Quirino v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 17-989V

Filed: December 18, 2023

Special Master Horner

JASON QUIRINO,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Andrew Downing, Downing, Allison & Jorgenson, Phoenix, AZ, for petitioner.

Mitchell Jones, U.S. Department of Justice, Washington, DC, for respondent.

RULING ON ENTITLEMENT 1

On July 21, 2017, petitioner filed a petition under the National Childhood Vaccine

Injury Act, 42 U.S.C. § 300aa-10, et seq. (2018), 2 alleging that the Hepatitis B (“Hep B”)

and Tetanus Diphtheria acellular Pertussis (“Tdap”) vaccines he received on July 28,

2014, caused him to suffer a “rheumatologic injury.” (ECF No. 1; see also ECF No. 35

(Amended Petition).) Petitioner later amended his petition to allege that he suffers from

an “atypical form” of Guillain-Barré Syndrome (“GBS”), “manifesting as an isolated small

fiber neuropathy.” (ECF No. 53, p. 1.) For the reasons set forth below, I conclude that

petitioner is entitled to compensation.

1

Because this document contains a reasoned explanation for the action taken in this case, it must be

made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or

at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government

Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic

Government Services). This means the document will be available to anyone with access to the

internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact

medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy.

If, upon review, I agree that the identified material fits within this definition, I will redact such material from

public access.

2

Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.

§ 300aa-10-34.

1

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 a number of factual demonstrations,

including showing that an individual received a vaccination covered by the statute;

received it in the United States; suffered a serious, long-standing injury; and has

received no previous award or settlement on account of the injury. Finally – and the key

question in most cases under the Program – the petitioner must also establish a causal

link between the vaccination and the injury. In some cases, the petitioner may simply

demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be

shown that the vaccine recipient suffered an injury of the type enumerated in the

“Vaccine Injury Table,” corresponding to the vaccination in question, within an

applicable time period following the vaccination also specified in the Table. If so, the

Table Injury is presumed to have been caused by the vaccination, and the petitioner is

automatically entitled to compensation, unless it is affirmatively shown that the injury

was caused by some factor other than the vaccination. §§ 300aa-13(a)(1)(A); 300 aa-

11(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, of course,

the presumptions available under the Vaccine Injury Table are inoperative. The burden

is on the petitioner to introduce evidence demonstrating that the vaccination actually

caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d

1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,

1525 (Fed. Cir. 1991).

The showing of “causation-in-fact” must satisfy the “preponderance of the

evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-

13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that

standard, the petitioner must show that it is “more probable than not” that the

vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need

not show that the vaccination was the sole cause of the injury or condition but must

demonstrate that the vaccination was at least a “substantial factor” in causing the

condition, and was a “but for” cause. Shyface 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).

2

In what has become the predominant framing of this burden of proof, the Althen

court described the “causation-in-fact” standard, as follows:

Concisely stated, Althen’s burden is to show by preponderant evidence that

the vaccination brought about her injury by providing: (1) a medical theory

causally connecting the vaccination and the injury; (2) a logical sequence

of cause and effect showing that the vaccination was the reason for the

injury; and (3) a showing of proximate temporal relationship between

vaccination and injury. If Althen satisfies this burden, she is entitled to

recover unless the [government] shows, also by a preponderance of the

evidence, that the injury was in fact caused by factors unrelated to the

vaccine.

Althen, 418 F.3d at 1278 (citations omitted). The 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 “sound and reliable.” Boatmon v.

Sec’y of Health & Human Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019) (citing

Knudsen ex rel. Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed.

Cir. 1994)). The Althen court also indicated, however, that a Program fact-finder may

rely upon “circumstantial evidence,” which the court found to be consistent with the

“system created by Congress, in which close calls regarding causation are resolved in

favor of injured claimants.” 418 F.3d at 1280.

In this case, petitioner has alleged that the Hep B and Tdap vaccines caused him

to suffer an atypical form of GBS, manifesting as an isolated small fiber neuropathy.

(ECF No. 53, p. 1.) Because this is not an injury listed on the Vaccine Injury Table

relative to the Hep B and/or Tdap vaccines, petitioner must satisfy the above-described

Althen test for establishing causation-in-fact.

II. Procedural History

Petitioner filed his petition on July 17, 2017, alleging that he received the Hep B

and Tdap vaccinations on July 28, 2014, which caused him to develop a “rheumatologic

injury.” (ECF No. 1.) This case was originally assigned to Special Master Moran. (ECF

No. 6.) On October 30, 2017, petitioner filed his vaccination record (Exhibit 1) and

medical records (Exhibits 2-4). (ECF No. 12.) On November 9, 2017, petitioner filed his

damages affidavit. (ECF No. 15 (Ex. 5).) Thereafter, the case was reassigned to

Special Master Sanders. (ECF No. 19-20.)

On January 4, 2018, petitioner filed updated medical records from UCLA Health

(Exhibit 6) and a statement of completion. (ECF No. 24.) On February 27, 2018,

respondent filed his Rule 4(c) report, arguing that the evidence presented did not meet

petitioner’s burden and recommending against compensation. (ECF No. 27.) On

March 26, 2018, petitioner filed additional medical records (Exhibit 7) and a response to

3

respondent’s Rule 4(c) report. (ECF No. 29-31.) On March 27, 2018, Special Master

Sanders issued a Rule 5 Order instructing petitioner to file an expert report addressing

(i) petitioner’s diagnosis, including whether sequela of that condition lasted for more

than six months following vaccination, and (ii) a causation theory relating petitioner’s

diagnosis to the vaccines he received. (ECF No. 32.)

On April 9, 2018, petitioner filed an affidavit (Exhibit 8), as well as his first

amended petition. (ECF Nos. 33-35.) On July 25, 2018, petitioner filed a consented

motion to substitute Andrew Downing as counsel, in place of Ronald Homer. (ECF No.

38.) On November 27, 2018, petitioner filed an expert report (Exhibit 10) and curriculum

vitae (Exhibit 11) of Dr. Laura S. Boylan. (ECF No. 41.) On December 17, 2018,

petitioner filed his remaining medical records (Exhibit 12) and a statement of

completion. (ECF No. 44-45.) On June 21, 2019, respondent filed a responsive expert

report by Dr. Jeffrey Gelfand (Exhibit C), as well as Dr. Gelfand’s curriculum vitae

(Exhibit D) and accompanying medical literature (Exhibits E-G). (ECF No. 46.)

Thereafter, this case was reassigned to my docket on August 29, 2019. (ECF No. 48-

49.)

On September 5, 2019, petitioner filed medical literature (Exhibits 13-28) cited in

Dr. Boylan’s first expert report. (ECF Nos. 50-51.) A status conference was held on

October 3, 2019, wherein I indicated that, although petitioner pled this case as a

“rheumatologic injury,” petitioner’s expert subsequently discussed his injury of small

fiber neuropathy (“SFN”). (ECF No. 52.) Related to the six-month sequela issue raised

by respondent, I indicated that my preliminary view was that the medical records

preponderantly evidence six months of numbness and tingling, which are consistent

with Dr. Boylan’s opinion of SFN. (Id.) Based on my review of the records, I indicated

that I was preliminarily inclined to find that the onset of petitioner’s alleged SFN

occurred 36-hours post vaccination. (Id.)

Subsequently, petitioner filed his second amended petition on December 9,

2019. (ECF No. 53.) On March 3, 2020, petitioner filed a Dr. Boylan’s supplemental

expert report (Exhibit 29). (ECF No. 57.) On June 8, 2020, respondent filed Dr.

Gelfand’s supplemental expert report (Exhibit H). (ECF No. 62.) On July 14, 2020,

petitioner filed a status report indicating that the matter was ready to be set for a hearing

on entitlement. (ECF No. 63.)

A one-day entitlement hearing was held remotely on October 6th, 2022, via

Zoom. (See ECF Nos. 75-86; see also Transcript of Proceedings (“Tr”), filed at ECF

No. 90.) On November 14, 2023, petitioner filed additional authority, including a citation

to an additional case that “specifically address[ed] vaccine-induced small fiber

neuropathy.” (ECF No. 95 (citing Fiske v. Sec’y of Health & Human Servs., No. 17-

1378V, 2023 WL 8352761 (Fed. Cl. Spec. Mstr. Nov. 13, 2023)).) This case is now ripe

for resolution of petitioner’s entitlement to compensation.

4

III. Factual History

a. As reflected in the medical records

On September 20, 2013, petitioner presented his primary care physician, Dr.

Jamie Polito. (Ex. 2, pp. 1-4.) Physical examination was notable for normal motor and

sensory function and normal reflexes. (Id. at 2-3.) He had a history of psoriasis and

had psoriatic patches observed on the scalp and shins. (Id. at 1.) His psoriasis was

treated topically without systemic immunosuppression. (Id. at 3-4.) He also had a

history of rheumatic fever. (Id. at 1.) The primary care evaluation also recorded a

complaint of low back pain, specifically “sciatica with flares.” (Id.) Petitioner was

referred to an orthopedic surgeon for further evaluation. (Id.)

On July 11, 2014, petitioner transferred care to a new primary care physician, Dr.

Judy Kim-Hwang. (Ex. 2, p. 4.) On physical examination, there was no numbness to

light touch. (Id. at 7.)

On July 28, 2014, he returned to Dr. Kim-Hwang for his annual physical

examination. (Ex. 2, p. 9.) On review of systems, petitioner reported post nasal drip,

dry cough, and episodic “sinus type” headaches, without any other neurological

symptoms. (Id. at 9-10.) His past medical history was notable for psoriasis, irritable

bowel syndrome, gastroesophageal reflux disease (“GERD”), anxiety, lattice

degeneration of the retina and lumbar disc herniation. (Id. at 10.) On physical

examination, strength was normal and there was no sensory loss to light touch. (Id. at

12-13.) Hemoglobin A1C was normal at 5.0, TSH was normal at 1.5, RPR was non-

reactive, HIV was non-reactive, and a complete blood count (no differential), creatinine,

sodium and liver function testing were normal. (Id. at 13-15).

At this annual appointment on July 28, 2014, petitioner received the subject Hep

B and Tdap vaccinations. (Ex. 1, p. 1; Ex. 2, pp. 15.) On July 29, 2014, petitioner sent a

message to Dr. Kim-Hwang, stating that he was “having a pretty rough time with [his]

vaccines.” (Ex. 7, p. 3.) He described how he “started feeling really sick Tuesday

morning about 18 hours after the injections.” (Id.) At this time, his symptoms included a

fever, headache, and achiness in his muscles and joints, especially in his neck,

shoulders, lower back, and legs. (Id.) On July 31, 2014, petitioner sent another

message to Dr. Kim-Hwang, stating that his fever had subsided, but he had developed

numbness or tingling in his hands and feet. (Id. at 4.) He further described how he

began to experience a general feeling of exhaustion late Tuesday night. (Id.) Later that

same day, Dr. Kim-Hwang documented a telephone note that:

I spoke to patient this morning regarding his mychart email. He states that

his fever is gone and he reports no weakness at all, though he has

lethargy/no energy. Went to work and is at work presently. But since

Tuesday has felt numbness in his bilateral hands (dorsal/ventral) and

slightly above the wrist. No facial numbness or difficulty breathing. He has

been reading about possible “autoimmune reaction/disease” that can

5

develop as a result of hepatitis B vaccination and wanted to discuss that

with me. I advised him that if at any point his numbness worsened or if

weakness developed or any respiratory/speech issues, he should go to the

ER immediately. He will see me tomorrow at 4:40PM for follow-up where I

will do a complete neurological exam.

(Ex. 6, p. 2.) Later that same day, petitioner returned a call to Dr. Kim-Hwang indicating

that his fever resolved, but still felt “generalized lethargy / low energy.” (Id.) Petitioner

also “agreed to see Dr. Cholfin at 9AM on 8/4/2014 for a neurology consultation

regarding numbness that developed after hepatitis B and tdap vaccination.” (Id.)

On August 1, 2014, petitioner presented to Dr. Kim-Hwang for an urgent care

visit. Dr. Kim-Hwang recorded the following history:

One day after vaccination, patient had developed fevers T 101F at home,

malaise/myalgias, fatigue and onset of what patient describes as

numbness/tingling in his LE/UE and now left side of the neck. . . . His

fevers/myalgias subsided. Denies focal weakness or respiratory problems.

Pt has been going to work and been able to work. Admittedly, he feels very

depressed and anxious about this reaction as he read on the internet that

the hepatitis B vaccine can cause/trigger various autoimmune conditions

including MS, SLE, and [GBS].

He is accompanied by his significant other who also lives with him.

According to her, he has been very anxious at night losing sleep over this

and thus she feels his fatigue is largely due to sleep deprivation. He admits

to a long-standing hx of anxiety.

He also notes that he sleeps on his stomach often with his bilateral

arms crossed. He notices his symptoms most markedly at night but notices

throughout the day. He describes the numbness as mild dense feeling over

the tips of his fingertips and his feet, but is not consistent, comes and goes.

The “tingling” sensation he describes is also a rare tingling he feels at

various parts of his upper extremities. He does admit that he has known

herniated disks in lumbar spine that has been recently acting up and he

admits to having low back pain.

He is concerned that he might be developing an autoimmune

condition and this is causing him significant amount of psychological

distress/anxiety. He was referred to Dr. Cholfin for evaluation and has an

appointment with him on Monday. He also notes that last evening he felt a

dull sensation over his left neck, which is now gone.

(Ex. 2, p. 17.) On physical examination, petitioner was afebrile, his blood pressure was

130/90, and his pulse was 74. (Id. at 18.) Dr. Kim-Hwang recorded normal cranial

nerves; normal and symmetrical sensation to light touch, temperature, pain, and

6

vibratory sense; normal deep tendon reflexes; full strength; and normal gait. (Id.) Dr.

Kim-Hwang’s assessment included diagnoses of anxiety and subjective

numbness/tingling. (Id. at 19.) Dr. Kim-Hwang informed petitioner “that it would be

atypical (but not impossible) for him to develop symptoms of [GBS] so soon after

vaccination.” (Id.) It was further noted that petitioner’s symptoms do not correlate with

SLE and his presentation was not initially concerning for MS. (Id.) Petitioner was

advised to see a neurologist. (Id.)

On August 4, 2014, petitioner presented to neurologist Dr. Jeremy Cholfin. (Ex.

2, p. 20.) Dr. Cholfin recorded the following history:

The patient went for a routine physical appointment and received DTaP and

HepC [sic] vaccines last Monday. The next morning he woke up with fever,

aches, pains. The next day the fever broke, but he started having some

unusual sensations in hands/feet, described as a hot feeling, itchy, with mild

pins and needles. No frank numbness in that he could [sic] normal

sensations, but more of a subjective sense of numbness. No weakness,

balance problems, nausea, vomiting. Still has residual hand & feet

numbness/tingling. Feels worse while in bed. However, he has been

continuing to work, feels tired during the day, but no significant dysfunction.

He is worried that it could be anxiety producing the symptoms, as he has a

history of anxiety.

(Id.) There was no noted history of bowel or bladder symptoms. (Id. at 21.) On

neurological examination, Dr. Cholfin recorded normal cranial nerve function; normal

motor function; normal sensation to light touch, pinprick, temperature, and vibration;

normal cortical sensory function; normal reflexes, including ankle reflexes; and a

negative Babinski response. (Id. at 23 (“Downgoing toes bilaterally”).) Coordination

was normal, gait was normal, and the Romberg sign was negative. (Id.)

Dr. Cholfin’s assessment was that petitioner had fever followed by “mild residual

paresthesia[] and subjective numbness of the hands/feet, with a feeling of heat

sensation in the feet that is bothersome at night.” (Ex. 2, pp. 24-25.) Dr. Cholfin went

on to write:

This likely represents a mild vaccine reaction with subjective

paresthesia[]/numbness. There is no objective evidence of deficit on exam.

The patient expresses concern about whether this could represent [GBS] or

MS. I provided reassurance that at this point there is no sign of either

disorder. There is no history of MS symptoms, the reflexes are completely

intact and there are no pathologic findings on exam that would point to either

disorder.

(Id. at 25.) The final diagnosis was dysesthesia, and Dr. Cholfin prescribed a low dose

of gabapentin at 100 mg at bedtime for symptomatic relief. (Id.)

7

On August 6, 2014, petitioner saw Dr. Kim-Hwang again in primary care. (Ex. 2,

p. 26.) He indicated that his anxiety was the primary symptom that kept him up at night,

causing fatigue during the day. (Id.) He further complained about an inability to

concentrate and feelings of depression due to his belief that “he could’ve potentially

saved himself from these symptoms by having declined the vaccinations.” (Id.)

Petitioner reported taking Xanax, “which was somewhat helpful,” but he declined a

prescription for Ambien “as he had difficult[ies] waking up.” (Id.) It was noted that

petitioner would “consider an antidepressant in the future;” however, in the interim, he

requested a “further work-up for his symptoms.” (Id.) Neurological examination was

again recorded as normal. (Id. at 28.) Vitamin B12 was normal at 459. (Id. at 163-64.)

ESR was normal at 3 and CRP was <0.3. (Id. at 165-66.) Dr. Kim-Hwang remarked,

“Though I do not think he has a neurological disease at this present time, I do not have

a definitive explanation for his symptoms at this present time.” (Id. at 29.)

On August 12, 2014, petitioner presented to neurologist Dr. Cholfin for a follow-

up. (Ex. 2, p. 30.) Petitioner reported “continued problems with tingling and numbness

in the fingers and toes bilaterally” since his initial neurology consultation on August 4,

2014. (Id. at 31.) He further described how the numbness had spread to his lips,

tongue, and neck, and how it “happened once since last visit, lasted a few hours and

went away.” (Id.) Petitioner reported feeling “tired with little energy, which is new for

him.” (Id.) He explained that, although he could still ride his bike and exercise, these

activities exhausted him more than normal. (Id.) In addition, he reported tiredness and

weakness in his thighs, arms, and shoulders, as well as “some tremor in the bilateral

hands.” (Id.) Neurological examination was again normal. (Id. at 32.) At this point, Dr.

Cholfin concluded that “[t]he localization given the intact reflexes and both upper and

lower extremity symptoms may relate to either the brain or cervical spine.” (Id. at 34.)

He ordered brain and cervical spine MRI with and without contrast but indicated that he

would thereafter order electromyography and nerve conduction studies (EMG/NCS) to

assess for peripheral nervous system pathology if the MRI results were not revealing.

(Id.) Dr. Cholfin diagnosed petitioner with dysesthesia and anxiety. 3 (Id. at 34-35.)

An MRI of the brain on August 21, 2014, showed “[u]nremarkable contrast

enhanced MRI of the brain. Small capillary telangiectasias, a benign finding. Incidental

microadenoma of the pituitary gland. No intracranial abnormality visualized.” (Ex. 2, p.

230.) There was no evidence of demyelinating disease. (Id.) An MRI of the cervical

spine on that same day revealed a “[c]ircumferential disc bulge at C3-C4 with no

associated spinal canal stenosis or neural foraminal stenosis. The remainder of the

vertebral levels are normal. There is no abnormal enhancement in the spinal canal.”

(Id. at 229.) There were no abnormal lesions within the cervical cord. (Id.)

On August 25, 2014, petitioner returned to see neurologist Dr. Cholfin. (Ex. 2, p.

35.) Dr. Cholfin recorded an interval history, which noted that petitioner had been

sleeping better and feeling “somewhat less anxiety” since his last visit. (Id.) Petitioner

3 Dr. Cholfin remarked that “no matter what the neurologic findings are, [petitioner’s] anxiety is out of

proportion to the situation and [he] recommended [petitioner] seek medical attention to help manage the

anxiety symptoms, as these are interfering with his life.” (Ex. 2, p. 34.)

8

described how his shoulders and arm felt “weighted” and how the feeling was

“noticeable in bed” but lessened during the day. (Id.) He further reported that he was

still experiencing “tightness/deadening feeling in hands/fingers, feet about the same.”

(Id.) However, he stated that he was experiencing less “[b]urning dysethesias,” which

he had not experienced for a week. (Id.) Petitioner described feeling “[m]ore

jittery/shaky while writing or manipulating fine objects” but having “[b]etter energy over

the weekend.” (Id.) It was noted that petitioner was running two miles every other day

for exercise and playing guitar without missing notes. (Id.) However, petitioner was

also experiencing dry mouth and tongue numbness. (Id.) He reported that he had

“[t]ried gabapentin 100mg x1,” but he “felt fatigued.” (Id.) Neurological examination was

normal with the exception of a note that sensation to light touch was “slightly reduced in

finger tips, vibration slightly reduced at toes bilaterally.” (Id. at 37.) In his assessment,

Dr. Cholfin “rule[d] out peripheral neuropathy” and advised petitioner that “diagnosis of

CIDP is unlikely” as “the diagnosis cannot be made in under 8 weeks after onset of

symptoms.” (Id. at 38.) However, petitioner expressed concern that he could have a

mild form of CIDP. (Id.)

On September 4, 2014, petitioner returned to Dr. Cholfin for follow-up. (Ex. 2, p.

39.) Dr. Cholfin documented that, since his last visit, petitioner’s “symptoms have been

the same.” (Id.) Petitioner again reported taking “gabapentin 100mg twice” and feeling

“sleepy.” (Id.) He stated that he had not felt like he needed it. (Id. at 39-40.) Petitioner

reported feeling “significant residual numbness of fingers and feet” and tiredness often,

although he continued to work and exercise. (Id. at 40.) On laboratory testing,

petitioner’s antinuclear antigen (“ANA”) was positive at 1:80, rheumatoid factor was

negative, Sjogren’s antibodies were negative, and SPEP was unremarkable. (Id. at 42.)

The neurological examination was reported as “Stable.” (Id. at 41.) EMG/NCS on that

same day revealed “[n]o electrodiagnostic evidence of a peripheral neuropathy, brachial

or lumbosacral plexopathy, cervical or lumbosacral radiculopathy or irritable myopathy.”

(Id.) Dr. Cholfin’s assessment was “[v]accine reaction with resulting numbness: stable

to slightly improved. No evidence of medium to large fiber neuropathy on EMG/NCS.”

(Id.) He referred petitioner for rheumatological consultation. (Id. at 44.)

On September 15, 2014, petitioner presented to rheumatologist Dr. Geraldine

Navarro. (Ex. 2, p. 44.) Dr. Navarro documented that petitioner “was in his usual state

of health, until about the 28th of July - had Hep B and Tdap vax, within 24 hrs he

developed chills, fevers x1 day,” as well as “numbness/tingling in his LE/UE and on the

L side of his neck.” (Id. at 45.) Dr. Navarro observed that petitioner “has a lot of health

anxiety” and that he was not sure whether his tingling was “due to anxiety vs a side

effect of the vaccine.” (Id.) It was further noted that petitioner had “been reading a lot

on the internet” and was feeling “anxious as has read Hep B vax can lead to neuro

sequelae.” (Id.) Petitioner described a “heavy sensation in the proximal muscles of his

LE and UE” that lasted “[f]or awhile.” (Id.) He further described feeling “quite heavy”

when trying to get up, feeling “a little prickly” in his feet when walking, and experiencing

a constant “tightness feeling/tingling over his hand and feet.” (Id.) Petitioner recalled

that “[a]bout 4-5 days later on 8/1/14 he started to feel as though his neck, lips, mouth,

and tongue if [sic] feels as though he is coming off the anesthetics.” (Id.) He further

9

recalled taking “gabapentin x 2 pills for the hot sensation.” (Id.) Dr. Navarro explained

to petitioner that patients “with Sjogrens and SLE can present with neuropathy. His

Sjogrens Abs were negative. Further recs pending ab wk up. I did explain[] that he has

[a] h/o autoimmune disease, Psoriasis, and that a + ANA does not mean that he has a

CTD.” (Id. at 49.) She added that “[a]bout 5% of the normal population can have a +

ANA w/o any manifestation” but ultimately agreed “that if continued symptoms he many

benefit from symptomatic tx.” (Id.)

On September 22, 2014, petitioner saw Dr. Navarro for follow-up. (Ex. 2, p. 50.)

Petitioner’s C3 (complement) was low; the rest of his rheumatological labs were

negative other than the ANA at 1:80. (Id. at 53-54.) This included negative extractable

nuclear antigens and antiphospholipid antibody testing. (Id. at 172-78.) Petitioner’s CK

was normal at 105. (Id. at 181.) Dr. Navarro recommended additional diagnostics and

ordered an MRI of the spine and pelvis. (Id. at 53-54.) During those repeat diagnostics

on October 17, 2014, petitioner’s cryoglobulins were negative. (Id. at 188.) Repeat C3

was slightly low again at 69 (normal 76-165). (Id. at 187.) Petitioner also underwent an

MRI of the pelvis on October 17, 2014, that revealed “[n]ormal MRI of the sacroiliac

joints.” (Id. at 231.) The MRI of the lumbar spine on that same day revealed “multilevel

disc degeneration. At L4-L5 there is a small extra foraminal disc protrusion on the left

which contacts the exited L4 nerve. There is also mild to moderate left foraminal

narrowing at L3-L4 and L4-L5. There is no spinal canal stenosis. No abnormal

enhancement is seen.” (Id. at 232-33.)

On November 24, 2014, petitioner saw Dr. Roland Sakiyama in Internal Medicine

Urgent Care and was diagnosed with pharyngitis (a sore throat) that was favored to be

viral. (Ex. 2, pp. 54-58.) Petitioner was also diagnosed with headache secondary to his

viral upper respiratory infection. (Id. at 57.)

On December 5, 2014, petitioner saw Dr. Cholfin in the neurology clinic. (Ex. 2,

p. 58.) Dr. Cholfin documented that petitioner was still experiencing “persistent

numbness of mid forearm to hand;” numbness in the area around his lips, tongue, and

jaw; and “heat” in his hands and feet in the evening. (Id.) It was also noted that

petitioner had started taking Lexapro two weeks prior but was no longer taking

gabapentin. (Id.) Regarding his vaccine reaction with resulting numbness/peripheral

neuropathy, Dr. Cholfin recorded that petitioner was “stable to slightly improved” and

that there was “[n]o evidence of medium to large fiber neuropathy on EMG/NCS.” (Id. at

62.) Dr. Cholfin further recorded that “ANA was mildly positive” and C3 was “mildly

low.” (Id.) It was noted that Dr. Cholfin suspected immune complex deposition 4 as a

4 Respondent contests this assessment in his Rule 4(c) report, arguing that Dr. Cholfin “provides no

support for this statement.” (ECF No. 27, p. 7, n.3.) An immune complex deposition involves “the binding

of antibodies to excess antigens, and subsequent deposition of the immune complexes in tissues, where

they can elicit complement activation and inflammation.” (Id.) Respondent stresses that “[t]his would

require high levels of circulating antibody as well as high levels of antigenic protein,” and that [t]he small

quantity of protein in present-day vaccines is unlikely to cause such reactions.” (Id.) Respondent

stresses that Kurul et al. found “that a large number and frequent doses of vaccines did not lead to

immune complex deposition in the choroid plexus, and did not significantly increase the deposition of

immune complexes in glomeruli in unilateral nephrectomized mice.” (Id. (citing Semra Kurul et al.,

10

“reaction to vaccine” but that petitioner’s symptoms were “stable overall.” (Id.) Dr.

Cholfin assessed petitioner with paresthesia, dysesthesia, ANA positive, peripheral

neuropathy, and “tremor, physiological.” (Id. at 58, 62.)

On December 26, 2014, petitioner presented to Dr. Rajan Patel complaining of a

cough, neck pain, and back pain. (Ex. 2, p. 63.) Petitioner did not notice any areas of

weakness or numbness. (Id.) Moreover, petitioner told Dr. Patel that he went on a trip

to Miami between December 12th through the 26th and was “moving a lot of heavy

items” and subsequently noticed “some soreness on the sides of his neck going down

his shoulders.” (Id.)

On January 27, 2016, petitioner presented to Dr. Alina Katsman to establish care

and with complaints of back and shoulder pain. (Ex. 2, p. 75.) Dr. Katsman noted that

petitioner was suffering from right shoulder pain for about two months that “[h]appened

when he was wrestling brother in Texas,” and that petitioner “[s]aw Dr. Garvey on

1/16/16 for back pain.” (Id. at 75-76.) She documented “[p]eripheral neuropathy after

vaccination (Hep B and Tdap) - neuropathy mostly in hands and feet. Feet get hot;

‘pins and needles’ sensation.” (Id. at 76.) She noted that petitioner saw Dr. Cholfin in

12/2014 and rheumatologist Dr. Navarro. (Id.) She further noted that petitioner did not

take Neurontin “too much” and all of his “labs were normal except for a low C3 level and

+ANA. (Id.)

From January 28, 2016, to June 18, 2017, petitioner treated with various medical

providers, but did not report any new symptoms related to his alleged vaccine injury.

(See Ex. 2, pp. 84-129; Ex. 4, pp. 13-30.) On June 19, 2017, petitioner was again seen

by Dr. Katsman for an annual exam. (Ex. 2, p. 119.) Dr. Katsman ordered lab testing,

which again showed a mildly positive ANA and a slightly low C3. (Id. at 221-22.) Other

rheumatologic lab testing was normal. (Id. at 219-27.)

On August 7, 2017, petitioner presented to the UCLA Department of Orthopaedic

Surgery After Hours Clinic for right knee pain after playing soccer. (Ex. 2, p. 134-38.)

An MRI of the knee showed a complex medial meniscus tear and small joint effusion.

(Id. at 236.) Thereafter, petitioner participated in physical therapy. (Ex. 4, pp. 3-10.)

Petitioner phoned UCLA Clinic on September 5, 2017, for a follow-up for atrial

fibrillation, and asked for a cardiology referral. (Ex. 6, p. 24.) Petitioner’s ECHO results

were normal – showing no evidence of rheumatic heart disease. (Id. at 25.)

Petitioner presented to Dr. Malcolm Smith on December 21, 2017, for a cold that

he developed while traveling in Spain. (Ex. 12, p. 22-24.) Petitioner’s records reflect

ongoing treatment for chronic cough that was thought to be viral, allergic and/or

asthmatic. (See id. at 22 (interval history), 26.)

Frequent Vaccination and Immune Complex Deposition in Unilateral Nephrectomized Mice, 19 PEDIATRIC

NEPHROLOGY 621 (2004) (Ex. B)).)

11

Petitioner’s remaining records detail his office visits and emails with his treating

physicians regarding his unrelated atrial fibrillation, right shoulder pain, and right knee

pain. (Ex. 12, pp. 28-262.) On May 9, 2018, petitioner presented to Dr. David

McAllister, complaining of right knee pain. (Id. at136.) Dr. McAllister noted that

“[p]atient is neurologically intact in the bilateral lower extremities. Specifically, the

patient is able to flex and extend the toes and ankle without any difficulty and sensation

is intact to light touch along the dorsal, plantar, medial and lateral aspects of both feet.”

(Id. at 139.) Petitioner’s “Problem List” continued to include peripheral neuropathy

through September 7, 2018. (See id. at 235.) No further records were filed.

b. As reflected in petitioner’s testimony

In addition to submitting an affidavit (Exhibit 8), petitioner testified at the hearing

that was held in this case. (See Transcript of Proceedings (“Tr.”) at ECF No. 90.)

Petitioner testified that, prior to the date of his vaccinations, he was “an active person,”

who “often engaged in hiking, jogging,” and bike riding. (Tr. 9-10.) He explained that,

prior to the vaccinations, he had no neurological complaints. (Id.) Petitioner explained

that he did have rheumatic fever when he was eight years old and experienced

“excruciating joint pain,” had a rash all over his body, and he was “mostly confined to a

bed during that time.” (Id. at 11-12.) He noted that his symptoms lasted for “the better

part of a year.” (Id. at 12.) In addition to rheumatic fever, petitioner testified that he was

diagnosed with psoriasis in his late teens. (Id. at 13.) Petitioner described having a

rash all over his body. (Id. at 13-14.) He testified that his psoriasis is under control and

is “mostly on [his] head and face.” (Id. at 14.) Petitioner also described his history with

irritable bowel syndrome and GERD. (Id. at 14-16.) Petitioner explained that his father

suffered from psoriasis and that his mother had rheumatic fever twice and had been

diagnosed with polymyalgia rheumatica and irritable bowel syndrome. (Id. at 16-18.)

Petitioner testified that he received the Tdap and Hep B vaccines on July 28,

2014, when he saw Dr. Kim-Hwang. (Tr. 17-18.) He recalled that he did not have “any

major concerns” during that visit. (Id. at 17.) Petitioner explained that he received the

vaccines around 10:00 AM on a Monday, the 28th. (Id. at 18.) He described that at

around 4:00 or 5:00 AM on July 29, 2014, he began to feel ill and developed flu-like

symptoms. (Id.) He called his doctor the next morning and told him that he “‘may have

had a pretty rough time with [his] vaccinations,’” and that he “started feeling really sick

Tuesday morning about 18 hours after the injections.” (Id. at 18-19 (citing Ex. 7, p. 3).)

At this point, petitioner noted that he had a fever of 101.3º and had a headache and was

experiencing “really bad muscle and joint aches.” (Id. at 19.) He described when he

woke up on Wednesday, he was experiencing a numbness, stinging, tingling, tightness,

and a deadening feeling in his hands and feet. (Id. at 20.) Petitioner testified that he

called his doctor again on July 31, 2014. (Id. at 20-21.) During this phone call, he

noted that, although his fever had resolved, he had now developed “a numbness or

tingling sensation in [his] hands and feet” and he felt “exhausted, very lethargic, and no

energy.” (Id. at 21 (discussing Ex. 7, p. 4).) Petitioner clarified that he “went to bed

fevery, sick on Tuesday,” and developed the sensory symptoms very early Wednesday

morning. (Id.)

12

Petitioner addressed the different symptoms he had throughout the course of his

injury. (Tr. 22.) He stated that the sensations he had felt in his hands and his feet

eventually expanded from the tips of his fingers to just below his elbows and up both of

his legs to just below his knees. (Id.) He described that these symptoms always

remained in his hands and feet but would come and go from the other areas he

described. (Id. at 23.) Petitioner noted that he called his doctor on August 1, 2014.

(Id.) He explained that the sensation he had been feeling in his hands and feet had now

moved to his chest, neck, and head. (Id. at 23-24 (citing Ex. 6, p. 3).) He described

how the feeling has “ebbed and flowed,” but has never completely gone away. (Id. at

23.)

Petitioner described his first visit to his doctor following the development of his

symptoms. (Tr. 25 (citing Ex. 2, p. 20).) Petitioner noted that the summary of this

appointment correctly described his onset of symptoms as two days following

vaccination and after his fever had already broken. (Id.) During this appointment,

petitioner’s doctor described his reaction as “a mild vaccine reaction with subjective

paresthesia/numbness.” (Id. at 26 (citing Ex. 2, p. 25).) Petitioner testified that his

physician “ultimately indicated to [him] that it was caused by the vaccine, [in] his

opinion,” and that petitioner’s condition would likely be permanent if it did not resolve

within a year. (Id. at 26-27.) Petitioner testified that his doctor had theorized that his

condition was likely due to the Hep B vaccine. (Id. at 27.) He noted that during that

appointment, he told his doctor that he was exhausted and “had absolutely no energy.”

(Id.) During an appointment on December 5, 2014, petitioner was diagnosed with

“[v]accine reaction with resulting numbness/peripheral neuropathy.” (Id. at 53.)

Petitioner testified that his symptoms have persisted, and he still feels extremely

tired. (Tr. 34-35.) He explained that his condition forced him to take days off of work

here and there. (Id. at 35.) Petitioner testified that, in particular, there are four

symptoms that have stayed with him: burning, fatigue, stinging/numbness, and

itchiness. (Id. at 35-36.) Petitioner testified that he has not regained full ability in his

hands. (Id. at 37.) Petitioner explained that his injury left him depressed and

frightened, especially when he did not have any answers. (Id. at 39.)

Petitioner also addressed his medical records and the references to his injury

being “related to anxiety.” (Tr. 50.) He explained that he had difficulty securing an

appointment and that he initially hoped “that it was just anxiety.” (Id. at 50-51.)

However, he was confident that his anxiety was not the cause of his symptoms. (Id. at

51-52.)

IV. Expert Opinions

a. Petitioner’s expert, Laura S. Boylan, M.D., 5 initial report, Exhibit 10

5 Dr. Boylan has been presented without objection as an expert in neurology. (Tr. 64.) Dr. Boylan

received her medical degree from Columbia University College of Physicians & Surgeons in 1994. (Ex.

11, p. 1.) She is currently an attending physician at Bellevue Hospital Medical Center in New York City,

13

Petitioner’s expert, Dr. Boylan, opines that petitioner “more likely than not, within

a reasonable degree of medical certainty,” suffers from an atypical form of GBS

manifesting as an isolated SFN, caused-in-fact by his Hep B and Tdap vaccinations.

(Ex. 10, p. 9.) She explains that damage to small nerve fibers typically accompanies

damages to larger nerve fibers, which commonly occurs in conditions like diabetic

peripheral neuropathy. (Id. at 7.) It is also associated with GBS, hepatitis, HIV, Lyme,

genetic and other systemic conditions. (Id. (citing J.D. England et al., Practice

Parameter: Evaluation of Distal Symmetric Polyneuropathy: Role of Autonomic Testing,

Nerve Biopsy, and Skin Biopsy (An Evidence-Based Review), 72 NEUROLOGY 177

(2009) (Ex. 15)).) She explains that GBS patients commonly experience SFN in

addition to the symptoms of pain and dysesthesia typically associated with GBS. (Id.)

Dr. Boylan cites a study by Pan et al., in which twenty patients with EMG/NCS and

clinically confirmed GBS underwent skin biopsies, as well as autonomic nervous system

testing. (Id. (citing Chun-Liang Pan et al., Cutaneous Innervation in Guillain-Barré

Syndrome: Pathology and Clinical Correlations, 126 BRAIN 386 (2003) (Ex. 17)).) She

stresses that more than half of the patients suffered small fiber nerve damage, in

addition to damage in larger diameter fibers, which can be detected on routine

EMG/NCS. (Id.)

Dr. Boylan explains that there are many variants of GBS, including twelve

different forms of GBS with varying clinical and electrodiagnostic presentations in

adults. (Ex. 10, p. 7 (citing Francine Vriesendorp, Guillain-Barré Syndrome in Adults:

Clinical Features and Diagnosis, UPTODATE (Jul. 19, 2022)

https://www.uptodate.com/contents/guillain-barre-syndrome-in-adults-pathogenesis-

clinical-features-and-diagnosis (Ex. 19).) Some authors have suggested that isolated

SFN is one such form of GBS and can similarly be caused by infection or vaccination.

(Id. at 8 (citing U. Seneviratne & S. Gunasekera, Acute Small Fibre Sensory

Neuropathy: Another Variant of Guillain-Barré Syndrome?, 72 J. NEUROLOGY

NEUROSURGERY PSYCHIATRY 540 (2002) (Ex. 20); Nobuhiro Yuki et al., Acute Painful

Autoimmune Neuropathy: A Variant of Guillain-Barré Syndrome, 57 MUSCLE & NERVE

320 (2018) (Ex. 21); Antonino Uncini & Nobuhiro Yuki, Sensory Guillain-Barré

Syndrome and Related Disorders: An Attempt at Systematization, 45 MUSCLE & NERVE

464 (2012) (Ex. 22)).) Dr. Boylan highlights one study where six patients presented with

acute onset numbness and dysesthesias of the arms and legs, and four were

considered “post infectious.” (Id. (citing Pan et al., supra, at Ex. 17).) Dr. Boylan

New York, and an Adjunct Professor of Neurology at the New York University School of Medicine. (Ex.

10, p. 1-2.) She also serves as an attending neurologist at the Albany Stratton VA Medical Center in

Albany, New York, and works as a neurohospitalist at Essential Health in Duluth, Minnesota. (Id. at 2.)

Dr. Boylan is board certified in neurology by the American Board of Psychiatry & Neurology. (Id.) She

completed clinical training in internal medicine at St. Vincent’s Hospital and Medical Center in New York

City and completed a residency in neurology at the Neurological Institute of Columbia-Presbyterian

Medical Center in New York City. (Id.) Dr. Boylan also completed fellowship training in Behavioral

Neurology and Neuropsychiatry at the Neurological Institute of Columbia-Presbyterian Hospital in

conjunction with the New York State Psychiatric Institute, both at Columbia University in New York City.

(Id.) Dr. Boylan testified that, in her practice as a neurologist, she has treated thousands of patients with

peripheral neuropathy. (Tr. 60.)

14

explains that “[a]nother study describes well documented cases of acute isolated small

fiber neuropathy within one day to two months following vaccinations for rabies,

varicella or Lyme disease.” (Id. (citing Nizar Souayah et al., Small Fiber Neuropathy

Following Vaccination for Rabies, Varicella or Lyme Disease, 27 VACCINE 7322 (2009)

(Ex. 25)).)

Dr. Boylan stresses that patients with “one auto-immune condition are prone to

develop other auto-immune conditions.” (Ex. 10, p. 9.) According to Dr. Boylan,

petitioner is “immunologically vulnerable.” (Id. at 10.) Petitioner developed rheumatic

fever as a young child while growing up in the suburbs of Los Angeles, California – at a

time and place where it was “exceedingly rare.” (Id. at 8-9 (citing Alberto Odio, The

Incidence of Acute Rheumatic Fever in a Suburban Area of Los Angeles, 144 W.J. MED.

179 (1986) (Ex. 26)).) Judging by the number of hospitalizations for rheumatic fever in

the area between 1971 and 1980, Dr. Boylan concludes that the overall risk of

rheumatic fever at that time was “approximately 2 in a million” in suburban Los Angeles.

(Id. (citing Odio, supra, at Ex. 26).) This suggests to Dr. Boylan that petitioner is

especially immunologically vulnerable. (See id. at 10.) Moreover, petitioner’s history of

joint hypermobility syndrome and psoriasis “are also consistent with abnormal

immune/inflammatory responses.” (Id.)

Dr. Boylan opines that petitioner’s development of atrial fibrillation following

vaccination is indicative of autonomic autoimmune neuropathy. (Ex. 10, p. 9.) She

explains that the autoimmune nervous system involves control of digestion, the heat,

adjustment of the eyes to different lighting, emotional responses, blood pressure, and

“many other ‘systemic’ and ‘non-specific’ symptoms.” (Id.) Autonomic autoimmune

neuropathy is a rare form of autoimmune neuropathy that effects only the nerves of the

autonomic nervous system, “which is associated with the AchR antibody.” (Id. (citing

Martha Kerr, Autonomic Autoimmune Neuropathy is an Antibody Mediated Disorder,

NEUROLOGY TODAY (Jan. 2004),

https://journals.lww.com/neurotodayonline/Fulltext/2004/01000/Autonomic_Autoimmune

_Neuropathy_Is_An.4.aspx (Ex. 27)).) Dr. Boylan explains that petitioner developed

atrial fibrillation post-vaccination, which is one of a variety of cardiac problems

associated with autonomic regulation. (Id. (citing Laura Boylan, Brain-Heart

Connections, NEUROLOGY.ORG (Mar. 28, 2018) (Ex. 28)).)

Dr. Boylan concludes that the “time course of [petitioner’s] illness is as expected

in GBS.” (Ex. 10, p. 10.) Petitioner had acutely acquired symptoms of non specific

inflammation followed within days by a series of classical symptoms of SFN: “glove and

stocking distribution of dysesthesias and pain and symptoms and signs of autonomic

dysfunction including abnormal cardiac rhythms, abnormal sweating, thermoregulation

and severe fatigue.” (Id.) The syndrome started immediately following petitioner’s

vaccinations, which Dr. Boylan opines is “unlikely to be coincidental.” (Id.)

15

b. Respondent’s expert, Jeffrey M. Gelfand, M.D., M.A.S., 6 initial report,

Exhibit C

Respondent’s expert, Dr. Gelfand, opines that petitioner more likely than not

suffers from a “sensory syndrome,” characterized by tingling, burning, itchiness, and

numbness in his hands and feet, which “likely involved isolated small fiber nerves.” (Ex.

C, pp. 6-7.) Onset, according to Dr. Gelfand, was within one day of Hep B and Tdap

vaccinations on July 24, 2014. (Id. at 7.) He explains that symptom onset was

associated with a transient fever as well as malaise and fatigue. (Id.)

Upon his review of records, Dr. Gelfand observed that petitioner’s neurological

examinations were repeatedly normal acutely, with the exception of one abnormal

exam, in which mild deficits to light touch in the fingertips and slightly reduced vibration

sense in the toes was noted on Dr. Cholfin’s August 25, 2019 exam, but not on his

August 4th or August 12th exams. (Ex C, p. 7.) Petitioner’s EMG/NCS on September

4, 2014, was normal, including no evidence of a large fiber sensory neuropathy,

neuronopathy, or radiculopathy. (Id.) Moreover, Dr. Gelfand noted that MRI of the brain

was unremarkable, including no evidence of demyelinating disease, and MRI of the

cervical spine showed relatively mild degenerative changes “that would not explain

[petitioner’s] clinical syndrome,” which Dr. Gelfand stresses is consistent with

petitioner’s treating neurologist’s interpretation. (Id.) MRI of the lumbar spine showed

mild degenerative changes, which Dr. Gelfand opines “would not explain his clinical

syndrome (which involved his upper limbs as well).” (Id.)

After detailed rheumatological investigation, Dr. Gelfand observes that petitioner

had a low grade positive anti-nuclear antibody and a mildly low C3 complement level on

blood testing. (Ex. C, p. 7.) He opines that both results are of uncertain and “probably

doubtful clinical significance – without other evidence for a systemic inflammatory /

rheumatological disease except for his known history of psoriasis.” (Id.) In Dr.

Gelfand’s opinion, petitioner’s neurological symptoms appeared to reach a nadir “within

days to a few weeks and partially improved over weeks to months, without any

documented evidence of neurological relapse or progression.” (Id.)

Dr. Gelfand opines that the record does not support a large fiber sensory

neuropathy, neuronopathy, or radiculopathy as the cause of petitioner’s clinical

syndrome. (Ex. C, p. 7.) Instead, he explains that GBS is an acute

polyradiculoneuropathy, and Brighton criteria are widely used to support this diagnosis

clinically and for epidemiological purposes. (Id. (citing Christiaan Fokke et al.,

6 Dr. Gelfand has been presented without objection as an expert in neurology. (Tr. 142-43.) Dr. Gelfand

received his medical degree from Harvard Medical School in 2006. (Ex. D.) He completed an internship

in internal medicine at University of California, San Francisco (“UCSF”), in 2007. (Id.) He also completed

his residency in neurology, as well as a subspecialty fellowship training in multiple sclerosis and

neuroimmunology, at UCSF. (Id.) Dr. Gelfand earned a Masters in Advanced Study (MAS) degree in

Clinical Research from UCSF in 2013. (Ex. C, p. 1.) He currently serves as an attending neurologist at

UCSF, and attends at both UCSF Medical Center and Zuckerberg San Francisco General Hospital, which

is UCSF affiliated. (Id.) Dr. Gelfand specializes in caring for patients with a wide range of

neuroinflammatory disorders and maintains an active clinical practice at UCSF. (Id.)

16

Diagnosis of Guillain-Barré Syndrome and Validation of Brighton Criteria, 137 BRAIN 33

(2014) (Ex. E)).) While petitioner’s clinical course was monophasic and onset to nadir

was more than 12 hours and perhaps not more than 28 days, “assuming that the

sensory change on Dr. Cholfin’s later neurological examination did not reflect true

progression but rather variability of mild findings,” Dr. Gelfand observes that petitioner

“never had documented bilateral or flaccid weakness of his limbs; decreased or absent

deep tendon reflexes in weak limbs; or nerve conduction study findings typical of GBS.”

(Id.) Dr. Gelfand stresses that these key features are needed to support a GBS

diagnosis. (Id.) Furthermore, Dr. Gelfand suggests that EMG/NCS studies were

conducted at a subacute enough timepoint following symptom onset and while petitioner

was still symptomatic, which is when abnormalities would be expected if GBS was the

correct diagnosis. (Id.) Lastly, he notes that petitioner never had a CSF examination.

(Id.)

Dr. Gelfand acknowledges that SFN is an important diagnostic consideration,

given petitioner’s history of new onset tingling, burning, itching and subjective

numbness in his hands and feet. (Ex. C, p. 7.) He explains that SFN refers to a

neuropathy characterized by involvement of peripheral afferent unmyelinated C-fibers

and thinly myelinated A-delta fibers. (Id. (citing Astrid Terkelsen et al., The Diagnostic

Challenge of Small Fibre Neuropathy: Clinical Presentations, Evaluations, and Causes,

16 LANCET NEUROLOGY 934 (2017) (Ex. F)).) However, Dr. Gelfand explains that,

“[u]nless large fiber nerves are involved as well as part of a mixed syndrome, isolated

small fiber neuropathies will not show abnormalities” on EMG/NCS. (Id.) Diagnosis of

isolated SFN is supported by key elements of the history and sometimes other evidence

of small fiber nerve dysfunction that may be discovered by quantitative sudomotor axon

reflex testing, which is “not routinely performed in clinical practice,” or skin biopsy

stained to evaluate for loss of intraepidermal nerve fibers. (Id. at 7-8 (citing Terkelsen et

al., supra, at Ex. F).) Dr. Gelfand explains that petitioner did not have these “specialty

diagnostics.” (Id.) Based on his experience, Dr. Gelfand notes that most small fiber

neuropathies present insidiously, over the course of months to years, or sometimes

subacutely, over the course of weeks to months. (Id. at 8.) In contrast, acute-onset

small fiber neuropathies are rare and not well understood. (Id.) According to Dr.

Gelfand, autoimmune causes for acute onset SFN have been postulated in select

cases, particularly in children and adolescents. (Id. (citing Anne Louise Oaklander,

Immunotherapy Prospects for Painful Small-Fiber Sensory Neuropathies and

Ganglionopathies, 13 NEUROTHERAPEUTICS 108 (2016) (Ex. G)).) He asserts that

petitioner did not have other known common causes of SFN, such as diabetes, heavy

alcohol use, B12 deficiency, thyroid dysfunction, chronic infection, or rheumatological

disease. (Id.) He further explained that psoriasis is not a known or accepted cause of

SFN, based on an updated search of the literature. (Id.)

Dr. Gelfand further acknowledges that sensory syndromes can also be a

somatoform reaction in the context of anxiety. (Ex. C, p. 8.) Although he notes that this

diagnosis was considered by petitioner’s treating physicians, Dr. Gelfand indicates that

“this would be a diagnosis of exclusion” and therefore cannot be supported, “beyond a

reasonable degree of medical certainty,” given the available evidence. (Id.)

17

On the question of vaccine-causation, Dr. Gelfand acknowledges that, “[a]n

isolated small fiber neuropathy, which could have been immune-mediated, is a possible

explanation for [petitioner’s] syndrome but the evidence to support this theory does not

meet the more likely than not standard [in his] opinion.” (Ex. C, p. 8.) Dr. Gelfand

indicates that there are no citations or peer-reviewed literature that support an

association of acute-onset isolated SFN following Hep B or Tdap vaccination

specifically. (Id. at 9.) Nor does Dr. Boylan cite any such literature. (Id.) Instead, Dr.

Boylan cites a paper reporting an association of SFN following vaccinations for rabies,

varicella, and Lyme disease. (Id.) Furthermore, Dr. Gelfand notes that Dr. Boylan

neither provides nor cites specific evidence to support how antigens in either the Hep B

vaccination or Tdap vaccination might cross-react with antigens in small fiber nerves or

whether injury is thought to relate to inflammation more generally (i.e., that is not

antigen-directed). (Id.) If this was GBS or GBS-like, Dr. Gelfand stresses that clinical

onset within one day would also be “too rapid [to] support a vaccine related cause of

neurological injury.” (Id.)

Even if we assume that petitioner’s sensory syndrome falls within the spectrum of

GBS as an atypical presentation, Dr. Gelfand stresses that the Institute of Medicine’s

(“IOM”) report in 2012 concluded, “The epidemiological evidence is insufficient or

absent to assess an association between [Tdap] and GBS.” (Ex. C, p. 9 (alteration in

original) (citing IOM report 2012, p. 557-58).) The IOM further concluded, “The

evidence is inadequate to accept or reject a causal relationship between [Tdap] and

GBS.” (Id. (alteration in original) (citing IOM report 2012, p. 557-58).) As for the Hep B

vaccine, the IOM concluded that “[t]he epidemiologic evidence is insufficient or absent

to assess an association between hepatitis B vaccine and GBS . . . [t]he evidence is

inadequate to accept or reject a causal relationship between hepatitis B vaccine and

GBS.” (Id. (citing IOM report 2012, p. 466).)

Therefore, Dr. Gelfand concludes that, “based on a reasonable degree of

medical probability, that the Petitioner suffered from acute onset sensory syndrome with

minimal objective findings on examination.” (Ex. C, p. 9.) Given that (1) “[s]upporting

evidence for a small fiber neuropathy, which could possibly be immune-mediated, rests

in this case entirely on history without other supporting diagnostics,” and (2) “[s]ymptom

onset occurred within 24 hours following Tdap and Hepatitis B vaccination,” there is not

sufficient evidence to support that petitioner’s vaccinations “more likely than not caused

a possible small fiber neuropathy.” (Id.)

c. Dr. Boylan’s supplemental report, Exhibit 29

In her supplemental report, Dr. Boylan relies on a review article by Dr.

Christopher Gibbons to suggest that SFN can be immune mediated. (Ex. 29, p. 1 (citing

Christopher Gibbons, Small Fiber Neuropathies, 20 CONTINUUM 1398 (2014) (Ex. 16)).)

Specifically, Dr. Boylan asserts that this article “outlines the evidence for auto-immune

etiologies of small fiber neuropathy.” (Id.)

18

Dr. Boylan agrees that petitioner’s symptoms reached nadir within days to a few

weeks of vaccination, which she explains is within the expected time frame under the

Brighton criteria for a diagnosis of GBS. (Ex. 29, p. 1 (citing James J. Sejvar et al.,

Guillain-Barré Syndrome and Fisher Syndrome: Case Definitions and Guidelines for

Collection, Analysis, and Presentation of Immunization Safety Data, 29 VACCINE 599

(2011) (Ex. 30)).) However, Dr. Boylan disagrees with Dr. Gelfand’s opinion that

petitioner’s onset of symptoms was “< 1 day following vaccination.” (Id. (citing Ex. C, p.

9).) Dr. Boylan stresses that petitioner had an “inflammatory prodrome (fever, aches,

pain, malaise) within hours following the vaccine.” (Id.) However, she emphasizes that

petitioner did not report symptoms of any sensory syndrome on the same day, or within

24 hours, of vaccine administration. (Id. (citing Ex. 7, pp. 3-4).)

Dr. Boylan stresses that petitioner’s sensory syndrome involved small fiber

nerves and that a diagnosis of SFN is often made without specialty diagnostic testing.

(Ex. 29, p. 1.) Dr. Boylan suggests that Dr. Gelfand either discounts or does not

acknowledge (1) the conclusions of petitioner’s treating neurologist Dr. Cholfin, (2)

petitioner’s abnormal sensory examination, (3) petitioner’s abnormal complement and

ANA blood tests, (4) petitioner’s symptoms of dysautonomia, (5) associations of SFN

with a history of autoimmune conditions, and (6) the caveats included within the

Brighton criteria for GBS. (Id. at 1-2.) Moreover, Dr. Boylan critiques Dr. Gelfand’s

report because he “does not offer an explicit opinion as to an alternate diagnosis.” (Id.

at 2.) Rather, Dr. Gelfand suggests that a somatoform, or psychological, disorder is

more likely than SFN. (Id.) Dr. Boylan stresses that this opinion lacks analysis or

explanation, beyond the fact that such a diagnosis was entertained by some of

petitioner’s treating physicians. (Id.) In fact, Dr. Boylan stresses that SFN has been

increasingly associated with conditions “long considered by many in the medical

community as being of psychological in origin,” such as fibromyalgia, chronic fatigue

syndrome, and complex regional pain syndrome. (Id. (citing Gibbons, supra, at Ex. 16;

Terkelsen et al., supra, at Ex. F; Anne Louise Oaklander & Maria Nolano, Scientific

Advances in and Clinical Approaches to Small-Fiber Polyneuropathy: A Review, 76

JAMA NEUROLOGY 1135 (2019) (Ex. 32)).)

Dr. Boylan cites one study involving a poly-ethnic U.S. sample of juveniles with

unexplained widespread pain. (Ex. 29, p. 2 (citing Anne Louise Oaklander & Max M.

Klein, Evidence of Small-Fiber Polyneuropathy in Unexplained, Juvenile-Onset,

Widespread Pain Syndromes, 131 PEDIATRICS e1091 (2013) (Ex. 33)).) Physical

examinations revealed no neurological abnormalities and electrodiagnostic studies were

noncontributory, except in the one case of a patient with a prior brachial plexitis. (Id.

(citing Oaklander & Klein, supra, at Ex. 33, p. 5).) Dr. Boylan notes that SFN was

identified as definite by clinical history and objective testing in 59% of this study group

and an additional 39% were considered to have possible or probable SFN. (Id. (citing

Oaklander & Klein, supra, at Ex. 33, p. 5).) Furthermore, a history of auto-immune

disease was identified in 33% of 41 patients. (Id. (citing Oaklander & Klein, supra, at

Ex. 33, pp. 1, 5).) Dr. Boylan emphasizes that petitioner has a history of auto-immune

diseases (i.e., rheumatic fever and psoriasis). (Id.) In the Oaklander & Klein study, a

wide range of autoimmune conditions were associated with small fiber polyneuropathy.

19

(Id. (citing Oaklander & Klein, supra, at Ex. 33, p. 5).) Dr. Boylan stresses that, like

petitioner, three participants had joint hypermobility (i.e., Ehlers-Danlos Syndrome). (Id.

(citing Oaklander & Klein, supra, at Ex. 33, p. 5).)

Dr. Boylan suggests that the Brighton criteria were developed for use in research

studies and exclude most clinical variants of GBS. (Ex. 29, p. 2 (citing Gibbons, supra,

at Ex. 16; Vriesendorp, supra, at Ex. 19; James Sejvar et al., supra, at Ex. 30).) She

explains that the Brighton criteria caution that case definitions differ based on “currently

available data, intended use and clinical setting.” (Id.) Moreover, the Brighton criteria

were designed to be strict, or “specific,” and Dr. Boylan contends that the criteria may

miss up to 1% of GBS cases. (Id.) She adds that “[i]t is recognized by the group that

the case definitions for GBS and Fisher Syndrome may not capture some of the clinical

variants that nonetheless may be related and are regarded by others to be forms of

‘GBS.’” (Id. (quoting Vriesendorp, supra, at Ex. 19).)

Dr. Boylan disagrees with Dr. Gelfand’s suggestion that a somatoform reaction is

a possible explanation of petitioner’s condition. (Ex. 29, pp. 2-3.) She claims that Dr.

Gelfand’s statement that a somatoform diagnosis is a diagnosis of exclusion is not in

line with the current thinking of leading neurologists with a special interest in this area.

(Id. at 3 (citing Jon Stone, Conversion Disorders in Adults: Clinical Features,

Assessment, and Comorbidity, UPTODATE (Jan. 7, 2020) (Ex. 35); Jon Stone,

Conversion Disorder in Adults: Terminology, Diagnosis, and Differential Diagnosis,

UPTODATE (Jan. 7, 2020) (Ex. 36); Alberto J. Espay et al., Current Concepts in

Diagnosis and Treatment of Functional Neurological Disorders, 75 JAMA NEUROLOGY

1132 (2018) (Ex. 37)).) Instead, Dr. Boylan explains that, when somatoform reactions

take the form of specific neurological conditions, they may be referred to as “functional

neurological disorders.” (Id. (citing Stone, supra, at Ex. 36).) According to Dr. Boylan,

“the area of functional neurological disorders involves inclusionary as well as

exclusionary features and does not rely on the presence or absence of psychological

stressors or suggestive historical clues.” (Id. (citing Stone, supra, at Ex. 36; Espay et al.,

supra, at Ex. 37).) In the case of sensory syndromes, Dr. Boylan opines that

inclusionary criteria include specific findings on the physical examination, such as

“precise splitting of the midline on vibrations sensation on the forehead or sternum,

sharply demarcated sensory loss at the groin or shoulder and certain abnormalities on

the testing of visual fields.” (Id.) She adds that there are additional “findings on

physical examination seen with functional neurological disorders which extend beyond

sensory syndromes to include problems with movement and strength.” (Id.) She

stresses that the diagnosis of functional neurological disorders in petitioner’s case is

“based on broad principles of inconsistency of symptoms over time and phenomenology

and incongruence of symptoms with known neurological disorders.” (Id.) Dr. Boylan

suggests that “[a]nxiety is ubiquitous in medical practice, particularly among patients

with unquestionably biologically based neurological or other medical illnesses.” (Id.)

In her clinical experience, Dr. Boylan contends that the “[f]ixed classical

symptoms” of SFN, in the absence of electrodiagnostic findings and/or established

peripheral neuropathy that is stable over years of time, is not common in clinical

20

practice. (Ex. 29, p. 3.) In her opinion, petitioner acquired an atypical form of GBS,

manifesting as an isolated SFN, that was caused-in-fact by his Hep B and Tdap

vaccines. (Id. at 4.)

d. Dr. Gelfand’s supplemental report, Exhibit H

In his supplemental report, Dr. Gelfand recalls that petitioner developed fever,

aches, and pain within 18 hours after vaccination. (Ex. H, pp. 2-3.) This was followed

by sensory complaints that appeared as early as Tuesday evening (July 29, 2014),

which Dr. Gelfand explains would put the onset of sensory symptoms between 24-48

hours postvaccination. (Id. (citing Ex. 7, p. 4; Ex. 6, p. 2; Ex. 2, pp. 17, 20).) Dr.

Gelfand suggests that if you include “the symptom complex as a whole (fevers, aches,

pain followed shortly after by sensory symptoms),” then symptom onset began as early

as about 18 hours post-vaccination. (Id. at 3.) However, if you exclude

fevers/aches/pains and only include sensory symptoms (as Dr. Boylan proposes), then

onset of was about 24-48 hours post-vaccination. (Id.) Dr. Gelfand concludes that a

timeframe of between 18-48 hours following vaccination “would be very quick to cause a

Guillain-Barre type syndrome.” (Id.)

Dr. Gelfand acknowledges that small fiber neuropathies may be considered

“Guillain-Barre-like” in that they resemble GBS “in time course and by being immune-

mediated;” however, he stresses that small fiber neuropathies “are best understood as

stand-alone conditions in terms of epidemiology and immunology.” (Ex. H, p. 3.) He

also acknowledges that Oaklander and Nolano and “others have proposed the

existence of small fiber–targeting inflammatory SFN, with acute and chronic

presentations temporally resembling Guillain-Barre syndrome and chronic inflammatory

demyelinating polyneuropathy, and preliminary evidence of episodic relapsing-remitting

courses.” (Id. (quoting Oaklander & Nolano, supra, at Ex. 32, p. 7).) However, Dr.

Gelfand explains that, unlike in GBS and chronic inflammatory demyelinating

polyneuropathy, “inflammatory cells are not prominent in SFN biopsies or cerebrospinal

fluid.” (Id. (quoting Oaklander & Nolano, supra, at Ex. 32, p. 7).) Dr. Gelfand also

contends that none of the 12 GBS variants listed in Vriesendorp’s article include “pure

small fiber neuropathy,” and petitioner never had absent reflexes or other evidence of a

concurrent large fiber neuropathy. (Id. (citing Vriessendorp, supra, at Ex. 19).)

Furthermore, he stresses that none of the medical literature supports an association of

an isolated SFN, specifically observed or reported with Hep B or Tdap vaccination, nor

is there specific evidence to support how antigens in either of those vaccinations might

cross-react with antigens in small fiber nerves. (Id.)

e. Dr. Boylan’s in court testimony

Dr. Boylan testified at the hearing on behalf of petitioner. (Tr. 54.) She defined

neuropathy as “a general term for injury to nerves,” which can include large, medium,

and small fibers. (Id. at 64.) Small fiber nerves specifically “deal with itching sensation,

pain, burning, [or] the types of things we generally refer to as neuropathic pain.” (Id. at

67.) Dr. Boylan explained that peripheral neuropathy is diagnosed through a review of

21

the patient’s history and physical examination, as well as through an EMG/NCS and

biopsy in more complicated or unusual cases. (Id. at 67-68.) However, she explained

that nerve conduction study may not detect all nerve issues, which is why an accurate

and thorough medical history is important in these cases. (Id. at 68.) In fact, a positive

nerve conduction study would, by definition, not be an isolated SFN, because only the

large and medium nerves show up on the nerve conduction study. (Id. at 68-69, 77, 89-

90.) Later in her testimony, Dr. Boylan clarified that SFN is a “clinical diagnosis” that is

determined by looking at a patient’s history, the time course of the neuropathy, and a

clinical examination to look for areflexia, which is “an early sign of” GBS. (Id. at 88.)

She specifically noted that acute onset suggests an “immune mediated event.” (Id. at

88.) She explained that some specialty centers will diagnose through a biopsy,

however, this is “not routine clinical care,” and the lack of a positive biopsy does not

necessarily mean the patient does not have SFN. (Id. at 89-91.) She also explained

that the clinical presentation for SFN would include stabbing, burning, palpitations,

dizziness, extreme fatigue, dry mouth, dry eyes, and dysmotility. (Id. at 92.)

Dr. Boylan reiterated her view that that “small fiber neuropathy is a form of GBS.”

(Tr. 77.) She relied on the article, Sensory Guillain Barré Syndrome and Related

Disorders: An Attempt at Systematization, to explain a proposal to classify this sensory

phenomenon into three subtypes under the umbrella of GBS: demyelinating

polyneuropathy that would be diagnosed on the basis of electrodiagnostic findings and

physical examination; “acute sensory large fiber axonopathy, ganglionopathy,” which

would also be diagnosed by electrodiagnostic study; and “acute sensory small fiber

neuropathy, ganglionopathy,” which would likely be characterized by normal

electrodiagnostic study. (Id. at 79-80 (citing Uncini & Yuki, supra, at Ex. 22, p. 1).) Dr.

Boylan also noted that the authors document “vaccine-induced neuropathy involving the

small fiber nerves.” (Id. at 81 (citing Uncini & Yuki, supra, at Ex. 22, p. 4).) However,

Dr. Boylan acknowledged that, unlike petitioner, these patients were ultimately

diagnosed though a biopsy. (Id.)

Dr. Boylan opined that vaccination, through the mechanism of molecular mimicry,

can cause SFN. (Tr. 82.) Although she acknowledged that there is not a consensus in

the scientific community as to how vaccines can cause SFN, Dr. Boylan asserts that

there is medical literature to support a theory of molecular mimicry between GBS and

Campylobacter jejuni. (Id. at 82-83.) She therefore suggested that it would be

“arbitrary” to classify small fibers “in a different category than the traditional . . . acute

motor axonal neuropathy and acute sensory axonal neuropathy variants.” (Id.) She

explained that there would need to be some homology between the vaccine and the

small fiber cells. (Id. at 85.) In addition, she opined that SFN can be immune mediated

and would therefore require an “immune system provocation” to trigger such response.

(Id. at 83-85.)

Dr. Boylan testified that, in her opinion, petitioner “has an autoimmune-mediated

small fiber neuropathy, isolated small fiber neuropathy, which is primarily but not

exclusively length dependent, caused by the vaccine or vaccines.” (Tr. 69.) She noted

that, prior to the subject vaccinations, petitioner “had a very striking autoimmune

22

response to a strep infection” and developed rheumatic fever, “one of the group A

streptococcal autoimmune conditions.” (Id. at 86-87.) Dr. Boylan opined that petitioner

had some genetic susceptibility to those conditions, making it more likely that he would

develop autoimmune disorders in the future. (Id. at 87-88.)

Dr. Boylan relied on petitioner’s medical records to explain his condition. (Tr.

92.) She testified that petitioner did not have any symptoms of peripheral neuropathy

during his July 28, 2014 appointment. (Id. at 92-93 (citing Ex. 2, pp. 9, 12-15).) She

noted that, during this appointment, petitioner received both the Hep B and Tdap

vaccines. (Id. at 94 (citing Ex. 2, p. 15).) She explained that, based on her review of

the records in this case, petitioner developed flu-like symptoms roughly 18 hours

following his vaccination. (Id. at 94-95.) Dr. Boylan explained that these symptoms

represent “signs that the inflammatory system has been activated.” (Id. at 95-96.)

However, she stated that petitioner’s neurological symptoms, including tingling and

numbness, then began two to three days after he received his vaccinations. (Id. at 96-

99 (citing Ex. 7, p. 4; Ex. 6, p. 2; Ex. 2, pp. 16-17, 19).) Dr. Boylan noted that

petitioner’s primary care physician then referred to him to a neurologist, Dr. Cholfin, who

documented petitioner’s symptoms as beginning after he received “the vaccinations.”

(Id. at 99-100.) She acknowledged Dr. Cholfin’s note there was no evidence of GBS,

and that petitioner’s symptoms were “subjective,” meaning “the patient feels it, but they

can’t find anything on exam.” (Id. at 100-01.) However, Dr. Boylan explained that the

neurologist did not test temperature, pinprick, or vibration, which implies that petitioner’s

paresthesias and numbness was more likely to be considered subjective. (Id. at 101-

02.) This complication in diagnosing SFN is supported by the medical literature

submitted by petitioner. (Id. at 102-03 (citing Oaklander & Nolano, supra, at Ex. 32).) In

addition, Dr. Boylan noted that petitioner’s symptoms continued to progress and

eventually petitioner began to suffer sensory loss. Accordingly, she suggests the

symptoms were not subjective and instead evidence of isolated small fiber neuropathy,

specifically an autoimmune mediated case. (Id. at 102 (citing Ex. 7, p. 12).)

Dr. Boylan later clarified that petitioner was, in fact, diagnosed with small fiber

neuropathy because his treating physician diagnosed neuropathy while noting that there

was no medium or large fiber neuropathy, which suggests he believed it was small fiber

neuropathy. Additionally, the treating physician proposed a “mechanism which could

damage small fibers, immune complex deposition.” (Tr. 110-11 (citing Ex. 2, p. 63).)

She explained that immune complex deposition is “when combinations of antibodies”

and “antigen deposits” get stuck to the vessel walls. (Id. at 111.) However, she

acknowledged that she is not an immunologist and could not further postulate on “an

endogenous antibody cross-reaction.” (Id.)

Dr. Boylan also addressed petitioner’s bloodwork. (Tr. 107-08 (citing Ex. 2, p.

62).) She noted that petitioner’s bloodwork showed an increase in ANA, which is

associated with a “rheumatologic and autoimmune disease.” (Id. at 108.) In addition,

petitioner’s bloodwork showed low complement protein C3, which is “part of the immune

inflammatory cascade” and can also suggest an autoimmune disease. (Id. at 108-09.)

23

Dr. Boylan opined that it is fair “to extrapolate medical literature and precedent

regarding what we know about the onset of immune-mediated GBS over to immune-

mediated small fiber neuropathy.” (Tr. 112.) She explained that the time course is

similar, and petitioner’s illness still followed the “expected trajectory in GBS,” despite a

latency of two days being “a little short.” (Id.) Dr. Boylan stated that she did not “see a

reason to exclude a small fiber variant” of GBS. (Id. at 112-13.) Dr. Boylan explained

that onset of symptoms can work on a bell curve, meaning that onset of 48 hours may

be fast for some patients while some outliers experience onset of symptoms even

faster. (Id. at 124.) She explained that an instantaneous response would not suggest

an autoimmune mediated phenomenon because that is too fast, however, 48 hours is

not outside of the realm of possibility. (Id. at 130-31.)

Although she indicated that she is unable to parse which of petitioner’s

vaccinations is causal, Dr. Boylan opined that it was “probably” the Hep B vaccine,

given the fact that hepatitis “is sometimes associated with a small fiber neuropathy.”

(Tr. 125.) She explained that this theory is based on medical literature that shows a

potential molecular connection between hepatitis and polyarteritis nodosa, which is a

“multisystemic disease” that is “one of the causes of a small fiber neuropathy.” (Id. at

128-29.)

f. Dr. Gelfand’s in court testimony

Dr. Gelfand testified at the hearing on behalf of respondent. (Tr. 143.) He began

his testimony by expressing his opinion that petitioner developed “an acute onset

sensory syndrome, and the evidence to support this is overwhelmingly clinical and

primarily based on the history without additional supporting diagnostics.” (Id.) He

acknowledged that petitioner did not have any diagnostic tests, “rather than tests that

were necessarily done and negative.” (Id. at 143-44.)

Dr. Gelfand defined small fiber neuropathy as an “impairment of small fiber

nerves,” which are “either thinly myelinated or unmyelinated small fiber nerves that

primarily involve sensation of pain, temperature, and those sensory functions.” (Tr.

144.) He explained that there are many causes of SFN, including diabetes, alcohol use,

infections, medications, genetics, and autoimmune conditions. (Id. at 146-147.) When

the cause cannot be determined, the SFN is referred to as idiopathic. (Id. at 147.)

Specifically, Dr. Gelfand opined that there is no evidence either the Hep B or Tdap

vaccine can cause SFN. (Id. at 149, 153.) However, Dr. Gelfand noted that “literature

establishes associations between several autoimmune conditions” and SFN. (Id. at

150-51.) He later admitted that the Hep B virus “is associated and probably causative

with certain kinds of peripheral neuropathy, in particular, polyneuropathy, meaning

there’s a component of large fiber neuropathy, including sometimes this association with

vasculitis type processes.” (Id. at 161.) Specifically, he explained that, while there can

be small fiber components “with large fiber polyneuropathies,” the relationship between

Hep B and SFN is “not as clear or established of an association.” (Id. at 162.) Dr.

Gelfand explained that there have been “antigenic features of the hepatitis B virus that

have been implicated as part of the immune response and proposed of the

24

pathogenesis.” (Id. at 163.) However, he noted that he does not recall the specific

literature concerning the surface antigen that is responsible for this association. (Id.)

Dr. Gelfand did admit that the Hep B vaccine uses parts of the hepatitis B virus “to

create this antigenic response.” (Id. at 164.)

Dr. Gelfand testified that he considers GBS and SFN to be distinct conditions.

(Tr. 147.) However, he acknowledged that there are analogies between the two “that

can be important.” (Id.) He explained that “an isolated small fiber neuropathy is not

established as a recognized stand-alone form” of GBS in the current medical literature.

(Id. at 148.) Dr. Gelfand noted that “the literature postulates whether there can be

immune causes of an isolated small fiber neuropathy” and that some of the literature

proposes that SFN be considered “an atypical variant” of GBS. (Id. at 148, 172.) Dr.

Gelfand explained, “I think that can be considered as its own etiologic or

pathophysiologic entity, and as sort of separate from what is established about classic

[GBS].” (Id. at 148.) He also agreed that SFN can be immune mediated. (Id. at 172-

73.)

Dr. Gelfand noted that petitioner never underwent a skin biopsy or QSART

testing. 7 (Tr. 149-50.) He opined that this is significant because, “[t]o diagnose small

fiber neuropathy, there needs to be a very strong clinical history, correlated with

physical examination, and then additional investigations to support what patterns of

nerves are involved.” (Id.) Although he admitted these tests are not necessary for

diagnosis, Dr. Gelfand emphasized that they “increase the confidence in diagnosis.”

(Id. at 150.) He agreed with petitioner’s expert that a normal nerve conduction study

simply means there is “no evidence of a large fiber neuropathy,” and that “[i]n routine

clinical practice, small fiber neuropathy is often diagnosed in some form based on

clinical history.” (Id. at 165-66; 168.) He also agreed that “[i]n routine clinical practice,

skin biopsies are not commonly ordered.” (Id. at 167.) He explained that petitioner’s

“neurologic examinations did not demonstrate evidence of weakness nor was there any

clear evidence of impairment of motor function.” (Id. at 151.) All of petitioner’s

“[r]eflexes were documented as normal.” (Id.) In addition, there is “no evidence of an

upper motor neuron pattern of involvement to suggest a central nervous system

localization.” (Id. at 152.) Dr. Gelfand did not explicitly opine as to petitioner’s

diagnosis; however, he explained, “I believe that a small fiber neuropathy is a

reasonable phenotypic consideration and is possible, but with the data and available

evidence, I cannot give a more specific diagnosis or support a diagnosis to a

reasonable degree of medical certainty.” (Id.) He later agreed that petitioner’s treating

physician did document sensory symptoms and that “small fiber neuropathy is a

reasonable but unconfirmed working diagnosis.” (Id. 156-57, 187-89.) Dr. Gelfand also

admitted that petitioner’s treating physician did describe his symptoms as a “vaccine

reaction.” (Id. at 190.)

7 Dr. Gelfand explained that QSART is a type of testing that analyzes automatic functions of the nervous

system and examine responses. (Tr. 150.) He acknowledged that the availability of this form of testing is

limited to “a few specialized centers.” (Id.) As such, Dr. Gelfand suggested that small fiber skin biopsy is

the form of testing that would be “most accessible to patients.” (Id.)

25

Dr. Gelfand also addressed the time frame proposed by petitioner’s expert. (Tr.

153.) He opined that there are two time frames: the first involved petitioner’s fever and

aching, which began 18 hours after vaccination; and the second is the sensory

syndrome that started about 48 hours after vaccination. (Id. at 153-54.) He opined that

an onset of 48 hours is plausible in some contexts, but the plausibility depends on the

time it takes for an immune response to form and cause a reaction. (Id. at 159-60.) He

also opined that, “[i]n general, it takes several days for an immune-mediated process,”

and that onset “somewhere between 72 hours to five days would be common in the

literature.” (Id. at 174-75.) Dr. Gelfand agreed that immune mediated SFN would

require some sort of immune response. (Id. at 181-82.) He further agreed that

petitioner’s symptoms that developed 18 hours after vaccination were evidence of a

“systemic inflammatory response.” (Id. at 182.)

V. Discussion

a. Althen prong one

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) (quoting

Pafford v. Sec’y of Health & Human Servs., No. 01-0165V, 2004 WL 1717359, at *4

(Fed. Cl. Spec. Mstr. July 16, 2004)). To satisfy this prong, petitioner’s theory must be

based on a “sound and reliable medical or scientific explanation.” Knudsen, 35 F.3d at

548. Such a theory must only be “legally probable, not medically or scientifically

certain.” Id. at 548-49. However, petitioners may satisfy the first Althen prong without

resort to medical literature, epidemiological studies, demonstration of a specific

mechanism, or a generally accepted medical theory. Andreu ex rel. Andreu v. Sec’y of

Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano v.

Sec’y of Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). Scientific

evidence offered to establish Althen prong one is viewed “not through the lens of the

laboratorian, but instead from the vantage point of the Vaccine Act's preponderant

evidence standard.” Id. at 1380.

Petitioner argues that GBS should be considered a “global neuropathy,” instead

of only a large fiber neuropathy, and, therefore, SFN should be considered a form of

GBS. (ECF No. 81 (citing Pan et al., supra, at Ex. 17; Seneviratne & Gunasekera,

supra, at Ex. 20; Yuki et al., supra, at Ex. 21; Unciini & Yuki, supra, at Ex. 22).) Dr.

Boylan submits that, because SFN is a form of GBS, the medical theories that underlie

the connections between GBS and vaccines, such as molecular mimicry, can be applied

here. (Tr. 82.) Specifically, petitioner notes that respondent’s expert has acknowledged

that, like GBS, SFN can be immune mediated. (Tr. 7; 160.) Petitioner cites a case in

which the special master accepted SFN as a GBS variant that affects small fibers.

(ECF No. 81, pp. 23-25 (discussing Swaiss v. Secretary of Health & Human Services,

No. 15-286V, 2019 WL 6520791 (Fed. Cl. Spec. Mstr. Nov. 4, 2019)). Additionally, the

special master concluded that SFN could be immune mediated and, therefore, there

was enough evidence to support the conclusion that the Tdap vaccine can cause SFN,

26

as a variant of GBS. (Id.) Dr. Boylan asserts that petitioner’s history of autoimmune

disorders made him more vulnerable to an immune mediated reaction to the

vaccination. (Ex. 10, pp. 6-9; Ex. 29, p. 2.)

Respondent disagrees. Instead, he argues, that petitioner “did not offer a theory

of causation that explained how the Tdap and/or Hep B vaccines can cause petitioner’s

alleged SFN.” (ECF No. 83, p. 18.) He further asserts that there is “no evidence to

support for Dr. Boylan’s opinion that the Hep B and Tdap vaccines could have caused

GBS, particularly a small fiber variant of GBS.” (Id. at 19 (citing Ex. C, p. 9).) In support

of this conclusion, respondent points to a 2012 IOM report that “concluded that the

‘epidemiological evidence is insufficient or absent to assess an association between

hepatitis B vaccine and GBS. . . . The evidence is inadequate to accept or reject a

causal relationship between hepatitis B vaccine and GBS.’” (Id. at 19-20 (quoting 2012

IOM Report).) Respondent contends that petitioner’s theory in this case is “too

generalized” to pertain to this specific case and, therefore, petitioner has failed to carry

his burden as to Althen prong one. (Id. at 20 (citing W.C. v. Sec’y of Health & Human

Servs., 704 F.3d 1352, 1360 (Fed. Cir. 2013).)

I have previously accepted that the sensory variant of GBS can be caused by flu

vaccination. See Goforth v. Sec’y of Health & Human Servs., No. 14-1128V, 2021 WL

6337672 (Fed. Cl. Spec. Mstr. Nov. 19, 2021). However, I have also previously found

that the causes of GBS standing alone are not informative of the cause(s) of SFN.

McGill v. Sec’y of Health & Human Servs., No. 15-1485V, 2023 WL 3813524, at *26-27

(Fed. Cl. Spec. Mstr. May 11, 2023.) The McGill petitioner had a presentation that

included SFN arising in the context of preexisting rheumatoid arthritis. Id. at *31-33.

Especially in that context, the multitude of causes of SFN, including a strong association

with rheumatic autoimmune conditions, coupled with the multitude of causes and

variants of GBS, confounded petitioner’s attempt to rely on analogy to GBS as the

primary support for her theory of causation. The literature filed in that case indicated

that only a subset of SFN presentations result from tissue-specific dysimmunity that

could potentially be compared to GBS. Id. at *26. In this case, both parties’ experts

have provided testimony that accords with that analysis. (Tr. 144-47 (Dr. Gelfand

explaining the list of causes of SFN is “very long” and includes a “wide range of

injuries”); Tr. 69-70 (Dr. Boylan discussing different forms of GBS with differing nerve

involvement); Tr. 87, 147 (both experts discussing causal relationship between

autoimmune rheumatic conditions and SFN).) In fact, Dr. Gelfand was also

respondent’s neurology expert in the McGill case.

Here, however, Dr. Boylan has specifically explained, not only that an acute

onset suggests an immunologically mediated event, but further that petitioner’s own

SFN fits the acute, monophasic pattern otherwise seen in GBS. (Id. at 88, 112-13.) Dr.

Gelfand likewise acknowledges the importance of this distinction in assessing the

strength of any analogy to GBS and agrees that petitioner’s condition was monophasic

and reached a nadir within days to weeks. (Id. at 147-48 (indicating that analogy

between GBS and SFN can be “important” but stressing the monophasic inflammatory

27

process targeting antigens in the peripheral (large fiber) nerves involved in GBS); Ex. C,

p. 7.)

Though Dr. Gelfand stresses that he would maintain the distinction between SFN

and GBS, he agrees on this record that, while SFN does not fall under the umbrella of

classic GBS, analogy with respect to the immune causes of GBS may be reasonable

and there may be similarities between the causes of GBS and SFN. (Tr. 173.) He

suggested that there is at least some degree to which the distinction is semantic. (Id. at

147-48, 172.) Regardless of the analogy, Dr. Gelfand agrees that infectious and

immune causes are among the proposed causes of SFN. (Id. at 146-47.) Both experts

also agreed that large fiber polyneuropathies can include small fiber components. (Id.

at 133; 162.) In that regard, Dr. Boylan opined that it is “arbitrary” to separate cases

with only small fiber involvement from “traditional” or large fiber involved neuropathies

when determining what pathogenic antibodies may be involved or what may trigger

those antibodies. (Id. at 82-83.) On this record, that opinion is effectively unrebutted,

despite Dr. Gelfand repeatedly noting the distinction between large and small fiber

involvement more generally. 8

Further to that, both experts agree that the hepatitis B virus can cause peripheral

neuropathies, most notably a demyelinating large fiber polyneuropathy known as

polyarteritis nodosa, but also acute large fiber polyneuropathies more generally. (Ex.

10, p. 3; Tr. 128; 161.) Polyarteritis nodosa is a multisystemic disease, but it is also

known to cause SFN. (Tr. 129.) Dr. Gelfand maintains that hepatitis B-related

polyneuropathies are a distinct clinical syndrome from GBS with separate supporting

associational evidence, but agreed they would share a similar immune mediated

mechanism. (Id. at 162; 173.) He acknowledged that GBS is a form of acute

inflammatory polyneuropathy for which the hepatitis B virus could be a “possible” but

“not well established” infectious cause. (Id. at 163.) He agreed that antigenic features

of the hepatitis B virus are implicated in the immune response pathogenic for

polyneuropathies. (Id.) Thus, Dr. Boylan opines that molecular mimicry, which has

otherwise been implicated with respect to GBS, is also a likely explanation for the

causal connection between the hepatitis B virus and peripheral neuropathies. Further,

she opines that this also supports molecular mimicry between the hepatitis B surface

antigen contained in the Hep B vaccine and the peripheral nerves as a cause of SFN.

(Id. at 133; 162-64.) Dr. Boylan explained that extrapolating from hepatitis B-induced

peripheral neuropathies is reasonable because molecular mimicry works like a lock and

key. (Id. at 133.) Where the same proteins and structures are at issue, the fit between

the lock and key will be the same. (See id.) Although Dr. Gelfand does not agree that

8 One factor discussed in McGill is that the small fibers are largely unmyelinated whereas myelin is often

identified as the key target of GBS injury when seeking to implicate vaccination as a cause. 2023 WL

3813524, at *30. The most commonly discussed form of GBS is acute inflammatory demyelinating

polyneuropathy. (Tr. 70.) However, as both experts indicated in this case, some of the small fibers are

lightly myelinated. (Id. at 61, 144.) Accordingly, the distinction is not necessarily dispositive on its own.

Moreover, when specifically asked about cross-reaction between campylobacter antigen (a known cause

of GBS) and myelin tissue, Dr. Gelfand was careful not to limit his response to myelin specifically, noting

that “different antigens have been identified and postulated within the spectrum of Guillain-Barre

syndrome, you know, depending on whether it’s myelin or axonal or others.” (Tr. 181.)

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the Hep B vaccine is a recognized cause of SFN, he acknowledged that the Hep B

vaccine uses “parts of the virus” to create an antigenic response and demurred on any

further specifics. (Id. at 149, 164.) Therefore, Dr. Boylan has provided largely

unrebutted expert testimony opining that hepatitis B surface antigen, as contained within

the Hep B vaccine, can cause peripheral neuropathies, including SFN.

In light of all of the above, I find Dr. Boylan’s theory of causation to be sound and

reliable within the context of this record. Therefore, petitioner has preponderantly

established that the Hep B vaccine can cause SFN. This is not necessarily surprising

given that prior cases have concluded that the Hep B vaccine can cause both GBS and

SFN. See, e.g., Shaw v. Sec’y of Health & Human Servs., No. 01-0707V, 2013 WL

2897425, at *15-16 (Fed. Cl. Spec. Mstr. May 24, 2013) (accepting that the Hep B

vaccine can cause SFN via molecular mimicry despite a lack of direct evidence); Peugh

v. Sec’y of Health & Human Servs., No. 99-638V, 2007 WL 1531666 (Fed Cl. Spec.

Mstr. May 8, 2007) (finding as part of the “Hepatitis B-Neurological Demyelinating

Omnibus Proceeding” that the Hep B vaccine can cause GBS).

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 v.

Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). In establishing

that a vaccine “did cause” injury, the opinions and views of the injured party’s treating

physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d

at 1326 (explaining 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’” (alteration in original) (quoting Althen, 418 F.3d at 1280)). Medical

records are generally viewed as particularly trustworthy evidence because they are

created contemporaneously with the treatment of the patient. Cucuras v. Sec’y of

Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

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 § 300aa-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 ex rel. Snyder v. Sec’y of Health &

Human Servs., 88 Fed. Cl. 706, 745 n.67 (2009) (explaining “there is nothing . . . that

mandates that the testimony of a treating physician is sacrosanct—that it must be

accepted in its entirety and cannot be rebutted”). As with expert testimony offered to

establish a theory of causation, the opinions or diagnoses of treating physicians are only

as trustworthy as the reasonableness of their suppositions or bases. The views of

treating physicians should also be weighed against other, contrary evidence also

present in the record, including conflicting opinions among such individuals. Hibbard v.

Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011) (concluding that it is not

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arbitrary or capricious for a special master to weigh competing treating physicians’

conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y

of Health & Human Servs., 100 Fed. Cl. 119, 136-37 (2011), aff’d, 463 Fed. App’x 932

(Fed. Cir. 2012); Veryzer v. Sec’y of Health & Human Servs., No. 06-522V, 2011 WL

1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), motion for review denied, 100

Fed. Cl. 344 (2011), aff’d per curiam sub nom. Veryzer v. United States, 475 Fed. App’x

765 (Fed. Cir. 2012).

Respondent raises two challenges to petitioner’s claim under Althen prong two.

(ECF No. 83, pp. 20-23.) First, respondent contends that petitioner did not actually

suffer SFN. (Id. at 21-22.) And, second, the treating physician opinions in the case

were limited to noting a temporal association and “none of petitioner’s treating

physicians could explain how the vaccinations can cause the symptoms alleged by

petitioner.” 9 (Id.) Ultimately, neither argument is persuasive.

During the hearing, both experts agreed that petitioner’s treating physician

diagnosed him with SFN. (Tr. 110-11; 189-90 (citing Ex. 2, p. 63).) In addition, both

experts ultimately agreed that a biopsy is not necessary to diagnosis someone with

SFN. 10 (Id. at 67-68; 150.) Both experts also agree that SFN will not show up on nerve

conduction studies because these only show large nerve dysfunction. (Id. at 89-90;

165-66, 168-69.) Ultimately, Dr. Gelfand agreed on respondent’s behalf that petitioner

experienced a sensory syndrome with neuropathic features for which SFN is a

“possible” diagnosis or a reasonable, but unconfirmed, working diagnosis. (Tr. 152,

156-57.) Considering the record as a whole, including the treating physician’s

diagnosis, Dr. Boylan’s opinion affirmatively endorsing the SFN diagnosis, and Dr.

Gefland’s more tentative partial agreement, I conclude that there is preponderant

evidence that petitioner suffered SFN.

Further to this, petitioner experienced an acute, post-vaccination reaction that

included fever, headache, and muscle and joint aches. (Ex. 7, p. 3.) On respondent’s

behalf, Dr. Gelfand agreed that this is evidence of a systemic inflammatory reaction.

(Tr. 182.) In that regard, petitioner’s treating neurologist, Dr. Cholfin, accepted that

petitioner suffered a vaccine reaction leading to paresthesia. (Ex. 2, p. 25.) Dr. Boylan

also noted that petitioner’s bloodwork showed an increase in ANA, which in isolation

would be inconsequential, however, when it is associated with a history of autoimmune

conditions, is evidence of an ongoing autoimmune response. (Tr. 108 (citing Ex. 2, p.

62).) In addition, petitioner’s bloodwork showed low complement protein C3 which is

“part of the immune inflammatory cascade,” and can also suggest an autoimmune

disease. (Id. at 108-09.) In fact, respondent himself distinguishes petitioner’s initial

presentation from the typical, months-to-years development of SFN. (ECF No. 83, p.

21.)

9 Part of respondent’s argument, to be sure, is the timing of onset. (ECF No. 83, pp. 21-22.) However,

this is addressed separately under Althen prong three.

10 A biopsy is the gold standard for diagnosing SFN, however that does not mean it is absolutely required

to diagnose SFN in all cases. (Gibbons, supra, at Ex. 16, p. 5.) In addition, “history and examination” are

important diagnostic tools. (Id. at 2.)

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Petitioner’s treating physicians repeatedly characterized his symptoms as a

vaccine injury throughout his treatment and noted a suspected “immune complex

deposition as reaction to vaccine.” (Ex. 2, pp. 49, 53, 61-62.) While respondent

challenged the value of this explanation in his prehearing brief (ECF No. 83, p. 22),

petitioner’s expert, Dr. Boylan, confirmed during the hearing that the immune complex

deposition cited by the treating physicians is consistent with both the accepted

mechanisms of causation for SFN (Tr. 110-12) and the mechanism by which the

hepatitis B antigen is understood to cause peripheral neuropathy in the form of

polyarteritis nodosa (Tr. 128-30), though immune complex deposition is not her own

theory of causation. Dr. Gelfand likewise identified “vasculitis type processes” as

“sometimes” present among the different immunologic causes of polyneuropathy. (Tr.

161-62.) Petitioner’s medical records also confirm that his physicians considered, but

rejected, the possibility that petitioner’s neuropathic symptoms were related to the type

of rheumatic conditions that can otherwise be associated with SFN. (Ex. 2, pp. 19, 49.)

In fact, this is a point stressed by respondent. (ECF No. 83, p. 22 (asserting that

petitioner “did not have other known common causes of small fiber neuropathy”).)

Thus, I do not agree that the treating physicians’ causal opinions were limited to noting

temporality.

For the reasons discussed above, petitioner has preponderantly established that

there is a logical sequence of cause and effect between his vaccination and his SFN.

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 1278. That term

has been equated to the phrase “medically-acceptable temporal relationship.” Id. at

1281. A petitioner must offer “preponderant proof that the onset of symptoms occurred

within a time frame for which, given the medical understanding of the disorder’s

etiology, it is medically acceptable to infer causation-in-fact.” de Bazan v. Sec’y of

Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for

what is a medically acceptable time frame must also 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); Koehn v.

Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877, at *26 (Fed. Cl.

Spec. Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

Petitioner’s testimony and medical records support the conclusion that

petitioner’s sensory symptoms developed 48 hours after he received his vaccinations.

Petitioner received his Hep B and Tdap vaccines on Monday, July 28, 2014. (Ex. 1.)

On July 31, 2014, petitioner called his doctor and complained that he had developed flu-

like symptoms and that he was feeling generally lethargic and had no energy. (Ex. 6, p.

2.) Petitioner explained that he had felt numbness in his hands since Tuesday and that

believed he was experiencing an autoimmune reaction to the Hep B vaccine. (Id.)

Later that same day, petitioner returned a call to Dr. Kim-Hwang and indicated that his

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fever had resolved, but he still felt “generalized lethargy / low energy.” (Id.) On August

1, 2014, petitioner presented to Dr. Kim-Hwang for an urgent care visit. (Ex. 2, pp. 16-

17.) Petitioner explained that he had developed a fever one day after receiving his

vaccinations, and then he had developed numbness and tingling on his left side. (Id.)

Finally, on August 4, 2014, petitioner presented to neurologist Dr. Cholfin. (Ex. 2, p.

20.) Dr. Cholfin also noted that petitioner developed flu-like symptoms one day after

receiving the vaccines. (Id.) He described that petitioner’s fever broke the following day

and, soon after, petitioner developed numbness and tingling in his hands and feet. (Id.)

Petitioner clarified this timeline at the hearing by explaining that his flu-like symptoms

developed one day after he received the vaccines, and his sensory symptoms began

when his fever broke very early (between 4:00 AM and 5:00 AM) Wednesday morning.

(Tr. 21.)

Dr. Boylan opined that the onset timeline for GBS could be used as the onset

timeline for SFN. (Ex. 10, p. 3.) She noted that there was usually a delay in post

vaccine related neurological syndromes “because the immune response system is a

complex cascade involving many different cells and chemical messengers.” (Id.)

During her testimony, Dr. Boylan explained that 48 hours was quick for a vaccine

induced neurological reaction, but “biology tends to work in bell curves,” meaning that

there may be outliers who experience reactions faster than one would normally

associate with a vaccine reaction. (Tr. 124.) She acknowledged that there is a cut off

on the left side of the bell curve and that instantaneous reactions would not support an

autoimmune mediated response; however, she opined that 48 hours was not an

unreasonable timeline. (Id. at 130-31.) For example, among the series of post-

vaccination SFN cases reported by Souayah et al., two had onset occurring within 24

hours of vaccination. (Souayah et al., supra, at Ex. 25, p. 3.) Petitioner’s own primary

care physician, Dr. Kim-Hwang, initially considered whether petitioner might have had

GBS and, in weighing that possibility, felt that the timing of onset was “atypical” but “not

impossible.” (Ex. 2, p. 19.)

Dr. Gelfand did not necessarily disagree with Dr. Boylan. He noted that there are

two different time frames in this case: the first involves petitioner developing flu-like

symptoms within 18 hours and the second involves petitioner developing sensory

symptoms within 48 hours. (ECF No. 83, p. 24 (citing Ex. H, p. 3); Tr. 153-54.) He

opined that, while “48 hours or less is very quick for traditional adaptive immune

responses,” he acknowledged that where exactly the line is drawn is somewhat

arbitrary. (Tr. 159-60.) He opined that, with what little is known about small fiber

neuropathies, he could not explicitly state the appropriate temporal association, though

he did explain that between 72 hours and 42 days would not be unreasonable. (Id. at

160.) He opined that all that matters is that there is enough “time for an immune

response to form.” (Id.) However, even when asked directly, at no point did Dr. Gelfand

opine that 48 hour falls below that threshold. Instead, he stated that a cut-off

“somewhere around three days is reasonable” and disclaimed any opinion that a 48-

hour onset is impossible. (Tr. 174-75.)

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The Federal Circuit has cautioned against using “hard and fast” deadlines

between vaccination and onset of symptoms. Paluck v. Sec’y of Health & Human

Servs., 786 F.3d 1373, 1383 (Fed. Cir. 2015). In light of all of the above, petitioner has

shown by preponderant evidence that there was a proximate temporal relationship

between his vaccination and development of SFN.

d. Factor unrelated to vaccination

Once petitioner has satisfied his own burden pursuant under the Althen test, the

burden shifts to respondent to demonstrate that petitioner’s injury was caused by factors

unrelated to vaccination. § 300aa-13(a)(1)(B); Deribeaux ex rel. Deribeaux v. Sec’y of

Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013). In this case, Dr.

Gelfand confirmed during the hearing that he is not proposing any alternative

explanation for petitioner’s condition. (Tr. 171-72.)

VI. Conclusion

Accordingly, for all the reasons described above, I find that petitioner is entitled to

compensation. Specifically, I find that petitioner has established by preponderant

evidence that he developed small fiber neuropathy as a result of his hepatitis B

vaccination. A separate damages order will be issued.

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

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