Greenslade v. Secretary of Health and Human Services

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. H, Tab 5); Stuart G. Tangye et al., Intrinsic Difference in the Proliferation of Naive

and Memory Human B Cells as a Mechanism for Enhanced Secondary Immune

Responses, 170 J. IMMUNOLOGY 686 (2003) (Ex. H, Tab 6)).) He explained that, in line

with the time frame for antibody response after re-vaccination with the flu vaccine, it

takes about 5-8 days “after boosting of memory B cells from the previous exposure until

antibody titers in the blood show a significant rise.” (Id. at 5 (citing Scharer et al., supra,

at Ex. H, Tab 5; Florian Krammer et al., Antibody Responses in Seropositive Persons

34

After a Single Dose of SARS-CoV-2 mRNA Vaccine, 384 NEW ENG. J. MED. 1372 (2021)

(Ex. H, Tab 7)).) He explained that, even in the case of cell-mediated skin reaction to

tuberculin injection, the infiltration of skin with inflammatory T cells still takes about 1-2

days. (Ex. B, p. 19; see also Ex. C, pp. 14-15.) Even assuming that epitope spreading

was underway, Dr. Forsthuber opined that this process does not support an onset within

24 hours either. (Tr. 410-11.)

Dr. Forsthuber criticized Dr. Tornatore’s reliance on case reports and reviews of

case reports that observed TM following vaccination with various vaccines. (Ex. G, p. 1;

Ex. H, p. 21.) Dr. Forsthuber explained that the information provided by these sources

is limited to a temporal relationship and that they overlooked critical confounding

factors. (Ex. G, p. 1.) For instance, the claims of the Akkad study were later called into

question when it was suggested that the patient may have had mycoplasma infection

prior to onset of TM. (Id. at 1-2 (citing Akkad, supra, at Ex. 86); Christopher S. Ambrose

et al., A Case Report of Transverse Myelitis Following Influenza Vaccination, 68

ARCHIVES NEUROLOGY 1085 (2011) (Ex. 87)).) Similarly, onset of the Korn-Lubetzki

patient’s TM was preceded by a two-day history of fever, suggesting an infectious

condition temporally related to the patient’s TM. (Id. at 2 (citing Korn-Lubetzki et al.,

supra, at Ex. 92).) Dr. Forsthuber pointed out that the IOM has concluded that the

“epidemiologic evidence was insufficient or absent to assess an association between

influenza vaccine and TM,” and that studies reporting onset of TM following vaccination,

including Bakshi & Mazziotta (supra, at Ex. 88) and Nakamura et al. (supra, at Ex. 93),

do not provide evidence beyond a temporal association. (Id.) Dr. Forsthuber cited two

large studies that he indicated found no association between the flu vaccine and TM.

(Id. (citing James D. Nordin et al., Maternal Safety of Trivalent Inactivated Influenza

Vaccine in Pregnant Women, 121 OBSTETRICS & GYNECOLOGY 519 (2013) (Ex. G, Tab

4); Roger Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-

Centered Analysis, 63 CLINICAL INFECTIOUS DISEASES 1456 (2016) (Ex. G, Tab 5)).) Dr.

Forsthuber further asserted that the flu vaccine has not been associated with MS, a

condition that is related to TM, explained that the National Multiple Sclerosis Society

recommend annual vaccination of MS patients with the inactivated seasonal flu vaccine.

(Id.) The French MS society concurred, concluding that “the available data on seasonal

influenza vaccination does not support an increased risk of relapse and disability in MS

patients.” (Id. at 2-3 (citing Christine Lebrun et al., Immunization and Multiple Sclerosis:

Recommendations from the French Multiple Sclerosis Society, 31 MULTIPLE SCLEROSIS

& RELATED DISORDERS 173 (2019) (Ex. G, Tab 6)).)

Regarding Dr. Tornatore’s fertile field theory and reliance on Talaat et al. (supra,

at Ex. 127), Dr. Forsthuber explained that the study was not reliable due to faulty

methodology. He opined that the authors did not perform scientifically reliable and

generally accepted calculations and instead used standard deviations that were too high

to properly determine statistical significance. (Ex. J, p. 3.) He further criticized the lack

of unvaccinated control group, which is necessary to control for random variations in

cytokine/chemokine levels in the subjects, as “even minimal changes may seemingly

appear statistically significant in lieu of proper groups sizes based on power

calculations.” (Id. at 3-4.) This failure is significant because the study observed

35

cytokine and chemokine levels that were similar to or lower than what can be observed

in healthy individuals. (Id.) Finally, Dr. Forsthuber noted that there was no way of

knowing whether the cytokine and chemokine levels were the result of the vaccine,

given that there were significant differences in injection site pain/myalgia before the

vaccination and at least one subject may have had concomitant conditions. (Id. at 4.)

Even if reliable, “the slight changes in the levels of serum cytokines reported by Talaat

et al. are irrelevant for the fertile field concept.” (Id. at 2.) Dr. Forsthuber explained that

the study observed cytokine and chemokine levels that were similar to or lower than

what would be observed in healthy individuals, and much lower than what would be

observed in autoimmune diseases or required for activation of immune cells. (Id. at 3,

7-11.) Some cytokine levels actually decreased post-vaccination, while there was “a

significant increase in the powerful anti-inflammatory cytokine IL-10 in the serum, which

would counter-regulate the effects of proinflammatory cytokines on immune cells.” (Id.

at 2.) Moreover, the results showed that cytokines thought to be important in TM are

either unaffected or decreased after vaccination. (Id. at 11 (citing Puneet Dixit et al.,

Cytokines and Matrix Matelloproteinases in the Cerebrospinal Fluid of Patients with

Acute Transverse Myelitis: An Outcome Analysis, 65 INFLAMMATION RESEARCH 125

(2016) (Ex. J, Tab 3)).) Dr. Forsthuber further explained that it took 10 days to develop

an autoimmune disease when testing the fertile field concept by immunizing animals

with a “strong adjuvant” that has a “highly inflammatory nature,” “severe adverse

effects,” and “cannot be used in humans.” (Id. at 13-15 (citing Diethilde J. Theil et al.,

Viruses Can Silently Prime for and Trigger Central Nervous System Autoimmune

Disease, 7 J. NEUROVIROLOGY 220 (2001) (Ex. J, Tab 11); Matthias G. von Herrath et

al., Microorganisms and Autoimmunity: Making the Barren Field Fertile?, 1 NATURE

REVS.: MICROBIOLOGY 151 (2003) (Ex. J, Tab 12)).)

Moreover, Dr. Forsthuber disputed Dr. Tornatore’s comparison of natural flu

infection and vaccines using live attenuated flu virus with the inactivated flu vaccine

received by petitioner as vaccines use live attenuated virus, not “live attenuated

antigens.” (Ex. G, p. 3 (emphasis omitted).) Dr. Forsthuber further disputed Dr.

Tornatore’s assertion that the response to vaccination is similar to the response to

infection because it overlooks fundamental differences between the two. (Id. at 3-4.)

For instance, the flu infection enters through the upper respiratory tract and induces

local and systemic protective immunity by generating CD+8 cytotoxic T cells, CD4+ T

cells, and antibodies directed against the flu virus, resulting in profound effects on the

immune cells in the lungs. (Id. at 3.) On the contrary, the inactivated flu vaccine

induces a systemic immune response primarily via protective antibodies; however, the

inactivated flu vaccine antigens “do not replicate and are poor at inducing cellular

immune responses, including CD+8 T cells response.” (Id. (citing Daniel F. Hoft et al.,

Live and Inactivated Influenza Vaccines Induce Similar Humoral Responses, but Only

Live Vaccines Induce Diverse T-Cell Responses in Young Children, 204 J. INFECTIOUS

DISEASES 845 (2011) (Ex. G, Tab 7)).)

Finally, Dr. Forsthuber challenged Dr. Tornatore’s claims regarding a proximate

temporal relationship between petitioner’s vaccination and onset of his TM. (Ex. G, pp.

4-8.) He began by noting that most case reports on the association between TM and flu

36

vaccination have reported an onset of 7 days post-vaccination, at the earliest. (Id. at 4

(citing N Agmon-Levin et al., supra, at Ex. A, Tab 5).) Dr. Forsthuber acknowledged

that the case report by Akkad et al. (supra, at Ex. 86) reported an onset that was

outside of this time frame but asserted that the report “is not a reliable case report.” (Id.

at n. 4.) He pointed to a study finding onset of clinical signs of EAE approximately 10-

11 days following immunization with autoantigens, with a disease peak approximately

15-21 days post-immunization. (Id. at 4-5 (citing Stefan Bittner et al., Myelin

Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune

Encephalomyelitis (EAE) in C57BL/6 Mice, 86 J. VISUALIZED EXPERIMENTS e51275

(2014) (Ex. G, Tab 13); Niannian Ji et al., Anaphylaxis and Mortality Induced by

Treatment of Mice with Anti–VLA-4 Antibody and Pertussis Toxin, 186 J. IMMUNOLOGY

2750 (2011) (Ex. G, Tab 14)).) Dr. Forsthuber provided a detailed explanation of the

time frame for a primary immune response. (Id. at 5-7; Tr. 346-50.) He asserted that,

following vaccination, it takes approximately 24-36 hours for the first antigen-specific T

cells to become activated in the lymph nodes. (Ex. G, p. 6.) It takes a further 3 days for

T cell immune responses to become detectable in the regional lymph nodes. (Id. at 6-

7.) Similarly, it takes about 2-3 days for B cells to become activated and produce

detectable levels of IgM antibodies, with peak levels after about 4-7 days and a decline

to minimal levels after about 2 weeks. (Id. at 7.) IgG antibodies, which have stronger

binding to target antigens, “peak approximately 2 weeks after infection/antigen counter.”

(Id.) This extensive adaptive immune response upon initial encounter creates a

secondary (memory) immune response that is accelerated and less severe when the

pathogen is re-encountered. (Id.) However, Dr. Forsthuber noted that “it will still take a

few days for a notable immune response to develop” because that memory T and B

cells must become activated and expand before they can generate an effective immune

response. (Id. at 7-8; Tr. 416-18 (suggesting a time frame of at least five days to mount

a memory B cell response).) He further noted that the time frame for immune response

is different from the time frame for onset of TM as it takes times for the autoimmune T

cells to proliferate and migrate to the CNS/spinal cord, damaging nerve and other cells

and inducing clinical symptoms of TM. (Ex. G, p. 8.) Dr. Forsthuber suggested that this

additional time frame “is probably best estimated at several days and up to a few

weeks” after an autoimmune response has formed on a cellular level. (Id.) He noted

that Liang & Loré (supra, at Ex. 101) “fully support” his proposed time frame. (Ex. H,

pp. 22-24.) Thus, Dr. Forsthuber opined that onset of petitioner’s TM was too soon to

be associated with an immune response to his flu vaccination. (Ex. G, p. 8.)

V. Analysis

Petitioner contends that his flu vaccination significantly aggravated his TM. (ECF

No. 144, pp. 1, 13.) He argues in the alternative that his TM was caused-in-fact by the

subject flu vaccination. (Id.) I will first address his significant aggravation claim under

the six part Loving test. Specifically, under Loving prongs one through three, I first

address the parties’ factual contentions and find that petitioner suffered a monophasic

acute TM with an onset that predated his vaccination. Taking Loving prong five out of

order, I further explain why there is no evidence to demonstrate that the vaccine

affected this condition. Turning to Loving prongs four and six, I assume for argument’s

37

sake that petitioner’s theories of causation are viable and turn directly to Loving prong

six, under which analysis I conclude that petitioner’s theories of causation cannot be

reliably invoked to explain a significant aggravation of TM occurring within 24 hours of

vaccination. Finding that petitioner has not met his burden of proof for a significant

aggravation claim, I then briefly confirm that his alternative cause-in-fact claim likewise

fails for some of the same reasons, especially the timing of onset. This case is complex

insofar as petitioner had an atypical presentation and the expert opinions were

premised on many differing factual assumptions in need of resolution. However, the

complete analysis below finds that, regardless of whether petitioner’s TM initially

predated the flu vaccine at issue, the one-day onset of post-vaccination symptoms

remains dispositive under either a Loving or Althen analysis.

a. Loving Prong One

The first Loving prong involves an examination of petitioner’s pre-vaccination

condition. Loving, 86 Fed. Cl. at 144. Although the parties agree petitioner ultimately

suffered TM, the parties dispute whether petitioner suffered TM prior to the subject flu

vaccination on November 23, 2011. (ECF No. 144, pp. 15-23; ECF No. 143, pp. 9-10.)

Petitioner asserts that his TM pre-dated his November 23, 2011 flu vaccination in a

“smoldering” form and that the initial onset of that condition occurred “in late October-

early November 2011.” (ECF No. 144, pp. 15-23.) Respondent disagrees, contending

that onset of petitioner’s TM occurred the day after his vaccination on November 24,

2011. (ECF No. 143, pp. 11-12.)

Resolving this difference requires an examination of four factual questions: (i)

whether petitioner’s November 23 report of neck, upper back, and shoulder pain is a

symptom of TM or a musculoskeletal complaint; (ii) whether petitioner’s November 23

report of an impaired ability to sense the need to defecate is a symptom of TM or of pre-

existing gastrointestinal issues; (iii) what, if any, significance should be placed on

petitioner’s later reports of a prior episode of identical symptoms; and (iv) how likely, if

at all, is it that petitioner’s later discovered non-enhancing spinal lesions pre-dated his

vaccination. After addressing each of these points in turn, it is necessary to briefly

discuss (v) in conclusion how they are interrelated.

i. Neck, upper back, and shoulder pain

On November 23, 2011, the date petitioner received his flu vaccination, he

reported a four-week history of pain in the posterior neck, back, and shoulders. (Ex. 1,

pp. 581-83.) He denied any preceding injury and reported that his symptoms were

improving without specific treatment. (Id. at 581.) This was noted to be a new problem.

(Id.) Although his primary care physician determined this pain “seems” to be

musculoskeletal in etiology (Id. at 582-83), she did not at that time have the benefit of

knowing what petitioner’s subsequent clinical course would entail. Additionally, while a

neurologic exam was documented relative to petitioner’s lower extremities, physical

exam of the neck and back was limited to noting tenderness over the trapezius and

38

cervical paraspinal muscles. (Id. at 582.) Therefore, little if anything confirms any

musculoskeletal explanation for these symptoms.

On petitioner’s behalf, both Drs. Tornatore and Steinman persuasively opine that

this new symptom was associated with petitioner’s TM, given his overall subsequent

history. (Tr. 33-34, 230.) Dr. Tornatore in particular explained that neurologic

symptoms are sometimes misdescribed as musculoskeletal pain (Ex. 81, pp. 17-18) and

that petitioner’s neck and upper back pain were otherwise a feature of his post-

vaccination condition, which is undisputed as a presentation of TM (Tr. 114). On behalf

of respondent, Dr. Gelfand attempts to tease out a musculoskeletal etiology of

petitioner’s reported shoulder and neck symptoms based on the specific descriptors

utilized by petitioner’s primary care physician. (Ex. A, p. 15; Tr. 249-50, 300.) However,

Dr. Gelfand concedes that neck and shoulder pain can have a cervical spine

localization, even if he would not diagnose an active myelitis based on this symptom

alone. (Ex. E, p. 7; Tr. 248-49.) Notably, when petitioner later presented for care of

what was ultimately determined to be TM, he reported that his symptoms began with

increased neck and shoulder soreness. (Ex. 1, p. 565.)

ii. Impaired ability to sense the need to defecate

Petitioner’s November 23, 2011 encounter record indicates, inter alia, that he

was experiencing a “lack of ability to sense the need to defecate,” which his experts

interpret as a sensory symptom referable to the spinal cord. (Ex. 1, p. 581; Tr. 36-37.)

Importantly, however, this history was in follow up for petitioner’s chronic abdominal

pain and early satiety in contrast to the neck and shoulder pain that was noted to be

“new since [last office visit].” (Ex. 1, p. 581.) During petitioner’s immediately preceding

office visit of September 21, 2011, it was specifically recorded that petitioner “since

surgery has felt that urge for BM impaired.” (Id. at 589.) The surgery in question was a

much earlier in life bowel resection (Id. at 588), meaning the impaired sense of the need

to defecate was chronic. Accordingly, while this symptom could potentially be

consistent with an evolving spinal injury (Tr. 36-38, 253-54), there is not preponderant

evidence that it is related to petitioner’s TM. (See id. at 254-55.) Much later, in April of

2012, petitioner’s primary care provider recorded that, despite predating his TM, his

inability to sense the urge to defecate did worsen following his injury. (Ex. 1, p. 164.)

However, when reviewing the records holistically, and, in particular, comparing the

encounter records for September 21 and November 23, 2011, there is not preponderant

evidence that petitioner reported this symptom as a new or acute symptom occurring at

that time.

iii. Reported prior episode of identical symptoms

On four separate occasions while being evaluated for possible TM, petitioner

reported an “identical” episode as occurring prior to his flu vaccination. (Ex. 1, pp. 316,

566, 579; Ex. 8, p. 48.) However, he was an inconsistent historian with respect to

timing. Specifically:

39

• A nurse triage note of November 28, 2011, indicates that petitioner “had

these muscle aches about one month ago and it went away.” (Ex. 1, p.

579.)

• On November 28, 2011, petitioner reported symptoms that began with

shoulder and neck soreness and progressed down his arms and legs to

then include sensory abnormalities and weakness. (Ex. 1, pp. 565-66.)

He indicated that he experienced “an identical episode” lasting 3-4 days

about two months prior, for which he did not seek medical attention. (Id.

at 566.)

• On December 6, 2011, petitioner had an encounter with Dr. Junck. Dr.

Junck reviewed the course of the symptoms that brought him to medical

attention on November 28, 2011, and then indicated, “Per report, he did

have an identical episode about two months ago.” (Ex. 8, p. 48.)

However, Dr. Junck further explained that “when questioned here today at

UofM, he states that it might have been only about 1-2 weeks ago. The

onset was identical and the entire symptomatology lasted 3-4 days and

then gradually resolved on its own. He did not seek medical attention at

that time, and he returned to his baseline without any lasting deficits.” 25

(Id.)

• On December 22, 2011, petitioner reported that his November 28

hospitalization represented his second episode of neck and shoulder pain

within a ten-day time span. (Ex. 1, p. 316.) This would place the onset of

the first episode around November 14. In that regard, the record further

specifies that the first episode occurred “in mid 11/2011” and left him bed-

bound for three days. (Id.) In both instances the pain “instantaneously

radiated down his body into legs and was associated with extreme

weakness.” (Id.)

Considering each of these notations and the record as a whole, I find that the

evidence preponderates in favor of a finding that petitioner did suffer an episode of

symptoms lasting 3-4 days that consisted of neck and extremity pain, weakness, and

sensory symptoms. Because Dr. Junck’s record explicitly reflects a conversation

intended to clarify this history, I find that it is more likely that the later December 6 and

25

Although Dr. Junck wrote that the prior episode occurred 1-2 weeks “ago,” potentially implying one to

two weeks prior to the encounter date of December 6, a holistic reading of his note suggests he more

likely meant 1-2 weeks prior to the second episode, which had begun on November 24. (See Ex. 8, p.

48.) Two weeks prior to December 6 would have been November 22, just two days prior to the beginning

of the second episode. However, Dr. Junck’s record makes clear that he understood there to be two

distinct episodes and that the first episode lasted 3-4 days before gradually resolving. (Id.) Given that Dr.

Junck was specifically seeking to clarify the report of a prior episode, it is unlikely that he would have

recorded a history incompatible with the presence of two episodes without remarking on that fact. Thus,

Dr. Junck was most likely indicating that petitioner had reported onset of his first episode occurring

sometime in mid-November, between about the 10th or 17th.

40

December 22 records are more accurate in placing this episode sometime in mid-

November, rather than one or two months prior. At a minimum, Dr. Junck clarified with

petitioner that the time course was more condensed than originally indicated.

Especially given that understanding, petitioner’s subsequent report that the two

episodes occurred ten days apart gives the clearest indication of the temporal

relationship between the two episodes. The December 22 history is also more detailed

in recording that petitioner specifically recalled being bed-ridden in mid-November,

rather than merely estimating how long ago the episode occurred. Further, if one

interprets Dr. Junck’s record as placing onset of the first episode in mid-November (see

supra note 25), the two records are entirely consistent whereas the other two records

are not (placing onset at one or two months prior respectively). Additionally, petitioner’s

telephone encounters of September 22, September 23, September 27, and October 12,

make it somewhat less likely this episode happened during that period. (Ex. 1, pp. 584-

86.)

Although petitioner’s deficits may have resolved such that he returned to a

functional baseline, his November 23, 2011 report of ongoing neck and shoulder pain

prevents a finding that his condition completely resolved. (Ex. 1, p. 581-83.) Moreover,

because petitioner was clear and consistent in providing a history wherein the neck and

shoulder pain heralded the onset of symptoms in both episodes, I find that it is most

likely that the neck and shoulder pain reported on November 23, 2011, began at around

the time of this first episode, rather than four weeks prior. This is consistent with

petitioner’s representation on November 23, 2011, that his symptoms were improving,

yet ongoing. (Id.)

Dr. Gelfand’s hesitation in crediting these reports as consistent with TM are

understandable, given that the prior episode was not discussed in detail but rather only

in overarching terms. (Ex. A, pp. 14-15; Ex. E, p. 5; Tr. 280-81.) However, he has not

persuaded me that the report can be disregarded.

[F]or many medical symptoms or events – such as a headache or other

pain, dizziness, nausea, vomiting – the patient’s or a parent’s testimony may

be the best, or only, direct evidence of their occurrence. Medical records

related to those symptoms would likely be based on the statements of those

who experienced them.

James-Cornelius ex rel. E.J. v. Sec’y of Health & Human Servs., 984 F.3d 1374, 1380

(Fed. Cir. 2021). “Medical records, in general, warrant consideration as trustworthy

evidence. The records contain information supplied to or by health professionals to

facilitate diagnosis and treatment of medical conditions. With proper treatment hanging

in the balance, accuracy has an extra premium. These records are also generally

contemporaneous to the medical events.” Cucuras ex rel. Cucuras v. Sec’y of Health &

Human Servs., 993 F.2d 1525, 1528 (Fed Cir. 1993). Petitioner’s persistence in

reporting this prior episode at a critical juncture in his diagnosis and treatment counsels

against disregarding the provided history.

41

Dr. Gelfand also finds it improbable that petitioner’s prior episode, being as

profound as it must have been, would have not come to medical attention and would

have had such a quick recovery. (Tr. 281-82.) This is based on an understanding that

what petitioner had described was coextensive with his ultimate inability to walk and

inability to use his arms to hold things. (Id. at 281.) However, that was not petitioner’s

presentation at the time he first reported his prior similar symptoms. As of November

28, when petitioner first characterized the prior episode as similar to his present

condition, he was still able to stand and ambulate, albeit unsteadily. (Ex. 1, p. 566.)

Moreover, though reporting the presence of the same symptoms, he also specified that

what he was experiencing beginning after his vaccination “is the worst it has been.” (Id.

at 579.) Although petitioner did report having previously been temporarily bed-bound, it

was not until after his hospitalization that his weakness became so profound as to

cause him to be unable to walk or perform any activities of daily living. (Id. at 316.) In

that regard, petitioner additionally denied in his affidavit that he experienced paralysis

prior to his flu vaccination. (Ex. 3, ¶ 2.) Dr. Gelfand agreed that paralysis would be on

a spectrum with weakness, i.e., weakness is a less severe form of impairment to the

motor pathways as compared to paralysis. (Tr. 336.) Thus, the evidence does not

favor the conclusion that petitioner’s initial episode, though including the same

symptoms, was as severe as his later presentation ultimately became.

iv. Presence of lesions pre-vaccination

On November 29, 2011, petitioner underwent an MRI study that revealed a

“small area of focal T2 signal prolongation in the ventral aspect of right hemi cord at C3

vertebral level, suggesting either demyelination or gliosis.” (Ex. 1, p. 806.) Repeat

study as of December 5 revealed stable findings. (Id. at 799, 801-02; Ex. 8, pp. 64-65.)

Ultimately, the experts agree that petitioner had two non-enhancing lesions consistent

with TM. Moreover, petitioner asserts that the MRI findings “link” his reported pre-

vaccination history of neck and shoulder pain and the T2 lesions. (ECF No. 144, pp.

17-18.) While Dr. Tornatore notes that the duration of lesion enhancement varies, he

opines that the lack of enhancement suggests that the lesions were at least 2-3 weeks

old when the first MRI study was performed on November 29, 2011. (Ex. 81, pp. 18-19

(citing Lai et al., supra, at Ex. 96; Cotton et al., supra, at Ex. 97); Tr. 133.) Although Dr.

Steinman is hesitant to associate a specific date with the non-enhancing lesions (Ex.

55, p. 3), Dr. Tornatore sought to reconcile their opinions by explaining that both experts

agree “that we don’t know how old they are, but we know that they’re not acute in onset”

(Tr. 128-29). Although Dr. Gelfand disagrees that non-enhancing lesions can be dated

with precision, he likewise acknowledges that non-enhancing lesions are generally

assumed to have been enhancing at some point in their course. (Id. at 275, 285.) He

stresses, however, that in this case there is no clinical association between petitioner’s

symptom presentation and any period of known florid lesion enhancement. (Id. at 284.)

The evidence is inadequate to definitively age petitioner’s lesions. However, all

the experts generally agree that non-enhancing lesions were likely enhancing at some

point and that enhancing lesions are a marker of inflammation that may be associated

with TM. (Ex. 81, pp. 18-19; Ex. 55, pp. 2-4; Ex. A, p. 11-12; Tr. 275-76, 285-86.)

42

Moreover, Dr. Tornatore is persuasive in placing at least some weight on the notion that

lesions typically enhance for about 2-3 weeks. (Cotton et al., supra, at Ex. 97, p. 3.)

Accordingly, given that the first MRI was performed only about six days post-

vaccination, I credit Dr. Tornatore’s opinion that it is more likely than not that the lesions

predated petitioner’s flu vaccination. Accord W.C., 704 F.3d at 1358-59 (accepting the

special master’s finding based on the unlikelihood that lesions would enhance for a

short duration). Notably, Dr. Tornatore’s approximation also potentially correlates the

likely lesion enhancement to petitioner’s reported first episode of symptoms. Dr.

Tornatore did testify based on his clinical experience that it is improbable that the two

lesions occurred simultaneously (Tr. 67); however, he was nonetheless clear and

explicit in opining that both lesions pre-dated petitioner’s flu vaccination. (Id. at 66.) For

his part, Dr. Gelfand opined that it is common for monophasic acute TM to have

multifocal lesions. (Id. at 274, 276.) Thus, there is preponderant evidence that both of

the spinal lesions associated with petitioner’s TM predated his flu vaccination.

v. Conclusion as to Loving prong one

In light of all of the above, I find that there is preponderant evidence that

petitioner suffered onset of his TM prior to administration of his November 23, 2011 flu

vaccination. The onset of petitioner’s TM likely occurred in mid-November and was

heralded by a more severe 3-4 day episode of neck and extremity pain, weakness, and

sensory symptoms. Although petitioner’s function returned to baseline, the TM did not

completely resolve, as evidenced by petitioner’s report of ongoing neck and shoulder

pain at the time of his flu vaccination. Petitioner’s spinal lesions more likely than not

(though not definitively) pre-dated his flu vaccination. In sum, petitioner was suffering

TM for approximately one to two weeks prior to the subject vaccination and was

continuing to suffer the attack at the time of the vaccination.

b. Loving Prong Two

The second Loving prong examines petitioner’s condition following vaccination.

Loving, 86 Fed. Cl. at 144. As noted above, at the time of vaccination, petitioner was

already suffering TM, which was manifesting at that time with ongoing neck and

shoulder pain. However, it is also undisputed that petitioner experienced a second

progression of more concerning symptoms consistent with TM following his flu

vaccination. (Ex. 81, p. 15; Ex. 12, p. 9; see also Ex. A, p. 11.)

The medical records reflect that petitioner first noticed increased shoulder and

neck soreness on November 24, 2011, one day post-vaccination. (See Ex. 1, pp. 565,

579.) At this time, petitioner also reported a new sensation of feeling as though he had

sand in his shoulders, which Dr. Tornatore interpreted as a sensory symptom. (Tr. 45-

46.) Petitioner described soreness spreading down his arms and legs over the next 24

hours or so and progressing to numbness and coldness in his extremities. (Ex. 1, p.

565.) Petitioner presented to the emergency department on November 28, 2011, five

days post-vaccination. By that time, petitioner was reporting sensory issues, including

an inability to feel changes in temperature below his head and neck and a “pins and

43

needles” feeling in his extremities. (Id. at 565-66.) He had also developed urinary

retention, requiring use of a catheter. (Id. at 550.) At some point during the five-day

interval between his vaccination on November 23, 2011, and when he presented to the

emergency department on November 28, 2011, petitioner experienced weakness and

difficulty standing, walking, and gripping. (Id. at 566, 578-80.) Although petitioner’s

clinical course confounded his treaters at times, he was ultimately diagnosed with TM.

(Id. at 1, 144-45, 199, 320, 445-46; 526, 549.) Drs. Tornatore and Gelfand agree that

this was the correct diagnosis. (Tr. 48, 263, 266-67; Ex. A, pp. 11, 13; Ex. 81, p. 23.)

At a follow-up neurology evaluation on December 1, 2011, it was noted that

petitioner’s symptoms, namely, his sensory changes and weakness, were progressing.

(Ex. 1, pp. 524-26.) Petitioner was administered IVIg Solu-Medrol with some

improvement. (Id. at 515, 519-20, 526.) However, by December 2, 2011, petitioner was

non-ambulatory due to extensive bilateral lower extremity weakness and suffering from

impaired sensation, decreased respiratory strength, and weakness in all extremities.

(Id. at 519-20; see also Ex. 1, p. 546 (mentioning a new symptom of shortness of breath

on November 30, 2011).) This represents the likely nadir of petitioner’s TM, from which

he ultimately never recovered despite a clinical course that continued to fluctuate. (Ex.

E, p. 9; Tr. 277-78.) Dr. Gelfand explained 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.” 26 (Ex. E, p. 7; Ex. I, p. 2; Tr. 277.)

“During his 16 day hospital course, his symptoms waxed and waned but he

continue[d] to have significant weakness . . . .” (Ex. 1, p. 7.) Repeated MRI studies

revealed stable findings (Ex. 1, pp. 797-802, 803-06; Ex. 8, pp. 63-65; see also Ex. 1,

pp. 1, 144.) After several weeks of physical therapy, petitioner was eventually able to

ambulate with the assistance of a front-wheeled walker and to perform most of his

activities of daily living without assistance. (Ex. 1, p. 235.) However, by mid-January

2012, petitioner was again reporting weakness and incontinence, and he was

dependent on a wheelchair. (Id. at 140-45.) And by 2014, petitioner was completely

wheelchair bound and reporting pain, weakness, spasticity, neurologic bowel and

bladder, and paraplegia. (Exs, 7, 76, 108-09.)

In sum, petitioner experienced a worsening of his symptoms of TM the day

following his vaccination. His condition continued to progress for approximately one

week post-vaccination. Once he reached his nadir, he continued to suffer a fluctuating

course and never recovered.

26

In his testimony, Dr. Gelfand indicated that petitioner’s clinical course continued to evolve “over several

days” after November 24. (Tr. 278.) In testimony, he suggested that the clinical nadir may then have

occurred “over a couple of weeks.” (Id.) This testimony is a bit unclear as a nadir would reflect a distinct

point in time. However, in his report at Exhibit E, Dr. Gelfand more clearly opined that a prior episode

occurring 1-2 weeks prior to his November 24, 2011 symptoms would constitute a single episode of TM

with a progression from onset to nadir occurring within the 21-day timeframe set by the diagnostic criteria.

(Ex. E, p. 8; see also Tr. 279-80.) This is consistent with the nadir occurring around December 2.

44

c. Loving Prong Three

The third Loving prong requires a showing that petitioner’s post-vaccination

condition constitutes a “significant aggravation” of his pre-vaccination condition. Loving,

86 Fed. Cl. at 144. The Vaccine Act defines “significant aggravation” as “any change

for the worse in a preexisting condition which results in markedly greater disability, pain,

or illness accompanied by substantial deterioration of health.” § 300aa-33(4). Loving

prong three only requires a comparison of petitioner’s pre- and post-vaccination

conditions. Loving, 86 Fed. Cl. at 143; Sharpe ex rel. L.M. v. Sec’y of Health & Human

Servs., 964 F.3d 1072, 1082 (Fed. Cir. 2020). Although he need not prove the

expected outcome of his pre-vaccination condition or that his post-vaccination condition

is worse than the expected outcome, Sharpe, 964 F.3d at 1082, petitioner still must

show that his post-vaccination condition was affected by his vaccination. Locane v.

Sec’y of

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