the differential, but the lack of
enhancement coupled with his largely normal CSF results (other than protein of 61)
would make this very unusual, as does his older age.” (Id. at 493.) Dr. Corey
recommended an additional two-day course of Solu-Medrol. (Id.) Because petitioner’s
symptoms had worsened since his initial cervical spine MRI, Dr. Corey recommended
an additional MRI of his brain and total spine to evaluate for any changes. (Id.) The
next day, petitioner was seen by neurology again and he reported his recent flu
vaccination. (Id. at 476.) It was noted that TM “has been reported after many

7
Solu-Medrol is as intramuscular or intravenous injection of synthetic glucocorticoid derived from
progesterone that is used as an anti-inflammatory and immunosuppressant in short-term emergency
treatment. Solu-Medrol, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=46174 (last visited June 5, 2024);
Methylprednisolone, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=31014 (last visited June 5, 2024);
Methylprednisolone Sodium Succinate, DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=89219 (last visited June 5, 2024).

9
vaccinations,” but the relationship between his vaccination and his condition was not
explored as petitioner’s “work-up has not been consistent with Transverse myelitis.”
(Id.)

Petitioner underwent a thoracic and cervical spine MRI on December 5, 2011.
(Ex. 1, pp. 797-802.) The MRI revealed “[s]table appearance of hyperintensity along the
anterior spinal cord at C2-C4 with stable cervical spondylosis” and “[i]ncreased thin
tumor flow-void along the posterior aspect of the spinal cord form mid thoracic spinal
cord down to L1, could represent a dural AV fistula” but there was “no associated
expansion of the spinal cord or T2 hyperintensity on the spinal cord.” (Id. at 802.) On
December 5, 2011, petitioner was transferred to the University of Michigan (“UofM”)
hospital for evaluation of a possible venous malformation in his spinal cord based on his
MRI findings from the previous day. (Id. at 443; Ex. 8, pp. 6-7.) Radiologists at the
UofM hospital reviewed the December 5, 2011 MRI and concluded:

On postcontrast imaging, patchy areas of abnormal contrast enhancement
are seen dorsal to the cord at T9-T10 to T12-L1 levels. No convincing
evidence for abnormal flow-voids is seen on T2 axial imaging. A venous
structure is seen exiting from right L1-L2 neuroforamen and can be traced
superiorly up to T11 level posterior to the conus. Between T9-T10 and T11,
no significant areas of enhancement are seen. This could represent a mildly
dilated venous channels. The possibility of dural AV fistula, even as less
likely, cannot be entirely excluded. Clinical correlation is recommended.

Intramedullary high T2 signal area is seen on the left at C7-T1 level,
concerning for plaques of demyelination versus transverse myelitis.
Smaller similar area is also seen on right C4-C5 level. Intramedullary high
T2 signal is seen from C2-C3 to C4-C5 levels.

(Ex. 8, pp. 64.) During a neurology consultation with Larry Junck, M.D., on December
6, 2011, it was noted that petitioner initially reported an identical episode as occurring
“about two months ago,” but “when questioned here today at UofM, he states that it
might have only been about 1-2 weeks ago.” (Id. at 48.) He maintained that “[t]he
onset was identical and the entire symptomatology lasted 3-4 days” before gradually
resolving on its own without medical intervention or lasting deficits. (Id.) Dr. Junck
reiterated that petitioner received a flu vaccine prior to the onset of his symptoms and
that while TM “has been reported after many vaccinations . . . [petitioner’s] work-up has
not been consistent with [TM].” (Id. at 50.) During a neurosurgical inpatient consult, it
was noted that petitioner’s MRI showed “multiple areas of T2 hyperintensity throughout
the cervical and thoracic cord,” “irregular enhancement of the dorsal caudal thoracic
spine,” and “mild degenerative disc changes,” but “no active neurosurgical issues at this
time.” (Id. at 24.) A spinal angiogram performed on December 8, 2011, ruled out a
dural venous fistula. (Id. at 66-69; Ex. 1, pp. 443, 447-48.)

On December 9, 2011, petitioner was transferred back to the VA Ann Arbor
Hospital. (Ex. 1, pp. 443-47.) Upon transfer, petitioner was seen by Dr. Corey with

10
reports of ongoing weakness. (Id.) Dr. Corey noted that “extensive workup to date
aside from aforementioned spinal cord lesions and low vitamin B12 (no s/p 2 days IV
replenishment) has been negative.” (Id. at 443.) Petitioner’s presumed diagnosis was
autoimmune myelitis, given his negative workup. (Id. at 447.) A brain MRI performed
on December 12, 2011, was normal. (Id. at 792-93.) By December 13, 2011, petitioner
had improved, but his symptoms continued to wax and wane. (Id. at 409.) Throughout
his hospital course, petitioner’s lack of definitive diagnosis was a persistent point of
frustration. (Id. at 398, 411, 421, 457, 528-29.)

Petitioner was discharged from VA Ann Arbor ER and transferred to the VA
Community Living Center on December 14, 2011. (Ex. 1, pp. 4-8.) Petitioner’s primary
diagnosis at discharge was weakness and spinal cord lesion. (Id. at 4; Ex. 4, pp. 7-8;
Ex. 2, pp. 5-9.) While at the VA Community Living Center, petitioner continued to attend
physical therapy sessions. (E.g., Ex. 1, pp. 382-83.) On December 22, 2011, petitioner
saw neurologist Ben Segal, M.D., who noted that petitioner “originally presented on
11/28/2011 after his 2nd episode of neck and shoulder pain (in 10 days) that
instantaneously radiated down his body into legs and was associated with extreme
weakness.” (Id. at 316.) Petitioner described how “[e]ach episode left him [bed] bound,
the first for 3 days in mid 11/2011 and the second led to pursuit of medical care on
11/28/2011.” (Id.) Dr. Segal assessed “myelopathy was most likely due to a
demyelinating event.” (Id. at 321.) Dr. Segal noted that a “[p]ossible cause is flu
vaccine several weeks before [petitioner’s] initial symptoms,” but later qualified that
“[t]he relationship between the myelopathy and his recent influenza vaccination is
uncertain.” (Id. at 320-21.) Petitioner continued to improve with inpatient rehabilitation,
and he remained at the VA Community Living Center until January 6, 2012, when he
was discharged home. (Ex. 4, pp. 1-3.) At the time of his discharge, petitioner could
ambulate with a front-wheeled walker but still needed a wheelchair at times. (Id. 3.) He
could also perform most of his activities of daily living without assistance. (Id.)
Petitioner’s discharge diagnosis was TM with unknown etiology. (Id. at 1.)

Following his discharge from inpatient rehabilitation, petitioner’s condition again
deteriorated. I have reviewed the remaining medical records; however, it is not
necessary to discuss petitioner’s subsequent course in detail. Neither the parties nor
their experts have asserted that the subsequent course of petitioner’s condition affects
their assessment of the alleged causal relationship to vaccination.

During a follow-up neurology visit on June 21, 2012, petitioner reported that he
was weak, incontinent, and dependent on his wheelchair, despite continued therapy.
(Ex. 1, pp. 140-45.) The attending physician noted that petitioner’s symptoms could be
attributed to TM that was resolving upon his initial presentation but it was unclear if
petitioner’s vaccinations “played any part [in] his disease process.” (Id. at 144-45.) The
physician further noted that petitioner’s condition “may have at least partially responded
to 5 day course of Solumedrol in early 12/2011.” (Id. at 144.) By 2014, petitioner had
become completely wheelchair dependent. (See e.g., Ex. 4, p. 50.) Additionally, he
developed pain and spasticity (increased tone and reflexes) in his extremities, continued

11
to suffer constipation, and had difficulty controlling his bladder function. (See e.g., id. at
43-44.)

In response to petitioner’s inquiry, Dr. Foster noted on October 28, 2023, that she
does not confirm that petitioner’s shingles vaccine was related to his paralysis, although
she noted his history of “presumed autoimmune myelitis with extensive, negative work
up in 11/2011.” (Ex. 108, pp. 44-45.)

Petitioner continues to suffer from sequela of his injury. He remains wheelchair
dependent and continues to suffer paraplegia, neurogenic bowel and bladder, pain,
spasticity, and weakness. (See e.g., Ex. 7; Ex. 76, p. 20; Ex. 108, pp. 12-13, 28, 46, 81;
Ex. 109, pp. 28-29, 49, 89, 97, 118-244, 258, 271, 295-331.) Petitioner also continues
to experience deficiencies in vitamins D and B12. (See e.g., Ex. 108, p. 82.)

b. As Reflected in the Affidavits

i. Affidavits of Petitioner

Petitioner filed two affidavits, marked as Exhibits 3 and 123. (ECF No. 136.) In
his affidavit, petitioner states that, prior to receipt of the subject flu vaccine on
November 23, 2011, he did not suffer “any signs or symptoms of paralysis,” was never
diagnosed with TM, was not wheelchair bound, and did not require in-home medical
care or physical therapy. (Ex. 3, ¶¶ 3, 8-9.) Following his vaccination, petitioner states
that he began to develop tingling and numbness in his lower extremities and was
incapable of moving his legs. (Id. ¶ 4.) He states that he went to the ER on November
28, 2011, with complaints of continued numbness, tingling, and difficulty moving his
lower extremities. 8 (Id. ¶ 5.) He explains that a CSF evaluation revealed that he “had a
myelin basic protein at 4.0” and he was subsequently diagnosed with TM. (Id. ¶¶ 6-7.)
As a result, petitioner states that he requires a wheelchair, in-home medical care, and
physical therapy. (Id. ¶ 10.) He further contends that he continues to suffer emotional
distress and physical injury as a result of the subject vaccination. (Id. ¶ 13.)

In his supplemental affidavit, petitioner clarifies that he was vaccinated in
November of 2011 and “was hospitalized within days.” (Ex. 123, ¶ 1.) He described
how he “started feeling unwell” after his vaccination and how he was paralyzed from the
neck down “shortly after” arriving at the ER. (Id.) He states that he remained in the
hospital for several months before returning home where he continued to have trouble
walking. (Id.)

Regarding residual symptoms, petitioner indicates that the cramping in his legs
progressed to point of spasticity, which has not abated. (Ex. 123, ¶¶ 1-2.) Petitioner
explains that his legs remain folded under him in a cramped position and he cannot use
or straighten them. (Id. ¶ 2.) Despite taking muscle relaxers on a daily basis, petitioner
states that he continues to feel constant pain, making sleep and daily activities difficult.
(Id.) Petitioner further explains that he is now confined to a wheelchair and struggles

8
The affidavit misstates the date as September 28 rather than November 28.

12
moving and transferring in and out of his wheelchair, compounding his difficulty
performing daily activities, such as cooking and cleaning. (Id. ¶ 4.) He is also no longer
able to drive a car. (Id.) Petitioner explains that he could previously “work on all sorts
of mechanical and construction projects,” but his spasticity has prevented him from
continuing to do so. (Id. ¶ 5.) Although he admits that he sustained a military injury
prior to vaccination, which resulted in difficulty with bowel movements, petitioner claims
that these symptoms have only gotten worse since vaccination. (Id. ¶ 3.) He states that
he developed an inability to urinate without the assistance of a catheter. (Id.) Lastly, he
describes the psychological toll of his injury, which he states is “terrible” and “has taken
the joy out of everything.” (Id. ¶ 5.) He further states that “know[ing] that nothing will
take this pain away makes [him] just want to die sometimes.” (Id.)

Petitioner states that he experienced some relief with massage therapy, but
Veteran’s Affairs has refused to cover such treatment. (Ex. 123, ¶ 6.) He further
explains that he must cover the cost of his medication and medical supplies with his
own income, “which is minimal at this point.” (Id.)

Notably, petitioner claims that he “experienced similar symptoms after receiving
different vaccine [a] few months earlier” and that “those symptoms were short lived and
resolved on their own.” (Ex. 123, ¶ 1.)

ii. Affidavit of Jessica Cushard

Petitioner filed an affidavit of Jessica Cushard, marked as Exhibit 124. (ECF No.
136.) In her affidavit, Ms. Cushard states that she is a friend of petitioner’s and that “it
has been very disturbing to see what has happened to him since being vaccinated.”
(Ex. 124, ¶ 1.) She explains that she transported petitioner to the ER when he began
experiencing difficulty walking and breathing following vaccination. (Id.) “During the
rest of that day and evening, [she] watched as he went from mostly functional to being
completely paralyzed from the neck down.” (Id.) Ms. Cushard describes how petitioner
remained in the hospital for several months and underwent “test after test with no
conclusions.” (Id.) She further describes how he could eventually walk with the
assistance of a walker and was discharged from the hospital. (Id.)

Ms. Cushard explains that, rather than improving upon discharge, petitioner’s
legs started cramping to the point that they were spastic and painful. (Ex. 124, ¶ 2.)
She states that he sought further testing, “but no solution was found for the problem”
and “[t]he best they could do was to prescribe a large amount of daily muscle relaxers to
try to help ease the cramping.” (Id.) Ms. Cushard describes how petitioner’s legs are
always folded together as if “he has constant charley horses in all of his leg muscles.”
(Id.) As a result, she explains that he is confined to a wheelchair, making “any normal
daily activities like cooking, cleaning, bathing, etc.” difficult. (Id.) She states that
petitioner experiences spasms on top of the cramping “if he moves just the wrong way.”
(Id.) His pain makes getting comfortable and sleeping difficult. (Id.)

13
Ms. Cushard goes on to describe how, “[a]round the same time that all of this
happened,” petitioner started to experience difficulty urinating and required the
assistance of a catheter. (Ex. 124, ¶ 3.) She further describes how petitioner’s difficult
with bowel movements caused him to lose about 65 pounds because he was afraid to
eat. (Id.) However, Ms. Cushard indicates that she is unsure of whether these
symptoms are “a result of the original problem or a side effect of so many muscle
relaxers.” (Id.)

Ms Cushard explains that, prior to vaccination, petitioner was a very active
person. (Ex. 124, ¶ 4.) She states that petitioner walked a lot and drove a car, but he
can no longer do either of these activities. (Id.) She suggests that petitioner spends
most of his time inside of his apartment because the battery power on his mobile
wheelchair dictates how far he can travel. (Id.) Ms. Cushard also states that petitioner
does not often go outside in the winter because the cold weather causes his legs to
spasm. (Id.) Ms. Cushard states that she can see why petitioner seems to be very
depressed most of the time. (Id.)

Finally, Ms. Cushard states that does not believe that there could have been any
other cause for petitioner’s condition as “[n]othing else notable happened around that
time.” (Ex. 124, ¶ 5.)

iii. Affidavit of Elmer S. Kittle, Jr.

Petitioner filed an affidavit of Elmer S. Kittle, Jr., marked as Exhibit 125. (ECF
No. 136.) In his affidavit, Mr. Kittle states that he has known petitioner “for many years.”
(Ex. 125, ¶ 1.) He explains that he would be devastated if he had to go through what
petitioner has gone through. (Id.) Mr. Kittle describes how petitioner “used to walk
everywhere” prior to the vaccinations. (Id. at ¶ 2.) Mr. Kittle explains that petitioner’s
condition “left him discouraged and in a wheelchair without hope of every walking
again.” (Id.)

14
IV. Expert Opinions

a. Petitioner’s Experts

i. Carlo Tornatore, M.D. 9

In support of his claim, petitioner presented the expert opinion of Carlo
Tornatore, M.D. Dr. Tornatore authored three expert reports in support of petitioner’s
claim. (Exs. 81, 98, 130.) Additionally, at the hearing, he was proffered without
objection as an expert in neurology with a special expertise in demyelinating diseases of
the CNS, including MS and TM. (Tr. 29, 32.)

Regarding the onset of petitioner’s condition, Dr. Tornatore opined that petitioner
experienced the first manifestations of his TM “several weeks prior to the 11/23/2011
influenza vaccination and that the vaccination profoundly aggravated the TM resulting in
the precipitous onset of quadriparesis.” (Ex. 81, p. 15; Tr. 33-34; see also Tr. 106-07
(opining that onset was “sometime in that three- to four-week period prior to the
influenza vaccination” and that the end of October to the beginning of November 2011
time frame “makes the most sense . . . from a historical standpoint”).) Dr. Tornatore
explained that, prior to the pneumococcal and zoster vaccinations, petitioner’s medical
condition was significant for gastrointestinal issues, as well as right posterior thigh and
calf pain and an apparent vitamin B12 deficiency; however, there was no record of
significant neurologic symptoms. (Tr. 34-36 (citing Ex. 1, pp. 597-600).) Nonetheless,
he noted that during a visit with Dr. Foster on November 23, 2011, petitioner reported
experiencing pain in the posterior neck and upper back and shoulders for the past four
weeks. (Tr. 36-38; Ex. 81, p. 16; see also Ex. 98, p. 3 (emphasizing that petitioner’s
neck and shoulder pain was present before he received the flu vaccine).) Dr. Tornatore
associated petitioner’s reports of neck, back, and shoulder pain with his TM. (Ex. 81,
pp. 17-18; Ex. 98, p. 3; see also Tr. 39, 112.) He stressed that a primary care physician
may not necessarily tease out neurologic symptoms (Tr. 119), and that “pain described
as musculoskeletal symptoms can have an origin in the central nervous system
demyelination.” (Ex. 81, pp. 17-18). He further noted that petitioner’s November 23,
2011 encounter included a new symptom – the lack of ability to sense the need to

9
Dr. Tornatore received his medical degree from Georgetown University School of Medicine before
completing an internship in internal medicine at Providence Hospital, his residency in neurology at
Georgetown University Hospital, and a fellowship in molecular virology at National Institutes of Health.
(Ex. 82, p. 2; Ex. 81, p. 2.) He is board certified in neurology and specializes in demyelinating conditions
of the CNS. (Ex. 82, p. 1, Tr. 30-31.) Dr. Tornatore currently works a professor and the Chair of the
Department of Neurology at Georgetown University Medical Center, as well as the Chair and Neurologist-
in-Chief of the Department of Neurology at Medstar Georgetown University Hospital. (Ex. 82, p. 3; Ex.
81, pp. 1-2; Tr. 29-30.) Additionally, he is the Director of Georgetown University Hospital’s Neurology
Clerkship Program, Multiple Sclerosis Clinic, and Spasticity Clinic. (Ex. 82, pp. 3-4; Ex. 81, pp. 1-2.) At
the hearing, Dr. Tornatore explained that he has been in practice for thirty years with most of his time
spent treating patients with “the whole spectrum” of neuroinflammatory disorders of the nervous system,
including transverse myelitis. (Tr. 30.) He further explained that he has over thirty years of experience
reading MRIs and spent around seventeen years teaching neurology residents and medical students how
to read MRIs. (Id. at 31.) Dr. Tornatore has published several articles on cell biology and pathology of
demyelinating disorders and diseases of the CNS. (Ex. 81, pp. 8-13.)

15
defecate, which he explained is a sign of sensory abnormalities in the spinal cord. (Tr.
36-38 (citing Ex. 1, pp. 591-93).)

On cross-examination, Dr. Tornatore acknowledged that petitioner had a
longstanding history of gastrointestinal issues (Tr. 112-14); however, he opined that the
significance of the new symptom became apparent after petitioner developed pain,
motor symptoms, and bowel and urinary incontinence as “evidence that there might be
something already indolent in the cervical spinal cord.” (Tr. 40-41, 115-16). Dr.
Tornatore also acknowledged that the degenerative disc disease seen on MRI could
potentially account for petitioner’s neck and shoulder pain, but he maintained that
petitioner’s neurologic symptoms suggest that his pain originated from “within the spinal
cord and not from nerve root impingement.” (Tr. 164-65.) Citing petitioner’s age, Dr.
Tornatore opined that the degree of degenerative changes would be expected and that
he did not believe that the two conditions could be acting synergistically. (Tr. 165.) Dr.
Tornatore noted that “inflammatory conditions of the spinal cord can be brief in duration
with remission back to baseline,” similar to what petitioner described to his treating
physicians. (Ex. 98, p. 3.) Dr. Tornatore concluded that in the weeks prior to
petitioner’s flu vaccination, “there were multiple references to transient as well as
ongoing symptoms referable to the cervical spinal cord.” (Id.)

Addressing petitioner’s MRIs of the cervical spine, Dr. Tornatore opined that
petitioner’s presentation on November 23, 2011, was consistent with the cervical spine
lesions seen on subsequent MRI. (Ex. 81, p. 18.) He explained that, once there is an
injury to the spinal cord, the presence of enhancement on MRI simply “tells us about the
timing, but it doesn’t really tell us anything about the symptoms themselves.” (Tr. 65.)
He explained that it is significant that the cervical spine lesions did not enhance with
contrast as a non-enhancing lesion on T2-weighted imaging indicates that the lesion is
generally at least 2-3 weeks old. (Ex. 81, pp. 18-19 (citing M. Lai et al., A Preliminary
Study into the Sensitivity of Disease Activity Detection by Serial Weekly Magnetic
Resonance Imaging in Multiple Sclerosis, 60 J. NEUROLOGY, NEUROSURGERY, &
PSYCHIATRY 339 (1996) (Ex. 96); Francois Cotton et al., MRI Contrast Uptake in New
Lesions in Relapsing-Remitting MS Followed at Weekly Intervals, 60 NEUROLOGY 640
(2003) (Ex. 97)); Tr. 56-59, 132-33.) Dr. Tornatore explained that a paper cited by Dr.
Gelfand, Bulut et al. (infra at Ex. E, Tab 3), also bolstered his opinion as that study
confirmed that an MRI within 10 days of symptom onset is more likely than not to have
gadolinium enhancement. (Ex. 98, p. 4; Tr. 82-84, 151-52.) Thus, Dr. Tornatore opined
that the MRI findings from November 29, 2011, indicate that the lesions likely developed
between November 7, 2011, and November 14, 2011, which overlaps with the onset of
petitioner’s cervical and shoulder symptoms. (Ex. 81, p. 18.) He added that petitioner’s
MRIs “revealed partial myelitis, not full thickness myelitis.” (Ex. 98, pp. 3-4; Tr. 76-79.)
He explained that partial myelitis involves an inflammatory process and “can result in
transient spinal cord symptoms,” which is consistent with petitioner’s reports to his
treating doctors. (Ex. 98, pp. 3-4; Tr. 76-79.) Dr. Tornatore further explained that the
pathology and kinetics of partial myelitis is comparable to multiple sclerosis (“MS”) as
partial myelitis is seen in over 60 percent of MS patients, and MS patients often

16
experience “a flare of transverse myelitis” that “can be absolutely identical to what
[petitioner] experienced.” (Tr. 86, 139, 176-77.)

Dr. Tornatore explained that, although there are some instances when clinicians
can parse out symptoms as being caused by one lesion or another, petitioner’s case is
“a little muddier.” (Tr. 59-61.) However, he opined that the inability to pinpoint a
specific lesion as causing a specific symptom “is less important than the fact that it’s all
referable to the cervical spinal cord.” (Tr. 61, 65.) Dr. Tornatore explained that “MRI
findings for transverse myelitis are nonspecific.” (Ex. 81, p. 20 (citing Rohit Bakshi &
John C. Mazziotta, Acute Transverse Myelitis After Influenza Vaccination: Magnetic
Resonance Imaging Findings, 6 J. NEUROIMAGING 248 (1996) (Ex. 88)).) Here, however,
Dr. Tornatore found it significant that there were two non-enhancing lesions on MRI. 10
(Tr. 67, 72-73.) Based on his clinical experience, Dr. Tornatore opined that it is highly
improbable for someone to develop two lesions at the same time and for both of the
lesions to lose their enhancement within less than 5 days. (Id. at 67, 81, 84, 137-38.)
He suggested that it could be argued petitioner had a “recurrent disease” due to there
being “two different lesions” and “two different episodes.” (Id. at 84, 107-08; see also
Tr. 140-42 (explaining that the location of petitioner’s lesions lends support for his
opinion that the lesions are distinct, given what we know about the kinetics of blood-
brain barrier breakdown).) When I asked why it would be the case that the second
lesion was unlikely to progress in the absence of the flu vaccination, Dr. Tornatore relied
on “the tempo” of petitioner’s reported symptoms. (Id. at 68, 170-72; see also Tr. 144
(explaining that the significance of the MRI studies showing non-enhancement is
informed by petitioner’s symptom course).) He explained that older patients experience
immunosenescence, and that petitioner’s advanced age, in combination with the lack of
enhancement and normal CSF, suggests that his neck pain likely would have resolved
on its own but for the flu vaccination. (Tr. 170-73.) Dr. Tornatore opined that “there’s
no question that the inflammation is in one area and is starting to spread to other areas
in the spinal cord, causing these other symptoms” (Id. at 70-71), and that petitioner’s
“clinical course is by far the most important” sign of augmented inflammation (Id. at
158). He explained that there need not be a robust amount of inflammation to cause
significant symptoms, given the relatively small size of the spinal cord, and that the
location of the inflammation can have an impact on the severity of the symptoms. (Id. at
71-72, 77-78, 93, 162-63.) He agreed that the clinical progression of the symptoms
itself “can demonstrate that the inflammatory process is progressing.” (Id. at 71.)

10
When asked about the December 5, 2011 MRI results, Dr. Tornatore explained that the results were
reviewed and determined to show “irregular areas of enhancement dorsal to the lower cord.” (Tr. 73-74
(citing Ex. 8, pp. 63-65).) He clarified that these results demonstrate that the “hazy enhancement” was in
the thoracic spine, rather than the cervical spine. (Id. at 74.) Either way, Dr. Tornatore explained that the
“patchy areas of abnormal contrast enhancement” referred to “blood vessels that were outside of the
spinal cord” and suggestive of mildly prominent venous channels; however, a subsequent angiogram
ruled out dural fistula. (Id. 74-75 (citing Ex. 8, p. 7).) Dr. Tornatore explained that the lesions seen on
subsequent MRI studies were “all there from the 29th onward,” and “[n]one of the lesions [were]
enhanced.” (Id. at 72.) In response to my question regarding whether his opinion would change if I were
to accept the initial impression of hazy enhancement, Dr. Tornatore explained that his opinion would not
change because the faintness of the enhancement would indicate that the “it’s starting to resolve” and
CSF analysis confirmed that there was no “bona fide enhancement.” (Tr. 167-68.)

17
Following the flu vaccination on November 23, 2011, petitioner reported “a
progression of the symptoms,” including worsening muscle aches, weakness, sensory
loss, and bowel and bladder issues. (Tr. 41-46 (citing Ex. 1, pp. 575-78, 588-90), 79;
Ex. 81, p. 16.) Dr. Tornatore opined that these symptoms are referable to the cervical
spinal cord as “part of a larger continuum of pain that becomes more diffuse.” (Tr. 43-
44 (citing Ex. 1, p. 590), 69-70 (citing Ex. 1, p. 577).) Although he acknowledges that
petitioner may not be an accurate historian, Dr. Tornatore emphasized petitioner’s
report of a prior “identical episode” and suggested that it is difficult to tease out whether
petitioner’s pre-vaccination symptoms had resolved or whether his post-vaccination
symptoms were part of the same continuum. 11 (Id. at 46-48, 75, 122.) Dr. Tornatore
acknowledged that petitioner’s affidavit includes a statement that he had not
experienced paralysis, numbness, or tingling prior to his flu vaccination; however, Dr.
Tornatore found the contemporaneous medical records to be more compelling than an
affidavit that was authored at least three years after the events. (Id. at 123-25, 177-78.)
He explained that the medical records confirm that, on four separate occasions,
petitioner told four different medical providers about his prior episode. (Id. at 124-25.)
Moreover, Dr. Tornatore submitted that the affidavit and the medical records were not
inherently inconsistent because petitioner did not report paralysis when describing his
prior episode to his providers and it is not entirely clear what petitioner meant when he
used the word “paralysis” in his affidavit. (Id. at 124, 178.)

Dr. Tornatore explained that petitioner’s CSF, which did not reveal any
inflammatory cells, indicates that the inflammatory process was not acute. (Tr. 50-52,
158-59.) The presence of elevated myelin basic protein, in combination with the lack of
elevated white blood cell count, further bolstered Dr. Tornatore’s belief that the
inflammatory injury was not new. (Id. at 50-52.) Dr. Tornatore explained that a study by
Talaat et al. demonstrates that there are “immune hyper-responders” that may
experience constitutional symptoms, despite lower absolute levels of the measured
serum factors. (Ex. 130, pp. 1-4 (citing Kawsar R. Talaat et al., Rapid Changes in
Serum Cytokines and Chemokines in Response to Inactivated Influenza Vaccination, 12
INFLUENZA & OTHER RESPIRATORY VIRUSES 202 (2018) (Ex. 127)); Tr. 442-43.) He
opined that “the absolute level of a measured soluble factor is less important that the
fact that there is a measurable clinical response to an antigenic challenge.” (Ex. 130, p.
5.) Dr. Tornatore further testified that non-enhancement on MRI suggests that the
blood-brain barrier has been reestablished; however, this does not mean that the
inflammation has subsided as the presence of a T2 lesion indicates that the
inflammation has gotten into the spinal cord and the reestablished blood-brain barrier
has sealed it in. (Tr. 153.) Because the spinal fluid is outside of the blood-brain barrier,
inflammation in the spinal cord will no longer be reflected in the CSF once the blood-
brain barrier has been reestablished. (Id. at 158-59.) Thus, petitioner “continues to
11
Dr. Tornatore evaluated Dr. Foster’s November 28, 2011 addendum, where she stated that petitioner
had developed symptoms including generalized weakness and myalgias since his visit the week before,
as her recognition of new symptomology since the November 23, 2011 encounter. (Tr. 43-44 (citing Ex.
1, p. 590). Additionally, Dr. Tornatore references a notation by petitioner’s treaters from the initial
hospitalization that petitioner had a previous identical episode as recognition that his subsequent
symptoms were a continuum. (Id. at 69-70 (citing Ex. 1, p. 577).)

18
have very significant neurologic issues” as the inflammation remains, despite
unremarkable CSF. (Id. at 78, 153-54.) Moreover, Dr. Tornatore opined that, while an
initial immune response may result in an increase in cytokines or chemokines, “the
subsequent triggering of the cellular and other portions of the humoral arm of the
immune system can result in downstream CNS inflammatory effects long after the
serum cytokine/chemokine levels have dropped to normal.” (Ex. 130, p. 4.)

Dr. Tornatore agreed with Dr. Steinman’s assessment that the flu vaccine can
cause a significant aggravation of TM. (Ex. 81, p. 19.) He added that TM has been
reported following flu vaccination and cited several case reports linking the flu vaccine
with TM. (Id. at 19-21 (citing Bakshi & Mazziotta, supra, at Ex. 88; Isabelle Korn-
Lubetzki et al., H1N1 Vaccine-Related Acute Transverse Myelitis, 13 ISR. MED. ASS’N J.
249 (2011) (Ex. 92); Wafa Akkad et al., Longitudinally Extensive Transverse Myelitis
Following Vaccination with Nasal Attenuated Novel Influenza A(H1N1) Vaccine, 67
ARCHIVES NEUROLOGY 1018 (2010) (Ex. 86); Naoko Nakamura et al., Neurologic
Complications Associated with Influenza Vaccination: Two Adult Cases, 42 INTERNAL
MED. 191 (2003) (Ex. 93)).) He explained that a person’s response to a vaccine, which
is initially produced to create protective immunity, is comparable to a person’s response
to infectious antigens, and therefore, the recombinant or live attenuated antigens used
in vaccines can similarly produce autoimmunity. (Id. at 21.) Dr. Tornatore identified
multiple mechanisms by which an infectious antigen may induce autoimmunity but
noted that molecular mimicry is the most common. (Id. at 21-22.) In addition to
molecular mimicry, Dr. Tornatore identified the potential mechanisms of epitope
spreading and polyclonal activation. (Id. at 22.)

Dr. Tornatore explained the concept of the “fertile field” model, in which an
antigen with sequence homology to self-proteins may prime autoreactive T-cells but not
initiate an adverse immune reaction on its own; however, later stimulation by a vaccine
– even one without cross-reactive antigens or sequence homology – can initiate an
autoimmune reaction in a susceptible person and lead to inflammatory demyelination.
(Ex. 81, p. 22 (citing William Huynh et al., Post-Vaccination Encephalomyelitis:
Literature Review and Illustrative Case, 15 J. CLINICAL NEUROSCIENCE 1315 (2008) (Ex.
90)).) He elaborated that a subsequent flu vaccination can induce a rapid increase of
cytokines and chemokines, resulting in augmented inflammation in hyper-responders,
(Tr. 442-43 (citing Talaat et al., supra, at Ex. 127)), and the fertile field concept can
explain why petitioner was experiencing constitutional symptoms despite a lack of
pleocytosis in the CSF. (Id. at 155-57.) He also pointed out that the National Multiple
Sclerosis Society recommends delaying vaccination of persons who are experiencing
ongoing CNS inflammation, out of concern that vaccination could aggravate the
underlying inflammatory condition. (Ex. 98, p. 5.)

Dr. Tornatore offered 1-63 days (with a mean of 16.5 days) as the appropriate
time frame for TM to be caused by flu vaccination. (Ex. 81, p. 23 (citing Bakshi &
Mazziotta, supra, at Ex. 88, p. 248).) However, the Institute of Medicine (“IOM”) has
recognized that the latency between subsequent exposure to the antigen and
development of the immune response will likely be shorter due to recognition of memory

19
B and T cells during the primary immune response. (Ex. 98, p. 8.) He pointed to a
study by Langer-Gould et al., in which researchers concluded that a vaccine can act as
a “proinflammatory cofactor in individuals with subclinical autoimmunity,” such that
vaccination may “hasten symptom[s] onset but not change the long-term risk of
developing MS.” (Tr. 89-92 (quoting Annette Langer-Gould et al., Vaccines and the
Risk of Multiple Sclerosis and Other Central Nervous System Demyelinating Diseases,
71 J. AM. MED. ASS’N NEUROLOGY 1506 (2014) (Ex. 102)).) He elaborated that the role
of adjuvants in triggering an immune response “affirms the concept that muscle tissue is
capable of mounting a rapid immune response, with antigen bearing cells quickly
evident in draining lymph nodes shortly after vaccination.” (Ex. 98, pp. 9-10 (citing
Frank Liang & Karin Loré, Local Innate Immune Responses in the Vaccine Adjuvant-
Injected Muscle, 5 CLINICAL & TRANSLAT’L IMMUNOLOGY e74 (2016) (Ex. 101)); Tr. 100-
03.) Dr. Tornatore further opined that vaccine-induced inflammation can aggravate
underlying CNS inflammation rapidly due to the kinetics and anatomy of “draining lymph
nodes and their proximity to the spinal cord.” (Ex. 98, pp. 8-11 (citing Laurent Jacob et
al., Anatomy and Function of the Vertebral Column Lymphatic Network in Mice, 10
NATURE COMMC’NS, no. 4594, 2019, at 1 (Ex. 99)); Tr. 96-100.) Thus, Dr. Tornatore
asserted that Dr. Forsthuber’s conclusion that it is improbable that the flu vaccine could
aggravate symptoms of TM within one or two days overlooks that petitioner had
preexisting CNS inflammation prior to receiving the flu vaccine and that aggravation of
CNS inflammation is “hastened” when the flu vaccine is a “pro-inflammatory cofactor,”
rather than the first induction to autoimmunity. (Ex. 98, pp. 7-8; Ex. 130, p. 3.)

Regarding his reliance on case reports, Dr. Tornatore submitted that “[c]ase
reports are exceedingly important teaching tools in clinical medicine given that the
bedside approach to every patient is essentially a case report.” (Ex. 98, p. 6.) To
demonstrate the importance of case reports, Dr. Tornatore noted that the criterion in
Johns Hopkins Transverse Myelitis Center’s model diagnostic approach, which directs
the consideration of recent vaccination or systemic illness, was based on the clinical
experience of practitioners at Johns Hopkins that noticed a clinical history of prior
vaccination within a month of presentation in around 30% of TM patients. (Id. (citing
Chitra Krishnan et al., Transverse Myelitis: Pathogenesis, Diagnosis and Treatment, 9
FRONTIERS BIOSCIENCE 1483 (2004) (Ex. 100)).) He further noted that the case studies
he relied upon went beyond simply recognizing a temporal relationship and further
recognized “a logical sequence of cause and effect which was biologically based.” (Id.)
Dr. Tornatore asserted that, by contrast, “epidemiology cannot disprove the presence of
a rare event” and that petitioner’s case is exceptionally rare. (Id. at 7.) Even so, Dr.
Tornatore asserted that Langer-Gould et al. provides epidemiologic evidence by noting
that a vaccine can act as a “pro-inflammatory cofactor” in susceptible individuals. (Id.
(citing Langer-Gould et al., supra, at Ex. 102).)

20
ii. Lawrence Steinman, M.D. 12

Petitioner also relied on the expert opinion of Lawrence Steinman, M.D. Dr.
Steinman authored five expert reports in support of petitioner’s claim. (See Exs. 12, 55,
64, 75, 103.) He also testified at the entitlement hearing, during which he was proffered
without objection as an expert in the fields of neurology and neuroimmunology. (Tr.
182.)

Regarding diagnosis, Dr. Steinman concurred with Dr. Tornatore’s analysis and
opined that petitioner most likely has TM. (Ex. 12, p. 9; Tr. 183.) He noted that
petitioner’s treating physicians explored several alternative diagnoses, and petitioner’s
testing was negative for infection, mass lesion, and vascular malformation. (Ex. 12, p.
9.) He noted that petitioner’s spinal angiography was negative, meaning petitioner did
not have a dural venous fistula malformation. (Ex. 55, pp. 2-3 (citing Ex. 8, p. 7).) He
explained that petitioner’s history of pain in his neck, upper back, and shoulders four
weeks before his flu vaccination is consistent with TM. (Ex. 12, p. 9 (citing Ex. 1, p.
581).) At the hearing, Dr. Steinman clarified that “the whole picture emerged” with
petitioner’s difficulty walking and sensory issues around the time he was first
hospitalized. (Tr. 218-19.) He added that petitioner’s Solu-Medrol therapy on
December 1, 2011, “might have masked the evolution of more pronounced inflammation
on subsequent MRI and on any subsequent examination of the spinal fluid.” (Ex. 12, p.
9; Tr. 206.) He further suggested that treaters may have performed the spinal tap too
soon to reveal pleocytosis in the spinal fluid. (Tr. 207.) Thus, Dr. Steinman contended
that petitioner’s TM was not idiopathic as Dr. Forsthuber and Dr. Gelfand suggested.
(Ex. 64, pp. 4, 8; Tr. 185, 207.)

Dr. Steinman opined that petitioner had “smoldering” myelitis as evidenced by
earlier episodes of symptoms that were identical to petitioner’s symptoms following his
flu vaccination. (Tr. 183; Ex. 12, p. 27.) To support his opinion, he pointed to a medical
history of “pain in the posterior neck and upper back and shoulders” for approximately 4
weeks prior to flu vaccination (Ex. 55, p. 2 (citing Ex. 1, p. 581); Ex. 12, p. 27) and
petitioner’s reports of an earlier “identical episode” (Ex. 12, p. 27 (citing Ex. 1, pp. 16,
326)). He claimed that petitioner’s “earlier episodes indicate that the transverse myelitis
was brewing and that his immune system was primed.” (Ex. 12, p. 27.) Dr. Steinman
clarified that, in using the descriptor “smoldering,” he was referring to a condition that

12
Dr. Steinman received his medical degree from Harvard University in 1973. (Ex. 65, p. 1.) He is board-
certified in neurology and has practiced adult and pediatric neurology at Stanford University. (Ex. 12, p.
7; Ex. 65, p. 2; Tr. 180.) For the first twenty years of his career, Dr. Steinman “saw all sorts of patients.”
(Tr. 180.) He specifically treated both adults and children who suffered from various forms of
inflammatory neuropathy, including TM, acute disseminated encephalomyelitis, neuromyelitis optica, MS,
and others. (Ex. 12, p. 7.) Although he still treats patients while attending a couple weeks per year, Dr.
Steinman mostly does referrals on patients with probable neuroinflammatory diseases. (Tr. 180.) He is
currently a professor of neurology at Stanford University. (Ex. 12, p. 7; Ex. 65, p. 1; Tr. 180.) Dr.
Steinman’s research focuses on how the immune system attacks the nervous system, and he has
published on various topics involving vaccines and neurological disorders, including molecular mimicry.
(Ex. 12, pp. 7-8; Ex. 65, pp. 5-45; Tr. 181-82.) He holds numerous American and European patents,
including several U.S. patents relating to vaccines. (Ex. 12, p. 8; Ex. 65, pp. 2-3.)

21
was neither fully developed nor subclinical. (Tr. 215-16.) He also opined that
petitioner’s “smoldering” myelitis had been initially triggered by his prior zoster
vaccination. (Id.; Ex. 12, p. 27.) Petitioner’s November 29, 2011 antibody test was
negative for zoster (Ex. 1, p. 777); however, Dr. Steinman opined that this is not
dispositive. (Tr. 217.) Dr. Steinman suggested that petitioner likely had immunity to
varicella-zoster due to his age. (Id. at 216.)

Dr. Steinman opined that it is biologically plausible that the flu vaccine can cause
or significantly aggravate TM by triggering immunity to myelin lipids and proteins via
molecular mimicry. 13 (Ex. 12, p. 10.) According to Dr. Steinman, the specific
components of the 2011-12 flu vaccine, which included an H1N1 virus, can trigger an
immune response to myelin proteins and various complex sugars called gangliosides. 14
(Id.; Tr. 184.) He noted that “[g]angliosides are key structures associated with the
pathogenesis of inflammatory polyneuropathy,” and described molecular mimicry

13
Dr. Steinman explained that molecular mimicry occurs when the same protein fragment (i.e., peptide
epitope) is recognized by T cell receptors that bind to slightly different portion of the self-antigen (e.g.,
myelin basic protein). (Ex. 12, pp. 14-15.) Dr. Steinman used a computer program and bioinformatic
search tool, known as BLAST, to compare a vaccine protein and a protein that is known to be targeted in
a disease with the goal of determining whether there is sufficient similarity. (Ex. 75, pp. 6, 9-14, Tr. 184,
209-12.) He used a “three-step filtration system” to identify molecular mimics between the subject
vaccines and antigens that are targeted in TM. (Ex. 103, pp. 5-8.) In the first step, Dr. Steinman
explained that a viral peptide with homology at five amino acids within a stretch of twelve amino acids can
induce clinical signs of experimental autoimmune encephalomyelitis (“EAE”) in mice. (Ex. 12, p. 14 (citing
Anand M. Gautam et al., A Viral Peptide with Limited Homology to a Self Peptide Can Induce Clinical
Signs of Experimental Autoimmune Encephalomyelitis, 161 J. IMMUNOLOGY 60 (1998) (Ex. 35); Anand M.
Gautam et al., Minimum Structural Requirements for Peptide Presentation by Major Histocompatibility
Complex Class II Molecules: Implications in Induction of Autoimmunity, 91 PROCEEDINGS NAT’L ACAD.
SCIS. USA 767 (1994) (Ex. 36)); see also Ex. 64, p. 6; Tr. 210-12.) He explained that the identical amino
acids need not be consecutive and that certain amino acid substitutions will have no effect on activation
of a response if such variation is within a certain degree of degeneracy. (Ex. 12, pp. 14, 18-19 (citing Kai
W. Wucherpfennig et al., Structure of Human T-Cell Receptors Specific for an Immunodominant Myelin
Basic Protein Peptide: Positioning of T-Cell Receptors on HLA-DR2/Peptide Complexes, 92 PROCEEDINGS
NAT’L ACAD. SCIS. USA 8896 (1995) (Ex. 38); Stefan Hausmann et al., Structural Features of Autoreactive
TCR that Determine the Degree of Degeneracy in Peptide Recognition, 162 J. IMMUNOLOGY 338 (1999)
(Ex. 40)).) Dr. Steinman explained that “[d]egeneracy refers to how structurally similar amino acids can
still be recognized by an auto immunogenic T cell receptor.” (Ex. 12, p. 18.) He noted that
Wucherpfennig et al. found that “various substitutions at key residues” did not interfere with T cell
recognition of myelin basic protein.” (Id. at 19 (citing Wucherpfennig et al., supra, at Ex. 38).) In the
second step, the areas of alignment are filtered based on three peer reviewed papers. (Ex. 103, p. 5
(citing Anand M. Gautam et al., supra, at Ex. 35; Anand M. Gautam et al., supra, at Ex. 36; Robert Root-
Bernstein, Rethinking Molecular Mimicry in Rheumatic Heart Disease and Autoimmune Myocarditis:
Laminin, Collagen IV, CAR, and B1AR as Initial Targets of Disease, 2 FRONTIERS PEDIATRICS, Aug. 2014,
at 1 (Ex. 107)).) He explained that this filtration eliminates homologies that are below the threshold for
inducing clinical symptoms of neuroinflammation. (Id. at 5-6.) In the last step, the peptide sequences are
further filtered so that only those that have been identified by the Immune Epitope Database or the
Influenza Research Database remain. (Id.)
14
In particular, Dr. Steinman relied on the fact that the vaccine petitioner received contained
A/California/7/09 (H1N1)-like virus, A/Perth/16/2009 (H3N2)-like virus, and B/Brisbane/60/2008. (Ex. 12,
p. 10 (citing U.S. FOOD & DRUG ADMIN., NEWS RELEASE: FDA APPROVES VACCINES FOR 2011-2012
INFLUENZA SEASON (July 18, 2011) (Ex. 23)).)

22
between gangliosides and Campylobacter jejuni (“C. jejuni”) as one of the best
examples of molecular mimicry. (Ex. 12, p. 11 (citing C.W. Ang et al., Structure of
Campylobacter jejuni Lipopolysaccharides Determines Antiganglioside Specificity and
Clinical Features of Guillain-Barré and Miller Fisher Patients, 70 INFECTION & IMMUNITY
1202 (2002) (Ex. 26); Y. Fukami et al., Anti-GQ1b Antibody Syndrome: Anti-Ganglioside
Complex Reactivity Determines Clinical Spectrum, EUR. J. NEUROLOGY, 2015, at 1 (Ex.
27); Lawrence Steinman, Autoimmune Disease: Misguided Assaults on the Self
Produce Multiple Sclerosis, Juvenile Diabetes and Other Chronic Illnesses. Promising
Therapies are Emerging, SCI. AM., Sept. 1993, at 107 (Ex. 28)).) He cited a study by
Wucherffpenig et al. that found that the flu virus shares molecular similarities with
myelin basic protein and that antibodies to myelin basic protein cross-react with flu
virus. (Id. at 14-15 (citing Wucherpffenig, supra, at Ex. 38).) This is important because
it has been shown that immunity to myelin basic protein is related to TM (Id. at 14 (citing
Oded Abramsky & Dvora Teitelbaum, The Autoimmune Features of Acute Transverse
Myelitis, 2 ANNALS NEUROLOGY 36 (1977) (Ex. 33)) and immune responses to
gangliosides are associated with neuroinflammation (Id. at 20 (citing Jennifer L. Kanter
et al., Lipid Microarrays Identify Key Mediators of Autoimmune Brain Inflammation, 12
NATURE MED. 138 (2006) (Ex. 41); Peggy P. Ho et al., Identification of Naturally
Occurring Fatty Acids of the Myelin Sheath That Resolve Neuroinflammation, 4 SCI.
TRANSLAT’L MED., June 6, 2012, at 1 (Ex. 42)).) Dr. Steinman identified molecular
mimics between the components of the 2011-12 influenza vaccine and myelin basic
protein that he opined are sufficient to trigger neuroinflammation. (Ex. 75, pp. 11-12; Tr.
214.) Comparing the hemagglutinin of A/California/7/09 H1N1 and myelin basic protein,
Dr. Steinman identified the sequence GTCYPGDFIDY with five of eleven identical
amino acids. 15 (Ex. 75, pp. 11-13; Tr. 214.)

Further to this, Dr. Steinman asserted that “the zoster vaccine contains a
molecular mimic to the same myelin protein that has molecular mimics in the 2011-12
vaccine.” (Ex. 12, p. 10; Tr. 184.) Specifically, Dr. Steinman found several potential

15
Following critique from respondent’s experts, Dr. Steinman defended his criteria for determining
whether there is sequence homology between a protein and a self-antigen in his supplemental reports
and testimony. He explained that a BLAST search is the preferred search tool of Silvanovich et al., who
derided the “sliding window” approach for finding rungs of consecutive amino acids in a protein that may
have immunogenicity. (Ex. 75, p. 6, 15 (citing Andre Silvanovich et al., The Value of Short Amino Acid
Sequence Matches for Prediction of Protein Allergenicity, 90 TOXICOLOGICAL SCIS. 252 (2006) (Ex. 116)).)
He further explained that he applied two peer reviewed papers, which were both published in the official
journal of the American Association of Immunologists and studied the effects of a molecular mimic of five
of twelve identical amino acids and required that the amino acids in the sequence be identical, but not
consecutive. (Ex. 64, pp. 6-7 (citing Gautam et al., supra, at Ex. 35; Gautam et al., supra, at Ex. 36); Tr.
427.) Even under this criteria, researchers found that 40% of mice displayed clinical signs of EAE, such
as paralysis, after injection with a viral peptide that had 5 of 11 identical and 3 consecutive amino acids
between the virus and myelin basic protein. (Ex. 64, pp. 6-7; see Ex. 12, p. 14.) Dr. Steinman further
defended his reliance on Wucherpffenig et al. by citing a paper by Ahmed et al., which found that the
vaccine contain hemagglutinin, as well as “a diversity of other influenza viral antigens and egg proteins,”
such as nucleoprotein. (Ex. 64, p. 7 (citing Syed Sohail Ahmed et al., Antibodies to Influenza
Nucleoprotein Cross-React with Human Hypocretin Receptor 2, 7 SCI. TRANSLAT’L MED., July 1, 2015, at 1
(Ex. 22)); Ex. 75, pp. 15-16.) Dr. Steinman also disputed the relevance of E values beyond determining
whether proteins are in a similar family. (Tr. 430.)

23
molecular mimics between components of the zoster vaccine and myelin basic protein,
which he opined are also sufficient to induce neuroinflammation. (Ex. 12, pp. 20-23.)
Specifically, Dr. Steinman identified a five of ten match and an eight of ten match with
similar and identical amino acids between myelin basic protein and Zoster ORF 47, and
a five of eight match between myelin basic protein and Zoster ORF 56. (Ex. 12, pp. 20-
23; see also Ex. 75, pp. 8-11; Tr. 213-14.) He further identified the following
homologies between the zoster vaccine and myelin basic protein: TKTGLPQR with a
five out of ten match and SLFLLKHGLTRD with a six out of twelve match. (Ex. 75, p. 8;
Tr. 214.) Dr. Steinman suggests that epitope spreading 16 can therefore result in a recall
response, despite two different vaccines being involved. He explained that “[t]hey both
have mimics of myelin basic protein and therefore by this molecular spreading,
determinant spreading, you get a recall response when [petitioner] gets the influenza
[vaccine].” (Tr. 195.) He explained that “epitope spreading[] can certainly explain how
one myelin basic protein region on zoster could spread via this mechanism to a different
region of myelin basic protein, and cause a recall response.” (Tr. 434.) Thus, based on
the components contained in the zoster vaccine and flu vaccine, Dr. Steinman opined
that the flu vaccine can trigger a “recall response” to myelin basic protein induced by an
earlier zoster or flu vaccination. 17 (Ex. 12, pp. 10, 23, 27; Tr. 195, 214-16.) Dr.
Steinman concluded that homology with myelin basic protein and both the zoster
vaccine and the flu vaccine was sufficient to possibly provoke TM (Tr. 184, 189-90) and
that petitioner’s flu vaccination likely “aggravated the smoldering symptoms initially
triggered by” petitioner’s zoster vaccine approximately two months earlier (Id. at 215-16;
Ex. 12, p. 27.). 18

16
Dr. Steinman explains “epitope spreading” as a concept by which a break in tolerance to a myelin
protein for one epitope precedes a break in tolerance to other components of the same myelin molecule.
(Ex. 12, p. 21 (citing Eli E. Sercarz, Arraying Autoimmunity Treatment, 21 NATURE 1017 (2003) (Ex. 44));
see also Ex. 75, p. 8.) He notes that the process of epitope spreading generally takes “a few weeks” and
that the “approximately two, two-and-a-half months [between receipt of the zoster and flu vaccines] . . .
would have been more than enough time for a recall response to have been mustered.” (Tr. 195.)
17
In his reports, Dr. Steinman suggested that petitioner may have also received the 2010-11 flu vaccine,
which contained an H1N1-like virus, or otherwise had significant immunity to flu due to viral exposure,
prior vaccination, or both. (Ex. 12 p. 10.) Although noting petitioner likely had immunity to flu and to
hemagglutinin due to his age, his tenure in the armed forces, and Dr. Steinman’s belief that he had
previously received a flu vaccine, Dr. Steinman clarified at the hearing that he was not relying on a prior
flu vaccination to support his opinion regarding a recall response. (Tr. 188-89; Ex. 12, p. 24.)
18
There was significant discussion in the reports regarding Dr. Steinman’s initial claim surrounding a
dominant peptide in the influenza A hemagglutinin: YVKQNTLKL, which Markovic-Plese et al. found to be
cross-reactive with human T cell clone, and a sequence in a component of the flu vaccine that petitioner
received (A/perth/16/2009 (H3N2)): YVKQNTLKL. (Ex. 12, pp. 12-13 (citing Silva Markovic-Plese et al.,
High Level of Cross-Reactivity in Influenza Virus Hemagglutinin-Specific CD4+ T-Cell Response:
Implications for the Initiation of Autoimmune Response in Multiple Sclerosis, 169 J. NEUROIMMUNOLOGY
31 (2005) (Ex. 29)).) He asserted that “this immune response triggers a cross-reactive immune response”
to two myelin mimics of myelin oligodendroglia glycoprotein (“MOG”) and a myelin mimic of 2,3 cyclic
nucleotide phosphodiesterase (“2,3 CNPase”). (Id. at 13.) In response, Dr. Forsthuber criticized Dr.
Steinman’s comparison between the sequence YVKQNTLKL from the Influenza Texas/77 hemagglutinin
with the YVKQNTLKL sequence from the Influenza A/perth/16/2009 virus as the “degree of similarity is
completely expected” given the fact that these are the same hemagglutinin protein in two flu viruses. (Ex.
B, p. 6.) He further noted that Dr. Steinman had mistaken MOG for oligodendrocyte myelin glycoprotein

24
Dr. Steinman opined that the time frame of symptom onset in less than 72 hours
of vaccination is “consistent with what is seen in a recall response to a common
antigen.” (Ex. 12, p. 2.) He explained that once a “recall response to myelin basic
protein induced by earlier immunization with earlier wild-type influenza virus or wild-type
zoster virus, and/or an earlier vaccine to either influenza or zoster” has mounted, “such
a response could occur in as short as a day.” (Id.; see also Ex. 12, pp. 24-25 (citing
Tiroumourougane V. Serane & Bhuvaneswari Kothendaraman, Tuberculin Test Can Be
Read After 24 Hours in Adolescent Children, 60 J. TROPICAL PEDIATRICS 157 (2014) (Ex.
47); Lin Fan et al., Variation of Mycobacterium Tuberculosis Antigen-Specific IFN-γ
Responses in Healthy Tuberculin Skin Test (TST)-Positive Human Subjects, 7 PUB.
LIBR. SCI. ONE e42716 (2012) (Ex. 48); T. Kardjito & J.M. Grange, Immunological and
Clinical Features of Smear-Positive Pulmonary Tuberculosis in East Java, 61 TUBERCLE
231 (1980) (Ex. 49)) (discussing tuberculin responses that peaked within 24 hours after
injection).) He cited an animal study, in which researchers found that myelin reactive
lymphocytes can penetrate the CNS “within hours” and were “deep in the ‘parenchyma’
or brain substance” within 60 hours. (Ex, 12, pp. 4-6 (citing Ingo Bartholomäus et al.,
Supplementary Information, Effector T Cell Interactions with Meningeal Vascular
Structures in Nascent Autoimmune CNS Lesions, 462 NATURE, at 1 (2009) (Ex. 16)); Tr.
432 (quoting Ingo Bartholomäus et al., Effector T Cell Interactions with Meningeal
Vascular Structures in Nascent Autoimmune CNS Lesions, 462 NATURE 94, 94 (2009)
(Ex. 17, p. 1)) (emphasizing that the 1-2.5 day time frame in Bartholomäus et al. was
based on clinical signs of neurologic issues, but “an experimental animal is unable to tell

(“OMGP”), which “are two completely unrelated proteins, with essentially no sequence homology, despite
the similar sounding names.” (Id. at 7 (emphasis omitted); Ex. C, p. 8.) Although Dr. Steinman
subsequently acknowledged that the sequence referenced by Markovic-Plese et al. was OMGP, not
MOG, he asserted that an immune attack on OMGP, triggered by cross-reaction between the flu virus and
OMGP, could worsen neuroinflammation. (Ex. 64, p. 5 (citing Xinhua Lee et al., Oligodendrocyte
Differentiation and Myelination Defects in OMGp Null Mice, 46 MOLECULAR & CELLULAR NEUROSCIENCE
752 (2011) (Ex. 68)); see also Ex. 75, p. 5; Tr. 208-09.) However, Dr. Forsthuber asserted that Dr.
Steinman’s reliance on Markovic-Plese et al. is misplaced as neither OMGP nor 2, 3 CNPase have been
associated with TM. (Ex. B, p. 7; Ex. C, p. 8; Ex. D, pp. 6-7 (explaining that Lee et al. does not support
Dr. Steinman position because the study specifically looked at how the absence of OMGP affected
oligodendrocytes and remyelination).)

Dr. Steinman ultimately asserted that “discussion of OMGP is largely irrelevant” as he has
provided “numerous molecular mimics between [myelin basic protein] and MOG and the components of
the influenza vaccine and zoster vaccines.” (Ex. 75, p. 6.) At the hearing, he further disclaimed any
intention of relying on MOG, instead choosing to rely on molecular mimics between myelin basic protein
and the zoster and flu vaccines. (Tr. 209 (“So the good news is I’m not pushing either MOG or OMGP.
We can just stick to myelin basic protein . . . .”); see also Tr. 215 (“There’s also a lot of discussion . . .
about MOG, but because of the error in the Markovic-Plese paper, I’m not even -- we don’t have to rely
on MOG. We should just stick to the myelin basic protein mimicry between zoster and influenza.”); Tr.
214 (Dr. Steinman indicating that “we should focus on” zoster and the hemagglutinin of influenza as
“myelin basic protein determinants”).) Based on his testimony, Dr. Steinman has abandoned his
arguments regarding MOG, OMGP, and 2, 3 CNPase, including his suggestion of molecular mimics
between the zoster vaccine and MOG. (See Ex. 12, p. 23.) Although Dr. Steinman decided to abandon
these arguments at the hearing, I have still reviewed all of the arguments and evidence presented in his
prior reports. However, in the interest of brevity, I will not herein address the specific arguments that Dr.
Steinman subsequently disclaimed.

25
you whether they’re having subtle neurologic signs”).) As another example of how
quickly the immune system responds in a recall response, Dr. Steinman cited a study by
Odoardi et al., that found exposure to myelin basic protein affected TMBP-GFP cells
throughout the spinal cord within about 1 hour. (Ex. 12, p. 7 (citing F. Odoardi et al.,
Blood-Borne Soluble Protein Antigen Intensifies T Cell Activation in Autoimmune CNS
Lesions and Exacerbates Clinical Disease, 47 PROCEEDINGS NAT’L SCIS. 18625 (2007)
(Ex. 18)).) He further cited a series of studies showing that a recall response to self-
antigens can manifest “within minutes.” (Id. at 26 (citing Rosetta Pedotti et al., An
Unexpected Version of Horror Autotoxicus: Anaphylactic Shock to a Self-Peptide, 2
NATURE IMMUNOLOGY 216 (2001) (Ex. 51); Rosetta Pedotti et al., Involvement of Both
‘Allergic’ and ‘Autoimmune’ Mechanisms in EAE, MS and Other Autoimmune Diseases,
24 TRENDS IMMUNOLOGY 479 (2003) (Ex. 52); Howard L. Weiner, The Fine Line Between
Autoimmune and Allergic Encephalomyelitis, 2 NATURE IMMUNOLOGY 193 (2001) (Ex.
53); Edwin Liu et al., Anti-Peptide Autoantibodies and Fatal Anaphylaxis in NOD Mice in
Response to Insulin Self-Peptides B:9-23 and B:13-23, 110 J. CLINICAL INVESTIGATION
1021 (2002) (Ex. 54)).)

In further support of a proximate temporal relationship, Dr. Steinman pointed to a
study by Schonberger et al., which found increased incidence of GBS within 0-1 days of
vaccination when compared to later intervals. (Ex. 12, pp. 2-3, 26 (citing Lawrence B.
Schonberger et al., Guillain-Barre Syndrome Following Vaccination in the National
Influenza Immunization Program, United States, 1976–1977, 110 AM. J. EPIDEMIOLOGY
105 (1979) (Ex. 13)); Ex. 64, p. 8.) He asserted that, despite exploring the relationship
between GBS and the flu vaccine, Schonberger is relevant to petitioner’s case. (See
Ex. 75, pp. 1-2.) Dr. Steinman suggests that the blood-brain barrier of the CNS is
similar to the blood-nerve barrier of the peripheral nervous system and, thus, analogy to
the time frame for breakdown of the blood-nerve barrier in GBS is instructive of a
reasonable time frame for breakdown of the blood-brain barrier in TM. (Ex. 12, p. 3
(citing Takashi Kanda, Biology of the Blood-Nerve Barrier and Its Alteration in Immune
Mediated Neuropathies, 84 J. NEUROLOGY NEUROSURGERY PSYCHIATRY 208 (2012) (Ex.
14)); Ex. 75, pp. 1-2.)

In supplemental reports, Dr. Steinman defended his theory of causation against
criticism from Drs. Forsthuber and Gelfand. (Ex. 64; Ex. 75.) Given that petitioner was
66 years old when he received the flu vaccine at issue, Dr. Steinman explained that he
likely possessed anti-ganglioside antibodies, and the flu vaccine therefore could have
triggered a recall response to these antibodies. (Ex. 64, p. 2; Ex. 75 pp. 2-3.) Dr.
Steinman further stated that Dr. Forsthuber overlooked that flu hemagglutinins are
“heavily glycosylated” and that the glycosylation “plays a significant role in the antigenic
drift and immunogenicity.” (Ex. 64, p. 3 (citing Athanasios Kossyvakis et al., Challenges
in Antigenic Characterization of Circulating Influenza A(H3N2) Viruses during the 2011-
2012 Influenza Season: An Ongoing Problem?, 53 J. CLINICAL MICROBIOLOGY 1493
(2015) (Ex 66)).) Dr. Steinman cited an article by Tate et al. to show the importance of
glycosylation of flu vaccine proteins. (Id. at 3-4 (citing Michelle D. Tate et al., Playing
Hide and Seek: How Glycosylation of the Influenza Virus Hemagglutinin Can Modulate
the Immune Response to Infection, 6 VIRUSES 1294 (2014) (Ex. 67)).)

26
b. Respondent’s Experts

i. Jeffrey Gelfand, M.D., M.A.S. 19

To defend against the claim, respondent offered an expert opinion of neurologist
Jeffrey Gelfand, M.D., M.A.S. Dr. Gelfand authored three expert reports on behalf of
respondent. (See Exs. A, E, I.) He also testified as the entitlement hearing, during
which, he was proffered without objection as an expert in the field of
neuroimmunology. 20 (Tr. 239, 243.)

Although he does not dispute petitioner’s diagnosis of TM (Ex. A, p. 11), Dr.
Gelfand opined that petitioner’s flu vaccination “did not cause or aggravate his
transverse myelitis to a more likely than not standard” (Tr. 244; see also Ex. E, p. 8),
and that petitioner instead suffered from an acute, idiopathic TM (Ex. A, pp. 11, 20). He
stated that petitioner’s history of evolving cervical spinal cord syndrome, neurological
examinations showing spinal cord localization, and MRI showing multifocal
enhancement and a T2 hypersensitivity in the cervical cord all support a diagnosis of
TM. 21 (Id. at 11.) Dr. Gelfand opined that petitioner experienced sensory dysfunction
that was attributable to the spinal cord, bilateral symptoms, and sensory impairment that

19
Dr. Gelfand received his medical degree from Harvard Medical School. (Ex. A, Tab 1, p. 1; Ex. F, p. 1;
Tr. 240.) He went on to complete an internship in Internal Medicine, a residency in Neurology, and a
fellowship in MS and Neuroimmunology at the University of California, San Francisco (“UCSF”). (Ex. A,
Tab 1, p. 1; Ex. F, p. 1; Tr. 240.) He also received a Master’s in Advanced Study in Clinical Research
from UCSF. (Ex. A, Tab 1, p. 1; Ex. F, p. 1; Tr. 240-41.) He is board-certified in neurology and maintains
an active medical license in California. (Ex. A, Tab 1, p. 1; Ex. A, p. 2; Ex. F, p. 1; Tr. 241.) He currently
works as an associate professor of clinical neurology and regularly sees patients at UCSF, and the
Zuckerberg San Francisco General Hospital. (Ex. A, Tab 1, p. 2; Ex. F, p. 2; Tr. 241.) Dr. Gelfand
regularly treats patients with myelitis of various causes, including TM. (Tr. 241-42.) He also works as the
Director of the Clinical Fellowship Program and the Assistant Medical Director at UCSF MS and
Neuroinflammation Center. (Ex. A Tab 1, p. 2; Ex. F, p. 2; Tr. 241.) Finally, Dr. Gelfand conducts clinical
research that is focused on neuroinflammatory disorders. (Ex. A, p. 3; Ex. A, Tab 1, pp. 13-14; Ex. F, p.
14; Tr. 242-43.) He has published 69 peer-reviewed publications, 30 review articles, and 7 books and
chapters on this subject. (Ex. F, pp. 16-24; Ex. A, Tab 1, pp. 15-20.)

Although Dr. Gelfand was offered as an expert in neuroimmunology, he deferred to Dr. Forsthuber’s
20

more in-depth immunology opinion. (Ex. A, p. 18; see also Tr. 318-20.)
21
More specifically, he explained that petitioner’s presentation “are consistent with accepted diagnostic
criteria” for TM, which includes (1) development of sensory, motor, or autonomic dysfunction attributable
to the spinal cord; (2) bilateral symptoms; (3) sensory impairment below a certain level; (4) exclusion of
extra-axial compressive etiology by neuroimaging; (5) inflammation within the spinal cord as
demonstrated by pleocytosis in the CSF, elevated IgG index, or gadolinium enhancement on MRI; and/or
(6) progression to nadir between 4 hours and 21 days following onset of symptoms. (Ex. A, p. 11-13; Tr.
244-78 (citing Transverse Myelitis Consortium Working Group, Proposed Diagnostic Criteria and
Nosology of Acute Transverse Myelitis, 59 NEUROLOGY 499 (2002) (Ex. A, Tab 2)).) Although the MRI
showed cervical spinal stenosis, the stenosis was not believed to be significant enough to merit surgical
decompression or explain his symptoms, and a spinal dural arterio-venous fistula or other spinal vascular
malformation was ruled out. (Ex. A, p. 12; Tr. 262.) Further, Dr. Gelfand opined that petitioner’s B12
deficiency did not fully explain his spinal cord syndrome, although it could have magnified some of
petitioner’s neurologic symptoms. (Ex. A, p. 12; Tr. 262.)

27
progressed in a manner consistent with what is expected of an evolving spinal cord
syndrome. (Tr. 247-48, 258.) That is, Dr. Gelfand submitted that petitioner’s clinical
syndrome evolved over several days before reaching a nadir over the course of a
couple weeks, fitting the standard for what would be expected of an acute TM. (Id. at
278.) Regarding inflammation of the spinal cord, Dr. Gelfand explained that, while the
CSF analysis revealed a mild protein elevation, there were no other CSF markers of
inflammation. (Id. at 263; Ex. A, pp. 11-12.) Dr. Gelfand explained that elevated myelin
basic protein is a nonspecific marker of an acute injury that is consistent with spinal cord
injury, and the fact that it was only mildly elevated does not suggest that it was
resolving. (Tr. 268-69.) He also noted that it is common for patients with monophasic
conditions, such as acute, idiopathic TM, to have multifocal lesions, and “that a non-
enhancing lesion could still be and often is the causative acute [TM] lesion when the
rest of the pieces fit.” (Id. at 274-76.) The monophasic characteristic of acute TM
suggests that the multifocal lesions are part of the same process. 22 (Id. at 274, 287;
see also Tr. 309.) Thus, Dr. Gelfand concluded that petitioner’s presentation and
testing supported an inflammatory cause of his symptoms and that the most appropriate
diagnosis of his condition is acute, idiopathic TM with an autoimmune origin. (Ex. A, p.
13; Tr. 263, 266-67.)

Regarding timing, Dr. Gelfand indicated that the medical records suggest that
petitioner first exhibited symptoms of TM on November 24, 2011, the day after his flu
vaccination. (Ex. A, pp.14-16; Tr. 247-48, 291-92.) He noted that petitioner did not
report any shoulder or back pain when he received his pneumococcal and zoster
vaccinations on September 21, 2011. (Ex. A, p. 14 (citing Ex. 1, pp. 586-88); Ex. E, p. 3
(citing Ex. 1, pp. 587-90.) Additionally, he cited telephone encounters with petitioner’s
primary care clinic on September 22, 2011, September 23, 2011, September 27, 2011,
and October 12, 2011, which do not document any symptoms suggestive of TM. (Ex. A,
p. 14 (citing Ex. 1, p. 584); Ex. E, p. 3 (citing Ex. 1, pp. 584-85.)

While Dr. Gelfand acknowledged that, on November 28, 2011, petitioner reported
an “identical” episode of neck and shoulder pain two months prior, he asserted that the
information contained in the medical records does not establish that these symptoms
were consistent with TM. (Ex. A, pp. 14-15; Ex. E, p. 5 (stating that “[t]here is no
additional documentation provided about what symptoms made the episode ‘identical’”);
see also Tr. 280-81.) Specifically, he noted that there was no detail as to “the character
and pattern” of the symptoms or whether petitioner experienced additional symptoms
such as “sensory changes or bowel or bladder involvement to support a spinal cord

22
Dr. Gelfand explained that some of petitioner’s treating neurologists were concerned about some
enhancement in the cervical spine, “but on official neuroradiology final reads, there was no definite
enhancement called.” (Tr. 288.) However, “there was definite enhancement called overlying the parts of
the thoracic cord.” (Id.) Dr. Gelfand explained that “[t]here’s nothing intrinsic that says only one part of
the nervous system can be affected at a time,” and concurred with Dr. Tornatore’s opinion that the
definite enhancement was “overlying the dorsal, the back part of the spinal cord, as opposed to being
within the spinal cord itself.” (Id. at 287-89.) Because dural arterio-venous fistula was ruled out by
conventional angiogram, Dr. Gelfand opined that the definite enhancement is either prominent vessels or
a component of focal inflammation, but “without follow-up imaging, I don’t think we can say more.” (Id. at
289.)

28
localization for those symptoms.” (Ex. A, pp. 14-15.) Dr. Gelfand also submitted that
petitioner’s episode of “identical” symptoms was not typical of acute TM, explaining that
“[t]he most common clinical presentation of acute transverse myelitis is an acute
neurological syndrome with continued progression to nadir followed either by gradual
recovery or statis persistence of neurological deficits.” (Ex. E, p. 7; see also Ex. I, p. 2;
Tr. 277.) He further explained that “[s]ymptoms of myelitis can sometimes appear to
stutter or manifest subtly,” but this typically occurs in the context of persistent symptom
progression “without rapid intervening complete remissions.” (Ex. E, p. 7.) Dr. Gelfand
explained that it would be “remarkable clinically” for a patient with such significant
neurologic dysfunction to not seek medical care, to not report these symptoms to any
provider, and for the symptoms to spontaneously resolve without medical intervention.
(Tr. 279-82, 311.) However, assuming that the court accepted petitioner’s claims of
experiencing a prior episode of “identical” symptoms, Dr. Gelfand conceded that those
reports “could be interpreted as consistent with myelitis.” (Tr. 304-05.) He explained
that the one- to two-week time frame “would likely be attributable to a single event of
TM;” however, a one- to two-month time frame “would fall far outside the expected
onset to nadir time frame typical of acute TM.” (Ex. E, p. 8; Tr. 279-80.) The latter point
is important because there is no evidence that petitioner had recurrent TM. (Ex. E, pp.
7-8.) Thus, Dr. Gelfand ultimately disagreed that petitioner had a preexisting
smoldering myelitis. (Ex. A, p. 19; Tr. 278.) However, Dr. Gelfand acknowledged that,
if the court credits petitioner’s reports of a prior episode, regardless of what time frame
was believed, then onset of petitioner’s TM would have predated his flu vaccine. (Tr.
306-07.)

Although Dr. Gelfand initially described neck and shoulder pain as a new
symptom as of November 23, 2011 (Tr. 293-95 (citing Ex. 1, pp. 591, 597)), and as
“clearly consistent” with TM (Ex. A, p. 15), he later qualified that “[n]eck and back pain
are also very common complaints that can be ascribed to many different etiologies, and
those symptoms are not specific for any one etiology.” (Ex. E, p. 7; Tr. 296). He
elaborated that it is possible for neck and shoulder pain to have a cervical spinal
localization, but “in the absence of other features, [he did] not believe that that was
reflective of an active myelitis to a more likely than not standard.” (Tr. 248-49, 296; Ex.
E, p. 7.) Although he provided, by way of example, descriptions of pain that would allow
a clinician to distinguish between neuropathic symptoms and musculoskeletal pain, Dr.
Gelfand testified that “[p]ain is an inherently subjective human experience,” and opined
that it was reasonable for petitioner’s primary care physician to conclude that
petitioner’s neck and shoulder pain on November 23, 2011, had a musculoskeletal
etiology. (Tr. 249-51; see also Tr. 296 (“Soreness is a relatively nonspecific or vague
term, so it really depends on what is meant by soreness.”); Tr. 326-28 (discussing
certain records of shoulder pain that demonstrate the clinical complexity of
distinguishing between new symptoms and comorbidities).) He explained that “one of
the challenges with interpretation [of the medical records] is the limited clinical
description that is available.” (Tr. 297.) Dr. Gelfand testified that, even “with the benefit
of hindsight and review of the record, I think that the description is -- what we have of it
is relatively nonspecific to invoke a neuropathic cause . . . given the available medical
record.” (Id. at 251.) Additionally, the physical examination on November 23, 2011,

29
revealed tenderness in the neck and back muscles. (Ex. A, p. 15. (citing Ex. 1, pp. 581-
83).) Although he acknowledged that soreness is generally accepted as “within the
spectrum of pain and discomfort” (Tr. 292), Dr. Gelfand opined that the
soreness/tenderness documented was more suggestive of a muscular cause and noted
that no other neurological symptoms were reported. (Ex. A, p. 15. (citing Ex. 1, pp. 581-
83); see also Ex. E, p. 4 (concluding that “[p]etitioner’s symptoms at that time were
muscular in nature”); Tr. 335-36 (citing Ex. 1, pp. 591-92).) However, he also concurred
with the radiology report that assessed petitioner as having degenerative disc disease,
rather than compressive myelopathy. (Tr. 259.) Ultimately, Dr. Gelfand admitted that
there is “no other explanation in the record for shoulder pain in late November . . .
beyond the myelitis.” (Id. at 298.)

Regarding petitioner’s inability to sense the need to defecate, Dr. Gelfand opined
that, based on the medical record as a whole, this symptom was more likely than not a
chronic symptom that predated the onset of petitioner’s TM. (Tr. 252-53, 257.) He
referenced a September 21, 2011 encounter, during which it was noted that petitioner
“felt the urge for bowel movement” had been “impaired” since his earlier surgery. (Id. at
254-55 (citing Ex. 1, pp. 597-99).) He cited another encounter from April 2012, in which
it was noted that this symptom predated onset of petitioner’s TM. (Id. at 256-57 (citing
Ex. 1, p. 174).) However, Dr. Gelfand admitted that the lack of ability to sense the need
to defecate could be a precursor to a later incontinence as a symptom of a spinal cord
dysfunction in the correct time frame and clinical context. (Id. at 254, 257-58.) He
further acknowledged that petitioner’s symptom worsened and eventually evolved to
include prominent neurogenic bowel symptoms. (Tr. 256-57 (citing Ex. 1, p. 174).)

Dr. Gelfand opined that petitioner’s TM “is most convincingly and compellingly
documented with the rapid onset and progression of severe shoulder pains with sand-
like sensory change (a neuropathic quality) and weakness with rapidly progressive
symptoms localizable to the cervical spinal cord on or around November 24, 2011.”
(Ex. E, p. 8.) Dr. Gelfand emphasized that the description of sand in the shoulders
“sounds different from the much vaguer descriptions of pain documented previously.”
(Ex. A, p. 15.) He stated that petitioner’s reported symptoms on November 25 and 28,
2011, confirm that he was experiencing symptoms of TM at that time. (Id. at 15-16
(citing Ex. 1, pp. 565, 572, 579).) He opined that the non-enhancing lesions seen on
MRI further confirm myelitis. (Tr. 308.) Thus, based on his review of the medical
records, Dr. Gelfand placed the onset of petitioner’s TM at one day post-vaccination on
November 24, 2011. (Id. at 247-48; Ex. A, p. 15.) However, Dr. Gelfand conceded that
petitioner was not seen by a doctor at any point between when he received the flu
vaccine on November 23, 2011, and when he presented to the ER on November 28,
2011. (Tr. 300-01.) He explained that, despite the lack of medical records during that
time frame, he credited the history provided by petitioner on November 28, 2011, which
correlated with physical examination findings. (Id.) Thus, Dr. Gelfand opined that onset
of petitioner’s TM was likely November 24, 2011, but his symptoms in the following days
confirm that petitioner’s documented neck and shoulder pain on November 24, 2011,
was associated with an evolving neuropathic syndrome. (Id. at 297-98.)

30
In response to Dr. Tornatore’s report, Dr. Gelfand challenged the proposition that
the non-enhancing T2 lesions seen on petitioner’s MRI indicates that the lesion was at
least two- to three-weeks old (Ex. E, pp. 9-10), and instead opined that the lesions likely
started no earlier than November 24, 2023, or five days before the MRI (Tr. 307). Dr.
Gelfand disputed the relevance of the literature Dr. Tornatore relied on to support his
opinion. (Ex. E, pp. 9-10.) He explained that neither the Lai study nor the Cotton study
analyzed spinal cord MRIs or spinal cord lesions. (Id. at 9 (citing Lai et al., supra, at Ex.
96; Francois Cotton et al., supra, at Ex. 97).) Additionally, he noted both studies
examined patients with MS, not acute TM. (Id.) Dr. Gelfand noted that studies focused
on spine imaging in acute TM cases have found “varied patterns of gadolinium
enhancement on baseline MRI.” (Id. at 10 (citing E. Bulut et al., MRI Predictors of
Recurrence and Outcome After Acute Transverse Myelitis of Unidentified Etiology, 40
AM. J. NEURORADIOLOGY 1427 (2019) (Ex. E, Tab 3); J. de Seze et al., Idiopathic Acute
Transverse Myelitis: Application of the Recent Diagnostic Criteria, 65 NEUROLOGY 1950
(2005) (Ex. E, Tab 4)).) He opined that the non-enhancing lesions cannot be dated with
any precision, given this variability. (Tr. 275, 314-15.) Although Dr. Gelfand explained
that the Transverse Myelitis Consortium Working Group’s proposed diagnostic criteria
was developed to aid in identifying the etiology of a condition, rather than to understand
the timing (Id. at 266-67), he further noted that the criteria for TM do not require contrast
enhancement on spinal MRI (Id. at 260; see also Ex. E, p. 10). He explained that
“enhancement is not always present when a patient has a bona fide acute transverse
myelitis” (Tr. 272-73 (citing Bulut et al, supra, at Ex. E, Tab 3)), and that, in the case of
monophasic acute TM, non-enhancement can mean that the lesion is older or that the
MRI is not uncovering a break in the blood-brain barrier due to the limitations of MRI
technology (Id. at 275-76, 285-86). However, he explained that it generally understood
that an autoimmune myelitis “takes time to build” and an immune process was likely
evolving “for some time.” (Id. at 317-18, 321-22.) He further acknowledged that, if the
lesions were present on November 23, 2011, the date of vaccination, then petitioner
likely had TM at that time. (Id. at 307-08.)

Concerning the lack of inflammatory markers in the CSF, Dr. Gelfand
acknowledged that there are some clinical contexts in which a lumbar puncture can be
performed too early in an inflammatory syndrome to reveal the true extent of the
inflammation. (Tr. 267.) However, he disagreed with Dr. Tornatore’s suggestion that
the blood-brain barrier healed, trapping the inflammation inside and resulting in the
absence of other clinical signs of inflammation. (Id. at 283.) In response to my question
regarding whether there would typically be a correlation between symptom progression
and lesion enhancement, Dr. Gelfand opined that, in the context of an acute
inflammatory process, it is counterintuitive for someone to experience a dramatically
worsening condition that is temporally associated with non-enhancing lesions. (Id. at
283-85.) And, although he testified that clinicians assume that lesions were enhanced
at some point in their course, he qualified his opinion by again acknowledging that, in
the case of an acute TM, there may not be enhancing lesions on MRI for a number of
reasons, including that the lesion is too small or too subtle, or that the MRI is not
sensitive enough to detect enhancement. (Id. at 284-86.)

31
Dr. Gelfand disagreed with Dr. Steinman’s causal theory and opinion regarding
an appropriate time frame for onset of TM following vaccination. (Ex. A, pp. 13-20.)
Given Dr. Gelfand’s opinion that petitioner’s TM first manifested on November 24, 2011,
he stated that a one-day interval between vaccination and onset “would be too soon to
invoke a post-influenza vaccination myelitis based purely on a molecular mimicry
theory.” (Id. at 17.) He referenced a review that described the minimum time interval
between flu vaccination and onset as being seven days. (Id. (citing N. Agmon-Levin et
al., Transverse Myelitis and Vaccines: A Multi-Analysis, 18 LUPUS 1198 (2009) (Ex. A,
Tab 5)).) Dr. Gelfand also disputed the applicability of the Schonberger article (supra,
at Ex. 13), noting that the article explored the flu vaccine’s relationship to GBS, an
inflammatory polyneuropathy/radiculopathy, not TM, which is an inflammatory spinal
cord syndrome with a distinct disease process from GBS. (Id. at 18-19.) Instead, Dr.
Gelfand pointed to two studies, which found that the measurable risk myelitis following
flu vaccination was “extremely low.” (Id. at 19 (citing Langer-Gould et al., supra, at Ex.
102; James D. Nordin et al., Maternal Safety of Trivalent Inactivated Influenza Vaccine
in Pregnant Women, 121 OBSTETRICS & GYNECOLOGY 519 (2013) (Ex. A, Tab 9)).)
Although he conceded that it is possible for myelitis to be aggravated, he explained that
“it depends on the specifics of the theory being proposed.” (Tr. 324.) Dr. Gelfand
ultimately opined that the evidence is insufficient to support that the flu vaccine more
likely than not aggravated petitioner’s TM. 23 (Id.; see also Ex. E, p. 12.)

ii. Thomas Forsthuber, M.D., Ph.D. 24

Dr. Forsthuber authored six expert reports in support of respondent’s position in
this case. (See Exs. B-D, G-H, J.) He also testified at the entitlement hearing during
which he was proffered without objection as an expert in the field of immunology. (Tr.
339, 345.) A significant portion of Dr. Forsthuber’s opinion includes his disagreement
that molecular mimicry is a plausible causal theory. However, because I did not find it
necessary to reach that question in order to resolve this case, it is not necessary to
summarize Dr. Forsthuber’s more detailed rebuttal to that proposed mechanism of
injury.

23
In his second supplemental report, Dr. Gelfand suggested that there were two possible scenarios in this
case. In his opinion, the “most likely scenario” places onset at one-day following vaccination. (Ex. I, p.
3.) However, he suggested that there is another “possible scenario, which requires some degree of
speculation given the available clinical record.” (Id.) In this second scenario, Dr. Gelfand suggested that
“petitioner’s TM began approximately two weeks prior to his flu vaccination, and worsened one day after
his flu vaccination.” (Id.) Dr. Gelfand ultimately maintained that petitioner’s flu vaccination did not
aggravate his TM to a more likely than not standard. (Id.)
24
Dr. Forstuber received his medical degree from the University of Tübingen. (Ex. B, Tab. 1, p. 1.) He is
board-certified in anatomical and clinical pathology. (Ex. B, p. 1; Tr. 340.) He specializes in immunology,
specifically autoimmune disease research and T cell immunology. (Ex. B, p. 1.) He spends about sixty
percent of his time conducting medical research. (Tr. 343.) He has published “a little over a hundred”
peer-reviewed publications and “a couple of book chapters.” (Id. at 343; Ex. K, pp. 24-35.) He is
currently employed as a professor of immunology and endowed chair of biotechnology at the University of
Texas at San Antonio as well as an adjunct professor of pathology, microbiology, and immunology at the
University of Texas Health Sciences Center, San Antonio. (Ex. B, p. 1; Tr. 339.)

32
Dr. Forsthuber explained that MS and TM are comparable neuroinflammatory
conditions. (Ex. G, p. 4.) He noted that researchers have studied whether the flu
vaccine can induce T cell responses to myelin basic protein in MS patients and found
that flu-vaccinated MS patients can mount immune responses against flu but not
against myelin basic protein. (Ex. H, p. 17 (citing N.F. Moriabadi et al., Influenza
Vaccination in MS: Absence of T-Cell Response Against White Matter Proteins, 56
NEUROLOGY 938 (2001) (Ex. H, Tab 15)).) That said, Dr. Forsthuber explained that
“there is no reliable evidence that a vaccine given during a flare induces MS or makes
MS flares worse, and the advice to delay vaccination is given out of abundance of
caution.” (Id. at 20.) He disagreed with Dr. Tornatore’s reliance on Langer-Gould et al.
(supra, at Ex. 102), noting that researchers found the flu vaccine neither increased the
risk of MS (or any other CNS demyelinating syndrome) nor accelerated or aggravated
relapses. (Id.) Further refuting Dr. Tornatore’s claims, Dr. Forsthuber cited a study by
Michielsens et al., in which researcher observed MRI studies of MS patients before and
after flu vaccination. (Id. (citing B. Michielsens et al., Serial Magnetic Resonance
Imaging Studies with Paramagnetic Contrast Medium: Assessment of Disease Activity
in Patients with Multiple Sclerosis Before and After Influenza Vaccination, 30 EUR.
NEUROLOGY 258 (1990) (Ex. H, Tab 16)).) The study concluded that vaccination had no
short-term clinical or subclinical effect on MS activity. (Id.)

Regarding the timeframe, Dr. Forsthuber opined that it was highly unlikely for an
individual to manifest disease within a one-day time interval after vaccination. (Ex. B, p.
20.) Dr. Forsthuber noted that the Bartholomäus study (supra, at Ex. 17) does not
demonstrate onset of disease before three days post-vaccination. (Id. at 18-20; Tr. 411-
13.) He explained that Dr. Steinman relied on studies that looked at T cells in “passive”
EAE, but this model creates an immune response that is “completely unlike” the
immune response that follows vaccination. (Ex. B, p. 18; Tr. 413.) He described his
own study, in which autoimmune demyelinating disease was induced by immunization
and onset of clinical signs of EAE coincided with an increase in inflammatory cells in the
CNS “approximately 10-11 days after active immunization” with disease peak
“approximately one week later, i.e. by 15-21 days.” (Ex. B, pp. 18-19 (citing Rebecca A.
Sosa et al., The Kinetics of Myelin Antigen Uptake by Myeloid Cells in the Central
Nervous System during Experimental Autoimmune Encephalitis, 191 J. IMMUNOLOGY
5848 (2013) (Ex. B, Tab 13).) Additionally, Dr. Forsthuber challenged the relevance of
the Schonberger article (supra, at Ex. 13) to this case, noting that the article focused on
GBS, which is different from TM in clinical features, pathogenesis, diagnostic features,
and efficacy of treatments. (Ex. B, p. 18 (citing Chitra Krishnan et al., Transverse
Myelitis: Pathogenesis, Diagnosis and Treatment, 9 FRONTIERS BIOSCIENCE 1483 (2004)
(Ex. B, Tab 2)); see also Ex. C, p. 1.)

In response to Dr. Steinman’s recall response theory, Dr. Forsthuber opined that
the flu vaccine cannot activate a recall response against an earlier zoster vaccine. (Ex.
B, pp. 17-19.) Dr. Forsthuber explained that Dr. Steinman’s causal theory turns on a
meaningful relationship between the zoster vaccine and the flu vaccine because,
without such relationship, there is no way for the flu vaccine to have activated zoster

33
specific T cells. (Tr. 400-01.) He explained that, in order for the flu vaccine to induce
memory T cells from the prior zoster vaccination, the flu vaccine would need “to contain
a peptide that is pretty much identical” to the peptide in the zoster vaccine that induced
a T cell response against myelin basic protein. (Id. at 401.) Dr. Forsthuber noted that,
although Dr. Steinman provided peptides in the zoster vaccine and in the flu vaccine
that could have sequence homology to myelin basic protein, he did not compare those
peptides to each other. (Id.) Dr. Forsthuber compared the peptides from the zoster and
flu vaccines and found that those peptides “have essentially no similarity.” (Id.) Dr.
Forsthuber stressed that there is no evidence that the flu vaccine can recall varicella-
zoster immunity as the flu vaccine “does not provide protection against a varicella-
zoster virus infection and vice versa,” and as such, “there is no significant sequence
homology between these unrelated viruses.” (Ex. B, p. 19 (emphasis omitted).) Dr.
Forsthuber emphasized that Dr. Steinman suggests the concept of epitope spreading to
explain how the flu vaccine could have reacted to additional epitopes that were spread
as a result of the zoster vaccine, even if the flu vaccine does not cross-react with an
epitope from the zoster vaccine; however, Dr. Forsthuber opined that it is “very difficult
to prove epitope spreading in humans” and that Dr. Steinman has not substantiated this
theory. (Tr. 403-05, 409.) He explained that epitope spreading requires “substantial
autoimmune disease” to release enough antigens that they will “become immunogenic
targets for a new set of autoimmune T cells.” (Id. at 405.) He further explained that, in
humans, this process can take months. (See id. at 410-11.) Dr. Forsthuber also
challenged Dr. Steinman’s claims that the zoster vaccine induced a “smoldering
myelitis.” (Ex. H, p. 2.) He explained that two doses of the varicella-zoster vaccine are
necessary to provide adequate immunity, and it is questionable whether petitioner’s
single dose was sufficient to produce a meaningful antibody and/or immune response,
especially in light of his negative varicella-zoster antibody titer. (Id. (citing J Breuer,
Vaccination to Prevent Varicella and Shingles, 54 J. CLINICAL PATHOLOGY 743 (2001)
(Ex. H, Tab 1)).)

Even if there was a recall response, Dr. Forsthuber suggested that it could not
result in an immune response in 24 hours. Dr. Forsthuber provided a detailed
explanation of the development of a recall response following vaccination and
concluded that it takes approximately 4-5 days for an antibody recall response to form.
(Ex. H, pp. 2-5 (citing Jens Wrammert et al., Rapid Cloning of High-Affinity Human
Monoclonal Antibodies Against Influenza Virus, 453 NATURE 667 (2008) (Ex. H, Tab 3);
Rebecca J. Cox et al., An Early Humoral Immune Response in Peripheral Blood
Following Parenteral Inactivated Influenza Vaccination, 12 VACCINE 993 (1994) (Ex. H,
Tab 4); Christopher D. Scharer et al., Plasma Cell Differentiation is Controlled by
Multiple Cell Division-Coupled Epigenetic Programs, 9 NATURE COMMC’NS 1698 (2018)
(Ex.

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10734690. Public record. Not legal advice.