VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-00989
Package ID: USCOURTS-cofc-1_17-vv-00989
Petitioner: Jason Quirino
Filed: 2017-07-17
Decided: 2024-01-12
Vaccine: Hepatitis B
Vaccination date: 2014-07-28
Condition: isolated small fiber neuropathy
Outcome: entitlement_granted_pending_damages
Award amount USD: 

AI-assisted case summary:
Jason Quirino, an adult, received Hepatitis B and Tdap vaccines on July 28, 2014. Within approximately 18-48 hours, he developed flu-like symptoms, followed by numbness, tingling, and fatigue in his hands and feet. He was diagnosed with an atypical form of Guillain-Barré Syndrome (GBS) manifesting as an isolated small fiber neuropathy (SFN). Quirino submitted medical records and expert testimony from Dr. Laura Boylan, who opined that the vaccines caused his SFN, potentially through molecular mimicry, and that SFN can be considered a variant of GBS. The respondent's expert, Dr. Jeffrey Gelfand, acknowledged that SFN is a possible diagnosis and that the vaccines could be immune-mediated but argued that the evidence did not meet the "more likely than not" standard for causation and that SFN is distinct from GBS. The court found that Quirino established a medical theory connecting the Hepatitis B vaccine to SFN, a logical sequence of cause and effect supported by his medical records and expert testimony, and a proximate temporal relationship between vaccination and symptom onset. The court concluded that Quirino is entitled to compensation for his small fiber neuropathy, with damages to be determined in a separate order.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-00989-2
Date issued/filed: 2024-01-12
Pages: 33
Docket text: PUBLIC ORDER/RULING (Originally filed: 12/18/2023) regarding 96 Ruling on Entitlement. Signed by Special Master Daniel T. Horner. (ksb) Service on parties made.
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Case 1:17-vv-00989-UNJ Document 98 Filed 01/12/24 Page 1 of 33
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 ENTITLEMENT1
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.
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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).
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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
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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.
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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
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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
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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.)
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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.)
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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
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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 deposition4 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.,
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“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)).)
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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.)
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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,
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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.)
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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.)
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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.)
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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.)
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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.)
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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.
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(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
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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
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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
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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.)
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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
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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.)
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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,
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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
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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
33

================================================================================
DOCUMENT 2: USCOURTS-cofc-1_17-vv-00989-3
Date issued/filed: 2025-02-04
Pages: 12
Docket text: PUBLIC DECISION (Originally filed: 1/8/2025) regarding 112 DECISION AWARDING DAMAGES. Signed by Special Master Daniel T. Horner. (cd) Service on parties made.
--------------------------------------------------------------------------------
Case 1:17-vv-00989-UNJ Document 116 Filed 02/04/25 Page 1 of 12
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-989V
Filed: January 8, 2025
Special Master Horner
JASON QUIRINO,
Petitioner,
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Andrew Donald Downing, Downing, Allison & Jorgenson, Phoenix, AZ, for petitioner.
Mitchell Jones, U.S. Department of Justice, Washington, DC, for respondent.
DECISION AWARDING DAMAGES1
On July 21, 2017, petitioner filed a petition under the National Childhood Vaccine
Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging that he suffered “a
rheumatologic injury” as a result of Hepatitis B (“Hep B”) and Tetanus-Diphtheria-
acellular-Pertussis (“Tdap”) vaccinations that he received on July 28, 2014. (ECF No. 1;
ECF No. 35.) Petitioner later amended his petition to allege he suffered from isolated
small fiber neuropathy, an atypical form of Guillain-Barré Syndrome (“GBS”). (ECF No.
53.) In December of 2023, I issued a Ruling on Entitlement finding petitioner entitled to
compensation. (ECF No. 96; see also No. 17-989V, 2023 WL 9229145 (Fed. Cl. Spec.
Mstr. Dec. 18, 2023).) For the reasons discussed below, I now conclude petitioner is
entitled to an award of $130,000.00 in compensation for actual pain and suffering.
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, et seq.
1

Case 1:17-vv-00989-UNJ Document 116 Filed 02/04/25 Page 2 of 12
I. Procedural History
After the Ruling on Entitlement3 was issued in this case, petitioner presented a
demand for damages to respondent on January 16, 2024. (ECF No. 99.) Respondent
did not present a counteroffer until about nine months later, on September 13, 2024.
(ECF No. 106.) At that time, petitioner reported that the parties were likely too far apart
in their valuation of damages to resolve the case informally, especially given the delay
in receiving respondent’s counteroffer. (Id.) Petitioner requested the undersigned
resolve damages based on the parties’ briefing. (Id.) Accordingly, the parties were
directed to submit briefing on the appropriate amount of damages. Petitioner filed a
brief on damages on October 1, 2024. (ECF No. 107.) Respondent filed a response on
November 7, 2024. (ECF No. 109.) Petitioner then filed a reply on November 21, 2024.
(ECF No. 110.) This matter is now ripe for resolution.
II. Factual History
a. Medical records4
On July 28, 2014, at an annual appointment with his primary care physician, Dr.
Judy Kim-Hwang, petitioner received the vaccines at issue in this case. (Ex. 1; Ex. 2, p.
15.) The day after receiving the vaccines, petitioner messaged his primary care
physician and reported that he developed flu-like symptoms, including fever, headache,
and muscle and joint aches, about eighteen hours after receiving his vaccinations. (Ex.
7, p. 3.) On July 31, 2014, petitioner called Dr. Kim-Hwang to report numbness in his
bilateral hands and above the wrist. (Ex. 6, p. 2.) The next day, on August 1, 2014,
petitioner reported “numbness/dull sensation” over his left neck area. (Id. at 3.) That
same day, petitioner had a follow up appointment with Dr. Kim-Hwang, during which he
reported that one day after receiving the vaccines at issue in this case, he developed a
fever, malaise/myalgias, fatigue, and numbness/tingling in his left upper extremities and
on the side of his neck. (Ex. 2, pp. 16-17.) At the time of the appointment, his fever and
myalgias had subsided; however, the numbness and tingling had continued
intermittently in his upper extremities and feet. (Id.) Petitioner’s neurological exam was
normal. (Id. at 18.)
Petitioner saw neurologist Dr. Jeremy Cholfin on August 4, 2014, and elaborated
on his symptoms. (Ex. 2, p. 20.) He described a hot, itchy, and “pins and needles”
sensation in his hands and feet. (Id.) It was noted that he had “normal sensations” and
“more of a subjective sense of numbness,” but “[n]o frank numbness.” (Id.) His
neurological exam was normal, and he was prescribed gabapentin. (Id. at 22-23, 25.)
Dr. Cholfin opined that petitioner was suffering from a “mild vaccine reaction with
subjective parathesias/numbness,” but there were no signs of GBS or multiple sclerosis.
(Id. at 25.) Petitioner called Dr. Kim-Hwang’s office on August 6, 2014, and reported
3 The procedural history leading to the Ruling on Entitlement is included within that ruling.
4 The medical records summarized here focus on those records relevant to the determination of
damages. A more detailed summary of the medical records is included in the Ruling on Entitlement.
2

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that his intermittent numbness had continued. (Ex. 6, p. 3.) Petitioner requested an
additional appointment and an MRI. (Id.) Petitioner presented to Dr. Kim-Hwang later
on August 6, 2014, and described his consultation with Dr. Cholfin two days earlier. (Id.
at 26.) Petitioner’s labs at this visit were normal. (Id. at 160-66.)
Petitioner had a follow up appointment with Dr. Cholfin on August 12, 2014,
during which he reported general fatigue and numbness/tingling in his bilateral fingers
and toes, as well as in his lips, tongue, and neck. (Ex. 2, p. 31.) Dr. Cholfin ordered
MRIs of the brain and cervical spine, which petitioner underwent on August 21, 2014.
(Id. at 34, 37-38, 228-29.) The MRIs revealed no abnormal enhancement. (Id. at 37-
38, 229.) Petitioner had his next follow up appointment with Dr. Cholfin on August 25,
2014; however, he still reported a numbness, tightness, and “deadening feeling” in his
arms, hands, and feet. (Id. at 35.) Additionally, he described a burning sensation, but
noted that it has decreased. (Id.) Petitioner also reported taking gabapentin. (Id.)
Petitioner’s bloodwork revealed he was ANA positive. (Id. at 172.)
On September 4, 2014, petitioner underwent a nerve conduction study and had a
follow up appointment with Dr. Cholfin. (Ex. 2, pp. 39, 267.) He reported that his
symptoms remained the same and that he was still experiencing significant numbness
in his fingers and feet. (Id. at 39-40.) He explained that he had taken gabapentin twice,
but felt sleepy and did not feel like he needed it. (Id.) Petitioner’s neurological exam
revealed a subjective decrease in sensation in his bilateral fingers and toes. (Id. at 43.)
Dr. Cholfin noted that petitioner’s condition was “stable to slightly improved.” (Id.) Dr.
Cholfin also noted that there was no evidence of medium to large fiber neuropathy on
petitioner’s nerve conduction study. (Id.)
Petitioner began seeing rheumatologist Geraldine Navarro, M.D., on September
15, 2014. (Ex. 2, p. 44.) Petitioner reported that, within 24 hours after receiving the
vaccines at issue in this case, he developed chills and a fever. (Id. at 45.) Additionally,
he reported that he developed numbness and tingling in his extremities and the left side
of his neck at about the same time. (Id.) Petitioner noted that he still felt constant
tightness and tingling “over his hand and feet.” (Id.) Petitioner also explained that he
developed a feeling like he was “coming off anesthetics” in his neck, lips, mouth, and
tongue. (Id.) Given petitioner’s positive ANA and unexplained paresthesia, Dr. Navarro
ordered a further workup. (Id. at 49.) Petitioner had a follow up appointment with Dr.
Navarro on September 22, 2014. (Id. at 50.) He reported continued numbness and
tingling in his fingers and toes; however, the burning sensation in his feet had resolved.
(Id. at 53.) Dr. Navarro noted that petitioner’s ANA was positive, but his workup was
otherwise unremarkable. (Id.) On October 17, 2014, petitioner underwent an MRI of
the pelvis to evaluate for sacroiliitis, which revealed “mild discogenic disease of the
lower lumbar spine.” (Id. at 231.)
Petitioner was seen at urgent care for an unrelated sore throat on November 24,
2014. (Ex. 2, p. 54.) Petitioner had a follow up with neurologist, Dr. Cholfin, on
December 5, 2014. (Id. at 58.) Petitioner reported continued numbness in his forearm,
hand, lips, tongue, and jaw area. (Id.) Additionally, he reported “heat in [his]
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hands/feet” every evening. (Id.) Dr. Cholfin noted that petitioner’s vaccine injury was
“stable to slightly improved.” (Id. at 62.) Dr. Cholfin reiterated that petitioner’s EMG
revealed no evidence of medium or large fiber neuropathy, that petitioner’s ANA was
slightly positive, and his C3 was mildly low. (Id.) Dr. Cholfin recommended that
petitioner undergo a glucose tolerance test “to rule out hyperglycemic component,”
encouraged petitioner to “exercise and [perform] dexterous activities such as guitar
playing,” and prescribed both magnesium oxide for petitioner’s paresthesias/tremors
and gabapentin as needed for neuropathic pain. (Id.) Petitioner was seen for an
unrelated cough on December 26, 2014. (Id. at 63.)
Petitioner was seen twice in May of 2015 for unrelated conditions. (Ex. 2, pp. 67-
72.) In January of 2016, petitioner began seeking treatment for back and shoulder pain.
(Id. at 72-75.) At his appointment on January 27, 2016 for back and shoulder pain,
petitioner reported a hotness and a “pins and needles” sensation in his hands and feet.
(Id. at 76.) He began physical therapy in February 2016 to treat his back and shoulder
pain. (Ex. 4, pp. 29-32.) He continued to seek this treatment through March of 2016.
(Id. at 13-28.) Petitioner was next seen on April 4, 2016 for an unrelated issue. (Ex. 2,
p. 80.) During this appointment, petitioner continued to report a “pins and needles”
sensation in his hands and feet due to neuropathy. (Id. at 81.)
Petitioner had an annual exam on June 14, 2016, during which he again reported
a “pins and needles” sensation. (Ex. 2, p. 85.) On December 20, 2016, petitioner had
an appointment for fatigue, rhinorrhea, cough, and an earache, during which his
neuropathy was not noted. (Id. at 92.) Petitioner was seen again for the same cough
on December 26, 2016, and again on January 17, 2017. (Id. at 95-101.) Petitioner’s
neuropathy was not mentioned during either of these appointments. (Id.) Petitioner
began seeing pulmonologist Malcolm Smith, M.D., on February 16, 2017, for his chronic
cough. (Id. at 101.) He did not report his neuropathy at this appointment. (Id. at 101-
05.) He continued to see Dr. Smith throughout the rest of 2017. (Id. at 110-18, 125-34;
Ex. 12, pp. 22-26.)
On June 19, 2017, petitioner had an annual exam, during which he reported that
he continued to experience hotness and a “pins and needles” sensation in his hands
and feet sometimes; however, “most days [he] doesn’t feel anything.” (Ex. 2, p. 119.)
In August, petitioner hurt his knee and was diagnosed with a posterior medial meniscus
tear, for which he underwent physical therapy until December 2017. (Id. at 134-38, 234-
36; Ex. 4, pp. 1-11; Ex. 12, pp. 11-14.) After December 2017, petitioner had two more
follow ups for his knee pain, one on February 26, 2018, and the final one on May 9,
2018. (Ex. 12, pp. 38-42, 136-40.) In September of 2017, petitioner began
experiencing an irregular heartbeat. (Ex. 7, p. 75.) Testing revealed no abnormalities.
(Ex. 12, pp. 81-128.) No additional medical records were filed in this case.
b. Testimony
Petitioner provided two affidavits and testified at an entitlement hearing in this
case in which he recounted his condition and the impact it has had on his life. (Exs. 5,
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8; Transcript of Proceedings (“Tr.”), at ECF No. 90.) Petitioner testified that, before
receiving the vaccines at issue in this case, he had no significant health problems. (Ex.
5, ¶ 3.) He testified that, within 24 hours after receiving the vaccines at issue in this
case, he developed flu-like symptoms. (Ex. 8, ¶ 2; Tr. 18-20.) He also experienced
“tingling and stinging sensations in [his] hands, arms, legs, feet, upper chest, neck and
face,” and “itching on the sides of [his] feet, as well as burning sensations in [his] feet
and hands.” (Ex. 5, ¶ 7.) Additionally, petitioner experienced fatigue, joint soreness,
and dry eyes and mouth. (Id.)
Petitioner testified that he is still experiencing symptoms to this day. (Ex. 5, ¶ 11;
Ex. 8, ¶ 4.) Specifically, petitioner noted that he still experiences numbness and
stinging in his “hands, arms, feet, legs, upper chest, neck and face,” and “extreme and
uncomfortable warmth in [his] hands and feet, especially when [he] tr[ies] to sleep.” (Ex.
5, ¶ 11.) Additionally, petitioner testified that his fatigue also continues to this day. (Tr.
35-36.) Petitioner acknowledged that between December 5, 2014, and January 6,
2016, he sought treatment for various other conditions and did not mention his
continued symptoms; however, he explained that, during these appointments, he was
there for different conditions and, given that his other doctors had failed to explain his
condition, he did not find it a pressing to mention these symptoms again. (Tr. 45-46,
49.) He explained that he felt like he just needed to cope with his symptoms and that
this was his new normal. (Id. at 49-50.)
Petitioner explained that his symptoms have had a substantial impact on his life
and have limited his ability to participate in certain activities. (Ex. 5, ¶ 10; Tr. 9-10.)
Specifically, he notes that the use of his hands has been limited. (Ex. 8, ¶ 5; Tr. 37-38.)
Additionally, the feeling in his feet has limited his ability to hike and jog. (Ex. 8, ¶ 6.)
Petitioner also explained that he continues to experience increased fatigue. (Id. ¶ 8.)
Petitioner’s other symptoms have subsided. (Id. ¶ 9.) Further, petitioner described the
significant mental toll this injury has taken. (Id. ¶ 11.)
III. Legal Standard
Compensation awarded pursuant to the Vaccine Act shall include “[f]or actual
and projected pain and suffering and emotional distress from the vaccine-related injury,
an award not to exceed $250,000.” § 300aa-15(a)(4). Additionally, a petitioner may
recover for unreimbursable expenses and loss of earning capacity. § 300aa-15(a)(1),
(3). In this case, however, petitioner requests only compensation for his pain and
suffering. (ECF Nos. 107, 110.) The petitioner bears the burden of proof with respect
to each element of compensation requested. Brewer v. Sec’y of Health & Human
Servs., No. 93-0092V, 1996 WL 147722, at *22-23 (Fed. Cl. Spec. Mstr. Mar. 18, 1996).
There is no mathematic formula for assigning a monetary value to a person’s
pain and suffering and emotional distress. I.D. v. Sec’y of Health & Human Servs., No.
04-1593V, 2013 WL 2448125, at *9 (Fed. Cl. Spec. Mstr. May 14, 2013) (reasoning that
“[a]wards for emotional distress are inherently subjective and cannot be determined by
using a mathematical formula”); Stansfield v. Sec’y of Health & Human Servs., No. 93-
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172V, 1996 WL 300594, at *3 (Fed. Cl. Spec. Mstr. May 22, 1996) (concluding that “the
assessment of pain and suffering is inherently a subjective evaluation”). In general,
factors to be considered when determining an award for pain and suffering include: 1)
awareness of the injury; 2) severity of the injury; and 3) duration of the suffering. I.D.,
2013 WL 2448125, at *9 (citing McAllister v. Sec’y of Health & Human Servs., No. 91-
1037V, 1993 WL 777030, at *3 (Fed. Cl. Spec. Mstr. Mar. 26, 1993), vacated and
remanded on other grounds, 70 F.3d 1240 (Fed. Cir. 1995)).
Special masters may also consider prior awards when determining what
constitutes an appropriate award of damages. See, e.g., Doe 34 v. Sec’y of Health &
Human Servs., 87 Fed. Cl. 758, 768 (2009) (finding that “there is nothing improper in
the chief special master’s decision to refer to damages for pain and suffering awarded in
other cases as an aid in determining the proper amount of damages in this case”);
Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 961 (Fed. Cir. 1993)
(explaining that Congress contemplated that special masters would use their
accumulated expertise in the field of vaccine injuries to judge the merits of individual
claims). However, while potentially persuasive, decisions regarding prior awards are
not binding. See Nance v. Sec’y of Health & Human Servs., No. 06-0730V, 2010 WL
3291896, at *8 (Fed. Cl. Spec. Mstr. July 30, 2010); Hanlon v. Sec’y of Health & Human
Servs., 40 Fed. Cl. 625, 630 (1998) (“Special masters are neither bound by their own
decisions nor by cases from the Court of Federal Claims, except, of course, in the same
case on remand.”), aff’d, 191 F.3d 1344 (Fed. Cir. 1999).
IV. Party Contentions
a. Petitioner’s motion
Petitioner requests $175,000.00 for past and ongoing pain and suffering. (ECF
No. 107, p. 11.) Petitioner explains that his pain and suffering has been significant and
continues to this day. (Id.) He encourages the court to “consider the nature of the
neurological injury coupled with the length of time the injury has persisted.” (Id. at 12.)
Additionally, petitioner encourages the court to “consider the procedural history of this
case, the delay in getting compensation to [petitioner], the severity of [petitioner’s]
injuries, and the fact that his injuries have persisted much longer than the stated
comparables in arriving at a damages number in this case.” (Id. at 13.) Petitioner cites
the following decisions as reflecting comparable facts: Coons v. Sec’y of Health &
Human Servs., No. 20-1067V, 2024 WL 4764001 (Fed. Cl. Spec. Mstr. Oct. 16, 2024)
(awarding $130,000.00 for pain and suffering based on a proffer)5; E.M. v. Sec’y of
Health & Human Servs., No. 14-753V, 2024 WL 844238 (Fed. Cl. Spec. Mstr. Feb. 13,
2024) (awarding $225,000.00 for pain and suffering based on a proffer); Drobbin v.
Sec’y of Health & Human Servs., No. 14-225V, 2023 WL 112268 (Fed. Cl. Spec. Mstr.
Jan. 5, 2023) (awarding $250,000.00 for pain and suffering based on a proffer); Dearing
v. Sec’y of Health & Human Servs., No. 14-289V, 2016 WL 3030148 (Fed. Cl. Spec.
Mstr. Mar. 11, 2016) (awarding $135,000.00 based on a stipulation); Rodrigues v. Sec’y
5 In his brief, petitioner misstates the amount awarded for pain and suffering in Coons as $135,000.00.
(ECF No. 107, p. 12.) The correct amount is $130,000.00.
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of Health & Human Servs., No. 21-1785V, 2024 WL 1434356 (Fed. Cl. Spec. Mstr. Mar.
5, 2024) (awarding $150,000.00 based on a stipulation).
b. Respondent’s response
Respondent proposes an award of $57,500.00 “as fair and reasonable
compensation for petitioner’s pain and suffering.” (ECF No. 109, p. 12.) He argues that
petitioner’s condition was “mild and limited.” (Id.) He explains that petitioner underwent
a “de-minimis course of care,” over a five-month period that included one course of
prescription medication. (Id. at 13.) During this time, petitioner was able to maintain an
active lifestyle. (Id.)
Respondent contends that the awards cited by petitioner are distinguishable from
the current case. (ECF No. 109, pp. 13-14.) Specifically, respondent notes that the
petitioners in Coons, E.M., and Drobbin suffered from the residual effects of their
condition for much longer and endured more extensive treatment than petitioner. (Id.
(citing Coons v. Sec’y of Health & Human Servs., No. 20-1067V, 2024 WL 1741619
(Fed. Cl. Spec. Mstr. Mar. 29, 2024); E.M., 2024 WL 844238; Drobbin, 2023 WL
112268).) Additionally, respondent notes that Dearing and Rodrigues were procedurally
distinct because they involved settlements.6 (Id. at 14 (citing Dearing, 2016 WL
3030148; Rodrigues, 2024 WL 1434356).) Respondent argues that “comparable cases
6 Neither party has cited any prior reasoned decision by a special master addressing the appropriate
amount of compensation for a small fiber neuropathy injury. Nor has the undersigned otherwise located
any prior reasoned decision on point. Reasoned decisions are generally more persuasive than cases
involving either stipulations or proffers. E.g., Smith v. Sec’y of Health & Human Servs., No. 19-0745V,
2021 WL 2652688, at *3 (Fed. Cl. Spec. Mstr. May 28, 2021) (observing that, “[w]hile ‘settled cases and
proffers provide some evidence of the kinds of awards received overall in comparable cases,’ they are not
as persuasive as reasoned decisions from a judicial neutral” (emphasis omitted)). Proffers and
stipulations differ in that proffers typically are presented in cases where entitlement to compensation has
been resolved and the government views the proffered amount as representing full compensation.
Stipulations, by contrast, typically are presented in cases where the parties have reached a compromise
based on litigative risk while significant issues remain unresolved regarding either entitlement to
compensation or the appropriate amount of damages. Respondent discounts prior stipulations because
they do not constitute admissions on respondent’s part as to what constitutes the full value of a given
claim. (ECF No. 109, n.1.) However, despite this distinction, both settlements and proffers are informal
resolutions by agreement of the parties, rather than reasoned adjudications. They can therefore be
influenced by factors beyond pin-pointing the appropriate amount of damages, especially in the context of
stipulations but also in the context of proffered awards. (For example, a given petitioner may disagree
that a proffered amount is full compensation, but opt to accept it anyway as a matter of expediency.)
Thus, when utilized in determining damages, stipulations and proffers are generally better viewed in
aggregate. E.g., Smith, 2021 WL 2652688, at * 3 (using data from prior SIRVA proffers and stipulations
“as a whole”). An additional issue with stipulations (and sometimes proffers) is that they may resolve
damages based on a top-line number only and do not break out the different elements of damages that
may be alleged. Furthermore, decisions adopting stipulations and proffers generally do not disclose the
facts of the case pertinent to the amount of the damages. In some proffered cases, such as those
discussed below, the facts of the case can be separately gleaned from a prior reasoned ruling on
entitlement. Nonetheless, despite these limitations, and especially given the lack of available reasoned
decisions on point, prior proffers and stipulations still provide some evidence of the awards given in
comparable cases.
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confirm that respondent’s proffer is reasonable, fair, and appropriate.” (Id. at 12-13.)
However, respondent does not actually identify any specific case(s) that he would
consider to be comparable.
c. Petitioner’s reply
Petitioner argues that his course of treatment was not mild, as respondent
contends, and that he pursued active treatment for four years and, to this day, eight
years after his injury, petitioner continues to experience the effects of his vaccine injury.
(ECF No. 110, pp. 1-4.) Therefore, while “each case has different facts,” petitioner’s
lasting symptoms entitle him to a “comparable amount for his pain and suffering to other
cases in this [p]rogram.” (Id. at 4.)
V. Analysis
I have reviewed damages awards for small fiber neuropathy, including those
cited by petitioner. However, I do not merely rely on analogy to any prior award to
determine the amount of petitioner’s damages in this case. Instead, I have reviewed
previous small fiber neuropathy awards, the arguments presented by the parties, and
the totality of the evidentiary record.
Petitioner alleges sensory symptoms, including pain, tingling, and numbness in
his hands, feet, neck, and face. (Ex. 8, ¶ 3.) However, his medical records demonstrate
that neither his strength, gait, nor reflexes were affected. (Ex. 2, pp. 16-19, 37.)
Respondent cites petitioner’s short active treatment timeline to draw attention to the
severity of petitioner’s injury, noting that petitioner was only actively treated for five
months and was able to maintain an active lifestyle during that time. (ECF No. 109, p.
13.) Nonetheless, petitioner established that he has suffered an overall course of small
fiber neuropathy persisting at this point for about a decade. Regarding the
discontinuance of active treatment, petitioner contends that he simply felt that his
doctors did not have an explanation for his condition and that his symptoms would be
his new normal. (Tr. 49-50.) Given the symptoms and condition at issue, this seems
reasonable.
However, petitioner is not persuasive in asserting that, despite symptom
fluctuations, his abnormal sensations “are always present.” (ECF No. 107, p. 8 (citing
Ex. 8, ¶ 4).) In discussing his fluctuating symptoms (noting good days and bad), his
medical records specifically confirm as of June 2017 that “most days [he] doesn’t feel
anything” vis-à-vis his reported sensations of burning, pins, and needles. (Ex. 2, p.
119.) Thus, while petitioner is credible in suggesting that his symptoms never entirely
resolved, petitioner’s medical records also support the conclusion that his symptoms
were relatively mild for a small fiber neuropathy and became intermittent during his
course of treatment. (See also ECF No. 107, pp. 7-8 (highlighting an assessment of
“mild” peripheral neuropathy as of December 5, 2014, at Ex. 2, p. 62, and a record
observing the neuropathy was “not progressive” as of January 27, 2016, at Ex. 2, p.
78).)
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Petitioner has cited five prior cases suggesting a range of pain and suffering
awards in small fiber neuropathy cases from $130,000.00 to the statutory maximum.
However, petitioner does not explicitly address the facts of any of these other cases.
(ECF Nos. 107, 110.) Instead, petitioner simply represents the listed cases to be a non-
comprehensive list of prior small fiber neuropathy awards and contends that “the time
frame that [petitioner]’s complaints have persisted is greater than any of these cases,
and the complaints are permanent. This warrants a higher amount for pain and
suffering.” (ECF No. 107, p. 12.) Nonetheless, respondent has not identified any
damages awards as comparable and has not substantiated the specific award he seeks
for this case. See Smith, 2021 WL 2652688, at *3 (Chief Special Master cautioning
respondent with respect to an award of pain and suffering that “[i]n arguing for a lower
pain and suffering figure herein, Respondent cited no prior reasoned decisions from the
Vaccine Program. During the proceeding held during the expedited Motions Day in this
case, I reminded Respondent’s counsel that if Respondent wants to prevail in future
cases, it is crucial that he offer comparable awards to support the argued for
amount(s).”).7
In Coons, wherein the petitioner received $130,000.00 for pain and suffering, the
petitioner suffered numbness, tingling, and burning sensations like this petitioner, but
her condition was severe enough to result in difficulty walking and progressed
throughout her treatment history, ultimately interfering with her ability to work.8 2024
WL 1741619, at *3-6. The Coons ruling on entitlement reviewed medical records for a
treatment history spanning about eleven months. Id. There is no indication within the
Coons ruling that petitioner ever saw any improvement in her symptoms. The decision
awarding damages was issued more than five years after the onset of the injury.
Coons, 2024 WL 4764001. Respondent argues that the Coons petitioner suffered a
more severe course of small fiber neuropathy because she was hospitalized, treated
with several prescriptions including amitriptyline, gabapentin, a Medrol dosepak, and
Keppra, and received consistent treatment for four years. (ECF No. 109, p. 13.) In
reply, petitioner contends, based on counsel’s familiarity with the case, that the Coons
7 Petitioner’s brief does acknowledge that his list of cited cases is “non-inclusive.” (ECF No. 107, p. 12.)
However, it is also worth noting that the undersigned’s own review of prior awards confirms that petitioner
has not identified a floor for small fiber neuropathy awards. See, e.g., Fiske v. Sec’y of Health & Human
Servs., No. 17-1378V, 2024 WL 4930687 (Fed. Cl. Spec. Mstr. May 21, 2024) (awarding $92,500.00 for
pain and suffering). Nonetheless, as noted in note 6, supra, prior awards based on stipulations and
proffers are better viewed in aggregate. Accordingly, especially in the absence of any effort by
respondent to identify any comparable cases, the undersigned will not endeavor to cherry-pick any
specific prior awards as additional points of comparison given that no prior reasoned decisions are
available.
8 The fact that an injury is severe or pervasive enough to interfere with employment can be a factor in
determining an award for pain and suffering separate and apart from an award of loss of earnings. E.g.
Hood v. Sec’y of Health & Human Servs., No.1601942V, 2021 WL 5755324, at *8-9 (Fed. Cl. Spec. Mstr.
Oct. 19, 2021) (considering the fact that a petitioner’s GBS interfered with his ability to work as evidence
going to the severity of the petitioner’s condition, as considered in determining an award for pain and
suffering).
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petitioner’s small fiber neuropathy was not more severe than this petitioner’s. However,
this assertion is not explained.9 (ECF No. 110, pp. 3-4.)
In E.M., the petitioner was compensated $225,000.00 for over twelve years of
pain and suffering. 2024 WL 844238.10 The E.M. petitioner suffered small fiber
neuropathy beginning in August of 2011. The condition generally stabilized during
2012, but remained ongoing and did include some “bad” flares thereafter. E.M. v. Sec’y
of Health & Human Servs., No. 14-753V, 2024 WL 10509841, at *3-6 (Fed. Cl. Spec.
Mstr. Dec. 27, 2023). Generally, petitioner’s ongoing symptoms included foot, trunk,
and arm pain made worse with activity, as well as a burning sensation, increased body
temperature (petitioner’s small fiber neuropathy included mild autonomic neuropathy),
and an inability to exercise. Id. Nerve conduction studies had been normal, but it was
later determined that petitioner had evidence of ganglionopathy. Id. Respondent
argues that the E.M. petitioner’s case was diagnostically more complex and significantly
impacted her career. (ECF No. 109, p. 14.) However, although the E.M. petitioner’s
treating physician had concluded that pain medication was ineffective and therefore
discussed with petitioner the need to rest and cut back on stressful work, the loss of
earnings capacity claim was ultimately rejected. 2024 WL 10509841, at 7, 22.
Moreover, the special maser specifically rejected the contention that the petitioner’s
broader, more complicated presentation was related to her small fiber neuropathy. Id.
at 20 (finding that symptoms of headache, eye pain, and blurred vision, were due to an
unrelated neuralgia). Nonetheless, the petitioner had testified that her symptoms
remained “severe” and were further aggravated by stress or fatigue. E.M. v. Sec’y of
Health & Human Servs., No. 14-753V, 2021 WL 3477837, at *12 (Fed. Cl. Spec. Mstr.
July 9, 2021). As noted above, petitioner did not explicitly address the facts of the E.M.
case.
The remainder of the cases cited by petitioner are less helpful. While taking
some limited notice of the fact of the stipulated awards in both Dearing and Rodrigues,
no publicly disclosed facts regarding the course of the alleged small fiber neuropathy
are available for comparison. Dearing, 2016 WL 3030148 (awarding $135,000.00);
Rodrigues, 2024 WL 1434356 (awarding $150,000.00). Neither party has attempted to
discuss the facts of either case. Notably, while the Rodrigues petitioner received a
higher award as compared to Dearing ($150,000.00 versus $135,000.00), the
Rodrigues petitioner had alleged bullous pemphigoid in addition to small fiber
9 As noted above, the ruling on entitlement in Coons only discusses medical records spanning
approximately eleven months. 2024 WL 1741619, at *3-6. Accordingly, respondent’s specific assertion
of a four-year treatment history cannot be confirmed based on the publicly available rulings and decisions
in the case. However, petitioner’s reply stresses that petitioner’s counsel was also counsel of record in
Coons, and petitioner’s reply does not dispute this assertion by respondent. (ECF No. 110, pp. 3-4.)
10 In addition to a decision awarding damages based on proffer, which is not factually informative, the
E.M. case also had a prior Ruling on Entitlement (No. 14-753V, 2021 WL 3477837 (Fed. Cl. Spec. Mstr.
July 9, 2021)) that discussed the facts of the case as relevant to determining entitlement to compensation
as well as a separate Ruling on Petitioner’s Lost Earnings Claim (No. 14-753V, 2023 WL 10509841 (Fed.
Cl. Spec. Mstr. Dec. 27, 2023)) that further discussed the medical facts, identified additional evidence
developed during the damages phase, and adjudicated certain factual aspects of the case.
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neuropathy. 2024 WL 1434356.11 The Drobbin case, though not involving a stipulation,
is also less helpful because the scope of the award for pain and suffering is not entirely
clear. The Drobbin petitioner was awarded $250,000.00 for pain and suffering, as well
as a significant amount for loss of earnings. 2023 WL 112268. Thus, respondent
stresses that the petitioner’s overall compensated condition was severe enough to
interfere with his employment. (ECF No. 109, p. 14.) However, Drobbin had alleged
not only small fiber neuropathy, but also a neuromuscular junction disorder and motor
polyneuropathy. 2023 WL 112268. In particular, during the course of the case,
petitioner sought to establish that he suffered a vaccine-caused mononeuritis multiplex.
Drobbin v. Sec’y of Health & Human Servs., No. 14-225V, 2020 WL 3799206, at *16
(Fed. Cl. Spec. Mstr. Jan. 21, 2020). Thus, even respondent’s expert, though
disagreeing with petitioner’s specific contentions, agreed that petitioner had a broader
constellation of symptoms beyond his confirmed small fiber neuropathy that were
difficult to classify. Id. at *11-14. Ultimately, in ruling that petitioner was entitled to
compensation, the special master found that petitioner had only demonstrated that he
suffered vaccine-caused small fiber neuropathy, specifically noting that petitioner had
not demonstrated causation as it related to mononeuritis multiplex. Id. at *17. Yet, in
separately resolving petitioner’s diagnosis, the special master also specifically
concluded that there was not preponderant evidence that petitioner suffered any
condition other than small fiber neuropathy. Id. at *16. Thus, while the Drobbin
petitioner’s overall clinical course was much more severe than this petitioner, it is
unclear what specific aspects of petitioner’s clinical history the parties considered when
informally resolving damages.
For the reasons discussed above, petitioner is not persuasive in contending that
his condition warrants higher compensation as compared to any of the other cases he
has cited. Neither party actually grappled with the facts of any of the cited cases in any
meaningful way. Yet, based on the undersigned’s own review, petitioner’s own case is
distinguishable from those prior cases. Petitioner, of course, bears the burden of proof
with respect to the damages he requests. Brewer, 1996 WL 147722, at *22-23.
However, even having concluded that petitioner’s injury was mild for a small fiber
neuropathy, a longstanding history of peripheral neuropathy is still a significant injury.
Thus, especially in light of respondent’s failure to meaningfully substantiate a lower
award, the undersigned finds that $130,000.00 represents a reasonable award of
compensation for petitioner’s pain and suffering. On the whole, while this case saw less
severe symptoms than the Coons case, the overall history supports a longer duration of
11 Notably, Rodrigues was on the undersigned’s own docket and it was the undersigned that issued the
decision awarding damages. However, bringing the undersigned’s own background knowledge to bear
within this decision would be problematic. Explicitly discussing previously undisclosed facts of the
Rodrigues case would violate the Rodrigues petitioner’s right under the Vaccine Act to seek redaction of
private medical information. However, relying on facts from the Rodrigues case without explicitly
disclosing them would risk prejudice to the parties. See Davis v. Sec’y of Health & Human Servs., 94
Fed. Cl. 53, 65-66 (2010) (indicating that a special master must “provide adequate notice to the parties of
evidentiary issues and matters” to be decided). Accordingly, nothing beyond the four corners of the
decision awarding damages in the Rodrigues case is considered herein.
11

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injury than was adjudicated in Coons. Absent a more robust defense of a lower
proposed award, the undersigned will not parse these factual differences.
VI. Conclusion
In light of the above, I award petitioner a lump sum payment of $130,000.00
for actual pain and suffering to be paid through an ACH deposit to petitioner’s
counsel’s IOLTA account for prompt distribution. This amount represents
compensation for all damages available under § 300aa-15(a).
The clerk of the court is directed to enter judgment in accordance with this
decision.12
IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
12 Pursuant to Vaccine Rule 11(a), entry of judgment can be expedited by the parties’ joint filing of notice
renouncing the right to seek review.
12