In the United States Court of Federal Claims 

OFFICE OF SPECIAL MASTERS

No. 15-1485V 

Filed: May 11, 2023

PUBLISHED

BETTINA MCGILL, 

 Petitioner,

v. 

SECRETARY OF HEALTH AND 

HUMAN SERVICES,

 Respondent.

 

Renee J. Gentry, George Washington University Law School, Washington, DC, for 

petitioners. 

Benjamin Patrick Warder, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

On December 8, 2015, petitioner filed a petition under the National Childhood 

Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012),

2 alleging that the 13-valent 

pneumococcal conjugate (“PCV13”) and trivalent influenza (“flu”) vaccines that she 

received on November 7, 2014, caused her to suffer a small fiber nerve injury and 

interstitial lung disease (“ILD”). (ECF No. 1.) Petitioner later amended her petition to 

specify that she suffered small fiber neuropathy, ILD, and myofascial pain syndrome

caused by her vaccinations. (ECF No. 62, p.2.) 

In her post-hearing brief, petitioner indicated that she no longer alleges that the 

vaccines caused her ILD and further confirmed that her claim is based on a diagnosis of 

small fiber neuropathy (“SFN”). (ECF No. 148, p. 23 n.7.) Although myofascial pain 

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 (2012) (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. 

Special Master Horner

Pneumococcal conjugate 

vaccine (“PCV13”); Influenza 

(“flu”) vaccine; Small fiber 

neuropathy (“SFN”)
2

syndrome is referenced within the differential diagnosis of some treating physicians, 

petitioner has not ultimately argued that she met her burden of proof with respect to a 

myofascial pain syndrome and her expert’s causal opinion is specifically predicated on 

SFN. 

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 timeframe 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); § 300 aa11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

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)(B); § 300aa-11(c)(1)(C)(ii). In such a situation 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 v. Sec’y of Health & Human Servs., 940 F.2d 1518, 

1525 (Fed. Cir. 1991). Because small fiber neuropathy is not listed as an injury on the 

Vaccine Injury Table, 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. § 300aa13(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 

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 
3

condition, and was a “but for” cause. 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 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, [petitioner’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 [petitioner] 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 Althen court noted that a petitioner 

need not necessarily supply evidence from medical literature supporting petitioner’s 

causation contention, so long as the petitioner supplies the medical opinion of an 

expert. Id. at 1279-80. That expert’s opinion must be based upon “sound and reliable” 

scientific explanation. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 

1359 (Fed. Cir. 2019) (quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 

543, 548-49 (Fed. Cir. 1994)). The Althen court also indicated that, in finding causation, 

a Program factfinder 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.” 418 F.3d at 1280.

II. Procedural History

This case was first assigned to Special Master Dorsey. (ECF No. 4.) Petitioner 

filed her medical records on a compact disc on May 19, 2016.3 (ECF No. 5.) On 

August 4, 2016, respondent filed his Rule 4(c) report, recommending against 

compensation. (ECF No. 28.) Respondent stated that petitioner’s ILD symptoms 

predated, and therefore could not have been caused by, her vaccinations. (Id. at 15-

16.) Respondent also indicated that petitioner had failed to provide a reputable 

3 This filing was later stricken from the record to avoid duplicative filings when petitioner submitted 

additional medical records later in this case. (See ECF No. 48; see also ECF Nos. 49-54.)
4

scientific or medical theory, and that she had ignored potential alternate causes of her 

condition. (Id. at 16-18.)

Petitioner moved to substitute attorney Renee Gentry in place of Dan Wilson 

Bolton III on January 19, 2017. (ECF No. 46.) She subsequently filed additional 

medical records on February 12, 2017, and expert reports from molecular virologist 

Judy A. Mikovits, Ph.D., and microbiologist Francis Ruscetti, Ph.D., on June 19, 2017.4 

(ECF Nos. 49-54, 60-61.) Following her filing of expert reports, petitioner filed additional 

medical records as well as an amended petition alleging her vaccine-caused injuries 

such as small fiber neuropathy (“SFN”), acute myofascial pain syndrome, and ILD. 

(ECF Nos. 62, 64.) Respondent then filed responsive expert reports by rheumatologist 

Chester Oddis, M.D., and immunologist J. Lindsay Whitton, M.B., Ch.B., Ph.D., on 

October 18, 2017. (ECF Nos. 67, 68.)

On November 29, 2017, Special Master Dorsey issued a Rule 5 Order, 

preliminarily concluding that petitioner’s ILD was a preexisting condition but noting that 

petitioner may be entitled to compensation for her SFN. (ECF No. 70.) Special Master 

Dorsey ordered petitioner to file an expert report from a neurologist, updated medical 

records, and outstanding medical literature cited by her previous experts. (Id.) 

Petitioner filed an expert report by neurologist Carlo Tornatore, M.D., on January 29, 

2018. (ECF No. 73.) Petitioner subsequently filed an affidavit regarding her VAERS 

investigation on February 16, 2018, and updated medical records on March 14, 2018. 

(ECF Nos. 77, 78.) In response to Dr. Tornatore’s report, respondent offered a report 

by neurologist Jeffrey M. Gelfand, M.D., M.A.S., on July 30, 2018. (ECF No. 85.) On 

November 5, 2018, petitioner presented a supplemental report by Dr. Tornatore. (ECF 

No. 89.) Respondent then filed a supplemental report by Dr. Gelfand on April 17, 2019. 

(ECF No. 96.) In a follow up status conference, Special Master Dorsey indicated that it 

was probable she would rule in petitioner’s favor based on Dr. Tornatore’s opinion, but 

without determining a specific diagnosis. (ECF No. 90.) However, on June 7, 2019, this 

case was instead reassigned to my docket. (ECF No. 100.) 

Thereafter, on August 5, 2019, I issued a scheduling order additionally urging the 

parties to consider informal resolution, explaining the previously presiding special 

master’s assessment and indicating that I agreed respondent maintained litigative risk. 

(ECF No. 104.) However, in contrast to the previous special master, I addressed the 

issue of diagnosis. In particular, I explained that Dr. Gelfand’s opinion, asserting that 

petitioner’s upper and lower extremity symptoms may be attributable to different

conditions, further complicated the case. (Id. at 2-3.) I later referred the case for 

mediation, but also scheduled an entitlement hearing. A two-day entitlement hearing 

was scheduled to commence July 14, 2021. (ECF No. 118.) This case was referred to 

alternative dispute resolution (“ADR”) on February 16, 2021. (ECF No. 123.) After 

multiple ADR conferences did not result in informal resolution, the case was removed 

from ADR on April 27, 2021. (ECF No. 128.) 

4 As discussed below, Dr. Mikovits’s and Dr. Ruscetti’s expert reports were later stricken from the record. 

(See ECF No. 142.)
5

During this period, the parties also continued to refine their presentations. 

Petitioner filed an additional supplemental report from Dr. Tornatore on July 25, 2019. 

(ECF No. 103.) Respondent filed a supplemental expert report from Dr. Whitton on 

April 6, 2020. (ECF No. 111.) Petitioner continued the exchange of expert reports with 

a supplemental report from Dr. Tornatore on August 9, 2020. (ECF No. 117.) 

Respondent filed a responsive expert report from Dr. Whitton on November 3, 2020. 

(ECF No. 119.) Petitioner then filed a final expert report from Dr. Tornatore on January 

11, 2021. (ECF No. 121.) Petitioner filed additional medical records on March 25, 

2021. (ECF No. 126.) On July 7, 2021, petitioner moved to strike Dr. Mikovits’s and Dr. 

Ruscetti’s expert reports and accompanying medical literature (Exs. 25-35). (ECF No. 

142.) Petitioner represented that she did not intend to rely on Drs. Mikovits and 

Ruscetti or their associated literature. (Id.) Respondent raised no objection. (Id.) 

Accordingly, Dr. Mikovits’s and Dr. Ruscetti’s expert reports and accompanying medical 

literature were stricken from the record. 

A two-day entitlement hearing was held on July 14 and 15 of 2021. (See 

Transcript of Proceedings (Tr.), ECF Nos. 145-46.) Petitioner, Dr. Tornatore, Dr. 

Whitton, and Dr. Gelfand testified. Following the hearing, a status conference was held 

on August 19, 2021. (See ECF No. 147.) I explained that post-hearing briefs were 

necessary to address three important issues: (i) whether the parties wished to 

supplement the record with regard to the Viega-Fernandes study discussed during the 

hearing; (ii) whether there were any relevant substantive differences between 

petitioner’s case and E.M., a recent ruling on entitlement in an SFN case with onset 

occurring in less than one day post-flu vaccination;5 and (iii) whether petitioner’s lower 

extremity condition could separately meet the Althen test for causation-in-fact in the 

absence of a finding that petitioner’s upper and lower extremity symptoms represent the 

same condition. (ECF No. 147.) I also instructed the parties to raise any procedural or 

substantive objections, if any, in reaching the third issue in the context of this case. (Id.) 

Petitioner filed her post-hearing brief on October 18, 2021. (ECF No. 148.) 

Respondent filed his post-hearing brief on December 17, 2021. (ECF No. 151.) 

Petitioner filed a reply on January 14, 2022. (ECF No. 152.)

With regard to the Viega-Fernandes study, contemporaneous with her posthearing brief, petitioner moved for leave to file the Veiga-Fernandes et al. article and an 

article by Lai et al. article. (ECF No. 149.) Respondent did not object to petitioner’s 

request to supplement the record with the Veiga-Fernandes and Lai articles. (Id. at 1; 

see also ECF No. 151, pp. 39-40.) Accordingly, I granted petitioner’s motion to 

supplement the record, and she filed the articles as Exhibits 64 and 65 on October 20, 

2021. (Henrique Veiga-Fernandes et al., Response of Naïve and Memory CD8+ T Cells 

to Antigen Stimulation In Vivo, 1 NATURE IMMUNOLOGY 47 (2000) (Ex. 64); Wendy Lai et 

al., Transcriptional Control of Rapid Recall by Memory CD4 T Cells, 187 J. IMMUNOLOGY

133 (2011) (Ex. 65).) 

5 See E.M. v. Sec’y of Health & Human Servs., No. 14-753V, 2021 WL 3477837 (Fed. Cl. Spec. Mstr. July 

9, 2021). 
6 

The parties offered their competing views of the ruling on entitlement in E.M. 

(Compare ECF No. 148, pp. 14-18 with ECF No. 151, pp. 40-45.) Ultimately, 

respondent is persuasive in contending that E.M. provides little guidance for this case, 

because the expert presentation differs significantly from this case and the outcome in 

E.M. cannot be separated from the special master’s credibility determination regarding 

respondent’s expert in that case – an expert who has not been presented in this case. 

(ECF No. 151, pp. 40-45.)

The parties also provided competing views on whether petitioner’s lower 

extremity symptoms could satisfy the Althen test standing alone. Although considering 

the lower extremity symptoms in isolation would change the timing of onset, and 

therefore also the Althen prong three analysis, respondent contends that petitioner’s 

claim would still fail under Althen prongs one and two. (ECF No. 151, pp. 45-50.) 

Petitioner asserts that her lower extremity symptoms would satisfy the Althen test if 

viewed in isolation (ECF No. 148, pp. 18-23.); however, she “asserts that her proper 

diagnosis is small fiber sensory neuropathy. Ms. McGill’s medical records cannot and 

should not be separated by extremity.” (ECF No. 152, p. 1.)

In light of all of the above, this case is now ripe for a resolution of entitlement. 

III. Factual History

a. As Reflected in the Medical Records

i. Pre-vaccination 

Prior to receiving the flu and pneumococcal conjugate vaccinations on November 

7, 2014, petitioner had received at least two flu vaccines and a “pneumonia” vaccine. 

(Ex. 3, p. 3.) Petitioner’s medical history was significant for autoimmune necrotizing 

myopathy or polymyositis, seropositive nonerosive rheumatoid arthritis (“RA”), 

neutrophilic dermatitis,

6 gastroesophageal reflux disease (“GERD”), depression, and 

significant upper respiratory symptoms including coughing, shortness of breath, and

“bilateral lung opacities.” (Ex. 15, pp. 4, 6, 29, 67-68, 71; Ex. 19, p. 158.) Petitioner 

initially sought treatment for her myopathy in September 2010, when she described six 

months of progressive symmetric proximal muscle weakness that primary affected her 

upper extremities. (Ex. 15, p. 91.) She received intravenous immunoglobulin (“IVIG”) 

therapy and a variety of immunosuppressive drugs including methotrexate, rituximab, 

prednisone, and CellCept for her autoimmune disorders. (Ex. 15, pp. 67, 83, 91.) 

On October 20, 2014, petitioner visited Nizar Chahin, M.D., who noted that in 

September 2010, petitioner’s creatine phosphokinase (“CK”), aspartate 

6 Neutrophilic dermatitis is “[a] type of neutrophilic dermatosis usually seen on the upper body of middleaged women, characterized by one or more large, rapidly extending, erythematous, tender or painful 

plaques, with fever and dense infiltration of neutrophilic leukocytes in the upper and middle dermis.” 

Acute Febrile Neutrophilic Dermatosis, DORLAND’S MEDICAL DICTIONARY ONLINE, 

https://www.dorlandsonline.com/dorland/definition?id=69376 (last accessed Nov. 7, 2022). 
7 

aminotransferase (“AST”), and alanine transaminase (“ALT”) levels were elevated. (Ex. 

15, p. 83.) Her myositis profile was negative, she was positive for antinuclear 

antibodies (“ANA”), rheumatoid factor (“RF”), and cyclic citrullinated peptide (“CCP”) 

antibodies, and negative for antineutrophil cytoplasmic antibodies (“ANCA”). (Id.) Dr. 

Chahin also noted that a September 2010 EMG and nerve conduction study performed

on petitioner’s right side showed normal sensory and motor responses but fibrillation 

potentials and positive sharp waves in her right deltoid, biceps, triceps, first dorsal 

interosseous, vastus medialis and the anterior tibialis. (Id.) Dr. Chahin noted that these 

findings were consistent with an inflammatory myopathy. (Id.) 

Petitioner presented to her primary care provider, Anna Conterato, M.D., on 

November 7, 2014, to follow up on her RA and myositis. (Ex. 15, p. 90.) At the time of 

this visit, petitioner was taking albuterol, a vitamin D supplement, Flexeril, fish oil, 

Prilosec, tramadol, and CellCept. (Id. at 91.) Dr. Conterato noted that petitioner’s RA 

and myopathy were stable, and that petitioner had not had an RA flare “in some time.” 

(Id.) During this visit, petitioner received the pneumococcal conjugate and influenza 

vaccine. (Ex. 2.) 

ii. Post-vaccination treatment

Nearly one week later, on November 13, 2014, petitioner presented to Russell J. 

Coletti, M.D., at the University of North Carolina (“UNC”) Internal Medicine Same Day 

Clinic with a complaint of “burning arm pain.” (Ex. 4, p. 2.) Petitioner was concerned 

that her arm pain was a reaction to her recent vaccinations and reported that six days 

prior, she had woken up with burning pain from her shoulders to her wrists, which was 

worse in the left arm. (Id. at 3.) She also noted that her symptoms were similar to her 

prior polymyositis symptoms. (Id. at 2.) Dr. Coletti noted that “[t]here does not appear 

to be any localized skin reaction around the site of the vaccination” and stated that her 

arm pain was “unlikely to be due to her vaccination.” (Id.) Upon examination, Dr. 

Coletti observed pain on abduction of the shoulder, slightly decreased bilateral deltoid 

strength, and blunted reflexes throughout. (Id. at 3.) He ordered petitioner to continue 

taking Tylenol and using ice packs. (Id. at 2.) He also ordered bloodwork to check

petitioner’s erythrocyte sedimentation rate (“ESR”) and CK to rule out a polymyositis 

flare. (Id.) 

The following day, petitioner reported to the UNC Emergency Department (“ED”) 

with a bilateral diffuse upper extremity burning sensation, ongoing for one week. (Ex. 4, 

p. 7.) She reported that the burning sensation began “the same day that she got both

her flu and pneumonia vaccines.” (Id.) She stated that the burning was “only in the 

arms and nowhere else in the body” and that she had never experienced similar 

symptoms before. (Id.) Her bloodwork from the day prior showed elevated CK levels 

and a slightly elevated ESR. (Id.) Sara Tarjan, M.D., evaluated petitioner and noted 

that her burning arm pain “may be related to her polymyositis or rheumatoid arthritis 

although the symptoms are not entirely typical.” (Id.) Upon examination, petitioner did 

not reveal any weakness or sensory loss in her upper extremities. (Id.) Dr. Tarjan 
8

observed that petitioner’s extremities were not swollen or tender to palpation, and that 

there was no rash. (Id. at 11.)

While in the UNC ED, petitioner requested to see attending physician Seth 

Glickman, M.D. (Ex. 4, p. 12.) Dr. Glickman noted that petitioner had normal vitals and 

a normal physical exam and that there were no signs of swelling or erythema in her 

arms. (Id. at 13.) He observed mild tenderness to palpation, but normal strength, 

sensation, and distal pulses in both arms. (Id.) His differential diagnosis was a local 

reaction to immunization versus myositis flare. (Id.) He recommended petitioner 

consult her rheumatologist about taking a steroid burst. (Id.) The discharge instructions 

indicate petitioner’s treating physicians were “unsure of the exact cause of [her] arm 

burning” and that “[i]t may be a flare of [her] RA or polymyositis.” (Id. at 17.) Petitioner 

declined steroids. (Id.) 

Petitioner had a neuromuscular consult with Elizabeth Jovanovich, M.D., on 

November 18, 2014. (Ex. 4, p. 29.) Petitioner reported that “[s]hortly after injection 

[she] developed redness and induration on [her] left deltoid” and “some minor erythema 

on the right side as well though not as severe.” (Id. at 31.) As of this visit, petitioner 

reported that the swelling at the injection sites “completely disappeared and that the 

pain in her right arm ha[d] improved slightly.” (Id.) On examination there was minimal 

swelling at deltoids bilaterally, but no evidence of discoloration; her deltoids were tender 

to palpation bilaterally, worse on the left; and there was no evidence of joint effusions or 

swelling or discoloration in hands, elbows, feet, or ankles. (Id. at 33.) Petitioner’s deep 

tendon reflexes and sensory exam were normal. (Id. at 34.) Dr. Jovanovich assessed 

petitioner with an arthus reaction to her vaccinations. (Id. at 30.) She prescribed a 

Medrol Dosepak and heat packs for symptomatic relief. (Id.)

The next day, petitioner returned to the UNC ED with a chief complaint of arm 

pain. (Ex. 4, p. 40.) She was treated by nurse practitioner Benjamin Linthicum, who 

observed decreased reflexes in the upper and lower extremities with no weakness and 

elevated CK and ESR levels (similar to her previous labs). (Id. at 40, 42.) He advised 

petitioner to continue using steroids and cold/hot compresses and to follow up with 

rheumatology and internal medicine. (Id. at 40.) Petitioner was prescribed Dilaudid for 

pain management. (Id. at 40, 44.)

Petitioner presented to rheumatologist Jake Ritt, M.D., at the UNC Blue Ridge 

Family Practice on November 20, 2014. (Ex. 4, p. 60.) Dr. Ritt noted that petitioner “did 

not think [her symptoms were] a flare of her myositis or her RA, but rather a reaction to 

the vaccination given a week prior.” (Id.) He noted that the on-call rheumatology fellow 

started petitioner on gabapentin for possible neuropathic pain during her stay in the ED, 

but that she was later seen by a neurologist who stopped the gabapentin in favor of 

corticosteroids for a possible arthus reaction. (Id.) Dr. Ritt believed that an arthus 

reaction “would be unlikely given [petitioner] was injected with two different potential 

antigens in two different areas (unless the medium the vaccines were carried in were 

similar and she had a hypersensitivity to that).” (Id. at 63.) Instead, he suspected that 

the more likely cause of petitioner’s pain was myofascial pain syndrome “triggered by 
9

the inciting event of the vaccinations.” (Id. at 63.) He noted that myofascial pain 

syndrome “is more common in patients with underlying chronic illness and a history of 

depression.” (Id.) He prescribed a higher dosage of gabapentin and home exercise to 

maintain range of motion in petitioner’s shoulders. (Id.) The same day, petitioner filed a 

VAERS report noting that she suffered from a “[b]urning sensation in both arms,” with 

an onset of November 8, 2014, at 12:30 AM. (Ex. 17, p. 2.)

Shortly after her visit to Dr. Ritt, on November 20, 2014, petitioner reported to the 

Duke Health ED with a chief complaint of “medical reaction” and paresthesia. (Ex. 18, p. 

1.) Petitioner informed the desk staff that “the pain in [her] arms ha[d] moved to [her] 

legs.” (Id. at 3.) Petitioner saw Amy Kumar, M.D., who noted that petitioner was “very 

upset with the conflicting answers being given to her and many medications being 

prescribed to her” and noted that petitioner came to the ED to see a neurologist and 

rheumatologist. (Id. at 4.) Petitioner’s physical examination did not reveal any 

significant abnormalities. (Id. at 5.) She referred petitioner to outpatient neurology and 

rheumatology. (Id.)

Petitioner was discharged from Duke ED early on November 21, 2014 (Ex. 18, p. 

7), but returned the following day with a chief complaint of “generalized pain” (Id. at 14). 

Seth Holt, M.D., and Nicholas Lauerman, M.D., examined petitioner and noted that her

burning arm pain had now progressed to her entire body. (Id. at 17.) Petitioner noted 

she was unable to walk as it “cause[d] diffuse pain and . . . generalized weakness” but 

showed full strength on her focal examination. Drs. Holt and Lauerman explained that 

petitioner had not been on gabapentin long enough to feel the effects. (Id.) The doctors 

recommended that petitioner continue gabapentin, attempt a trial of Ativan for anxiety, 

and follow up with her rheumatologist. (Id.)

Petitioner then presented to Kimberly Yarnall, M.D., at Duke Primary Care Blue 

Ridge on November 24, 2014, to establish care. (Ex. 18, p. 29.) At the time of this visit 

petitioner carried a diagnosis of myositis, depression, GERD, RA, and seasonal allergic 

rhinitis. (Id.) Petitioner informed Dr. Yarnall that she had recently become weak to the 

point that she was using a walker. (Id.) Dr. Yarnall encouraged petitioner to continue 

taking gabapentin for her nerve pain. (Id. at 36.) 

On November 25, 2014, petitioner presented to Duke rheumatologist Melissa 

Wells, M.D., for an evaluation of “burning sensation throughout [her] body.” (Ex. 7, p. 

2.) Petitioner reported that her pain progressed from being unilateral in her left arm, to 

bilateral, to her entire body. (Id.) She had experienced progressive weakness in her 

lower extremities and was using a walker after experiencing “a couple of almost falls.” 

(Id.) The weekend prior, petitioner had discontinued her narcotic medications and 

restarted gabapentin. (Id.) Upon examination, Dr. Wells observed that petitioner could

complete full shoulder abduction with active range of motion, but was unwilling to 

complete other range of motion tests due to her pain. (Id. at 5.) Petitioner exhibited full 

passive range of motion and bilateral tenderness to palpation on the anterior and lateral 

shoulders. (Id.) Her right knee was tender along the medial aspect, her left knee was 

diffusely tender along the lateral malleolus, and both knees showed full passive range of 
10

motion. (Id.) All other joints were normal. (Id.) Dr. Wells observed that petitioner had 

difficulty following simple instructions such as shrugging her shoulders. (Id.) Petitioner 

was noted to “get anxious and agitated when discussing the course of her illness.” (Id.) 

Dr. Wells assessed petitioner with inconsistent diffuse pain, left greater trochanteric 

bursitis, history of RA and myositis, and chronic immunosuppression. (Id. at 6.) 

During this visit, Dr. Wells noted that there was no documentation showing a 

localized reaction at the injection site, and although petitioner originally reported a 

localized reaction when reporting to UNC ED, she denied any localized reaction at this 

visit. (Ex. 7, p. 6.) Dr. Wells was “unable to determine if the onset of pain is related to 

the injection or not.” (Id.) She stressed however, that she was “not entirely sure” about 

other potential causes of petitioner’s pain because her symptoms did “not follow any 

typical dermatomal or neurological patterns.” (Id.) She noted that petitioner’s RA and 

myositis appeared to be well-controlled given that her strength was normal and there 

were no signs of synovitis. (Id.) Dr. Wells could not find any evidence of vasculitis, and 

petitioner denied any systemic symptoms, which made an underlying inflammatory 

process less likely. (Id.) Additionally, petitioner’s presentation was inconsistent with 

fibromyalgia and GBS. (Id.) Dr. Wells suspected that the more likely cause of 

petitioner’s pain was SFN because it “can present in atypical patterns.” (Id.) Dr. Wells 

deferred further evaluation to petitioner’s neurologist and ordered c-reactive protein 

(“CRP”) and CK labs. (Id.)

On December 2, 2014, petitioner visited neurologist Justin Mhoon, M.D., at Duke 

Health Center with a chief complaint of “numbness.” (Ex. 18, p. 64.) Petitioner reported 

feeling “very unsteady on her feet and as if her legs [were] going to give out.” (Id. at 

66.) On examination, Dr. Mhoon observed full strength bilaterally in petitioner’s upper 

and lower extremities. (Id. at 70.) She demonstrated normal pinprick, temperature, 

vibration, and proprioception in her upper and lower extremities, and had allodynia with 

light touch over the bilateral upper extremities. (Id.) Petitioner’s coordination was good 

but slow, and her deep tendon reflexes were decreased and symmetric bilaterally. (Id.) 

Petitioner staggered upon standing and reported that she felt like she was going to fall, 

that her knees may give out, and that she could not walk without a walker. (Id.) Even 

when using the walker, Dr. Mhoon noted that petitioner “still takes very awkward steps.” 

(Id.) Dr. Mhoon’s differential diagnosis included sensory neuritis due to a vaccine 

reaction, toe axial subluxation, and autoimmune demyelinating disease. (Id.) Dr. 

Mhoon recommended a brain and cervical spine MRI, cervical spine X-ray, and an 

electromyography (“EMG”)/nerve conduction study (“NCS”) to evaluate for mononeuritis 

multiplex, and if all tests were normal, a skin biopsy to evaluate for SFN. (Id. at 70-71.) 

Over a week later, on December 10, 2014, petitioner called Dr. Mhoon complaining that 

her right arm was “very weak” and that she could not lay it flat, and that her shoulders 

and back were very painful. (Id. at 108-09.)

Petitioner underwent brain and cervical spine MRIs with and without contrast on 

December 17, 2014. (Ex. 18, pp. 110-11.) Petitioner’s cervical spine MRI showed

some mildly enlarged cervical nodes, some spurring at the C3-C4 level, and some 

minor disc degeneration at C3-C4 and C5-C6. (Ex. 5, p. 3.) Petitioner’s brain MRI 
11

showed some scattered T2 hyperintense foci involving the white matter that were 

nonspecific and “could be sequela of prior infection/inflammation including Lyme’s 

disease, minor chronic microvascular disease or demyelinating disease” though none of 

the lesions revealed restricted diffusion or abnormal enhancement. (Id. at 4-5.) 

Petitioner underwent an EMG and NCS on December 31, 2014, both of which were 

normal. (Id. at 6.) Dr. Mhoon noted that there was no evidence of “a widespread large 

fiber peripheral neuropathy or myopathy” and that petitioner could undergo a skin 

biopsy to measure the intra-epidermal nerve fiber density to test for SFN. (Ex. 5, p. 6.) 

On December 31, 2014, petitioner presented to Dr. Mhoon to discuss her recent 

EMG, NCS, and MRI studies. (Ex. 18, p. 133.) Dr. Mhoon noted that petitioner’s 

neurologic exam revealed normal strength and sensation besides allodynia in her upper 

extremities, and that there was no evidence of peripheral neuropathy or active myositis. 

(Id.) He concluded petitioner may have neuritis or SFN, noting that “if this was a 

vaccine related neuritis it should improve on its own over time.” (Id.) Dr. Mhoon stated 

that petitioner could try tapering her gabapentin dose if her pain did not increase. (Id.) 

Petitioner underwent skin biopsies of her left thigh and left calf on January 27, 

2015. (Ex. 21, p. 1.) Her left thigh biopsy was normal, but her left calf showed 

significantly reduced epidermal nerve fiber density, consistent with SFN. (Id.) There 

was no evidence of vasculitis or other histological abnormalities. (Id.) Dr. Mhoon 

confirmed this diagnosis via an email to petitioner on February 17, 2015, explaining that 

SFN is “[o]ften associated with rheumatologic conditions such as yours.” (Ex. 13, p. 4.) 

On March 4, 2015, Dr. Mhoon responded via email to petitioner’s questions about her 

SFN diagnosis. (Id. at 3.) In response to petitioner’s request for Dr. Mhoon to update 

her chart to reflect a reaction to the flu and pneumococcal vaccines, Dr. Mhoon wrote,

“CANNOT PROVE A DIRECT CAUSATION OF THE VACCINES BUT IF YOU NEED A 

NOTE AT SOME POINT TO AVOID THE FLU SHOT LET ME KNOW.” (Id.)

On February 6, 2015, petitioner saw Dr. Yarnall for right shoulder pain, back pain 

that had moved to her right side, and chest pain. (Ex. 18, p. 178.) Petitioner explained 

that she had pain in her right side around her rotator cuff for several days. (Id. at 182.) 

Aside from her back and shoulder pain, petitioner’s examination was normal. (Id. at 

183.) Dr. Yarnall ordered chest and shoulder X-rays, referred petitioner to orthopedic 

surgery, and prescribed tizanidine. (Id.) Petitioner’s shoulder X-ray revealed a 9 mm 

sclerotic focus proximal humeral diaphysis, which “in the absence of known malignancy 

may represent an incidental bone island.” (Id. at 190.) Petitioner’s chest X-ray showed 

no significant degenerative changes in the thoracic spine; normal pulmonary 

vasculature; bibasilar interstitial prominence, most conspicuous on lateral radiograph 

and mildly improved; questionable retrocardiac airspace disease; and no pleural 

effusion. (Id.) 

Nearly one week later, on February 12, 2015, petitioner presented to

rheumatologist Amanda Nelson, M.D., for a follow up on her RA and myositis. (Ex. 7, p. 

15.) Besides the pain that petitioner had reported since her vaccinations, her 

examination was “entirely unremarkable.” (Id. at 17.) Dr. Nelson recommended 
12

maintaining the current CellCept dosage and a physical therapy evaluation to increase 

petitioner’s strength and conditioning. (Id.) Petitioner was advised to see a pulmonary 

specialist and began using an albuterol inhaler again. (Id. at 15.)

The next day, on February 13, 2015, petitioner presented to Hilda Metjian, M.D.,

at Duke Medicine. (Ex. 8, p. 2.) Petitioner reported that after experiencing some flu-like 

symptoms in January, her breathing had not been normal. (Id.) Dr. Metjian believed 

that petitioner’s restrictive lung disease is likely related to interstitial lung disease “for 

her autoimmune process.” (Id. at 4.) She noted that petitioner had an elevated CK, 

rheumatoid factor (“RF”), and an interstitial pattern on her chest X-ray. (Id.) Petitioner 

followed up with Dr. Metjian on March 5, 2015, where she received a chest CT that 

revealed findings consistent with non-specific interstitial pneumonia (NSIP), “most likely 

autoimmune in etiology.” (Ex. 18, p. 237.) Dr. Metjian diagnosed petitioner with ILD, 

referred her to pulmonary rehabilitation, and ordered petitioner to continue taking 

CellCept. (Id.) Petitioner attended pulmonary rehab sessions from April 13, 2015, to 

May 7, 2015, during which her pulmonary functions and conditioning slowly progressed. 

(See Ex. 24, pp. 13-129; Ex. 18, p. 419.)

Petitioner followed up with Dr. Mhoon on April 27, 2015, to discuss her ongoing 

complaints of pain and weakness. (Ex. 6, p. 51.) Petitioner had begun taking alpha 

lipoic acid in addition to gabapentin and appeared “[o]verall stable.” (Id.) She explained 

that she had a recent RA flare and was placed on prednisone, which she discontinued 

after it caused diarrhea. (Id.) Petitioner’s examination remained unchanged from prior 

examinations. (Id. at 53-54.) Dr. Mhoon believed that petitioner’s SFN “may be 

sequelae from rheumatoid arthritis” but also considered “vaccination neuritis” as another 

potential cause. (Id. at 60.) He recommended that petitioner continue taking

gabapentin and alpha lipoic acid. (Id.) 

iii. Later medical records

Petitioner has an extensive additional medical history. The remainder of her 

medical records are less informative with respect to the issues discussed by the experts 

in this case, but discussion of these records is included in the interest of completeness 

given that they include additional evaluation of her autoimmune conditions.

Between May and August of 2015, petitioner presented for care numerous times 

for musculoskeletal complaints relating to her shoulder and wrist. (Ex. 18, pp. 395-409, 

442-46, 486, 501-12, 526, 535-46, 638-39; Ex. 9, p. 2-3; Ex. 24, pp. 692-97.) There 

was some suspicion that petitioner’s wrist pain was a flare of RA, but this assessment 

was not shared by all of the treating physicians. (Ex. 18, pp. 551, 595.) She was 

diagnosed as having a frozen shoulder. (Ex. 18, pp. 638-39.) She also presented 

during this period with right leg pain that was consistent with a lumbar spinal disc bulge 

that was observed on MRI. (Ex. 18, pp. 672, 692, 719, 724, 789.)

On June 2, 2015, petitioner presented to neurologist Samuel Moon, M.D., at 

Duke Neurology. (Ex. 6, p. 62.) Dr. Moon observed a positive RF and noted that it was 
13

unclear whether petitioner’s various symptoms were caused by a single autoimmune 

disorder. (Id. at 66.) Petitioner declined acupuncture due to cost constraints, but Dr. 

Moon sent a chart message suggesting that petitioner’s physical therapy team conduct 

dry needling, a procedure similar to acupuncture. (Id.)

On June 18, 2015, petitioner saw Dr. Nelson at UNC Healthcare to transfer her 

rheumatology care to Duke. (Ex. 4, pp. 66-67.) Dr. Nelson noted that petitioner’s RA 

seemed to be under control outside of the most recent flare, and that rituximab may be 

a viable treatment option as she had responded well to it in the past. (Id. at 69.) 

Petitioner’s CK levels were improving, and Dr. Nelson considered lowering her CellCept 

dosage once her active issues resolved. (Id. at 69-70.) She ordered repeat CK and 

liver function labs. (Id.) Dr. Nelson advised petitioner to continue her current 

medications and follow up with her various specialists at Duke. (Id. at 70.) 

On September 22, 2015, petitioner presented to Melissa Reed, M.D., at Duke 

Primary Care for flu-like symptoms, including fatigue, nausea, dehydration, and chest 

pressure. (Ex. 18, pp. 939, 942.) Petitioner was concerned that her symptoms were 

caused by mold. (Id. at 942.) Dr. Reed diagnosed petitioner with autoimmune disease, 

fatigue, ILD, and anemia. (Id. at 946.) She ordered lab work, a thyroid profile, 

urinalysis, and chest X-rays. (Id.) Petitioner’s lab work showed that she was less 

anemic compared to earlier labs, and her chest X-rays did not show pneumonia. (Id. at 

969.) Dr. Reed believed that petitioner’s flu-like symptoms were caused by an 

autoimmune flare following a viral infection. (Id.) 

Petitioner reported to the Duke ED on September 26, 2015, with complaints of 

abdominal pain and fatigue. (Ex. 18, p. 971.) She reported that she had been 

experiencing generalized abdominal pain all week and that she was unable to eat. (Id. 

at 975.) Petitioner reported trouble walking and left leg spasms, with increased pain. 

(Id.) Petitioner was given a gastrointestinal cocktail of Zofran and normal saline. (Id.) 

Her treating physicians recommended that she continue to take iron supplements to 

manage her anemia and follow up with her primary care provider. (Id. at 978.) 

Petitioner followed up with Dr. Yarnall on September 29, 2015. (Ex. 18, p. 1033.) 

Dr. Yarnall assessed petitioner with GERD, nausea, autoimmune disease, generalized 

abdominal pain, and prediabetes. (Id. at 1007.) Dr. Yarnall noted that the cause of 

petitioner’s nausea was unclear and referred her to a GI specialist. (Id.) On October 2, 

2015, petitioner presented for initial consult for her GI issues with Melissa Teitelman, 

M.D., and Sarah Coppolino, PA. (Id. at 1018.) PA Coppolino ordered bloodwork for H 

pylori, an esophagogastroduodenoscopy (“EGD”) to assess for esophageal and gastric 

ulcerations and inflammation, and an abdominal ultrasound to assess for gallstones or 

chronic inflammation of the gallbladder. (Id. at 1024.) Petitioner’s abdominal ultrasound 

was normal aside from some fatty infiltration of petitioner’s liver. (Id. at 1036.) On 

November 11, 2015, petitioner later underwent an endoscopy, which revealed that the 

lumen of the lower third of her esophagus was mildly dilated, but was otherwise normal. 

(Ex. 18, p. 1226.) 
14

On October 13, 2015, petitioner returned to Dr. Wells. (Ex. 18, p. 1046.) 

Petitioner reported more frequent and intense RA flares. (Id. at 1050.) Dr. Wells did not 

identify any signs of an active flare on examination. (Id. at 1054.) Dr. Wells noted that 

petitioner’s report of unilateral wrist pain is somewhat atypical for RA and more often 

associated with gout or pseudogout. (Id.) Dr. Wells did not observe any signs of 

chondrocalcinosis on petitioner’s X-ray and ordered CK, ESR, CRP, uric acid, and BNP 

labs to monitor petitioner’s RA and screen for gout and hypertension. (Id.) She also 

ordered an electrocardiogram for additional hypertension screening. (Id.) 

Petitioner returned to NP Aitken on October 14, 2015, for a follow up on her left 

frozen shoulder. (Ex. 18, p. 1074-81.) Petitioner’s exam revealed full strength and 

range of motion and she was encouraged to continue her physical therapy and home 

exercises. (Id. at 1081.) Petitioner saw Dr. Liu on November 13, 2015, to follow up on 

her right leg and neck pain. (Ex. 18, p. 1253.) Petitioner reported that she was pain 

free aside from occasional back pain. (Id. at 1256.) Petitioner was walking but had 

decreased range of motion on her lumbar spine exam. (Id.) Dr. Liu recommended a 

trial of home exercises to help manage petitioner’s pain. (Id. at 1257.)

On December 2, 2012, petitioner saw Dr. Moon for a follow-up on her neuropathy 

and immune disorder. (Ex. 18, p. 1288.) Dr. Moon noted that gallstones were found on 

petitioner’s abdominal ultrasound and recommended that she follow up with a GI 

specialist and consider cholecystectomy. (Id. at 1291-92.) Petitioner also returned to 

the Duke Gastroenterology Clinic on December 17, 2015, and saw PA Coppolino. (Ex. 

18, p. 1334.) 

On January 5, 2016, petitioner returned to Dr. Wells for left shoulder and left-side 

neck pain believed to be caused by her myositis. (Ex. 18, p. 1351.) Dr. Wells noted 

that petitioner was doing very well and showed no weakness or signs of active synovitis. 

Petitioner declined additional prescriptions for her RA. (Id. at 1360.) Dr. Wells ordered 

CBC, ALT, AST, CK, Creatine, ESR, CRP, Sm antibody, RNP, and anti-SCL70 labs, 

and recommended that petitioner continue to follow up with her pulmonary specialists. 

(Id. at 1360, 1363.)

On March 2, 2016, petitioner returned to Dr. Moon to follow up on her pain and 

immune disorders. (Ex. 18, p. 1430.) Petitioner’s anemia was borderline, and her pain 

was variable but seemed to worsen with certain activities. (Id. at 1435.) Dr. Moon 

advised petitioner to rest every afternoon to deal with her chronic fatigue. (Id.) 

Petitioner called Dr. Wells’ office on March 7, 2016, complaining of pain and stiffness in 

her right shoulder and intermittent stabbing pain and stiffness in her right hand. (Ex. 18, 

p. 1464.) Dr. Wells believed this was an RA flare and recommended either prednisone 

or the maximum dose of Tylenol and ibuprofen. (Id.)

On March 14, 2016, petitioner presented to Dr. Metjian for follow up on her ILD. 

(Ex. 18, p. 1466.) Petitioner denied any worsening in her ILD symptoms. (Id. at 1470-

71.) Petitioner’s lung volumes were consistent with severe restrictive lung disease, her 
15

carbon monoxide diffusing capacity was substantially reduced, and “the potential effect 

of anemia on reducing carbon monoxide uptake [could not] be ruled out.” (Id. at 1473.)

Petitioner returned to Dr. Wells for a follow up of her chronic pain symptoms on 

April 4, 2016. (Ex. 18, p. 1479.) Petitioner reported that her previous hand pain had 

resolved but she now suffered from elbow pain for one day, right-side knee pain since 

March, and occasional back pain. (Id. at 1483.) Dr. Wells noted that petitioner was 

“doing great from a myositis standpoint,” but was concerned about underlying RA 

activity. (Id.) Petitioner’s examination was generally unremarkable, but she did show 

some tender joints. (Id. at 1488.) Dr. Wells noted that she believed petitioner’s right 

knee pain was due to bursitis and that her elbow pain stemmed from her right shoulder 

since it mostly occurred with right shoulder movement. (Id.) Petitioner’s X-ray showed 

a collapse of the proximal capitate with underlying vague lucencies and extensive 

sclerosis most consistent with osteonecrosis and collapse, but no definite erosions. (Id.

at 1493.) 

Petitioner presented to David Attarian, M.D., and PA Chanel Copeland at Duke 

Orthopaedics on April 8, 2016, for evaluation of left shoulder pain. (Ex. 18, p. 1521.) 

Petitioner reported that her shoulder pain began after her visit to Dr. Wells four days 

prior and that she was waiting on authorization to fill an indomethacin prescription. (Id.

1524.) Petitioner’s left shoulder examination showed generalized tenderness to 

palpation with extremely limited range of motion and strength. (Id. at 1525.) PA 

Copeland assessed petitioner with chronic left shoulder pain and adhesive capsulitis 

and ordered an increased Toradol injection along with a series of left shoulder X-rays. 

(Id. at 1526.) Petitioner’s left shoulder X-ray revealed mild AC joint degeneration. (Id.

at 1528.)

Petitioner next reported to Dr. Liu on June 10, 2016, for back pain. (Ex. 24, p. 

1546.) Petitioner reported that her back pain began following her epidural injection in 

August 2015, and that it was primarily in her lower back but radiated to her leg 

occasionally. (Id.) She further explained that stretching, Tylenol, and Flexeril helped to 

alleviate severe pain but that she otherwise experienced a dull pain. (Id. at 1550.) Dr. 

Liu noted that petitioner’s pain was likely a symptom of a disc bulge abutting the S1 

nerves in the spinal canal and recommended a series of home exercises. (Id.)

On July 7, 2016, petitioner reported to Katherine Kaufman, M.D., to follow up on 

her RA and ILD. (Ex. 24, p. 1580.) Petitioner’s myositis seemed to be under control 

due to her normal strength on examination. (Id. at 1586.) Petitioner’s ESR and CRP 

levels were elevated, but not more than usual, Dr. Kaufman recommended Plaquenil to 

assist with petitioner’s RA symptoms. (Id. at 1605.) 

Petitioner next visited PT Alan Sirk for disability evaluation and testing on 

September 12, 2016. (Ex. 24, p. 1711.) PT Sirk concluded that petitioner was 

incapable of performing the physical demands of her target job of Tax-Record Clerk. 

(Id. at 1721-22.) PT Sirk’s conclusion was primarily based on petitioner’s significant 

upper extremity impairment and positional intolerance limitations. (Id.)
16

Petitioner followed up on her ILD with Dr. Metjian on September 14, 2016. (Ex. 

24, p. 1742.) Petitioner reported ongoing dyspnea with walking upstairs or walking for 

several minutes and noted that she experienced shortness of breath, tightness in her 

legs, and numbness in her feet. (Id. at 1746.) Dr. Metjian observed that petitioner’s 

lung function had declined, indicating a progressive disease. (Id. at 1748.)

On September 19, 2016, petitioner presented to the Duke ED on September 19, 

2016, with a chief complaint of “[g]eneralized dysmotility of intestine.” (Ex. 24, p. 1773.) 

Upon initial examination, Kevin Gurysh, M.D., noted that petitioner’s labs were 

remarkable for leukocytosis (high white blood cell count) and electrolyte abnormalities, 

and that her CT imaging revealed colitis of her transverse colon. (Id. at 1786.) Dr. 

Gurysh considered infectious versus inflammatory processes, and, while less likely, 

ischemia as the cause of petitioner’s GI pain. (Id.) A subsequent abdominal angiogram 

was normal, which ruled out vasculitis, while a colonoscopy and biopsy suggested 

possible ischemic colitis. (Id. at 1794.) Petitioner’s bowel functions improved, but her 

abdominal pain did not, and a repeat CT revealed ongoing inflammation and new 

enteritis. (Id.) On October 6, 2016, a push enteroscopy showed “generalized slow 

transit consistent with scleroderma-related disease and ulcers most consistent with 

small intestinal bacterial overgrowth (“SIBO”). (Id.) Her discharge summary notes that 

after ten days of antibiotics and little improvement, inflammatory bowel disease (“IBD”) 

and vasculitis “remained high on the differential.” (Id.) 

On October 20, 2016, petitioner presented to Christopher Eckstein, M.D., at the 

Duke Neuroscience Center seeking an expert opinion in this case. (Ex. 24, p. 4352.) 

Dr. Eckstein noted that petitioner’s extensive rheumatologic and autoimmune history 

could predispose her to SFN, but that he “it is possible that the vaccination could have 

exacerbated her underlying autoimmunity, which would predispose her to the 

neuropathy, though this would be difficult to prove definitively.” (Id. at 4358.)

Petitioner did not submit any records documenting her treatment from October 

20, 2016, to February 22, 2018. 

Petitioner returned to Dr. Kaufman on February 22, 2018, to follow up on her RA. 

(Ex. 63, p. 47.) Dr. Kaufman noted that petitioner continued to have significantly active 

RA. (Id. at 53.) On March 8, 2018, petitioner saw PA Neil Ewing for bilateral shoulder 

pain. (Ex. 63, p. 113.) PA Ewing believed that petitioner’s shoulder pain was due to a 

RA flare, as she had stopped taking her RA medications. (Id. at 125.) Petitioner saw 

Dr. Kaufman with complaints of left shoulder, knee, hand, and foot pain on May 24, 

2018. (Ex. 63, p. 452.) Dr. Kaufman considered petitioner’s pain to be an active RA 

flare a prescribed a depomedrol injection, with a Medrol Dosepak to be administered if 

the injection failed to address petitioner’s pain. (Id. at 457.) She returned to Dr. 

Kaufman on August 24, 2018. (Id. at 524.) Petitioner reported that she was feeling 

better since starting rituximab, but she continued to show signs of active RA on her 

examination. (Id.) Dr. Kaufman also observed that petitioner’s lung and muscle 
17

disease seemed stable. (Id.) Petitioner did not exhibit any weakness on her 

examination, and based on her subjective reports, her ILD appeared stable. (Id.)

On October 18, 2018, petitioner visited Dr. Mhoon for a follow up on her SFN. 

(Ex. 63, p. 660.) Petitioner reported that her neuropathy was overall stable with limited 

dysesthesias and only occasional burning pain in her arms. (Id. at 666.) Dr. Mhoon 

noted that petitioner’s SFN “may have been a reaction to the vaccination or sequelae 

from rheumatoid arthritis.” (Id. at 673.) 

On December 6, 2018, petitioner visited Lake Morrison, M.D., at Duke 

Pulmonology for pulmonary function testing. (Ex. 63, p. 785.) Her testing revealed a 

restrictive process and substantially reduced diffusing capacity, which was the same as 

her prior pulmonary test results. (Id. at 741.) Dr. Morrison noted that petitioner’s ILD 

was generally stable and that there was no need to adjust her medication. (Id. at 781, 

773.) An updated CT showed progression of asymmetric right greater than left ILD with 

increased interstitial consolidation and bronchiectasis as compared to her earlier chest 

CT from March 5, 2015. (Id. at 773-74.) This was interpreted as representing an NSIP 

pattern of fibrosis, most likely in the setting of connective tissue disease. (Id.) 

Petitioner next saw Eugene Friedman, M.D., on January 25, 2019, for additional 

pulmonary testing, which had remained unchanged from her previous study. (Ex. 63, p. 

937.) 

Petitioner returned to Dr. Mhoon on October 18, 2019, to follow up on her SFN. 

(Ex. 63, p. 1506.) Petitioner reported that her SFN seemed stable overall and that she 

had no significant neuropathic pain other than some cramping in her toes. (Id. at 1512.) 

Petitioner underwent additional pulmonary function testing on December 2, 2019, 

which remained unchanged from her previous test. (Ex. 63, pp. 1698-99.) That same 

day, petitioner followed up on her ILD with Dr. Morrison. (Id. at 1729.) Dr. Morrison 

noted that petitioner was stable from a pulmonary perspective, recommended a twelvemonth follow up appointment and additional physical activity. (Id. at 1732-33.)

On May 21, 2020, petitioner emailed Dr. Mhoon reporting that she was 

experiencing a burning sensation in her left arm similar to that which she experienced 

following her vaccinations in 2014. In response, Dr. Mhoon’s assistant recommended 

an essential oils topical lotion. (Ex. 63, p. 2054.)

The remainder of petitioner’s medical records focus on treatment of her frozen 

shoulder, routine visits, and unrelated illnesses. (See generally Ex. 63, pp. 2056-3870.)

b. As Reflected in Petitioner’s Affidavits

Petitioner filed her first statement on February 12, 2017. (Ex. 3.) This “affidavit” 

(signed, but not sworn) was a comprehensive filing and contained a chronology of 

petitioner’s medical treatment, and several statements addressing the basic elements of 
18

a claim for entitlement in the program. Petitioner’s extensive description of her specific 

medical encounters, though reviewed, will not be repeated herein.

Petitioner explains that she received her immunizations on November 7, 2014, at 

the UNC Internal Medicine primary care clinic. (Ex. 3, p. 2.) She states that she was in 

fair health prior to the immunizations due to her RA and polymyositis. (Id.) She was 

taking CellCept, Omeperazole for heartburn, and other prescription as needed. (Id.) 

Petitioner notes that her RA and myositis were stable prior to her vaccinations. (Id.) 

She states that her quality of life, independence, and daily living activities were 

improving, and she was tolerating consistent workouts. (Id.) Petitioner received 

previous flu vaccines in 2012 and 2013 on her doctor’s recommendation, and at some 

point also received a pneumonia vaccination. (Id. at 3.)

Petitioner notes that she received the flu vaccine in her left deltoid, and the 

pneumococcal vaccine in her right. (Ex. 3, p. 3.) Petitioner recounts that she was 

awakened by a “horrible, burning sensation in both arms,” on November 8, 2014. (Id. at 

4.) From November 8 to November 11, petitioner received at-home care until calling the 

UNC Nurse Advice Line and being advised to make an appointment with her primary 

care physician. (Id.) Petitioner reports that the burning sensation started in her 

shoulders and shot down to her forearms. Both of petitioner’s arms were sore and 

swollen at the injection sites, and moving her arms caused pain that woke her from 

sleep. (Id.) Petitioner used Tylenol, Tramadol, Flexeril, and Oxycodone to manage her 

pain, but none of her medications alleviated the burning sensation. (Id.)

Petitioner notes that as of the date she wrote her affidavit, she continued to 

experience neck, left shoulder, left wrist, and upper back pain described as “painful 

burning sensation[s], knife stabbing, [and] something crawling on my skin and 

numbness.” (Id.)

Petitioner further explains in her affidavit that she is unable to complete light 

household chores without pain, that she spends much of her time resting because it is 

how she can get the most relief, that her sleeping patterns are inconsistent, and that her 

inability to resolve her issues or find a unifying diagnosis has “been very traumatizing, 

dramatic, and painful for me.” (Id.)

Petitioner describes the burden that her need for care has placed on her family. 

(Id. at 17.) She explains that she no longer works, has lost her independence, and 

lacks emotional support due to her distance from family. (Id. at 17-18.) Petitioner 

concludes her affidavit by stating:

I know my pain and suffering was directly caused by the Flu and Pneumonia 

vaccines received. The pain started the night of Nov. 7th, 2014 after the 

shots and has continued for the past 8 months to the present. I believe I 

had no conditions previous to the vaccine that could have caused the pain 

I have experienced and continue to experience.” 
19

(Id. at 18.) 

Petitioner filed a brief affidavit on February 16, 2018, explaining that she received 

the pneumococcal conjugate 3-valient vaccine and influenza vaccine at Duke Medical 

Clinic on November 7, 2014. She also notes that she “experienced persistent, painful 

burning sensation in [her] extremities after receiving the vaccination, for which [she] 

sought medical treatment.” (Ex. 48.) She further explains that she filed a VAERS report 

on December 2, 2014. Finally, petitioner attests that she has not received any 

additional documentation regarding the investigation of her initial VAERS report. (Id.)

c. As Reflected in Petitioner’s Testimony

Petitioner testified at the entitlement hearing on July 14, 2021. Petitioner recalled 

being diagnosed with autoimmune necrotizing myopathy and seropositive RA in 2010. 

(Tr. 6.) Between 2010 and 2014, before receiving the flu and pneumococcal 

vaccinations, petitioner testified that her autoimmune necrotizing myopathy caused 

muscle weakness throughout her body and muscle aches. (Id.) She also recalled 

having pain in her shoulders and back related to sitting or standing for prolonged 

periods. (Id. at 6-7.) Regarding her RA, she recalled experiencing symptoms of 

swelling and stiffness as well as limited range of motion in her wrists and hands. (Id. at 

7.) She testified that these conditions made her permanently disabled and unable to 

work. (Id.) Prior to receiving the vaccinations at issue, petitioner testified that her 

myopathy and RA were stable. (Tr. 7.) Although she still had physical limitations, she 

was able to cook meals with assistance, wash dished, sweep the floor, do laundry, go 

for walks, and participate in activities with friends and family. (Id. at 7-8.) However, 

she recalled that her energy levels would “depreciate throughout the day.” (Id. at 8.) 

Petitioner testified that she received the pneumococcal and flu vaccinations in 

separate arms on November 7, 2014, when she was visiting her primary care provider. 

(Tr. 8-9, 25.) She recalled that she was not feeling any pain and was able to drive 

herself to the doctor and walk into the office without using a cane, walker, or wheelchair. 

(Id. at 9.) After leaving the doctor’s office, she recalled feeling some soreness. (Id. at 

9-10.) She testified that she was visiting her son after the appointment but had to “cut 

the visit short” because the soreness in her arm was getting worse. (Id. at 10.) After 

going to bed, she woke up in the middle of the night screaming and crying “because 

[she] felt like the inside of [her] body was on fire.” (Id.; see also id. at 25-26.) She 

described feeling a painful burning sensation in her arms. (Id. at 10.) 

Over the next week, petitioner could not “get the burning sensation to go away.” 

(Tr. 10.) She self-treated the pain with ice and Tylenol, which did not help. (Id.) She 

could not sleep due to the pain, which was worse at night. (Id.) She described the 

burning in her arms as “sharp in one arm and then it would get real intense in the other 

one.” (Id.) At that point, she decided to see the doctor for her symptoms. (Id.) As the 

burning sensation progressed in her arms over the next week, she began feeling it in 

her back, neck, and shoulders, followed by her legs and feet. (Id. at 11; see also id. at 

29-31 (stating that she “felt like [she] was on fire in different parts of [her] body” and that 
20

the burning pain would move from one part of her body to another).) She remembered 

telling an ER nurse that the burning sensation was moving down to her leg. (Id. at 11.) 

She also began feeling anxious, scared, and confused. (Id.)

Petitioner differentiated the post-vaccination burning sensation from symptoms 

caused by her myopathy and RA. (Tr. 11.) She explained that with her muscle disease 

and RA, her muscles would “sting,” her hands would “throb,” and she would have 

stiffness in her joints. (Id. at 11-12.) Conversely, she described her post-vaccination 

symptoms as feeling like “the inside of [her] body [was] on fire.” (Id. at 12.) She noted 

that her skin was not hot to the touch and that she did not have a fever despite feeling 

like the inside of her body was on fire. (Id.) Petitioner remembered seeing Dr. Mhoon 

on December 2, 2014. (Tr. 12.) She stated that Dr. Mhoon ordered blood tests, two 

MRIs, and a skin biopsy to rule out other autoimmune diseases. (Id.) She testified that 

her skin biopsy was positive for small fiber neuropathy, which was the first time she 

heard that diagnosis. (Id. at 13.) She further recalled telling her treating doctors that 

her SFN symptoms were different from her preexisting conditions. (Id. at 13, 33.) She 

elaborated that when she saw Dr. Mhoon, she told him that she “never felt this before.” 

(Id. at 13.)

At the time of the hearing, petitioner testified that she continued to experience 

symptoms of SFN, though more sporadically. (Id.) She explained that she experiences 

the burning sensation in her arms intermittently. (Id.) She explained that the SFN 

impacted her sleep, caused fatigue, prevented her from being as involved with her 

children, and made her unable to exercise or drive. (Id. at 18.) She described 

experiencing painful flares, having a frozen shoulder, and having a swollen wrist. (Id. at 

18-19.) She testified that her condition caused her to lose her independence. (Id. at 

19.) She further stated that her SFN caused her to suffer depression. (Id. at 20.) She 

averred that her health has not gotten back to the place it was prior to vaccination. (Id.)

IV. Expert Opinions

a. Petitioner’s Expert, Carlo Tornatore, M.D.

Petitioner filed several reports from neurologist Dr. Tornatore to support her 

claim. (Exs. 36, 50, 54, 60; ECF No. 89.7) Dr. Tornatore also testified during the 

hearing. (Tr. 35-107, 213-26.) Dr. Tornatore was proffered without challenge as an 

expert in neurology.8 (Tr. 41.)

7 Dr. Tornatore’s second report was marked with an exhibit number (26) that was duplicate and out of 

sequence. It will therefore be referred to by its docket entry – “ECF No. 89.”

8 Dr. Tornatore received his medical degree from Georgetown University School of Medicine in 1986. 

(Ex. 37, p. 2.) In 1987, he completed an internship in internal medicine at Providence Hospital in 

Washington, DC. (Id.) He completed his residency in Neurology at Georgetown University Hospital in 

1990, followed by a fellowship in molecular virology at the National Institute of Health from 1990 to 1994. 

(Id.) He current serves as interim chairman for the department of neurology at Medstar Georgetown 

University Hospital, as well as chairman of the department of neurology at Georgetown University Medical 

Center and as Professor of Neurology at Georgetown University Medical Center. (Id. at 3.) Previously, 
21

i. Diagnosis

Dr. Tornatore described small fiber neuropathy as an injury to “the unmyelinated 

C-fibers, thinly myelinated A-deltas, and postganglionic sympathetics,” also known as 

“small fibers.” (Ex. 36, p. 8 (citing Anne Louise Oaklander, Immunotherapy Prospects 

for Painful Small-fiber Sensory Neuropathies and Ganglionopathies, 13

NEUROTHERAPEUTICS 108 (2016) (Ex. 38)).) He notes that “the small fibers sense pain 

and itch, innervate internal organs and tissues, and modulate the inflammatory and 

immune responses.” (Id.) He explained that symptoms of the condition include “chronic 

pain and itch, sensory impairment, edema, and skin color, temperature, and sweating 

changes.” (Id.) Small fiber polyneuropathy may also cause “cardiovascular, [GI], and 

urological symptoms, the neurologic origin of which often remains unrecognized.” (Id.) 

According to Dr. Tornatore, the time course and etiology of SFN is “strikingly similar to 

Guillain-Barre [syndrome (“GBS”)]” and “characterized by autonomic and sensory 

impairment without motor dysfunction that reaches its nadir within a short period of time. 

(Ex. 36, p. 8.) The monophasic clinical course and frequent presence of a history of 

antecedent infections suggest a participation of immune mechanisms.” (Id. (citing 

Haruki Koike & Gen Sobue, Autoimmune Autonomic Ganglionopathy, 53 RINSHO 

SHINKEIGAKU 1326 (2013) (Ex. 44)).) Skin biopsies are a key diagnostic technique 

because routine electrodiagnostic studies fail to detect SFN. (Ex. 38, p. 8.) Dr. 

Tornatore also reports that corticosteroids and immunoglobulins have been effective in 

treating SFN. (Id.) 

In response to Dr. Gelfand’s assertion that brachial neuritis may provide a better 

explanation for petitioner’s upper extremity symptoms, Dr. Tornatore noted that Dr. 

Gelfand conceded that “[i]n rare cases, small fiber neuropathy follows a non-length 

dependent distribution in which symptoms may be manifested predominately in the 

arms, face or trunk . . . [and that] non-length dependent patterns occur rarely including 

in presumed dysimmune causes.” (ECF No. 89, p. 2.) Dr. Tornatore interpreted this 

statement to mean that Dr. Gelfand conceded that petitioner’s upper extremity 

symptoms could be consistent with a dysimmune sensory neuropathy. (Id.) Dr. 

Tornatore also addressed Dr. Gelfand’s contention that petitioner’s lower extremity 

condition was a comorbidity independent of the process that was causing the burning 

sensation in her upper extremities. (Ex. 50, p. 3). Although Dr. Gelfand opined that “an 

acute small fiber neuropathy involving the proximal upper extremities (a non-length 

dependent pattern) would be atypical” (Ex. J, p. 9), Dr. Tornatore noted that petitioner’s 

skin biopsy report stated that “[o]ccasionally, patients with a length dependent 

neuropathy can feel symptoms in the hands before the lower extremities” (Ex. 50, p. 3). 

Thus, Dr. Tornatore concluded that petitioner’s upper extremity symptoms are 

attributable to SFN. 

 

Dr. Tornatore has held positions as vice chairman of the department of neurology at Medstar Georgetown 

University Hospital, Associate Professor at Georgetown University Medical Center, and Assistant 

Professor in the department of neurology at Georgetown University Medical Center. (Id.) Dr. Tornatore 

has also published 63 original papers and book chapters on neurology and virology. (Id. at 8-14.)
22

ii. Causation

1. Molecular Mimicry 

Dr. Tornatore opined that there are two possibilities that would explain 

petitioner’s painful neuropathic sensory symptoms. First, he posited that petitioner was 

predisposed to autoimmune disorders and developed “[d]e novo” autoimmune small 

fiber sensory neuropathy shortly after an antigen challenge from her vaccinations. (Ex. 

36, pp. 7-8; Tr. 50, 97-98.) Second, he opined that an “indolent, asymptomatic 

autoimmune small fiber neuropathy . . . was profoundly aggravated” following the 

antigen challenge from her vaccinations. (Ex. 36, pp. 7-8; Tr. 50, 97-98.) In either 

event, Dr. Tornatore concluded that “the vaccinations were the inciting factor.” (Ex. 36, 

pp. 7-8.) 

With respect to the mechanism by which the vaccinations petitioner received can 

cause SFN, Dr. Tornatore offered molecular mimicry. (Ex. 36, pp. 8-9.) Dr. Tornatore 

explained that the process of molecular mimicry triggers an autoimmune response that 

may result in inflammatory polyneuropathies, including small fiber neuropathy. (Id.) Dr. 

Tornatore opined that when antigens “present on the vaccine share any homology with 

host antigens . . . the immune response will be directed at both the injected antigens 

and host antigens, leading to an autoimmune response.” (Id. at 9 (citing Michael B.A. 

Oldstone, Molecular Mimicry, Microbial Infection and Autoimmune Disease: Evolution of 

the Concept, 296 CURRENT TOPICS IN MICROBIOLOGY & IMMUNOLOGY 1 (2005) (Ex. 47)).)

Dr. Tornatore further opined that “vaccines have been recognized to trigger 

autoimmune responses, albeit rarely, that lead to autoimmune response directed

against antigens on peripheral nerves, resulting in inflammatory polyneuropathies.” (Ex. 

36, p. 9 (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. 46); J.D. Pollard & G. Selby, Relapsing 

Neuropathy Due to Tetanus Toxoid, 37 J. NEUROLOGIC SCIS. 113 (1978) (Ex. 39)).) Dr. 

Tornatore also noted that there are numerous case reports of autoimmune peripheral 

neuropathies following other vaccinations, including rabies, varicella, Lyme, and HPV. 

(Id. (citing Frederic E. Shaw, JR. et al., Postmarketing Surveillance for Neurologic 

Adverse Events Reported After Hepatitis B Vaccination, 127 AM. J. EPIDEMIOLOGY 337

(1988) (Ex. 45); Nizar Souayah et al., Small Fiber Neuropathy Following Vaccination for 

Rabies, Varicella or Lyme Disease, 27 VACCINE 7322 (2009) (Ex. 40); Svetlana 

Blitshteyn, Postural Tachycardia Syndrome Following Human Papillomavirus 

Vaccination, 21 EUR. J. NEUROLOGY 135 (2014) (Ex. 42)).) According to Dr. Tornatore, it 

is not only a homology in amino acid sequences where exogenous antigens may induce 

an autoimmune response, but receptors on B and T cells are now known to recognize 

peptide sequences that share no homology and in turn mount an autoimmune response 

on the nervous system through a process known as ‘degeneracy.’ (Id. (citing Don 

Mason, A Very High Level of Crossreactivity Is an Essential Feature of the T-Cell 

Receptor, 19 IMMUNOLOGY TODAY 395 (1998) (Ex. 41)).)
23

Dr. Tornatore agreed with Dr. Gelfand’s assertion that to prove molecular 

mimicry, sequence homology between neuronal and vaccinal antigens must be shown. 

(Ex. 89, p. 2.) However, Dr. Tornatore stressed that sufficient sequence homology has 

already been demonstrated. Dr. Tornatore cited an article that found homologies 

between myelin proteins and viral proteins including measles, Epstein-Barr, influenza A 

and B, and others that cause upper respiratory infections. (Id. (citing Ulrike Jahnke et 

al., Sequence Homology between Certain Viral Proteins and Proteins Related to 

Encephalomyelitis and Neuritis, 229 SCIENCE 282 (1985) (Ex. 51)).) Dr. Tornatore 

further noted that Dr. Gelfand authored a paper stating that “acute disseminated 

encephalomyelitis . . . can be preceded by an acute systemic infection or vaccination,” 

acknowledging that vaccination can lead to molecular mimicry-induced autoimmunity. 

(Ex. 54, p. 5.)

Dr. Tornatore also addressed Dr. Whitton’s contention that “[t]here are, however, 

no clear examples of a human disease caused by molecular mimicry.” (Ex. 89, p. 4.) 

Dr. Tornatore explained that this is incorrect, as rheumatic fever and Sydenham’s 

chorea have been recognized “as the classic examples of molecular mimicry in clinical 

medicine for over a century.” (Id.) Dr. Tornatore cited a paper by Carapetis and others,

which found that after a group A streptococcal infection (“GAS”) of the pharynx in 

susceptible individuals, “the host response against GAS will trigger autoimmune 

reactions against host tissues mediated by both Streptococcus-specific antibodies and 

T cells through a process called molecular mimicry.” (Id. (citing Jonathan R. Carapetis 

et al., Acute Rheumatic Fever and Rheumatic Heart Disease, 2 NATURE REV. DISEASE 

PRIMERS 15084 (2016) (Ex. 57)).) He explains that after GAS infections, children may 

develop antibodies against dopamine receptors, which are cross reactive with 

streptococcus epitopes. (Ex. 54, p. 5.) 

Regarding petitioner’s rapid onset, Dr. Tornatore explained that “small fiber 

sensory neuropathy can occur abruptly.” (Ex. 36, p. 8.) Further, he opined that 

petitioner’s previous flu vaccinations could cause “a subsequent re-challenge to mount 

a brisk and rapid immune response.” (Id. at 8, 9.) He cited a report from the Institute of 

Medicine that shows that the latency or lag phase for an autoimmune response 

following exposure to “many antigens” is between seven and ten days, while “the 

latency between subsequent exposure to the antigen and the immune response will 

usually be shorter . . . generally one to three days; the logarithmic phase of the 

secondary antibody response occurs over the next three to five days.” (Id. (citing INST.

OF MED., EVALUATING BIOLOGICAL MECHANISMS OF ADVERSE EVENTS 51-52 (2011) (Ex. 

43)).)

In the context of molecular mimicry, Dr. Tornatore opined that the “secondary 

immune response” phenomenon explains petitioner’s rapid onset. The phenomenon is 

described as

a markedly enhance[d] response that is characterized by the accelerated 

appearance of immunocompetent T and B cells referred to as “memory 

cells” that collaborate to generate an enhanced production of antibody. The 
24

latent period is much shorter during the secondary immune response since 

the memory cells are present at a higher frequency and are available to be 

stimulated quickly . . . this is the basis for the IOMs recognition that the 

second exposure to a vaccination may result in a markedly shorter time of 

onset of an immune response to administration of an exogenous antigen.

(Ex. 50, p. 3.)

Therefore, Dr. Tornatore concluded that it was medically plausible that 

petitioner’s flu and/or pneumococcal vaccine caused her SFN via molecular 

mimicry. 

2. Interferon Gamma (“IFN- γ”) Theory

In his later reports, Dr. Tornatore offered another explanation for how the 

vaccines petitioner received can cause SFN in a rapid timeframe. (Exs. 54, 60.) Dr. 

Tornatore explained that the rapid onset in this case is due to a cytokine reaction 

producing interferon gamma (“IFN- γ”), a modulator of neuropathic pain. (See generally 

id.) He described an experiment conducted by Dr. Whitton where naïve mice were 

exposed to viral antigens and an inoculation against that antigen. In the experiment, the 

mice began producing IFN- γ, a signal that the immune response had been activated, 

within 6-12 hours. (Ex. 54, p. 1.) The mice were exposed to the same viral antigens 

and inoculated roughly a year later, and began producing IFN- γ within hours of 

exposure. (Id. at 1-2.) Dr. Tornatore explained that these results show that “within 

hours of activation, the immune system can produce interferon-gamma, a known 

mediator of chronic pain . . . consistent with [petitioner’s] clinical symptoms.” (Id. at 2.) 

Dr. Tornatore theorized that a vaccination could cause the systemic dissemination of 

viral antigens that could cross into the dorsal root ganglia (“DRG”) due to the lack of a 

blood-brain barrier. (Id. at 3.) He discussed how the vaccination could stimulate 

resident lymphocytes of the DRG that produce IFN- γ, thus resulting in the sensation of 

pain in a dermatomal distribution. (Id.) He asserted that within days, “there will be 

replication of the lymphocytes with further injury to the DRG ultimately resulting in loss 

of the sensory projections from the DRG into the extremity . . . .” (Id.)

Dr. Tornatore further noted that “the sensory component of the nervous system 

has a very low threshold to stimulation in the face of a noxious event.” (Ex. 54, p. 2.) 

Citing the diagram in his report, he explains that “there are dermatomes over the 

extremities that represent the innervation from a single nerve root. If one looks at the C7 

nerve, irritation or inflammation of that nerve root will result in sensory changes that 

involve a significant part of the arm.” (Id. at 2-3.) Dr. Tornatore explains that the DRG 

is where the cell bodies of sensory nerves lie, they are very small, and have a unique 

interface between accumulations of sensory neurons and blood vessels, specifically, 

that they lack a blood-brain barrier which allows blood borne molecules to directly enter 

the DRG and interact with neuronal and non-neuronal cells. (Id. at 2 (citing Rainer 

Viktor Harberger et al., Human Dorsal Root Ganglia, 13 FRONTIERS IN CELLULAR 

NEUROSCIENCE 271 (2019) (Ex. 56)).) The non-neuronal cells contained within the DRG 
25

include a group of immune cells consisting mainly of macrophages and T-lymphocytes, 

with a lower number of B-lymphocytes. (Id.) Dr. Tornatore simplifies this concept, 

noting that in the case of the DRG: 

[W]e have a very small structure with an absent blood-brain barrier that 

contains not only neurons but also lymphoid and myeloid cells, that can 

mediate pain and other sensory modalities over a large area. As such, it is 

biologically plausible that the administration of a vaccine could result in the 

systemic dissemination of viral antigens that could easily cross into the 

dorsal root ganglia given the lack of blood brain barrier, stimulate resident 

lymphocytes of the dorsal root ganglia that then produce IFN-gamma 

resulting in the sensation of pain in a dermatomal distribution, e.g. the length 

of the arm, as was the case with [petitioner]. 

(Id. at 3.)

Dr. Tornatore agreed with Dr. Whitton that “within days there will be replication of 

the lymphocytes with further injury to the DRG ultimately resulting in loss of the sensory 

projections from the DRG into the extremity, as was the case in Ms. McGill’s punch 

biopsy.” (Ex. 54, p. 3.) He stated that he and Dr. Whitton were “in agreement that the 

immune system has the capability of being stimulated quickly and producing soluble 

factors such as interferon gamma.” (Ex. 60, p. 2.) He further opined that “immune cells 

can be quickly activated by exogenous antigens to provide sensory symptoms referable 

to the nervous system.” (Id. at 3.) Thus, Dr. Tornatore reasoned that because memory 

T cells can produce IFN- γ within hours of exposure to viral antigen, it is biologically 

plausible that the vaccines petitioner received caused her to develop SFN 8.75 hours 

after administration. (See Ex. 54, pp 1-2.) 

b. Respondent’s Experts9

i. J. Lindsay Whitton, M.D., Ph.D.

Respondent also filed several reports from immunologist Dr. Whitton to support 

his position. (Exs. C, M, N.) Dr. Whitton also testified at the hearing. (Tr. 144-213.) He 

was proffered without objection as an expert in immunology.10 (Tr. 153.)

9 Respondent also filed an expert report from rheumatologist Chester Oddis, M.D. (Ex. A.) However, 

respondent confirmed in his prehearing brief that he did not intend to present live testimony from Dr. 

Oddis given that he addressed petitioner’s claims of ILD and myofascial pain syndrome. (ECF No. 135, 

p. 3. n.4.) Based on petitioner’s intent to proceed solely with her claim for SFN and abandon her claim for 

ILD and myofascial pain syndrome (ECF No. 148, p. 23, n.7), discussion of Dr. Oddis’ report has been 

omitted from this decision. 

10 Dr. Whitton received his medical degree from the University of Glasgow in 1979, and his Ph.D. from the 

same university in 1984. (Ex. D, p. 1.) He currently serves as a professor in the department of 

immunology and microbial science at Scripps Research Institute, and previously held positions as a 

professor in the department of neuropharmacology, and molecular and integrative neurosciences at 

Scripps as well. (Id.) He is a member of several professional societies including the American 
26

1. Causation

a. Molecular Mimicry

Dr. Whitton stated that although that molecular mimicry is a biological 

phenomenon, it is not a reliable theory for how the flu or pneumococcal vaccines can 

cause SFN. (Ex. M, p. 10.) Dr. Whitton pointed out that a report from the IOM cited by 

Dr. Tornatore notes, “[w]hile molecular mimicry is a well-established mechanism in 

selected animal models, its relevance to human autoimmune disease remains in most 

cases to be convincingly proven.” (Id. (quoting INST. OF MED., supra, at Ex. 43, p. 12).) 

The IOM publication further states:

[W]e found little clinical evidence (e.g., challenge/rechallenge), diagnostic 

evidence (e.g., presence of antigen or relevant immune complexes in 

affected tissue), or experimental evidence (e.g., in vitro evidence of crossreactive T-cells derived from a site of tissue injury) that could be 

consistent with the hypothesis of molecular mimicry in rare and selected 

case reports . . . . Based on the literature reviewed, molecular mimicry 

was not confirmed to be a mechanism leading to the development of the 

adverse events postvaccination.

(Id. (citing INST. OF MED., supra, at Ex. 43, p. 13).) 

Dr. Whitton also asserted that “it is very difficult to cause disease via molecular 

mimicry.” (Id. at 12; see also Tr. 157-58 (stating that the term “molecular mimicry” 

should not be equated with disease, as disease is a distinct step, and it is rare for 

molecular mimicry to cause disease).) He explained several difficulties in showing that 

viral infections can lead to molecular mimicry in animals. (Ex. M, pp. 11-12.) Dr. 

Whitton further noted that he was unaware of any medical literature confirming 

molecular mimicry as a mechanism by which the flu or pneumococcal vaccines can 

cause adverse events. (Tr. 167.) Likewise, he was unaware of any sequences in the 

flu or pneumococcal vaccines that could mimic antigens in small fiber nerves as 

required for molecular mimicry to occur. (Id. at 168.) Thus, Dr. Whitton concluded that 

neither the flu vaccine nor the pneumococcal vaccine is a recognized cause of SFN. 

(Id. at 197.)

Moreover, Dr. Whitton found it significant that prior to the vaccinations at issue, 

petitioner had been diagnosed with multiple autoimmune diseases, including ANM, RA, 

and ILD. He asserted that “SFN is often associated with autoimmune diseases, and 

some cases have been successfully treated using immunosuppressants.” (Ex. C, p. 9.) 

Thus, Dr. Whitton concluded that petitioner’s SFN is more likely “another manifestation 

Association of Pathologists, the American Association of Immunologists, the American Society of 

Virology, and the American Society of Microbiology. (Id.) He currently serves on the editorial boards of 

three different medical journals and holds the position of editor for the Virology medical journal. (Id. at 1-

2.) Dr. Whitton has published 191 different pieces of medical literature focusing on virology, immunology, 

and molecular biology. (Id. at 2-14.)
27

of her susceptibility to autoimmune processes” and that petitioner’s preexisting 

autoimmune diseases “provid[e] a likely explanation for her the eventual appearance of 

SFN.” (Ex. C, p. 12.)

Regarding the appropriate timing for molecular mimicry, Dr. Whitton opined that 

the lag phase for a primary immune response following vaccination is seven to ten days, 

while the lag phase for a secondary immune response following vaccination is one to 

three days. (Ex. M, p. 6.) He asserted that both time intervals “far exceed” the 8.75-

hour timeframe between petitioner’s administration of the flu and pneumococcal 

vaccines and the onset of the burning sensation in her arms. (Id. at 6-8; Tr. 177.) Dr. 

Whitton noted that he was unaware of any “reliable mechanism” by which vaccinations 

could trigger SFN in only 8.75 hours. (Tr. 177; Ex. C, p. 12.) Dr. Whitton stressed that 

autoimmune diseases “take time to develop,” and an antibody-mediated autoimmune 

neurological disease takes days to manifest, even in a previously immunized individual. 

(Ex. M, pp. 7-9, 12 (discussing how animal models show that an autoimmune 

neurological disease takes days to weeks to develop, even if the animal had been 

previously exposed to the inciting antigen).) Thus, even applying the appropriate 

interval for a secondary immune response, an 8.75-hour onset is too rapid to be 

plausible. (Id. at 7-8.) 

Dr. Whitton further described the process of how T cells begin to divide in 

response to an antigen. (Ex. M, p. 9.) He explained that “T cells can respond to 

antigen challenge, in vivo, very rapidly – within hours.” (Id.; see also Tr. 180-81 (noting 

that T cells can make cytokines, such as such as IFN-γ, within hours in response to an 

antigen challenge).) However, he emphasized that the T cells “do not begin to 

proliferate for several days (probably ~3-4 days).” (Ex. M, p. 9; Tr. 180-81.) He also 

clarified that this days-long lag phase applies to memory T cells. (Ex. M, p. 9; Tr. 181.) 

He elaborated:

To cause systemic neurological disease, the T cells would have to (i) start 

to divide (which doesn’t happen until ~3 days post-vaccination); (ii) divide 

multiple times over several more days to reach a sufficient number to 

cause harm; (iii) migrate to the nerves; and (iv) exert their effector 

functions thereupon, causing the signs and symptoms of SFN. So, it is 

implausible to suggest that a locally-injected vaccine could lead to a 

systemic T-cell mediated disease in only 83⁄4 hours.

(Ex. M, pp. 9-10 (citing Jason K. Whitmire, Boreth Eam, & J. Lindsay Whitton, Tentative 

T Cells: Memory Cells Are Quick to Respond, but Slow to Divide, 4 PLOS PATHOGENS

e1000041 (2008) (Ex. M, Tab 4)).) 

Although Dr. Whitton acknowledged that the timeframe may lessen as increasing 

numbers of booster injections are administered, he contended that “biology dictates that 

there be a minimum interval of several days.” (Id. at 12.) Dr. Whitton maintained that 

petitioner’s previous flu vaccinations would not shorten the required lag phase of 1-3 
28

days for a secondary immune response because T cells take three days to start 

dividing. (Tr. 178.) 

b. IFN- γ Theory

Dr. Whitton described Dr. Tornatore’s IFN- γ hypothesis as asserting that 

“vaccine-specific memory T cells, activated after the vaccination, shed sufficient IFN- γ 

to trigger neuropathic pain.” (Ex. N, p. 3.) Thus, he explained that Dr. Tornatore’s IFNγ theory has two parts: (1) antigens are disseminated systemically and enter the DRG 

where they trigger IFN-γ, causing pain; and (2) the antigen-bearing cells carry antigens 

into the lymphatics. (Tr. 185-86; see also Ex. N, p. 3.) He stated that Dr. Tornatore 

hypothesized that the IFN-γ caused neuropathic pain in the DRG. (Tr. 187.) He 

distinguished the IFN- γ theory from molecular mimicry, noting that molecular mimicry 

necessitates the induction of an immune response and the cross-reaction of the 

immune response with a self-antigen. (Id. at 187-88.) The IFN- γ theory is different 

from molecular mimicry as it does not involve a host antigen. (Id.) Further, Dr. Whitton 

explained that the IFN- γ theory is not autoimmune as an autoimmune response would 

require recognition of a self-antigen. (Id. at 188.) 

Regarding the role of memory T cell responses in Dr. Tornatore’s IFN- γ theory, 

Dr. Whitton explained that “it is a common misunderstanding that memory T cell 

responses, being ‘faster and stronger,’ must cause more discomfort / disease to the 

host.” (Ex. N, p. 4.) In contrast, Dr. Whitton explained that “the primary T cell response 

to infection causes more systemic signs and symptoms than does the memory T cell 

response, which is faster and more biologically-beneficial.” (Id.) He stressed that “T 

cells (both primary and memory) very tightly regulate the production of cytokines, 

including IFN- γ.” (Id.) He explained that memory T cells prevent a virus from 

multiplying, and as a result, “very little virus antigen is produced,” and the T cells can

therefore terminate cytokine production quickly after a subsequent exposure. (Id. at 5.)

For Dr. Tornatore’s IFN- γ theory to be feasible, Dr. Whitton opined that the 

proteins in a vaccination would need to diffuse from the site of administration, enter the 

DRG, and be taken up by an antigen presenting cell (“APC”). (Ex. N, p. 6.) Once inside 

the APC, the proteins would be degraded into short epitope peptides that are 

complexed with major histocompatibility complex (“MHC”) molecules into the APC 

cytoplasm. (Id.) The MHC/peptide complexes would then travel to the surface of the 

APC, where they would activate vaccine-specific T cells in the DRG. (Id.) The T cells 

would then produce IFN-γ that acted on nerve cells through the IFN-γ receptor to cause 

petitioner’s burning sensation. (Id. at 6, 9.) Dr. Whitton asserted that this process has 

never been demonstrated and was purely speculative. (Id. at 9; Tr. 191.) Dr. Whitton 

also noted that Dr. Tornatore did not provide any clinical or experimental support for this 

theory. (Ex. N, p. 9.)

Dr. Whitton also noted that petitioner’s clinical presentation was inconsistent with 

Dr. Tornatore’s IFN- γ theory. He opined that if the bilateral burning sensation in 

petitioner’s arms were caused by the overproduction of IFN-γ by vaccine-specific T-
29

cells, he would have expected petitioner to have presented with inflammation, redness, 

and induration at the UNC Same Day Clinic on November 13, 2014. (Tr. 196.) Given 

that petitioner did not have a fever or swelling in either arm (Ex. 4, p. 3), Dr. Whitton 

concluded that a vaccine-mediated event was unlikely (Tr. 196; Ex. N, p. 6). 

Further, Dr. Whitton argued that even if Dr. Tornatore’s IFN- γ theory was 

possible, it would occur “extraordinarily rarely.” (Ex. N, p. 6.) He noted, “Despite 

billions of doses of vaccine[s] having been administered, there is no recognized risk of 

antigen diffusing into DRG, causing severe burning neuropathic pain.” (Id. at 9; see 

also Tr. 196.) Dr. Whitton concluded that Dr. Tornatore abandoned molecular mimicry 

as a feasible theory and offered “a completely new biological mechanism, antigen 

diffusing into DRG, for which he presents no evidence, and which makes little biological 

sense.” (Ex. N, p. 8.)

Regarding the appropriate timeframe, Dr. Whitton agreed that the immune 

system can be activated rapidly following exposure to viral elements. (Ex. N, p. 3.) 

However, he emphasized the distinction between activation of the immune system and 

occurrence of neurological injury, which he stressed are “two completely separate 

biological events.” (Id. at 2.) Dr. Whitton acknowledged that when a person has 

memory T cells due to previous exposure to a virus and reencounters that virus, “those 

T cells very quickly (within hours) are activated by antigen contact a at which point, they 

immediately produce cytokines (including IFN- γ) that shut down the virus’ ability to 

multiply.” (Id. at 5; see also Tr. pp. 180-81.) Although Dr. Whitton acknowledged that 

memory T cells can respond to antigen challenge by making cytokines within hours, he 

explained that those T cells still take about three days to proliferate, after which they 

begin to “divide explosively and exponentially.” (Tr. 180-81.) Thus, although memory T 

cells can respond to antigen challenge within hours, Dr. Whitton maintained that both 

primary and memory T cells have a lag phase of about three days, and “the process of 

division is about the same.” (Id. (citing Whitmire, Eam, & Whitton, supra, at Ex. M, Tab 

4).) Thus, Dr. Whitton concluded that Dr. Tornatore’s IFN- γ theory would not explain 

petitioner’s rapid onset. 

ii. Jeffrey M. Gelfand, M.D., MAS, FAAN 

Respondent also filed two reports from neurologist Dr. Jeffrey Gelfand to support 

his position. (Exs. J, L.) Dr. Gelfand also testified at the hearing. (Tr. 107-139.) He 

was proffered without objection as an expert in both neurology and neuroimmunology.11

(Tr. 111.) 

11 Dr. Gelfand received his medical degree from Harvard Medical School in 2006, he completed his 

internship in internal medicine at the University of California, San Francisco (“UCSF”), followed by a 

residency in neurology at the same hospital in 2010. (Ex. K, p. 1.) Dr. Gelfand was chief resident from 

2009 to 2010 and held a fellowship in multiple sclerosis and neuroimmunology from 2010 to 2012 at 

UCSF. (Id.) He is licensed by the state of California, and board certified in neurology by the American 

Board of Neurology and Psychiatry. (Id.) Dr. Gelfand currently serves as an associate professor of 

clinical neurology at UCSF, previously he was an assistant professor of clinical neurology and a HS 

clinical instructor. (Id. at 2.) Dr. Gelfand has published 49 peer reviewed articles, 27 review articles, and 

6 books and book chapters on various neurological diseases. (Id. at 13-19.)
30

1. Diagnosis

Dr. Gelfand disputed that SFN explains petitioner’s symptoms. Although he 

acknowledged that petitioner’s skin biopsy on her leg showed evidence of SFN, he 

contended that there was no evidence of a concomitant large fiber polyneuropathy. (Ex. 

J, p. 8.) He opined that petitioner’s medical records fail to establish that her acute upper 

extremity symptoms can be attributed to SFN. (Id.) He noted that petitioner’s treating 

physicians raised SFN as a diagnosis based on petitioner’s left calf biopsy results but 

stressed that no evidence supported the presence of other manifestations of SFN, such 

as autonomic dysfunction. (Id.) 

Dr. Gelfand further emphasized that petitioner’s left calf biopsy showed evidence 

of SFN, but not her left thigh, which suggests a length-dependent pattern of SFN in her 

legs. (Ex. J, pp. 8-9; Tr. 121.) However, he noted that petitioner’s upper extremity 

symptoms are incompatible with a length-dependent pattern of SFN because they 

began in her proximal upper extremities, not her fingertips and hands. (Ex. J, p. 9; Tr. 

122.) He acknowledged that small fiber neuropathy may follow a non-length dependent 

pattern where symptoms manifest primary in the arms, face, or trunk. (Ex. J, p. 9.) 

However, he emphasized that this is rare, and it is also rare for a patient to have a more 

typical pattern in the legs and an atypical pattern in the arms. (Id.) He stressed that a 

non-length-dependent pattern would be “atypical, rare, and diagnostically speculative.” 

(Ex. L, p. 1.) 

Dr. Gelfand offered neuralgic amyotrophy (“NA”), also called brachial neuritis, as 

a potential explanation for petitioner’s acute bilateral upper extremity pain. (Ex. J, p. 7.) 

He explained that NA is a brachial plexus neuropathy that involves large fiber peripheral 

nerves of the brachial plexus innervating the upper extremities and can cause severe 

bilateral shoulder pain. (Id.) Dr. Gelfand opined that petitioner’s symptoms may be 

better attributed to NA given that her bilateral shoulder pain was acute, severe, and out 

of proportion to any possible weakness. (Id.) He distinguished NA from SFN, noting 

that NA is a “different diagnostic entity than autoimmune SFN, as it involves large and 

small fiber nerves in the brachial plexus.” (Ex. L, p. 1.) Based on the evidence, 

however, Dr. Gelfand conceded that he could not determine that petitioner’s upper 

extremity condition was more likely than not caused by NA. (Tr. 123.) He testified that 

he merely wanted to “credit” NA as part of a differential diagnosis for petitioner. (Id.) 

Dr. Gelfand further noted that “the evidence is insufficient to support a vaccine-induced 

cause of NA, if that is in fact what the diagnosis was.” (Ex. L, p. 1.)

Dr. Gelfand acknowledged that petitioner had SFN in her distal lower extremities. 

(Tr. 132.) Although he conceded that SFN was an “important diagnostic consideration” 

for petitioner, he did not offer a final diagnosis for petitioner’s condition. (Id. at 126-27.) 

He noted that it was difficult to establish a diagnosis “for the etiology of [petitioner’s] 

acute pain syndrome to a more-likely-than-not standard.” (Id. at 124.) Thus, Dr. 

Gelfand concluded that petitioner’s upper extremity symptoms were not attributable to 

SFN.
31

2. Causation

a. Molecular Mimicry 

In response to Dr. Tornatore’s molecular mimicry theory, Dr. Gelfand noted that 

Dr. Tornatore did not offer evidence demonstrating how getting another flu vaccination 

would create an immune response leading to SFN. (Ex. J, p. 10.) Dr. Gelfand also 

stated that Dr. Tornatore failed to provide sequences in the flu or pneumococcal 

vaccines that could mimic antigens in small fiber nerves that would demonstrate 

sufficient homology for molecular mimicry. (Id.) He contended that Dr. Tornatore’s 

reports “only offer general statements about antigens that may be in the vaccine or its 

adjuvants that could cause an inflammatory response generally.” (Id.) 

Further, Dr. Gelfand explained that SFN has several potential causes and 

associations, including diabetes/prediabetes, endocrine disease (i.e., thyroid 

abnormalities), vitamin deficiencies (i.e., B12 deficiency), toxic exposure (i.e., alcohol), 

chronic infection (i.e., HIV), autoimmune disease, paraproteinemia, and inherited or 

genetic factors. (Ex. J, p. 9.) He also noted that petitioner’s history of RA and 

propensity to autoimmune disease are potential causes of SFN. (Id. (citing Astrid J. 

Terkelsen et al., The Diagnostic Challenge of Small Fibre Neuropathy: Clinical 

Presentations, Evaluations, and Causes, 16 LANCET NEUROLOGY 934, 939 (2016) (Ex. J, 

Tab 2)); see also Tr. 118-20 (stating that individuals with autoimmune disease can be 

susceptible to other autoimmune diseases, and that SFN can be caused by an 

autoimmune process).) Additionally, in 30-50% of SFN cases, the underlying cause is 

unknown. (Terkelsen et al., supra, at Ex. J, Tab 2, p. 939.) Further, Dr. Gelfand 

maintained that neither the flu vaccine nor the pneumococcal vaccine is a recognized 

cause of SFN. (Tr. 115-16.) He stressed that Dr. Tornatore did not provide medical 

literature supporting either the flu or pneumococcal vaccine as a cause of SFN, as SFN 

is a “distinct pathophysiological entity from large fiber neuropathy.” (Ex. J, p. 10; Tr. 

128.)

Dr. Gelfand also criticized the relevance of the literature offered by Dr. Tornatore. 

He asserted that none of the literature associated the flu or pneumococcal vaccines with 

SFN. (Ex. J, pp. 10-11.) Rather, Pollard & Selby (supra, at Ex. 39) involved a large 

fiber demyelinating neuropathy following the tetanus toxoid; Shaw et al. (supra, at Ex. 

45) involved cases of SFN temporally associated with rabies, Lyme disease, and live 

varicella vaccines; Blitshteyn (supra, at Ex. 42) involved POTS following the HPV 

vaccine; and Koike & Sobue (supra, at Ex. 44) involved autoimmune autonomic 

ganglionopathy. (Ex. J, pp. 10-11.) Thus, Dr. Gelfand concluded that Dr. Tornatore 

provided no evidence to support a causal association between SFN and the flu or 

pneumococcal vaccines. 

With respect to the timing involved in molecular mimicry, Dr. Gelfand opined that 

the appropriate timeframe for onset of an autoimmune condition following a triggering 

event would be “over days to a few weeks.” (Tr. 133.) He further contended that Dr. 

Tornatore did not “explain how to reconcile the quite severe and acute onset of 
32

[petitioner’s] pain within hours to a day after vaccination and the several days of lag time 

he discusses as a possible medical theory for the immune response to develop even 

with prior influenza vaccination.” (Ex. J, p. 10.) He elaborated that the onset of 

petitioner’s “clinical syndrome, which came on profoundly within hours to 1 day of 

vaccination, would be too fast to support a vaccine-induced cause beyond a reasonable 

degree of medical certainty.” (Ex. L, p. 2.) 

b. IFN- γ Theory

During the entitlement hearing, Dr. Gelfand briefly addressed Dr. Tornatore’s 

IFN- γ theory. He testified that there was no recognized risk of vaccines causing 

severe, burning neuropathic pain within mere hours of administration. (Tr. 124.) He 

further stated that IFN- γ would be routinely expressed as part of many systemic 

infections and vaccinations. (Id. at 137-38.) He explained that acute, burning 

neuropathic pain is not a routine or expected adverse reaction that is seen with “sort of 

a standard vaccination” like a flu or pneumococcal vaccination. (Id.) Thus, Dr. Gelfand 

contested the reliability of Dr. Tornatore’s IFN- γ theory. 

V. Discussion

a. Althen prong one12

i. Dr. Tornatore’s theory includes two necessary components

Dr. Tornatore filed five separate expert reports in this case and also testified 

during the entitlement hearing. Although he has consistently opined that petitioner 

suffered vaccine-caused SFN, his theory of causation has evolved. In his initial reports, 

he asserted that molecular mimicry between vaccine components and peripheral nerve 

myelin tissue can result in inflammatory polyneuropathies, either by direct homology or 

by T cell degeneracy. (Ex. 36, p. 9; ECF No. 89, pp. 2-3.) He suggested this could be 

applied in the context of petitioner’s upper extremity symptoms occurring mere hours

after vaccination. (Id.) However, after being challenged on that theory with respect to 

timing, Dr. Tornatore stressed that IFN- γ, which can be produced by T cells within 

hours of infection, is “a well-known modulator of pain.” (Ex. 54, p. 2.) He theorized that 

“it is biologically plausible that the administration of a vaccine could result in the 

systemic dissemination of viral antigens that could easily cross into the dorsal root 

ganglia given the lack of a blood brain barrier, stimulate resident lymphocytes of the 

dorsal root ganglia that then produce IFN- [γ] resulting in the sensation of pain in a 

12 There is some suggestion from Dr. Tornatore’s reports that he could alternatively opine that petitioner’s 

vaccinations significantly aggravated an indolent SFN. (Ex. 36, pp. 7-8.) However, there is no evidence 

to suggest that petitioner actually was suffering such a condition prior to vaccination. And, in any event, 

Dr. Tornatore indicated that his theory would still be the same. (Tr. 97-98.) In her post-hearing briefs, 

petitioner references that aspect of Dr. Tornatore’s opinion that posited the possibility that indolent SFN 

may have been aggravated; however, she couched her claim specifically as meeting the Althen test and 

did not advocate for any separate analysis of significant aggravation under the Loving test. Accordingly, it 

is not necessary to do a separate Loving analysis.
33

dermatomal distribution, e.g. the length of the arm, as was the case with Ms. McGill.”13

(Id. at 3.) Nonetheless he also continued to maintain his opinion with respect to 

molecular mimicry. (Id. at 4-5.) 

During the hearing I asked Dr. Tornatore to clarify the relationship between these 

two theories. Specifically, I asked him “do these two theories work independently as 

alternatives or do you need both to explain petitioner’s condition?” (Tr. 223.) He 

responded “[t]hey do not work independently.” (Id. (emphasis added).) He testified that:

you can have those soluble factors, chemokines, cytokines, gamma 

interferon produced early on in the immune response that causes one set 

of symptoms, and then as the immune response continues to develop, you 

see the full impact of that immune response . . . So somebody may develop, 

in this case, symptoms, the neuropathic pain, as a result of the gamma 

interferon, but that gamma interferon is the fingerprint, if you will. It’s the 

canary in the coal mine that there is an autoimmune process via molecular 

mimicry which then may then smolder and then cause that neuronal demise 

to happen. So no, they are – I think they’re not two separate issues. They 

are all one mechanism.

(Tr. 223-24.) 

ii. Dr. Tornatore’s explanation is not sound and reliable

Under Althen prong one, petitioner must provide a “reputable medical theory,” 

demonstrating that the vaccine received can cause the type of injury alleged. Pafford v. 

Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (citations 

omitted). Such a theory must only be “legally probable, not medically or scientifically 

certain.” Knudsen, 35 F.3d at 549. Petitioner may satisfy the first Althen prong without 

resort to medical literature, epidemiological studies, demonstration of a specific 

mechanism, or a generally accepted medical theory. Andreu, 569 F.3d at 1378-79 

(citing Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 

2006)). However, “[a] petitioner must provide a ‘reputable medical or scientific 

explanation’ for [her] theory. While it does not require medical or scientific certainty, it 

must still be ‘sound and reliable.’”14 Boatmon, 941 F.3d at 1359 (quoting Knudsen, 35 

F.3d at 548-49). 

13 During the hearing, Dr. Whitton broke Dr. Tornatore’s INF- γ theory down into two further hypotheses 

based on variations in the way Dr. Tornatore expressed it. In his report at Exhibit 54, Dr. Tornatore 

proposed that systemic dissemination of vaccine antigens could cross into the DRG. (Tr. 184; Ex. 54, p. 

3.) In his report at Exhibit 60, Dr. Tornatore indicated that antigen bearing cells from draining lymphatics 

could reach the DRG. (Tr. 186; Ex. 60, pp. 5-7.) In either event, INF- γ within the DRG is activated to 

cause neuropathic pain. (Tr. 187.)

14 In their post-hearing briefs, the parties devote significant attention to their differing views on the 

question of whether petitioner’s burden under Althen prong one is limited to establishing a “plausible” or 

“biologically plausible” theory of causation. (ECF No. 148, pp. 11-13; ECF No. 151, pp. 19, 23; ECF No. 

152, pp. 4-5.) The parties appear to use the terms “plausible” and “biologically plausible” 

interchangeably, which has the effect of placing two Federal Circuit decisions, Andreu and Boatmon, in 
34

On this particular record, Dr. Tornatore stands alone in seeking to specifically 

hypothesize that either the flu vaccine or the pneumococcal vaccine can cause SFN. 

There is, however, at least some circumstantial support for this suggestion. As Dr. 

Tornatore indicated, at least some cases of SFN are considered to be autoimmune. 

(Oaklander, supra, at Ex. 38, p. 1.) Additionally, Dr. Tornatore has submitted literature 

identifying some other vaccines not at issue in this case as suspected causes of 

neurologic adverse events, including small fiber neuropathy. (See Souayah et al., 

supra, at Ex. 40 (case reports of SFN following rabies, varicella, or Lyme disease 

vaccinations); Shaw et al., supra, at Ex. 45 (neurologic adverse events following 

Hepatitis B vaccine). And, finally, some literature contends that SFN may, in at least 

some cases, be compared in its presentation to Guillain-Barre Syndrome which has, in 

turn, been linked to the certain formulations of the flu vaccine. (Oaklander, supra, at Ex. 

38 p. 6; Schonberger et al., supra, at Ex. 46.) With regard to the IFN- γ /DRG aspect of 

Dr. Tornatore’s theory, it is also the case that ganglionopathy has been identified as one 

mechanism by which peripheral sensory neuropathies may manifest. (Oaklander, 

supra, at Ex. 38, p. 2.) Additionally, Dr. Tornatore has support for the proposition, as a 

general matter, that IFN- γ may mediate chronic neuropathic pain. (Mayumi Sonekatsu 

et al., Interferon-gamma Potentiates NMDA Receptor Signaling in Spinal Dorsal Horn 

Neurons via Microglia-neuron Interaction, 12 MOLECULAR PAIN 1 (2016) (Ex. 55).) 

tension. In Andreu, the Federal Circuit accepted a theory as meeting Althen prong one based on the 

lower court’s determination that the theory was “biologically plausible.” 569 F.3d at 1375. In Boatmon, 

the Federal Circuit rejected a theory that was “at best ‘plausible’,” as in merely “possible,” as not meeting 

the preponderant evidence standard. 941 F.3d at 1360. Whereas the “biologically plausible” theory in 

Andreu was consistent with a preponderant showing, the Federal Circuit concluded that the Boatmon

special master had applied a “reasonable” burden of proof that fell below preponderant evidence. Id. at 

1359. However, both Federal Circuit decisions cite the same standard with respect to petitioner’s burden 

of proof. Both explain that a petitioner’s burden of proof is to present a theory that is supported by 

“reputable medical or scientific explanation.” Andreu, 569 at 1379 (quoting Althen, 418 F.3d at 1278); 

Boatmon, 941 F.3d at 1359 (quoting Moberly, 592 F.3d at 1322).) And both decisions further explicitly 

cite the prior Knudsen decision for the proposition that this means that the underlying scientific 

explanation must be “sound and reliable.” Andreu, 569 at 1379 (citing 35 F.3d at 548); Boatmon, 941 

F.3d at 1359 (same). Nothing in Andreu implies that the “biologically plausible” theory presented in that 

case constituted anything less than preponderant evidence or that a theory that is not “sound and 

reliable” could be considered “biologically plausible.” Nor, on the other hand, does Boatmon hold that any 

theory deemed “biologically plausible” is per se inadequate to meet the preponderant evidence standard. 

The Federal Circuit explained in Knudsen that “[c]ausation in fact under the Vaccine Act is thus based on 

the circumstances of the particular case, having no hard and fast per se scientific or medical rules.” 35 

F.3d at 548. Thus, it is not necessary to apply the specific “biologically plausible” terminology referenced 

in Andreu. Nor, however, should an expert’s use of the term “biologically plausible” be taken as a fatal 

concession without regard to context. On the whole, prior Federal Circuit decisions have instead focused 

on contrasting petitioner’s preponderant burden of proof against either the merely “possible” or 

“plausible,” which is insufficient, and “scientific certainty,” which is too burdensome. E.g. Moberly v. Sec’y 

of Health & Human Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010)(explaining at turns first that petitioners 

argued in favor of “something closer to proof of a ‘plausible’ or ‘possible’ causal link between the vaccine 

and the injury, which is not the statutory standard” and then that petitioners also argued that the term 

“cause-in-fact” implies scientific certainty “[b]ut this court has regularly used that term to describe the 

causal requirement for off-Table injuries and has made clear that the applicable level of proof is not 

certainty . . .”)
35

Based on all of this, Dr. Tornatore contends that he is “not making a stretch” in 

opining that the flu vaccine can be the cause of SFN. (Tr. 76.) However, this is not 

ultimately persuasive. Considering the record as a whole, the above points at best set 

the stage for his theory to be possible without evidence supporting it as probable. In 

contrast to Dr. Tornatore’s opinion, Dr. Gelfand and Dr. Whitton both contest that either 

the flu or pneumococcal vaccines are recognized causes of SFN and Dr. Gelfand 

further suggests the notion is speculative. (Tr. 115-16 (Gelfand); Tr. 57 (Whitton).) A 

close examination reveals for the reasons discussed in the sections that follow that 

there are too many unsupported gaps in Dr. Tornatore’s opinion for it to be considered 

sound and reliable. Nothing requires the acceptance of an expert’s conclusion 

“connected to existing data only by the ipse dixit of the expert,” especially if “there is 

simply too great an analytical gap between the data and the opinion proffered.” Snyder 

v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. 

v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health & Human Servs., 

No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for 

rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 999 (Fed. Cir. 2013). 

iii. Dr. Tornatore’s comparison of SFN to GBS is unpersuasive

 While Dr. Tornatore is correct that there is some overlap between GBS and SFN, 

he is not persuasive in equating the causes of GBS to the causes of SFN. In contrast to 

GBS, SFN is generally considered to be caused by underlying systemic conditions, 

including autoimmune conditions, diabetes, and toxic causes. (Oaklander, supra, at Ex. 

38, p. 5.) Only a subset of idiopathic SFN cases is suspected to result from tissuespecific dysimmunity in a manner that could potentially be compared to GBS. (Id. at 6.) 

However, even in that context, nothing on this record confirms the implicated tissue is 

necessarily the same. Whereas Dr. Tornatore specifically discuses myelin tissue as the 

likely target of autoimmune attack in the context of post-vaccination GBS (Tr. 55), the 

small fibers are largely not myelinated.15 The small fibers consist of both unmyelinated 

C-fibers and “lightly” or “thinly” myelinated A-delta fibers. (Oaklander, supra, at Ex. 38, 

p. 1; Tr. 96-97.) In an ordinary clinical setting (including this case), the specific small 

fiber(s) at issue in SFN are not distinguished. (Tr. 96-97, 135-37.) Dr. Tornatore has not 

provided evidence establishing that SFN itself is a demyelinating condition.

At base, Dr. Tornatore effectively asserts that because GBS in some instances 

affects the small fibers, then whatever causes GBS can also cause SFN. (Tr. 78.) In his 

testimony, however, Dr. Tornatore appeared to acknowledge that SFN is associated 

with other autoimmune processes, including GBS, “for reason that are unclear.” (Tr. 84-

85.) Indeed, in his first report, Dr. Tornatore quotes the literature as explaining that:

15 As noted above, Dr. Tornatore additionally asserts a role for an immune process affecting the DRG. In 

that regard, he notes that the DRG is also “very loosely” myelinated. (Tr. 96-97.) However, he confirmed 

the DRG aspect of his theory is cytokine driven rather than proposing molecular mimicry. (Tr. 92-94.)
36

The best-known peripheral neuropathies are those affecting the large, 

myelinated motor and sensor fibers. These have well-established 

immunological causes and therapies. Far less is known about the somatic 

and autonomic “small fibers”; the unmyelinated C-fibers, thinly myelinated 

A-delas, and postganglionic sympathetics.” 

(Ex. 36, p. 8 (quoting Oaklander, supra, at Ex. 38, p. 1.) Moreover, Dr. Gelfand 

persuasively urges that even if GBS can sometimes include small fiber symptomology, it 

is still defined by its large fiber involvement, which is necessarily absent in SFN.

16 (Tr. 

114-15, 135-37.) Thus, on the whole, Dr. Tornatore is unpersuasive on this record in 

suggesting that the cause(s) of GBS represent significant evidence concerning the 

causes of SFN.17 

iv. Molecular mimicry is not supported on this record

Setting aside the flawed analogy to GBS, Dr. Tornatore has not otherwise offered

evidence supporting homology between components of the vaccine(s) at issue in this 

case and the tissues affected by SFN despite specifically invoking molecular mimicry. 

Nor is there evidence of record to support cross-reaction or development of disease 

from a relevant mimic. Nor has Dr. Tornatore offered evidence more broadly implicating 

either the flu or pneumococcal vaccine(s) as causes of SFN. Considering the body of 

16 For a more thorough discussion of the many variants of GBS, see Swaiss v. Sec’y of Health & Human 

Servs., No. 15-286V, 2019 WL 6520791, at *12-18 (Fed. Cl. Spec. Mstr. Nov. 4, 2019). In Swaiss, the 

special master concluded, based on evidence not included within this record, that petitioner had 

established that a form of immune-mediated SFN could be said to represent a “small fiber GBS variant.” 

Id. at 18. Importantly, however, the Swaiss special master discussed “GBS” as an “umbrella term” for 

which the nosological limits remain unclear. Id. at 14. This uncertainty does not assist petitioner in 

meeting her burden. Rather, it underscores that the “S” in GBS stands for “syndrome.” Considered as a 

group, the GBS variants are generally believed to have a multitude of both clinical presentations and 

causes; however, the degree to which a cause of one condition placed under that umbrella could be said 

to apply to all conditions under the umbrella is an open question. The association between the flu 

vaccine and GBS is largely understood to be based specifically on a large fiber demyelinating form of 

polyneuropathy. While the Schonberger study did not specifically define GBS, it did specifically explain 

that subject cases were screened to require objective evidence of muscle involvement. (Schonberger et 

al., supra, at Ex. 46, p. 3.) Thus, cases of SFN, any pure sensory variant, or the “small fiber GBS 

variant” accepted in Swaiss, necessarily would have been excluded. 

17 Another special master has also previously reached the same conclusion. E.g. Fantini v. Sec'y of 

Health & Human Servs., No. 15-1332V, 2022 WL 1760730, *22 (Fed. Cl. Spec. Mstr. May 2, 2022) 

(explaining that “[t]he fact that reliable science establishes an association between GBS and the flu 

vaccine . . . does not inerrantly lead to the conclusion that SFNs can also be deemed to be similarlyassociated, given the facial differences in the nature of these conditions . . .” and further concluding 

molecular mimicry was not supported.); accord Mason v. Sec’y of Health & Human Servs., No. 17-1383V, 

2022 WL 600415, at *26 (similarly explaining in a different context that “I am unwilling to find that 

Petitioner has preponderantly established a causal relationship between the flu vaccine and CIDP merely 

because that theory has been accepted in the Program's past. Review of prior relevant cases suggests 

that more often than not, that determination has been based upon the faulty supposition that GBS and 

CIDP are two sides of the same coin.”); but see Jones v. Sec'y of Health & Human Servs., No. 15-1239V, 

2018 WL 7139212, at *13 (Fed. Cl. Spec. Mstr. Dec. 21, 2018) (accepting that vaccines, including the flu 

vaccine, can cause SFN based on analogy to GBS).
37

literature he cites as a whole, it serves mainly to underscore the speculation involved in 

Dr. Tornatore’s reliance on molecular mimicry. Dr. Tornatore has submitted literature 

that merely shows that various autoimmune targets have been suspected in various 

autoimmune injuries, none of which implicate the vaccines at issue in this case as 

causes of the SFN at issue in this case.18 This leaves his application of molecular 

mimicry to this case wholly unsupported. Respondent’s experts are persuasive in 

cautioning against unsupported inferential leaps in the context of molecular mimicry. In 

particular, Dr. Whitton explained that molecular mimicry cannot in itself be equated with 

disease (Tr. 157), that disease-causing molecular mimicry is much rarer than molecular 

mimicry itself (Tr. 204), that molecular mimicry involves a specific interaction that is not 

generalizable across differing contexts19 (Tr. 165-66), that molecular mimicry is not the 

cause of all autoimmune disease (Tr. 204-05), and that autoimmune disease should not 

be assumed to require any external trigger at all (id.).

“Of course, petitioners are never required to establish mechanism – but they 

often attempt to do so, and therefore it is reasonable to evaluate their success in in their 

effort.” Howard v. Sec’y of Health & Human Servs., No. 16-1592V, 2022 WL 4869354, 

at *24 (Fed Cl. Spec. Mstr. Aug. 31, 2022). There is no debate in this case that 

molecular mimicry is, in general, a genuine hypothesis to explain at least some 

autoimmune conditions. However, as has been observed in prior cases, “[t]hough

molecular mimicry is a generally accepted scientific principle, mere invocation of the 

scientific term does not carry a petitioner’s burden in a Program case.” Deshler v. Sec'y 

of Health & Human Servs., No. 16-1070V, 2020 WL 4593162, at *20 (Fed. Cl. Spec. 

Mstr. July 1, 2020) (citing Forrest v. Sec’y of Health & Human Servs., No. 14-1046V, 

2019 WL 925495, at *3 (Fed. Cl. Spec. Mstr. Jan. 18, 2019)). Here, Dr. Tornatore’s 

inability to substantiate the proposed molecular mimicry is significant because he has 

not otherwise been persuasive in suggesting that his theory is supported 

circumstantially. Moreover, because Dr. Tornatore confirms that his INF- γ

ganglionopathy theory does not operate independently of this molecular mimicry theory, 

his references to INF- γ do not cure his inability to persuasively support the molecular 

mimicry aspect of this theory. 

Dr. Tornatore does suggest that the concept of T cell degeneracy can explain the 

presence of molecular mimicry without the need to identify a specific homology. 

18 When prompted during the hearing to discuss the salient points of his cited literature with respect to 

molecular mimicry, Dr. Tornatore highlighted the following: Exhibit 47 is a study by Oldstone that 

examined molecular mimicry in rabbits between polymerase of hepatitis B and myelin-related protein (Tr. 

54-55); Exhibit 39 is a case report by Pollard and Selby examining post-tetanus GBS (Tr. 55-56);Exhibit 

46 is a study by Schonberger, et al., finding epidemiologic evidence of GBS following vaccination with a 

swine flu vaccination. (Tr. 55); and Exhibit 40 is a paper by Souayah, et al., presenting five case reports 

of SFN following vaccination with either rabies, varicella, or Lyme disease vaccinations (Tr. 56). Dr. 

Tornatore himself characterized this as reflecting evidence relating to a “hodgepodge” of vaccines. (Tr. 

56.)

19 That is, Dr. Whitton explained that in the case of GBS one specific bacterium (Campylobacter jejuni) 

has been shown to have caused GBS via molecular mimicry. Otherwise, the epidemiological evidence 

supporting the swine flu vaccine as a cause of GBS does not in itself demonstrate molecular mimicry. To 

suggest that all cases of GBS are explained by molecular mimicry is an unsupported “leap.” (Tr. 166.)
38

Specifically, he opines that “[r]eceptors on B and T cells that were once thought to have 

a high level of specificity for individual foreign antigens are now known to recognize 

peptide sequences that share no homology. . . Hence, microbiological antigen from a 

bacteria or virus which bears no similarity to nervous system antigen could active a B or 

T cells receptor which would then cause the B or T cell to mount an autoimmune 

response in the nervous system.” (Ex. 36, p. 9 (citing Don Mason, A Very High Level of 

Crossreactivity is an Essential Feature of the T-cell Receptor, 19 IMMUNOLOGY TODAY

395 (1998) (Ex. 41).) According to Dr. Tornatore, this concept, referred to in the cited 

literature as resulting in “unfocused cross reactivity,” allows him to rely on evidence 

relating to a “hodgepodge” of vaccines so long as they are ultimately implicated in the 

same outcome. (Tr. 56.) 

If accepted, the degeneracy concept might suggest that it is less important to 

demonstrate a specific homology in those cases where some other evidence suggests 

that a vaccine can cause a particular autoimmune injury. However, even if I accepted 

both Dr. Tornatore’s reliance on T cell degeneracy and his reliance on analogy to GBS, 

I would still conclude that this would be too speculative on this record to provide 

preponderant support for petitioner’s theory. In the absence of some evidence specific 

to SFN, accepting T cell degeneracy as the primary support for Dr. Tornatore’s opinion 

would mean effectively accepting that anything is possible – that any vaccine can be 

said to cause any autoimmune condition without any definable limit.20 

v. IFN- γ is not supported as a post-vaccination initiator of SFN

Turning to the other aspect of Dr. Tornatore’s theory, even though Dr. Tornatore 

has support in identifying IFN- γ as a possible mediator of neuropathic pain, nothing in 

the available literature suggests, as Dr. Tornatore urges, that it would be an initiator of 

SFN symptoms. Rather, the primary study Dr. Tornatore cites stresses that the effects 

of IFN- γ on the dorsal horn are unclear. That study discusses IFN- γ as an enhancer 

rather than initiator of neuropathic pain, suggesting only that it may be a causative 

agent with respect to the chronicity of neuropathic pain. In fact, the authors discuss the

production of IFN- γ in the dorsal horn as a consequence of otherwise manifesting 

nerve injury. (Sonekatsu et al, supra, at Ex. 55, p. 8 (Fig. 8).) Nothing in Dr. Tornatore’s 

supporting literature evidences the idea that IFN- γ would function as Dr. Tornatore 

20 Regardless, Dr. Tornatore’s application of the degeneracy concept does not appear to be sound for 

several other reasons. First, the article he relies on for this concept presents mathematical analyses only 

and disclaims the ability to determine whether the type of “unfocused” cross reactivity proposed actually 

predominates in the body. Second, the author further hypothesizes that this “unfocused” T cell cross 

reactivity, if it is occurring, would likely reduce the number of autoreactive T cells resulting from a foreign 

antigen. (Mason, supra, at Ex. 41, p. 9.) This appears to propose that cross reactivity may be more 

common, but far less significant, than previously thought. That idea is more supportive of Dr. Whitton’s 

testimony that cross reactive autoimmune responses do not invariably lead to disease (Tr. 156-57, 188-

89) than it is supportive of Dr. Tornatore’s theory. Dr. Whitton explained that while molecular mimicry 

rarely causes disease, molecular mimicry is not in itself rare. (Tr. 204.) And, in any event, even while 

discounting the need for specific homology, this paper still stands for the proposition that autoimmune 

disease results from cross reactivity. Yet there is still no persuasive evidence that such cross reactivity is 

occurring in the present context. Therefore, Dr. Tornatore’s theory of T cell degeneracy would still be 

speculative without more
39

suggests in the overall context of his theory, constituting the preceding “fingerprint” of a

later developing vaccine-caused autoimmune nerve damage. In contrast, Dr. Gefland 

testified that while IFN- γ is part of an inflammatory response, including in response to 

vaccination, he disagrees that there is evidence to support IFN- γ as a cause of acute, 

burning neuropathic pain. (Tr. 138.) Dr. Whitton likewise suggests that Dr. Tornatore’s 

specific explanation of how this would happen has never been demonstrated to actually 

occur. (Tr. 191.) He further stresses that INF- γ is commonly produced by the body in 

response to vaccination and infection, and yet neuropathic pain is not seen as a typical 

response. (Tr. 194-95.)

Dr. Whitton explains that rather than continuously producing INF- γ, T cells 

produce cytokines only upon contact with an antigen. Thus, the degree of cytokine 

response produced by a vaccination is more limited compared to a replicating viral 

infection. (Ex. N, p. 5.) For example, respondent filed a study by Cohen, et al., that 

demonstrated that INF- γ was elevated following administration of the Smallpox 

vaccine.21 (Jeffrey I. Cohen et al., Kinetics of Serum Cytokines after Primary or Repeat 

Vaccination with the Smallpox Vaccine, 201 THE J. OF INFECTIOUS DISEASES 1183 (2010) 

(Ex. N, Tab 2, p. 1).) However, subjects experienced only transitory symptoms 

including fatigue, lymphadenopathy, myalgia, headache, pruritis, loss of appetite, chills, 

and fever. (Id. at p. 2 (Fig. 1), 3 (Tab. 1).) According to Dr. Whitton, if Dr. Tornatore’s 

DRG/ INF- γ theory were correct, these study subjects should have experienced 

neuropathic pain. (Tr. 192.) Also notable, while INF- γ was associated with fatigue, 

lymphadenopathy, and myalgia, it was not associated with pruritis, which is the only 

symptom observed in the study that would appear to implicate the sensory small fibers. 

(Cohen et al., supra, at Ex. N, Tab 2, p. 6 (Tab. 3).) A single study of 42 subjects 

standing alone is inadequate to refute Dr. Tornatore’s theory; however, it does strongly 

suggest Dr. Tornatore’s theory is less likely to be accurate in a real-world context, 

reducing its overall reliability. 

vi. Conclusion as to Althen prong one

For all the reasons discussed above, petitioner has failed to preponderantly 

establish that either the flu vaccine or pneumococcal vaccine can cause SFN. 

Additionally, because Dr. Tornatore has confirmed that the two parts of this theory – 

molecular mimicry and IFN- γ – do not work independently, and because I have 

determined that neither aspect of the theory is sufficiently supported, this analysis 

prevents petitioner from meeting her burden under Althen prong one regardless of 

whether one examines her condition as relating to her upper extremities alone, her 

lower extremities alone, or both together.22

21 However, it is stressed that “[t]he smallpox vaccine is associated with more serious adverse events 

than any other live attenuated vaccine in use today,” suggesting caution would be needed in generalizing 

these findings to any other vaccination. (Cohen et al., supra, at Ex. N, Tab 2, p. 1.)

22 Prior cases present a mixed record with respect to whether the vaccines at issue in this case can cause 

SFN. Compare Fantini, 2022 WL 1760730, *22 (petitioner did not satisfy Althen prong one with respect to 

SFN allegedly caused by the flu vaccine.); Todd v. Sec'y of Health & Human Servs., No. 15-860V, 2020 

WL 727973, at *22 (Fed. Cl. Jan. 8, 2020) (finding that petitioner did not meet Althen prong one with 
40

b. Althen prong two

The second Althen prong requires proof of a logical sequence of cause and 

effect, usually supported by facts derived from a petitioner’s medical records. Althen, 

418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant, 

956 F.2d at 1148. In establishing that a vaccine “did cause” injury, the opinions and 

views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 

F.3d at 1367; Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1280) (stating 

that “medical records and medical opinion testimony are favored in vaccine cases, as 

treating physicians are likely to be in the best position to determine whether a ‘logical 

sequence of cause and effect show[s] that the vaccination was the reason for the 

injury’”). However, medical records and/or statements of a treating physician’s views do 

not per se bind the special master to adopt the conclusions of such an individual, even if 

they must be considered and carefully evaluated. See Section 13(b)(1) (providing that 

“[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be 

binding on the special master or court”); Snyder v. Sec’y of Health & Human Servs., 88 

Fed. Cl. 706, 746 n.67 (2009) (stating that “there is nothing . . . that mandates that the 

testimony of a treating physician is sacrosanct—that it must be accepted in its entirety 

and cannot be rebutted”). Ultimately, petitioner may support her claim either through 

her medical records or by expert opinion. § 300aa-13(a)(1).

i. Treating physician opinions do not preponderantly support 

petitioner’s claim

In this case, it is clear that petitioner’s treating physicians took seriously the 

suspicion of vaccine causation. However, careful review of the entire body of medical 

records shows that the treating physicians were equivocal in their opinions and never 

actually concluded that petitioner suffered vaccine-caused SFN. Ultimately, when 

considering the records as a whole, petitioner’s treating physicians did not express a 

view that petitioner’s SFN symptoms were more likely to be vaccine-caused than they 

were to be sequela of her preexisting autoimmune conditions.

When petitioner first reported her upper extremity symptoms to Dr. Coletti at a 

same-day clinic, she described them as similar to her preexisting polymyositis. (Ex. 4, p. 

2.) Dr. Coletti confirmed the lack of any local injection site reaction and concluded that 

vaccine-causation of her symptoms was “unlikely.” (Id.) The next day, an emergency 

respect to demonstrating a theory that the flu vaccine can cause SFN) with E.M., 2021 WL 3477837, at

*36 (finding the flu vaccine can cause SFN where petitioner’s expert demonstrated homology between 

components of the flu vaccine and alpha 3 AChR, which is associated with SFN, and respondent 

countered only by citing a lack of epidemiologic support); Jones., 2018 WL 7139212, at *13 (accepting 

that vaccines, including the flu vaccine, can cause SFN based on analogy to GBS); Doe v. Sec'y of 

Health & Human Servs., 2007 WL 3120297 (Fed. Cl. Spec. Mstr. Oct. 18, 2007) (finding the flu vaccine 

caused petitioner’s SFN). Of those cases finding the flu vaccine can cause SFN, I note that the prior E.M. 

case in particular had a substantially more detailed showing of molecular mimicry to support petitioner’s 

theory under Althen prong one and that showing was not predicated on homology to myelin proteins.
41

department physician, Dr. Tarjan recorded petitioner’s history of a post-vaccination 

onset, but concluded that her symptoms may be related to either her polymyositis or her 

rheumatoid arthritis. (Id. at 7.) Another emergency department physician, Dr. Glickman, 

was the first to include a reaction to immunization in a differential diagnosis set against 

a myositis flare. (Id. at 13.) However, the discharge summary confirms the physicians 

were “unsure” of the cause of her symptoms, maintaining they may be related to her 

polymyositis or rheumatoid arthritis. (Id. at 17.) Subsequently, petitioner saw a 

neuromuscular specialist, Dr. Jovanich, who assessed an arthus reaction to vaccination. 

(Ex. 4, p. 30.) However, when petitioner then followed up with a rheumatologist, Dr. 

Ritt, he felt that an arthus reaction was “unlikely” and instead suggested a more likely 

explanation would be myofascial pain syndrome triggered by vaccination. (Id. at 63.) 

Neither physician indicated any suspicion of SFN. By November 25, 2014, petitioner 

saw a second rheumatologist, Dr. Wells, now complaining of symptoms in both her 

upper and lower extremities. Dr. Wells was the first to suggest petitioner’s symptoms 

may be due to SFN; however, she was “unable to determine if the onset of pain is 

related to the injection or not.” (Ex. 7, p. 6.)

Thereafter, petitioner began consulting with neurologist Justin Mhoon. Of all of 

petitioner’s treating physicians, Dr. Mhoon’s causal assessment is the most thoroughly 

documented and the most consistent with petitioner’s claim; however, it is also highly 

equivocal. When petitioner first presented to Dr. Mhoon on December 2, 2014, he 

provided a differential diagnosis including both sensory neuritis due to a vaccine 

reaction and an unspecified form of autoimmune demyelinating disease. (Ex. 18, p. 70.) 

Later, however, after petitioner had undergone additional testing, including EMG and 

NCS that ruled out large fiber peripheral neuropathy, Dr. Mhoon changed his differential 

to either neuritis or SFN, but noted that “if this was a vaccine related neuritis it should 

improve on its own over time.” (Id. at 133.) Once Dr. Mhoon confirmed SFN based on 

petitioner’s skin biopsy, he indicated that SFN is “[o]ften associated with rheumatologic 

conditions such as yours” and further indicated when pressed by petitioner’s follow up 

questioning that he “cannot prove a direct causation of the vaccines.” (Ex. 13, pp. 3-4.) 

In subsequent records, Dr. Mhoon continued to equivocate as to whether petitioner’s 

condition was explained as sequela of her pre-existing rheumatoid arthritis or as a 

separate vaccine-caused neuritis.23 (Ex. 6, p. 60; Ex. 63, p. 673.) 

In October of 2016, petitioner additionally saw Dr. Eckstein at the Duke 

Neuroscience Center, who provided an opinion comparable to that of Dr. Mhoon. (Ex. 

23 In her post-hearing brief, petitioner stresses that Dr. Mhoon recommended that petitioner avoid flu and 

pneumococcal vaccinations in the future. (ECF No. 148, pp. 33-34 (citing Ex. 6, p. 60).) Petitioner argues 

the decision to withhold vaccination can be probative evidence. (Id. (quoting Andreu, 418 F.3d at 1376).) 

While this general proposition is true, it is important to note that the Andreu court specifically considered 

the fact that the referenced treating physician testified and, consistent with his determination to withhold 

vaccination, never disclaimed having a causal opinion favoring vaccine causation. Andreu, 418 F.3d at n. 

3. In contrast, Dr. Mhoon’s records in this case include an explicit statement that he cannot reach a 

conclusion that petitioner’s vaccines caused her condition. (Ex. 13, pp. 3-4.) Dr. Mhoon’s additional 

indication that it may be “reasonable” for petitioner to avoid vaccination does not contradict that explicit 

causal opinion nor does it in any way help to resolve the equivocation evident throughout Dr. Mhoon’s 

records.
42

24, p. 4358.) When pressed by petitioner with regard to whether her SFN was vaccinecaused, he stressed that petitioner’s preexisting autoimmune disease predisposed her 

to SFN, but added that “I suppose it is possible that the vaccinations could have 

exacerbated her underlying autoimmunity . . . though this would be difficult to prove 

definitively.” (Id. (emphasis added).)

These treating physician opinions do not preponderantly support petitioner’s 

claim. Accord Stapleford v. Sec’y of Health and Human Servs., No. 03-234V, 2009 WL 

1456441, at *17 n.24 (Fed. Cl. Spec. Mstr. May 1, 2009) (explaining that medical 

records may include notations where a physician “may well be indicating a question in 

the physician’s mind whether there is a causal relationship, or a suspicion that there 

might be a causal relationship. However, that is quite different from an indication that 

such physician has reached a conclusion concerning a causal relationship”) (emphasis 

in original), aff’d, 89 Fed. Cl. 456 (Fed. Cl. 2009). When viewing the record as a whole, 

the treating physician’s opinions supporting vaccine-causation are tentative at best, and 

largely fail to move beyond suspicion. Moreover, apart from recognizing temporality, 

they are not consistent in either diagnosis or rationale. However, “[a] treating 

physician’s recognition of a temporal relationship does not advance the analysis of 

causation.” Isaac v. Sec’y of Health and Human Servs., No. 08-601V, 2012 WL 

3609993, at *26 (Fed. Cl. Spec. Mstr. July 30, 2012).

ii. Dr. Tornatore is unpersuasive in opining petitioner’s vaccinations 

are a necessary trigger of her SFN

Because I have separately determined that the onset of upper extremity 

symptoms in this case is too fast relative to vaccination to allow for a causal inference 

(see Althen three, below), Dr. Tornatore’s specific reliance on the abruptness and short 

latency of the upper extremity symptoms to arrive at his causal assessment renders his 

opinion less persuasive. Importantly, but for Dr. Tornatore’s stressing of an abrupt 

onset, both parties’ experts otherwise agree that petitioner’s SFN is consistent with her 

preexisting autoimmune conditions,24 a point that is also repeatedly raised by the 

treating physicians. In fact, Dr. Tornatore’s seeming hesitation in completely ruling out 

an indolent and asymptomatic SFN predating the vaccination, despite himself placing 

symptom onset post-vaccination, underlines this very point. (Ex. 36, pp. 7-8; Tr. 97-98.) 

It should also be noted that the Cohen, et al., study presented by Dr. Whitton

introduces a degree of tension between Dr. Tornatore’s theory and petitioner’s own 

clinical history. Dr. Tornatore relies primarily on the INF-γ aspect of this theory to 

explain the minimal latency between vaccination and onset of SFN. However, while 

experimental studies filed in this case do show that memory T cells produce INF-γ more 

24 Specifically, see Tr. 114 (Dr. Gelfand explaining SFN is associated with rheumatologic and other 

autoimmune diseases); Tr. 97-98 (Dr. Tornatore agreeing “we totally recognize that primary autoimmune 

diseases whether Sjorgren’s or rheumatoid or lupus, can have small fiber sensory neuropathy as a part of 

that general autoimmunity that the patient has . . .”); Tr. 70-71 (Dr. Tornatore acknowledging SFN can be 

autoimmune in nature but discussing likelihood of vaccine being a logical trigger); Tr. 82-83 (Dr. 

Tornatore disagreeing with Dr. Mhoon that SFN was sequela to RA due to abrupt onset); Tr. 84-85 

(acknowledging people with RA can develop SFN). 
43

quickly than naïve T cells, in Cohen, et al.’s human study, only first-time vaccine 

recipients mounted a significant INF- γ response at all. (Cohen et al., supra, at Ex. N, 

Tab 2, p. 5 (Fig. 3(A)).) Dr. Whitton explains that this is because the “more biologically 

beneficial” memory T cell response generally produces fewer cytokines before the 

antigen at issue is neutralized. (Ex. N, pp. 3-5.) Thus, the proposed INF- γ response Dr. 

Tornatore relies upon (perhaps counterintuitively) is less likely in the scenario of a 

repeat exposure and recall response, which is the scenario actually present in this case. 

In any event, Dr. Tornatore is not persuasive in suggesting that an abrupt onset 

in itself distinguishes petitioner’s SFN as more likely to have been triggered by 

vaccination. This also helps to explain why petitioner’s treating physicians were unable 

eliminate petitioner’s preexisting autoimmune conditions from their differential diagnosis 

despite the abrupt onset. In asserting that onset of SFN within hours of vaccination is 

medically reasonable, a significant part of Dr. Tornatore’s rationale is that the small 

fibers are exquisitely sensitive and that the symptoms of a SFN would be the very first 

to be felt or recognized by a patient even in a broader neuropathy. (Tr. 51-52.) 

However, this rationale would apply equally regardless of the underlying cause of 

petitioner’s SFN. Indeed, contrary to Dr. Tornatore’s stated view, the literature he

provides suggests that SFN related to preexisting autoimmunity may be due to sensory 

ganglionopathies, which can be distinguished from distal sensory axonopathies both by 

patchy and often proximal symptoms and by the more rapid onset. (Oaklander, supra, at 

Ex. 38, p. 2; Jinny Tavee & Lan Zhou, Small Fiber Neuropathy: A burning Problem, 76 

CLEVELAND CLINIC J. OF MEDICINE 298 (2009) (Ex. A, Tab 3, p. 4).) For example, Sjogren 

syndrome in particular is known to result in sudden unexplained neuropathic pain from 

ganglionitis. (Oaklander, supra, at Ex. 38, p. 2.) Notably, consistent with this 

description, the experts’ disagreement as to petitioner’s correct diagnosis in this case 

has been driven in significant part by her rapid and atypical (i.e. not length dependent) 

onset of symptoms. In contrast, Dr. Whitton additionally stresses that petitioner’s onset 

of SFN was not accompanied by any of the clinical signs of a robust cytokine response 

as would be likely if Dr. Tornatore’s theory was accurate. (Tr. 56.) 

iii. Petitioner cannot meet Althen prong two based on her lower 

extremity symptoms alone

Both petitioner and Dr. Tornatore contend first and foremost that her upper and 

lower extremity symptoms should together be viewed as constituting SFN and should 

not be separated. (Tr. 89-90; ECF No. 152, pp. 1-1.) Additionally, following the 

hearing, I ultimately conclude that Dr. Gelfand’s testimony regarding the nature of 

petitioner’s upper extremity symptoms is too equivocal to cast substantial doubt on the 

SFN diagnosis favored by petitioner as a unifying explanation of the upper and lower 

extremity symptoms. (Tr. 123, 126-27, 132.) If one were to look exclusively at the lower 

extremity symptoms, then the later timing of onset would potentially be consistent with 

an inference of vaccine causation. However, this would detract from Dr. Tornatore’s 

stated rationale that a particularly “striking” and “abrupt” onset of upper extremity 

symptoms helps inform his overall assessment of a logical sequence of cause-andeffect implicating petitioner’s vaccinations despite otherwise having conditions 
44

predisposing her to SFN. (Ex. 60, pp.1- 2.) In any event, without more, a medically 

acceptable onset is not persuasive as a means to assert vaccine-causation. 

Devonshire v. Sec’y of Health and Human Servs., No. 99-031V, 2006 WL 2970418, at 

*19 (Fed. Cl. Spec. Mstr. Sept. 28, 2006) (medical expert’s “post hoc ergo proptor hoc 

reasoning...has been consistently rejected by the Court and is ‘regarded as neither 

good logic nor good law’”) (quoting Fricano v. U.S., 22 Cl. Ct. 796, 800 (1991) 

(emphasis in original)). The Federal Circuit has explained that “neither a mere showing 

of a proximate temporal relationship between vaccination and injury, nor a simplistic 

elimination of other potential causes of the injury suffices, without more, to meet the 

burden of showing actual causation.” Althen, 418 F.3d at 1278 (citing Grant, 956 F.2d at 

1149). Thus, even limiting the question to petitioner’s lower extremity symptoms, her 

preexisting autoimmune conditions would still constitute a likely explanation for 

petitioner’s SFN based on both the treating physicians’ observations and the expert 

opinions presented in the case. 

iv. Conclusion as to Althen prong two

For all these reasons, petitioner has not preponderantly established Althen prong 

two. This analysis prevents petitioner from meeting her burden under Althen prong two 

regardless of whether one examines her condition as relating to her upper extremities 

alone, her lower extremities alone, or both together.

c. Althen prong three

The third Althen prong requires establishing a “proximate temporal relationship” 

between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term 

has been equated to the phrase “medically-acceptable temporal relationship.” Id. A 

petitioner must offer “preponderant proof that the onset of symptoms occurred within a 

timeframe which, given the medical understanding of the disorder’s etiology, it is 

medically acceptable to infer causation.” de Bazan v. Sec’y of Health & Human Servs.,

539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically 

acceptable timeframe must coincide with the theory of how the relevant vaccine can 

cause an injury (Althen prong one's requirement). Id. at 1352; Shapiro v. Sec’y of 

Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 

Fed. Cl. 353 (2012), aff’d mem., 503 Fed. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of 

Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 

2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 

2014).

In this case discussion of two periods of onset is warranted. Petitioner began 

experiencing upper extremity symptoms of SFN within hours of her vaccination. 

Specifically, the subject vaccines were administered at a medical appointment that 

began at about 3:30pm (Ex. 15, p. 93) and she reported onset of symptoms occurring 

either the “same day” (Ex. 4, p. 7) or as waking her in the middle of the night (Ex. 4, p. 

2; Tr. 25). In her VAERS report she placed onset at 12:30AM. (Ex. 17, p. 2.) Thus, for 

purposes of discussing causation, the experts generally relied upon an onset of about 8-
45

9 hours. (Tr. 74, 103 (Dr. Tornatore); Tr. 126 (Dr. Gelfand); Tr. 177 (Dr. Whitton).) 

Petitioner’s initial treatment records confirmed her condition was limited to her arms (Ex. 

4, p. 7) and she later reported as of November 20, 2014, that her symptoms had moved 

to her legs (Ex. 18, p. 3). Thus, onset of lower extremity symptoms is placed at about 

twelve days post-vaccination.

i. Upper extremity onset

1. Molecular Mimicry

With respect to his molecular mimicry theory, Dr. Tornatore opined that the onset 

of petitioner’s burning sensation of her arms 8-9 hours after vaccination is medically 

appropriate because of petitioner’s history of vaccination. (See Ex. 36, p. 8.) He 

explained that petitioner’s previous flu vaccinations could cause a rapid recall 

response.” (Id. at 8, 9.) He further opined that the secondary or memory immune 

response phenomenon explains petitioner’s rapid onset as “the memory cells are 

present at a higher frequency and are available to be stimulated quickly.” (Ex. 50, p. 3.) 

In support of his contention, he cited an IOM report that he argued shows that a “second 

exposure to a vaccination may result in a markedly short time of onset of an immune 

response to administration of an exogenous antigen.” (Id. (citing INST. OF MED., supra, 

at Ex. 43).) After the hearing, petitioner also supplemented the record with the VeigaFernandes article (Veiga-Fernandes et al., supra, at Ex. 64.) The Veiga-Fernandes 

study found that in immunocompromised mice, “[b]lastogenesis occurred early in 

memory cells; increased size was detected by 8 h[ours] and all cells had become blasts 

24 h[ours] after in vivo transfer.” (Id. at 48.) 

Dr. Whitton contested Dr. Tornatore’s rapid recall response theory, noting that 

the IOM explained there is a lag phase of 7-10 days for a primary immune response and 

1-3 days for a memory immune response. (Ex. M, p. 6.) He emphasized that both of 

those lag phases “far exceed” the nearly 9-hour interval between petitioner’s vaccine 

administration and the onset of the burning sensation in her arms. (Id. at 6-8; see also

Tr. 177.) Dr. Gelfand Similarly opined. (Ex. J, p. 10; see also Ex. L, p. 2.) According to 

Dr. Whitton, the so-called “lag phase” is not likely to be injurious. (Tr. 174.)

Dr. Whitton also persuasively explained that his murine immunology research

further confirms that 8-9 hours is too rapid for a vaccine to cause disease via molecular 

mimicry. (Ex. M, pp. 9-10.) Although he acknowledged that T cells can respond to 

antigen challenge within hours, he stressed that the cells do not begin to proliferate for 

several days. (Id.) He further explained that this “lag phase” also applies to memory T 

cells. (Id.) Thus, for a vaccine to cause disease via molecular mimicry, the T cells 

would have to begin dividing over a period of about three days post-vaccine, then divide 

several times over more days to reach the required number to cause harm, travel to the 

nerves, and “exert their effector function thereupon, causing the signs and symptoms of 

SFN.” (Id. (citing Whitmire, Eam, & Whitton, supra, at Ex. M, Tab 4).) Dr. Whitton 

further explained that animal models show that even if an animal had been previously 

exposed to the inciting antigen, it takes “days or weeks” for an autoimmune neurological 
46

disease to develop. (Id. at 12.) Although he acknowledged that the time interval 

between vaccination and disease may decrease as booster injections are administered, 

“biology dictates that there be a minimum interval of several days.” (Id.; see also Tr. 

178.) 

Based on Dr. Whitton’s detailed explanation of how T cells respond to antigen 

challenge, 8-9 hours is not a medically appropriate timeframe for a vaccine to cause an 

autoimmune injury via molecular mimicry. Thus, Dr. Tornatore’s molecular mimicry 

theory is incompatible with an onset of 8-9 hours post-vaccination.25 

2. IFN- γ Theory

Dr. Tornatore also opined that in the context of his IFN- γ theory, “the immune 

system has the capability of being stimulated quickly and producing soluble factors such 

as interferon gamma.” (Ex. 60, p. 2.) He elaborated that memory T cells “can be 

quickly activated by exogenous antigens to produce sensory symptoms referable to the 

nervous system.” (See id. at 3.) Dr. Tornatore further indicated that an animal study 

conducted by Dr. Whitton supported his opinion because the mice exposed to viral 

antigens and an inoculation against that antigen began producing IFN- γ within 6-12 

hours. (Ex. 54, p. 1 (citing Whitmire, Eam, & Whitton, supra, at Ex. M, Tab 4).) Thus, 

Dr. Tornatore opined that “within hours of activation, the immune system can produce 

interferon-gamma, a known mediator of chronic pain . . . consistent with [petitioner’s] 

clinical symptoms.” (Id. at 2.) After the hearing, petitioner presented the Lai study in

support of this theory. (Lai et al., supra, at Ex. 65.) The Lai study examined IFN- γ 

production and found that memory T cell activation occurred within 6-8 hours. (Id. at 

Ex. 65, p. 135 (Fig. 1).)

As discussed under Althen prong one, Dr. Tornatore’s suggestion that postvaccination IFN- γ would be an initiator or “fingerprint” or an autoimmune SFN is largely 

25 While I find Dr. Whitton persuasive regarding the need for a latency period greater than the 9 hours 

seen in this case, I additionally note that I do not treat Dr. Whitton’s explanation of “days to weeks” long 

latency as constituting a bright line. Accord Paluck v. Se’cy of Health & Human Servs., 786 F.3d 1373, 

1383-84 (Fed. Cir. 2015) (finding that “[t]he special master further erred in setting a hard and fast 

deadline” for onset and noting that the medical literature filed in the case “do not purport to establish any 

definitive timeframe for onset of clinical symptoms.”). For example, in a prior case I have given at least 

some weight to the recall response as favoring a more rapid onset for an adaptive immune response and 

resulting autoimmune injury. That case involved GBS occurring one day post-vaccination. Harris v. Sec’y 

of Health & Human Servs., No. 18-944V, 2023 WL 2583393 (Fed. Cl. Spec. Mstr. Feb. 21, 2023). 

However, the difference between a 1-day onset and a less than 9-hour onset still remains significant. In 

that prior case I observed that “[w]hile the petitioner in this case has preponderantly satisfied Althen prong 

three despite an atypically rapid onset of just one day, this is a close call and the conclusion is a function 

of the specific record in this case. The conclusion that a one-day onset is medically appropriate for postvaccination GBS is not unprecedented, but neither is it the norm. Of the few GBS non-Table claims 

adjudicated in the Program where onset occurred earlier than three days after vaccination most have not 

succeeded.” Harris, 2023 WL 2583393, at *35; see also Rowan v. Sec’y of Health & Human Servs., No. 

17-760V, 2020 WL 2954954, at *19 (Fed. Cl. Spec. Mstr. Apr. 28, 2020) (concluding that “[p]etitioner’s 

claim must be dismissed because it has not been demonstrated that the flu vaccine could cause GBS in a 

30 to 36-hour timeframe).
47

unsupported on this record. Moreover, as discussed with respect to Althen prong two, 

Dr. Whitton demonstrated that only a primary vaccine exposure, and not a secondary 

exposure leading to a recall response, is likely to generate meaningful levels of IFN- γ. 

Thus, Dr. Tornatore’s reliance on experimental studies showing memory T cells to 

generate IFN- γ more quickly is not persuasive in the context of this case.

However, even if this aspect of the theory were better supported, Dr. Whitton 

also explains that the process would still be unlikely to unfold within 8-9 hours. Dr. 

Whitton emphasized that activation of the immune system and occurrence of 

neurological injury are distinct biological events. (Ex. N, p. 2.) Neither Dr. Whitton’s 

own article (Whitmire, Eam, & Whitton, supra, at Ex. M, Tab 4.) nor the Lai article (Lai et 

al., supra, at Ex. 65) support Dr. Tornatore’s opinion because they merely show that T 

cells can respond to antigen challenge within a matter of hours. (Ex. N, pp. 3, 5; Tr. 

180-81.) According to Dr. Whitton, the Whitmire study Dr. Tornatore relies upon 

actually shows that memory T cells are “quick to respond but slow to divide,” as is 

required to cause neurological injury. (Whitmire, Eam, & Whitton, supra, at Ex. M, Tab 

4.) This would likewise affect the overall production of IFN- γ. Thus, for example, the 

above discussed Cohen, et al, study that measured IFN- γ levels in actual human 

vaccinees following smallpox vaccination found both that cytokine levels, including IFNγ, “typically” did not begin to rise until 4-5 days post-vaccination and that symptom 

presentation correlated to cytokine level over time. (Cohen et al., supra, at Ex. N, Tab 2, 

p. 6, 7 (Figs. 4(A)-(B)).) The Cohen study is the only evidence of record in this case 

that addresses the timing of IFN- γ production in actual patients. It suggests that the 

mouse models must be viewed with caution.

Thus, petitioner has not established that it is medically reasonable to conclude

that petitioner’s vaccinations caused her to suffer SFN within just 8-9 hours of 

administration due to IFN- γ induced neuropathic pain. Accordingly, petitioner has failed 

to satisfy her burden under Althen prong three based on the assumption that her upper 

and lower extremities represent the same condition.

3. Comparison to E.M.

Special masters are not bound by the decisions of other special masters and are 

also not obligated to distinguish prior cases. Boatmon, 941 F.3d at 1358 (explaining 

that “[t]o the extent the Court of Federal Claims required that special masters cite and 

distinguish decisions of other special masters, it was incorrect.”) Nonetheless, in this 

case it might be helpful. Similar to this case, petitioner’s expert in E.M. relied on recall 

response to explain how memory T cells can cause SFN within four to six hours postvaccination. 2021 WL 3477837, at *42. This was based in significant part on citation to 

two papers, Lai, et al., and Schonberger, et al., both of which this petitioner has also 

filed in this case. The Lai paper addresses the time for memory T cells to respond to an 

antigen and the Schonberger is an epidemiologic paper examining incidences of postSwine flu vaccine GBS.
48

The E.M. special master credited petitioner’s expert’s reliance on these articles at 

least in part because (1) he had superior credentials in immunology as compared to 

respondent’s neurology expert and (2) respondent’s expert had changed his 

assessment of onset during the hearing, prompting her to observe that she would not 

give his opinion “much, if any, weight.” Id. at *43. In this case, Dr. Whitton – who is well 

qualified to opine and who does not present any credibility issue comparable to what 

was seen in E.M. – has offered expert opinion evidence thoroughly and persuasively 

rebutting Dr. Tornatore’s opinion with regard to the timing of onset. I have also 

explained above why this rebuttal applies specifically to the Lai paper and, with regard 

to the Schonberger paper, have explained why I do not find GBS to be a helpful analog 

with respect to vaccine causation. Even accepting arguendo that comparison to GBS 

could be informative, the Schonberger article provides only scant evidence of any rapid 

onset and lacks the granularity that would be necessary to demonstrate a mere hourslong onset in any case, let alone that causation could be ascribed in such outlier cases. 

Without more it would be unpersuasive in this case even absent Dr. Whitton’s 

testimony. 

ii. Lower extremity onset

Alternatively, if one were to assume that only petitioner’s lower extremity 

symptoms were confirmed to be a part of her SFN as Dr. Gelfand opined, then Althen

prong three would no longer present an issue. Under that scenario, respondent 

acknowledges that an onset of SFN twelve days after vaccination would be medically 

appropriate to infer causation. (ECF No. 151, p. 49, n.17.) However, the analysis above 

confirms that petitioner has likewise failed to meet Althen prongs one and two, which 

means that petitioner still cannot be compensated. Hibbard v. Sec’y of Health & Human 

Servs., 698 F.3d 1355, 1364-65 (Fed. Cir. 2012) (holding the special master did not err 

in resolving the case pursuant to prong two when respondent conceded that petitioner 

met prong three). 

VI. Conclusion

Petitioner has clearly suffered and she has my sympathy. Moreover, it is 

understandable that she would come to personally believe that pain arising so close in 

time to her vaccination would be related to those vaccinations. However, for all the 

reasons described above, petitioner has not preponderantly demonstrated that she 

actually suffered a vaccine-caused injury and is therefore not entitled to compensation. 

Accordingly, this case is dismissed.26

IT IS SO ORDERED.

 s/Daniel T. Horner

 Daniel T. Horner

 Special Master

26 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter 

judgment accordingly.